PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
27298228-7	2016	A further TGF-beta1 increase was induced by Arg silencing with siRNA, as with the Arg tyrosine kinase inhibitor Imatinib.	imatinib	112-120	transforming growth factor beta 1	Homo sapiens	10-19
28978170-1	2017	Resistance to imatinib has been recurrently reported in systemic mastocytosis (SM) carrying exon 17 KIT mutations.	imatinib	14-22	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	100-103
27467080-4	2016	In particular, the mutation V560G in KIT increases its sensitivity to Imatinib, while the D816V in KIT, and D802V in CSF-1R, triggers resistance to the drug.	imatinib	70-78	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	37-40
27467080-5	2016	We analyzed the Imatinib binding affinity to the native and mutated KIT (mutations V560G, S628N and D816V) and CSF-1R (mutation D802V) by using molecular dynamics simulations and energy calculations of Imatinib target complexes.	imatinib	16-24	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	68-71
27467080-6	2016	Further, we evaluated the sensitivity of the studied KIT receptors to Imatinib by measuring the inhibition of KIT phosphorylation.	imatinib	70-78	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	53-56
27467080-6	2016	Further, we evaluated the sensitivity of the studied KIT receptors to Imatinib by measuring the inhibition of KIT phosphorylation.	imatinib	70-78	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	110-113
27467080-7	2016	Our study showed that (i) the binding free energy of Imatinib to the targets is highly correlated with their experimentally measured sensitivity; (ii) the electrostatic interactions are a decisive factor affecting the binding energy; (iii) the most deleterious impact to the Imatinib sensitivity is promoted by D802V (CSF-1R) and D816V (KIT) mutations; (iv) the role of the juxtamembrane region, JMR, in the imatinib binding is accessory.	imatinib	53-61	colony stimulating factor 1 receptor	Homo sapiens	318-324
27467080-7	2016	Our study showed that (i) the binding free energy of Imatinib to the targets is highly correlated with their experimentally measured sensitivity; (ii) the electrostatic interactions are a decisive factor affecting the binding energy; (iii) the most deleterious impact to the Imatinib sensitivity is promoted by D802V (CSF-1R) and D816V (KIT) mutations; (iv) the role of the juxtamembrane region, JMR, in the imatinib binding is accessory.	imatinib	53-61	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	337-340
27467080-7	2016	Our study showed that (i) the binding free energy of Imatinib to the targets is highly correlated with their experimentally measured sensitivity; (ii) the electrostatic interactions are a decisive factor affecting the binding energy; (iii) the most deleterious impact to the Imatinib sensitivity is promoted by D802V (CSF-1R) and D816V (KIT) mutations; (iv) the role of the juxtamembrane region, JMR, in the imatinib binding is accessory.	imatinib	275-283	colony stimulating factor 1 receptor	Homo sapiens	318-324
27467080-7	2016	Our study showed that (i) the binding free energy of Imatinib to the targets is highly correlated with their experimentally measured sensitivity; (ii) the electrostatic interactions are a decisive factor affecting the binding energy; (iii) the most deleterious impact to the Imatinib sensitivity is promoted by D802V (CSF-1R) and D816V (KIT) mutations; (iv) the role of the juxtamembrane region, JMR, in the imatinib binding is accessory.	imatinib	275-283	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	337-340
27467080-7	2016	Our study showed that (i) the binding free energy of Imatinib to the targets is highly correlated with their experimentally measured sensitivity; (ii) the electrostatic interactions are a decisive factor affecting the binding energy; (iii) the most deleterious impact to the Imatinib sensitivity is promoted by D802V (CSF-1R) and D816V (KIT) mutations; (iv) the role of the juxtamembrane region, JMR, in the imatinib binding is accessory.	imatinib	408-416	colony stimulating factor 1 receptor	Homo sapiens	318-324
27467080-7	2016	Our study showed that (i) the binding free energy of Imatinib to the targets is highly correlated with their experimentally measured sensitivity; (ii) the electrostatic interactions are a decisive factor affecting the binding energy; (iii) the most deleterious impact to the Imatinib sensitivity is promoted by D802V (CSF-1R) and D816V (KIT) mutations; (iv) the role of the juxtamembrane region, JMR, in the imatinib binding is accessory.	imatinib	408-416	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	337-340
27483254-7	2016	Imatinib, a MATE inhibitor, inhibited [3H]dopamine uptake by hMATE1-, hMATE2-K- and mMATE1-expressing cells in a concentration-dependent manner.	imatinib	0-8	solute carrier family 47 member 1	Homo sapiens	61-67
27483254-7	2016	Imatinib, a MATE inhibitor, inhibited [3H]dopamine uptake by hMATE1-, hMATE2-K- and mMATE1-expressing cells in a concentration-dependent manner.	imatinib	0-8	solute carrier family 47 member 2	Homo sapiens	70-76
27483254-7	2016	Imatinib, a MATE inhibitor, inhibited [3H]dopamine uptake by hMATE1-, hMATE2-K- and mMATE1-expressing cells in a concentration-dependent manner.	imatinib	0-8	solute carrier family 47, member 1	Mus musculus	84-90
27483254-8	2016	At clinically-relevant concentrations, imatinib inhibited [3H]dopamine uptake by hMATE1- and hMATE2-K-expressing cells.	imatinib	39-47	solute carrier family 47 member 1	Homo sapiens	81-87
27483254-8	2016	At clinically-relevant concentrations, imatinib inhibited [3H]dopamine uptake by hMATE1- and hMATE2-K-expressing cells.	imatinib	39-47	solute carrier family 47 member 2	Homo sapiens	93-99
28978170-10	2017	These results together with previous data from the literature support the relevance of the KIT mutational status in selecting SM patients who are candidates for imatinib therapy.	imatinib	161-169	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	91-94
26841308-5	2016	In addition, peroxisome proliferator-activated receptors ligands increased imatinib uptake by upregulating the expression of human organic cation transporter 1.	imatinib	75-83	solute carrier family 22 member 1	Homo sapiens	131-159
27405085-0	2016	Impact of ABCB1 1236C > T-2677G > T-3435C > T polymorphisms on the anti-proliferative activity of imatinib, nilotinib, dasatinib and ponatinib.	imatinib	107-115	ATP binding cassette subfamily B member 1	Homo sapiens	10-15
27405085-3	2016	The most common ABCB1 variants are 1236C > T, 2677G > T, 3435C > T and have been associated with clinical response to imatinib in chronic myelogenous leukaemia (CML) in some studies.	imatinib	127-135	ATP binding cassette subfamily B member 1	Homo sapiens	16-21
27405085-6	2016	Imatinib anti-proliferative effect and accumulation were decreased to a larger extent in cells expressing the ABCB1 wild-type protein compared with the 1236T-2677T-3435T variant relatively to control cells.	imatinib	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	110-115
27405085-8	2016	In conclusion, our data suggest that wild-type ABCB1 exports imatinib more efficiently than the 1236T-2677T-3435T variant protein, providing a molecular basis for the reported association between ABCB1 polymorphisms and the response to imatinib in CML.	imatinib	61-69	ATP binding cassette subfamily B member 1	Homo sapiens	47-52
27405085-8	2016	In conclusion, our data suggest that wild-type ABCB1 exports imatinib more efficiently than the 1236T-2677T-3435T variant protein, providing a molecular basis for the reported association between ABCB1 polymorphisms and the response to imatinib in CML.	imatinib	61-69	ATP binding cassette subfamily B member 1	Homo sapiens	196-201
27405085-8	2016	In conclusion, our data suggest that wild-type ABCB1 exports imatinib more efficiently than the 1236T-2677T-3435T variant protein, providing a molecular basis for the reported association between ABCB1 polymorphisms and the response to imatinib in CML.	imatinib	236-244	ATP binding cassette subfamily B member 1	Homo sapiens	47-52
27405085-8	2016	In conclusion, our data suggest that wild-type ABCB1 exports imatinib more efficiently than the 1236T-2677T-3435T variant protein, providing a molecular basis for the reported association between ABCB1 polymorphisms and the response to imatinib in CML.	imatinib	236-244	ATP binding cassette subfamily B member 1	Homo sapiens	196-201
27167336-11	2016	Combinational treatment with KIT inhibitors (imatinib, regorafenib) enhanced the proapoptotic effect.	imatinib	45-53	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	29-32
26982239-5	2016	During treatment with the c-KIT inhibitor imatinib, she developed severe therapy-limiting skin toxicity.	imatinib	42-50	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	26-31
27282569-0	2016	EphB4-VAV1 signaling pathway is associated with imatinib resistance in chronic myeloid leukemia cells.	imatinib	48-56	EPH receptor B4	Homo sapiens	0-5
27282569-0	2016	EphB4-VAV1 signaling pathway is associated with imatinib resistance in chronic myeloid leukemia cells.	imatinib	48-56	vav guanine nucleotide exchange factor 1	Homo sapiens	6-10
26657156-4	2016	We demonstrate that specifically inhibiting the interaction between CBP and catenin with ICG-001 results in the differentiation of quiescent drug-resistant chronic myelogenous leukemia-initiating cells (CML LICs), thereby sensitizing them to BCR-ABL tyrosine kinase inhibitors, for example, Imatinib.	imatinib	291-299	CREB binding protein	Homo sapiens	68-71
27259262-7	2016	Moreover, AF1q up-regulated tyrosine kinase signaling through PDGFR signaling, which was blockable by imatinib.	imatinib	102-110	MLLT11 transcription factor 7 cofactor	Homo sapiens	10-14
27259262-7	2016	Moreover, AF1q up-regulated tyrosine kinase signaling through PDGFR signaling, which was blockable by imatinib.	imatinib	102-110	platelet derived growth factor receptor beta	Homo sapiens	62-67
27217448-4	2016	Cumulative rates of major molecular response and molecular responses with a 4.0- or 4.5-log reduction in BCR-ABL1 transcripts from baseline by 5 years remained statistically significantly higher for dasatinib compared with imatinib.	imatinib	223-231	BCR activator of RhoGEF and GTPase	Homo sapiens	105-113
27217448-6	2016	In patients who achieved BCR-ABL1 <= 10% at 3 months (dasatinib, 84%; imatinib, 64%), improvements in progression-free and overall survival and lower rates of transformation to accelerated/blast phase were reported compared with patients with BCR-ABL1 greater than 10% at 3 months.	imatinib	73-81	BCR activator of RhoGEF and GTPase	Homo sapiens	25-33
27217448-6	2016	In patients who achieved BCR-ABL1 <= 10% at 3 months (dasatinib, 84%; imatinib, 64%), improvements in progression-free and overall survival and lower rates of transformation to accelerated/blast phase were reported compared with patients with BCR-ABL1 greater than 10% at 3 months.	imatinib	73-81	BCR activator of RhoGEF and GTPase	Homo sapiens	246-254
27217448-8	2016	Fifteen dasatinib-treated and 19 imatinib-treated patients had BCR-ABL1 mutations identified at discontinuation.	imatinib	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-71
27166836-1	2016	The major mechanism of imatinib (IM) resistance of CML is the reactivation of ABL kinase either through BCR-ABL gene amplification or mutation.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
27293031-3	2016	Imatinib and nilotinib-induced tyrosine phosphorylation was dependent on expression of p130Cas and FAK activity and was independent of known imatinib targets including Abl, platelet derived growth factor receptor beta (PDGFRbeta) and the collagen receptor DDR1.	imatinib	0-8	BCAR1 scaffold protein, Cas family member	Homo sapiens	87-94
27156227-1	2016	BACKGROUND: Gastrointestinal stromal tumours (GIST) treated with the tyrosine kinase inhibitor (TKI) imatinib can become resistant when additional mutations in the receptor tyrosine kinases KIT or PDGFRA block imatinib activity.	imatinib	101-109	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	190-193
27156227-1	2016	BACKGROUND: Gastrointestinal stromal tumours (GIST) treated with the tyrosine kinase inhibitor (TKI) imatinib can become resistant when additional mutations in the receptor tyrosine kinases KIT or PDGFRA block imatinib activity.	imatinib	101-109	platelet derived growth factor receptor alpha	Homo sapiens	197-203
27156227-1	2016	BACKGROUND: Gastrointestinal stromal tumours (GIST) treated with the tyrosine kinase inhibitor (TKI) imatinib can become resistant when additional mutations in the receptor tyrosine kinases KIT or PDGFRA block imatinib activity.	imatinib	210-218	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	190-193
27156227-10	2016	Nine patients (35%) had a best response of stable disease, including two patients who had KIT mutations known to be associated with resistance to imatinib and sunitinib.	imatinib	146-154	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	90-93
27156227-12	2016	One patient with PDGFRA-mutant GIST had a partial response for more than 376 d. CONCLUSION: The combination of onalespib plus imatinib was well tolerated but exhibited limited antitumour activity as dosed in this TKI-resistant GIST patient population.	imatinib	126-134	platelet derived growth factor receptor alpha	Homo sapiens	17-23
29404138-6	2016	We herein report a patient with "complex undefined HES" who had disease resistant to corticosteroids, but who had a significant response after treatment with imatinib.	imatinib	158-166	ribosome binding protein 1	Homo sapiens	51-55
27329306-0	2016	The chimeric ubiquitin ligase SH2-U-box inhibits the growth of imatinib-sensitive and resistant CML by targeting the native and T315I-mutant BCR-ABL.	imatinib	63-71	sperm hammerhead 2	Mus musculus	30-33
27329306-6	2016	Moreover, SH2-U-box worked in concert with imatinib in K562 cells.	imatinib	43-51	sperm hammerhead 2	Mus musculus	10-13
27329306-8	2016	Collectively, by degrading the native and T315I-mutant BCR-ABL, the chimeric ubiquitin ligase SH2-U-box may serve as a potential therapy for both imatinib-sensitive and resistant CML.	imatinib	146-154	sperm hammerhead 2	Mus musculus	94-97
27281222-4	2016	Here we show--using proteomics, transcriptomics and network analyses--that in human LSCs, aberrantly expressed proteins, in both imatinib-responder and non-responder patients, are modulated in concert with p53 (also known as TP53) and c-MYC regulation.	imatinib	129-137	tumor protein p53	Homo sapiens	206-209
27281222-4	2016	Here we show--using proteomics, transcriptomics and network analyses--that in human LSCs, aberrantly expressed proteins, in both imatinib-responder and non-responder patients, are modulated in concert with p53 (also known as TP53) and c-MYC regulation.	imatinib	129-137	tumor protein p53	Homo sapiens	225-229
27281222-4	2016	Here we show--using proteomics, transcriptomics and network analyses--that in human LSCs, aberrantly expressed proteins, in both imatinib-responder and non-responder patients, are modulated in concert with p53 (also known as TP53) and c-MYC regulation.	imatinib	129-137	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	235-240
27153560-10	2016	Moreover, in the neoadjuvant setting, decline of ANO1 expression level correlated with the response of imatinib.	imatinib	103-111	anoctamin 1	Homo sapiens	49-53
27153560-14	2016	CONCLUSION: ANO1 detection by qRT-PCR in peripheral blood is of clinical potential for monitoring recurrence and evaluating therapeutic efficacy of imatinib for GIST patients.	imatinib	148-156	anoctamin 1	Homo sapiens	12-16
27044711-1	2016	Chronic myeloid leukemia (CML) patients who relapse on imatinib due to acquired ABL1 kinase domain mutations are successfully treated with second-generation ABL1-tyrosine kinase inhibitors (ABL-TKIs) such as dasatinib, nilotinib or ponatinib.	imatinib	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-84
27044711-1	2016	Chronic myeloid leukemia (CML) patients who relapse on imatinib due to acquired ABL1 kinase domain mutations are successfully treated with second-generation ABL1-tyrosine kinase inhibitors (ABL-TKIs) such as dasatinib, nilotinib or ponatinib.	imatinib	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-161
27044711-1	2016	Chronic myeloid leukemia (CML) patients who relapse on imatinib due to acquired ABL1 kinase domain mutations are successfully treated with second-generation ABL1-tyrosine kinase inhibitors (ABL-TKIs) such as dasatinib, nilotinib or ponatinib.	imatinib	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
27044711-3	2016	To identify these mechanisms of resistance and potential treatment options, we generated ABL-TKI-resistant K562 cells through prolonged sequential exposure to imatinib and dasatinib.	imatinib	159-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-92
27347169-0	2016	Concomitant essential thrombocythemia with JAK2 V617F mutation in a patient with chronic myeloid leukemia with major molecular response with imatinib and long-term follow-up.	imatinib	141-149	Janus kinase 2	Homo sapiens	43-47
27350795-1	2016	BACKGROUND: BCR-ABL1 fusion proteins contain constitutively active tyrosine kinases that are potential candidates for targeted therapy with tyrosine kinase inhibitors such as imatinib in chronic myeloid leukemia (CML).	imatinib	175-183	BCR activator of RhoGEF and GTPase	Homo sapiens	12-20
26455322-0	2016	PDGFRB mutants found in patients with familial infantile myofibromatosis or overgrowth syndrome are oncogenic and sensitive to imatinib.	imatinib	127-135	platelet derived growth factor receptor beta	Homo sapiens	0-6
27293031-0	2016	Imatinib and Nilotinib increase glioblastoma cell invasion via Abl-independent stimulation of p130Cas and FAK signalling.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-66
27293031-0	2016	Imatinib and Nilotinib increase glioblastoma cell invasion via Abl-independent stimulation of p130Cas and FAK signalling.	imatinib	0-8	BCAR1 scaffold protein, Cas family member	Homo sapiens	94-101
27293031-2	2016	We show that treatment of human glioblastoma multiforme (GBM) tumour cells with imatinib and the closely-related drug, nilotinib, strikingly increases tyrosine phosphorylation of p130Cas, focal adhesion kinase (FAK) and the downstream adaptor protein paxillin (PXN), resulting in enhanced cell migration and invasion.	imatinib	80-88	BCAR1 scaffold protein, Cas family member	Homo sapiens	179-186
27293031-2	2016	We show that treatment of human glioblastoma multiforme (GBM) tumour cells with imatinib and the closely-related drug, nilotinib, strikingly increases tyrosine phosphorylation of p130Cas, focal adhesion kinase (FAK) and the downstream adaptor protein paxillin (PXN), resulting in enhanced cell migration and invasion.	imatinib	80-88	protein tyrosine kinase 2	Homo sapiens	188-209
27293031-2	2016	We show that treatment of human glioblastoma multiforme (GBM) tumour cells with imatinib and the closely-related drug, nilotinib, strikingly increases tyrosine phosphorylation of p130Cas, focal adhesion kinase (FAK) and the downstream adaptor protein paxillin (PXN), resulting in enhanced cell migration and invasion.	imatinib	80-88	protein tyrosine kinase 2	Homo sapiens	211-214
27293031-3	2016	Imatinib and nilotinib-induced tyrosine phosphorylation was dependent on expression of p130Cas and FAK activity and was independent of known imatinib targets including Abl, platelet derived growth factor receptor beta (PDGFRbeta) and the collagen receptor DDR1.	imatinib	0-8	protein tyrosine kinase 2	Homo sapiens	99-102
27293031-3	2016	Imatinib and nilotinib-induced tyrosine phosphorylation was dependent on expression of p130Cas and FAK activity and was independent of known imatinib targets including Abl, platelet derived growth factor receptor beta (PDGFRbeta) and the collagen receptor DDR1.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	173-217
27293031-3	2016	Imatinib and nilotinib-induced tyrosine phosphorylation was dependent on expression of p130Cas and FAK activity and was independent of known imatinib targets including Abl, platelet derived growth factor receptor beta (PDGFRbeta) and the collagen receptor DDR1.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	219-228
27293031-3	2016	Imatinib and nilotinib-induced tyrosine phosphorylation was dependent on expression of p130Cas and FAK activity and was independent of known imatinib targets including Abl, platelet derived growth factor receptor beta (PDGFRbeta) and the collagen receptor DDR1.	imatinib	0-8	discoidin domain receptor tyrosine kinase 1	Homo sapiens	256-260
27293031-5	2016	In addition, silencing of p130Cas and inhibition of FAK activity both strongly reduced imatinib and nilotinib stimulated invasion.	imatinib	87-95	BCAR1 scaffold protein, Cas family member	Homo sapiens	26-33
27293031-2	2016	We show that treatment of human glioblastoma multiforme (GBM) tumour cells with imatinib and the closely-related drug, nilotinib, strikingly increases tyrosine phosphorylation of p130Cas, focal adhesion kinase (FAK) and the downstream adaptor protein paxillin (PXN), resulting in enhanced cell migration and invasion.	imatinib	80-88	paxillin	Homo sapiens	251-259
27293031-2	2016	We show that treatment of human glioblastoma multiforme (GBM) tumour cells with imatinib and the closely-related drug, nilotinib, strikingly increases tyrosine phosphorylation of p130Cas, focal adhesion kinase (FAK) and the downstream adaptor protein paxillin (PXN), resulting in enhanced cell migration and invasion.	imatinib	80-88	paxillin	Homo sapiens	261-264
27293031-5	2016	In addition, silencing of p130Cas and inhibition of FAK activity both strongly reduced imatinib and nilotinib stimulated invasion.	imatinib	87-95	protein tyrosine kinase 2	Homo sapiens	52-55
27293031-6	2016	Importantly, imatinib and nilotinib increased tyrosine phosphorylation of p130Cas, FAK, PXN and radial spheroid invasion in stem cell lines isolated from human glioma biopsies.	imatinib	13-21	BCAR1 scaffold protein, Cas family member	Homo sapiens	74-81
27293031-6	2016	Importantly, imatinib and nilotinib increased tyrosine phosphorylation of p130Cas, FAK, PXN and radial spheroid invasion in stem cell lines isolated from human glioma biopsies.	imatinib	13-21	protein tyrosine kinase 2	Homo sapiens	83-86
27293031-6	2016	Importantly, imatinib and nilotinib increased tyrosine phosphorylation of p130Cas, FAK, PXN and radial spheroid invasion in stem cell lines isolated from human glioma biopsies.	imatinib	13-21	paxillin	Homo sapiens	88-91
26971721-3	2016	We report on a phase 2 study that was designed to evaluate efficacy and safety of a treatment alternating nilotinib and imatinib, in newly diagnosed BCR-ABL1 positive, chronic phase, CML patients.	imatinib	120-128	BCR activator of RhoGEF and GTPase	Homo sapiens	149-157
26797802-0	2016	Clinical features predict responsiveness to imatinib in platelet-derived growth factor receptor-alpha-negative hypereosinophilic syndrome.	imatinib	44-52	platelet derived growth factor receptor alpha	Homo sapiens	56-101
26797802-10	2016	CONCLUSIONS: Clinical features of MHES predict imatinib response in PDGFRA-negative HES.	imatinib	47-55	platelet derived growth factor receptor alpha	Homo sapiens	68-74
27272772-3	2016	In the early 2000s, the ability of imatinib mesylate, a tyrosine kinase inhibitor, to inhibit KIT established a new paradigm for cancer treatment.	imatinib	35-52	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	94-97
26861905-0	2016	Correlation of CTNNB1 Mutation Status with Progression Arrest Rate in RECIST Progressive Desmoid-Type Fibromatosis Treated with Imatinib: Translational Research Results from a Phase 2 Study of the German Interdisciplinary Sarcoma Group (GISG-01).	imatinib	128-136	catenin beta 1	Homo sapiens	15-21
26861905-3	2016	For the current study, the CTNNB1 mutation status was analyzed in DF samples from the prospective German Interdisciplinary Sarcoma Group (GISG) phase 2 study evaluating imatinib to induce progression arrest in DF Response Evaluation Criteria In Solid Tumors (RECIST) progressive patients.	imatinib	169-177	catenin beta 1	Homo sapiens	27-33
26861905-13	2016	The positive correlation of CTNNB1 mutation status with the progression arrest rate after imatinib therapy supports the idea of a potential predictive impact of the mutation status on DF treatment decision making.	imatinib	90-98	catenin beta 1	Homo sapiens	28-34
26912059-0	2016	ZFX Facilitates Cell Proliferation and Imatinib Resistance in Chronic Myeloid Leukemia Cells.	imatinib	39-47	zinc finger protein X-linked	Homo sapiens	0-3
27085160-2	2016	Imatinib is a selective inhibitor of several tyrosine kinases, including PDGF receptors, Abl, and c-kit.	imatinib	0-8	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	89-92
27085160-2	2016	Imatinib is a selective inhibitor of several tyrosine kinases, including PDGF receptors, Abl, and c-kit.	imatinib	0-8	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	98-103
27085160-7	2016	Imatinib treatment in AngII infused mice resulted in a reduced cellular infiltration of CD3epsilon positive T lymphocytes by 86% and reduced gene expression of mast cell chymase by 50% compared with AngII infused mice lacking imatinib.	imatinib	0-8	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	22-27
27085160-7	2016	Imatinib treatment in AngII infused mice resulted in a reduced cellular infiltration of CD3epsilon positive T lymphocytes by 86% and reduced gene expression of mast cell chymase by 50% compared with AngII infused mice lacking imatinib.	imatinib	0-8	CD3 antigen, epsilon polypeptide	Mus musculus	88-98
27085160-8	2016	Gene expression analysis of SMC marker SM22alpha demonstrated an increase by 48% together with a more intact medial layer after treatment with imatinib as evaluated with SM22alpha immunostaining.	imatinib	143-151	transgelin	Mus musculus	39-48
27085160-8	2016	Gene expression analysis of SMC marker SM22alpha demonstrated an increase by 48% together with a more intact medial layer after treatment with imatinib as evaluated with SM22alpha immunostaining.	imatinib	143-151	transgelin	Mus musculus	170-179
26875015-8	2016	Pretreatment with imatinib, a PDGF receptor activity blocker, in HT rats reduced the alphaSMA-positive cell proliferation and fibrosis in the PVs and also induced a significant reduction in VEGF expression.	imatinib	18-26	vascular endothelial growth factor A	Rattus norvegicus	190-194
27002306-7	2016	Moreover, Y-632 efficiently overcame imatinib resistance mediated by Bcr-Abl point mutations both in vitro and in vivo.	imatinib	37-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
26912059-5	2016	In addition, ZFX silencing sensitized CML cells to imatinib treatment.	imatinib	51-59	zinc finger protein X-linked	Homo sapiens	13-16
26912059-7	2016	In summary, our data suggest that ZFX is a novel oncogene promoting cell proliferation and inducing imatinib resistance via PI3K/Akt signaling pathway.	imatinib	100-108	zinc finger protein X-linked	Homo sapiens	34-37
27002306-8	2016	We believe that Y-632, acting as a novel small-molecule inhibitor of the Hsp90-Hsp70/Hsp90 organizing protein complex, has great potential to be a promising Hsp90 inhibitor for cancer therapy, such as for imatinib-resistant leukemia.	imatinib	205-213	heat shock protein 90 alpha family class A member 1	Homo sapiens	73-78
27002306-8	2016	We believe that Y-632, acting as a novel small-molecule inhibitor of the Hsp90-Hsp70/Hsp90 organizing protein complex, has great potential to be a promising Hsp90 inhibitor for cancer therapy, such as for imatinib-resistant leukemia.	imatinib	205-213	heat shock protein 90 alpha family class A member 1	Homo sapiens	85-90
27002306-8	2016	We believe that Y-632, acting as a novel small-molecule inhibitor of the Hsp90-Hsp70/Hsp90 organizing protein complex, has great potential to be a promising Hsp90 inhibitor for cancer therapy, such as for imatinib-resistant leukemia.	imatinib	205-213	heat shock protein 90 alpha family class A member 1	Homo sapiens	85-90
27133948-2	2016	However, imatinib, the first approved BCR-ABL inhibitor, must be discontinued in many patients because of resistance or intolerance.	imatinib	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
26503642-0	2016	Delayed diagnosis leading to accelerated-phase chronic eosinophilic leukemia due to a cytogenetically cryptic, imatinib-responsive TNIP1-PDFGRB fusion gene.	imatinib	111-119	TNFAIP3 interacting protein 1	Homo sapiens	131-136
26965514-1	2016	PURPOSE: Cyclosporine A (CsA) and imatinib are both CYP3A4 and P-glycoprotein substrates.	imatinib	34-42	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	52-58
26965514-6	2016	The average dose-corrected CsA concentration was calculated before and after initiation of imatinib.	imatinib	91-99	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	27-30
26965514-7	2016	RESULTS: The average dose-corrected CsA concentration increased during imatinib use in all patients, on average by 94 % (p < 0.001).	imatinib	71-79	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	36-39
26965514-8	2016	Based on measured drug concentrations, the CsA dosage needed to be reduced, on average, by 27 % after initiation of imatinib (p = 0.004).	imatinib	116-124	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	43-46
26965514-9	2016	CONCLUSIONS: Imatinib significantly increases CsA concentrations in HSCT patients, putting these patients at increased risk of CsA toxicity.	imatinib	13-21	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	46-49
26965514-9	2016	CONCLUSIONS: Imatinib significantly increases CsA concentrations in HSCT patients, putting these patients at increased risk of CsA toxicity.	imatinib	13-21	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	127-130
26965514-10	2016	We recommend intensive monitoring of CsA concentrations after initiation of imatinib; a pre-emptive CsA dose reduction of 25 % might be considered.	imatinib	76-84	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	37-40
26898188-1	2016	Early molecular response (EMR, BCR-ABL1 (IS)<=10% at 3 months) is a strong predictor of outcome in imatinib-treated chronic phase chronic myeloid leukemia (CP-CML) patients, but for patients who transform early, 3 months may be too late for effective therapeutic intervention.	imatinib	102-110	BCR activator of RhoGEF and GTPase	Homo sapiens	31-39
26987906-1	2016	Cancerous inhibitor of protein phosphatase 2A (CIP2A) is a predictive biomarker of disease progression in many malignancies, including imatinib-treated chronic myeloid leukemia (CML).	imatinib	135-143	cellular inhibitor of PP2A	Homo sapiens	0-45
26987906-1	2016	Cancerous inhibitor of protein phosphatase 2A (CIP2A) is a predictive biomarker of disease progression in many malignancies, including imatinib-treated chronic myeloid leukemia (CML).	imatinib	135-143	cellular inhibitor of PP2A	Homo sapiens	47-52
26987906-5	2016	Disrupting this antiapoptotic phenotype by inhibition of BCL-XL via RNA interference or A-1331852, a novel, potent and BCL-XL-selective inhibitor, resulted in extensive apoptosis either alone or in combination with imatinib, dasatinib or nilotinib, both in cell lines and in primary CD34(+) cells from patients with high levels of CIP2A.	imatinib	215-223	BCL2 like 1	Homo sapiens	57-63
26950487-0	2016	PIK3C2A is a gene-specific target of microRNA-518a-5p in imatinib mesylate-resistant gastrointestinal stromal tumor.	imatinib	57-74	phosphatidylinositol-4-phosphate 3-kinase catalytic subunit type 2 alpha	Homo sapiens	0-7
26950487-2	2016	In this study, we investigated the relationship between microRNAs (miRNAs) and imatinib-resistant GISTs, and the effect of miR-518a-5p on PIK3C2A in imatinib-resistant GISTs.	imatinib	149-157	phosphatidylinositol-4-phosphate 3-kinase catalytic subunit type 2 alpha	Homo sapiens	138-145
26950487-16	2016	In conclusion, PIK3C2A is a gene-specific target of miR-518a-5p in imatinib mesylate-resistant GISTs.	imatinib	67-84	phosphatidylinositol-4-phosphate 3-kinase catalytic subunit type 2 alpha	Homo sapiens	15-22
30695330-3	2016	Molecular targeted therapy is widely utilized against malignancies, such as imatinib for chronic myelogenous leukemia blocking BCR-ABL tyrosine kinase, gefitinib for non-small cell lung cancer interrupt- ing signal transduction through EGFR, and trastuzumab for HER2-positive breast cancer.	imatinib	76-84	epidermal growth factor receptor	Homo sapiens	236-240
27268766-0	2016	ABCB1 1199G>A polymorphism (rs2229109) affects the transport of imatinib, nilotinib and dasatinib.	imatinib	67-75	ATP binding cassette subfamily B member 1	Homo sapiens	0-5
27268766-2	2016	The purpose of this study was to evaluate in vitro the influence of the ABCB1 1199G>A SNP on ABCB1 transport activity toward selected TKIs (imatinib, nilotinib and dasatinib) that are currently used in chronic myelogenous leukemia.	imatinib	143-151	ATP binding cassette subfamily B member 1	Homo sapiens	72-77
27268766-2	2016	The purpose of this study was to evaluate in vitro the influence of the ABCB1 1199G>A SNP on ABCB1 transport activity toward selected TKIs (imatinib, nilotinib and dasatinib) that are currently used in chronic myelogenous leukemia.	imatinib	143-151	ATP binding cassette subfamily B member 1	Homo sapiens	96-101
27268766-7	2016	CONCLUSION: Imatinib, nilotinib and dasatinib are transported more efficiently by the ABCB1 variant (Asn400) compared with the wild-type (Ser400) protein.	imatinib	12-20	ATP binding cassette subfamily B member 1	Homo sapiens	86-91
27228340-0	2016	MicroRNA-1301-Mediated RanGAP1 Downregulation Induces BCR-ABL Nuclear Entrapment to Enhance Imatinib Efficacy in Chronic Myeloid Leukemia Cells.	imatinib	92-100	Ran GTPase activating protein 1	Homo sapiens	23-30
27120808-0	2016	Long-term outcomes of imatinib in patients with FIP1L1/ PDGFRA associated chronic eosinophilic leukemia: experience of a single center in China.	imatinib	22-30	factor interacting with PAPOLA and CPSF1	Homo sapiens	48-54
27120808-0	2016	Long-term outcomes of imatinib in patients with FIP1L1/ PDGFRA associated chronic eosinophilic leukemia: experience of a single center in China.	imatinib	22-30	platelet derived growth factor receptor alpha	Homo sapiens	56-62
26944313-0	2016	NUMB inactivation confers resistance to imatinib in chronic myeloid leukemia cells.	imatinib	40-48	NUMB endocytic adaptor protein	Homo sapiens	0-4
27228340-0	2016	MicroRNA-1301-Mediated RanGAP1 Downregulation Induces BCR-ABL Nuclear Entrapment to Enhance Imatinib Efficacy in Chronic Myeloid Leukemia Cells.	imatinib	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
27097112-2	2016	A recent description of KIT and BRAF mutations co-occurring in an untreated GIST has challenged the concept of their being mutually exclusive and may account for ab initio resistance to Imatinib, even in the presence of Imatinib-sensitive KIT mutations.	imatinib	186-194	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	24-27
26848617-8	2016	Eleven patients treated with imatinib were evaluable for clinical response, and 2 of 3 patients with KIT mutations achieved partial response (PR), while only 1 of 8 patients without KIT mutations reached PR.	imatinib	29-37	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	101-104
27097112-1	2016	AIM: The BRAF mutation is a rare pathogenetic alternative to KIT/PDGFRA mutation in GIST and causes Imatinib resistance.	imatinib	100-108	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	9-13
27097112-2	2016	A recent description of KIT and BRAF mutations co-occurring in an untreated GIST has challenged the concept of their being mutually exclusive and may account for ab initio resistance to Imatinib, even in the presence of Imatinib-sensitive KIT mutations.	imatinib	186-194	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	32-36
27097112-1	2016	AIM: The BRAF mutation is a rare pathogenetic alternative to KIT/PDGFRA mutation in GIST and causes Imatinib resistance.	imatinib	100-108	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	61-64
27097112-1	2016	AIM: The BRAF mutation is a rare pathogenetic alternative to KIT/PDGFRA mutation in GIST and causes Imatinib resistance.	imatinib	100-108	platelet derived growth factor receptor alpha	Homo sapiens	65-71
27097112-2	2016	A recent description of KIT and BRAF mutations co-occurring in an untreated GIST has challenged the concept of their being mutually exclusive and may account for ab initio resistance to Imatinib, even in the presence of Imatinib-sensitive KIT mutations.	imatinib	220-228	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	24-27
27097112-2	2016	A recent description of KIT and BRAF mutations co-occurring in an untreated GIST has challenged the concept of their being mutually exclusive and may account for ab initio resistance to Imatinib, even in the presence of Imatinib-sensitive KIT mutations.	imatinib	220-228	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	32-36
27044748-8	2016	When combined with imatinib therapy, genetic targeting of Tcf1 and Lef1 potently diminished LSCs and conferred better protection to the CML recipients.	imatinib	19-27	transcription factor 7	Homo sapiens	58-62
26872634-7	2016	There are reports of EBF1-PDGFRB-positive patients who are refractory to conventional chemotherapy who achieve complete response when treated with the tyrosine kinase inhibitor imatinib.	imatinib	177-185	EBF transcription factor 1	Homo sapiens	21-25
27044748-8	2016	When combined with imatinib therapy, genetic targeting of Tcf1 and Lef1 potently diminished LSCs and conferred better protection to the CML recipients.	imatinib	19-27	lymphoid enhancer binding factor 1	Homo sapiens	67-71
26872634-7	2016	There are reports of EBF1-PDGFRB-positive patients who are refractory to conventional chemotherapy who achieve complete response when treated with the tyrosine kinase inhibitor imatinib.	imatinib	177-185	platelet derived growth factor receptor beta	Homo sapiens	26-32
26872634-9	2016	Two UKALL 2011 patients, positive for EBF1-PDGFRB, received imatinib; 1 died 6 months after a matched unrelated bone marrow transplant as a result of undefined encephalopathy, and the other remained in remission 10 months after diagnosis.	imatinib	60-68	EBF transcription factor 1	Homo sapiens	38-42
26872634-9	2016	Two UKALL 2011 patients, positive for EBF1-PDGFRB, received imatinib; 1 died 6 months after a matched unrelated bone marrow transplant as a result of undefined encephalopathy, and the other remained in remission 10 months after diagnosis.	imatinib	60-68	platelet derived growth factor receptor beta	Homo sapiens	43-49
27050374-1	2016	Multidrug resistance protein-1 (MDR1) has been proven to be associated with the development of chemoresistance to imatinib (Glivec, STI571) which displays high efficacy in treatment of BCR-ABL-positive chronic myelogenous leukemia (CML).	imatinib	114-122	ATP binding cassette subfamily B member 1	Homo sapiens	0-30
27027430-8	2016	Furthermore, DIF-3 potently inhibited the growth of imatinib-sensitive and imatinib-resistant K562 cells.	imatinib	52-60	gametogenetin binding protein 2	Homo sapiens	13-18
27027430-8	2016	Furthermore, DIF-3 potently inhibited the growth of imatinib-sensitive and imatinib-resistant K562 cells.	imatinib	75-83	gametogenetin binding protein 2	Homo sapiens	13-18
26942271-0	2016	p.(L576P) -KIT mutation in GIST: Favorable prognosis and sensitive to imatinib?	imatinib	70-78	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	11-14
26942271-1	2016	Exon 11 KIT mutations are found in a majority of gastrointestinal stromal tumors (GIST) and are usually predictive of response to imatinib, a KIT, PDGFRA and ABL inhibitor.	imatinib	130-138	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	8-11
26942271-1	2016	Exon 11 KIT mutations are found in a majority of gastrointestinal stromal tumors (GIST) and are usually predictive of response to imatinib, a KIT, PDGFRA and ABL inhibitor.	imatinib	130-138	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	142-145
26942271-1	2016	Exon 11 KIT mutations are found in a majority of gastrointestinal stromal tumors (GIST) and are usually predictive of response to imatinib, a KIT, PDGFRA and ABL inhibitor.	imatinib	130-138	platelet derived growth factor receptor alpha	Homo sapiens	147-153
26942271-1	2016	Exon 11 KIT mutations are found in a majority of gastrointestinal stromal tumors (GIST) and are usually predictive of response to imatinib, a KIT, PDGFRA and ABL inhibitor.	imatinib	130-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-161
26942271-3	2016	In silico and in vitro studies suggested a decreased binding affinity for imatinib in p.(L576P) KIT mutations, thereby offering an explanation for their poor outcome and poor response to standard therapy.	imatinib	74-82	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	96-99
26942271-5	2016	However, we describe the favorable response to imatinib and outcome in 5 p.(L576P)-KIT mutant GIST patients treated at a tertiary sarcoma referral center.	imatinib	47-55	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	83-86
26942271-6	2016	The sensitivity of p.(L576P)-KIT mutations to imatinib, and the prognostic impact of this mutation need to be further evaluated in a larger cohort.	imatinib	46-54	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	29-32
27050374-1	2016	Multidrug resistance protein-1 (MDR1) has been proven to be associated with the development of chemoresistance to imatinib (Glivec, STI571) which displays high efficacy in treatment of BCR-ABL-positive chronic myelogenous leukemia (CML).	imatinib	114-122	ATP binding cassette subfamily B member 1	Homo sapiens	32-36
27050374-1	2016	Multidrug resistance protein-1 (MDR1) has been proven to be associated with the development of chemoresistance to imatinib (Glivec, STI571) which displays high efficacy in treatment of BCR-ABL-positive chronic myelogenous leukemia (CML).	imatinib	114-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	185-192
27050374-6	2016	Galectin-1 might be considered as a novel target for combined modality therapy for enhancing the efficacy of CML treatment with imatinib.	imatinib	128-136	galectin 1	Homo sapiens	0-10
26985855-4	2016	Our results demonstrate that cellular location of p18(INK4c) and p57(Kip2) seems to be implicated in the antiproliferative activity of Imatinib and Dasatinib in CML cells and also suggest that the permanence of quiescent stem cells after TKI treatment could be associated with a decrease in p18(INK4c) and p57(Kip2) nuclear location.	imatinib	135-143	cyclin dependent kinase inhibitor 2C	Homo sapiens	50-53
27080051-6	2016	RESULTS: For large GIST at unfavorable anatomical locations, which are not amenable to organ-sparing resection, neoadjuvant imatinib therapy is the standard upfront treatment prior to surgery in the case of imatinib-sensitive mutations in the c-KIT protooncogene.	imatinib	124-132	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	243-248
26985855-4	2016	Our results demonstrate that cellular location of p18(INK4c) and p57(Kip2) seems to be implicated in the antiproliferative activity of Imatinib and Dasatinib in CML cells and also suggest that the permanence of quiescent stem cells after TKI treatment could be associated with a decrease in p18(INK4c) and p57(Kip2) nuclear location.	imatinib	135-143	cyclin dependent kinase inhibitor 2C	Homo sapiens	54-59
26985855-4	2016	Our results demonstrate that cellular location of p18(INK4c) and p57(Kip2) seems to be implicated in the antiproliferative activity of Imatinib and Dasatinib in CML cells and also suggest that the permanence of quiescent stem cells after TKI treatment could be associated with a decrease in p18(INK4c) and p57(Kip2) nuclear location.	imatinib	135-143	cyclin dependent kinase inhibitor 1C	Homo sapiens	65-68
26985855-4	2016	Our results demonstrate that cellular location of p18(INK4c) and p57(Kip2) seems to be implicated in the antiproliferative activity of Imatinib and Dasatinib in CML cells and also suggest that the permanence of quiescent stem cells after TKI treatment could be associated with a decrease in p18(INK4c) and p57(Kip2) nuclear location.	imatinib	135-143	cyclin dependent kinase inhibitor 1C	Homo sapiens	69-73
26985855-4	2016	Our results demonstrate that cellular location of p18(INK4c) and p57(Kip2) seems to be implicated in the antiproliferative activity of Imatinib and Dasatinib in CML cells and also suggest that the permanence of quiescent stem cells after TKI treatment could be associated with a decrease in p18(INK4c) and p57(Kip2) nuclear location.	imatinib	135-143	cyclin dependent kinase inhibitor 2C	Homo sapiens	291-294
26985855-4	2016	Our results demonstrate that cellular location of p18(INK4c) and p57(Kip2) seems to be implicated in the antiproliferative activity of Imatinib and Dasatinib in CML cells and also suggest that the permanence of quiescent stem cells after TKI treatment could be associated with a decrease in p18(INK4c) and p57(Kip2) nuclear location.	imatinib	135-143	cyclin dependent kinase inhibitor 2C	Homo sapiens	295-300
26985855-4	2016	Our results demonstrate that cellular location of p18(INK4c) and p57(Kip2) seems to be implicated in the antiproliferative activity of Imatinib and Dasatinib in CML cells and also suggest that the permanence of quiescent stem cells after TKI treatment could be associated with a decrease in p18(INK4c) and p57(Kip2) nuclear location.	imatinib	135-143	cyclin dependent kinase inhibitor 1C	Homo sapiens	306-309
26985855-4	2016	Our results demonstrate that cellular location of p18(INK4c) and p57(Kip2) seems to be implicated in the antiproliferative activity of Imatinib and Dasatinib in CML cells and also suggest that the permanence of quiescent stem cells after TKI treatment could be associated with a decrease in p18(INK4c) and p57(Kip2) nuclear location.	imatinib	135-143	cyclin dependent kinase inhibitor 1C	Homo sapiens	310-314
26865419-2	2016	We previously found that carcinoma-associated fibroblasts (CAFs) expressed platelet-derived growth factor receptor-beta (PDGFR-beta) and that PDGFR targeted therapy using imatinib or nilotinib inhibited stromal reaction.	imatinib	171-179	platelet derived growth factor receptor beta	Homo sapiens	121-126
27168851-0	2016	Association between the concentration of imatinib in bone marrow mononuclear cells, mutation status of ABCB1 and therapeutic response in patients with chronic myelogenous leukemia.	imatinib	41-49	ATP binding cassette subfamily B member 1	Homo sapiens	103-108
26154982-1	2016	Binding of tyrosine kinase inhibitors such as imatinib was shown to induce a novel open-inhibited conformation of BCR-ABL, in which Tyr245 is exposed and prone to phosphorylation.	imatinib	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
27168851-1	2016	Low concentrations of imatinib (IM) in bone marrow cells have been linked with poor prognosis in patients with chronic myeloid leukemia (CML), which may be caused by the emergence of ATP-binding cassette transporter B1 (ABCB1) mutations.	imatinib	22-30	ATP binding cassette subfamily B member 1	Homo sapiens	183-218
27168851-1	2016	Low concentrations of imatinib (IM) in bone marrow cells have been linked with poor prognosis in patients with chronic myeloid leukemia (CML), which may be caused by the emergence of ATP-binding cassette transporter B1 (ABCB1) mutations.	imatinib	22-30	ATP binding cassette subfamily B member 1	Homo sapiens	220-225
27226777-0	2016	EphB4/ephrinB2 Contributes to Imatinib Resistance in Chronic Myeloid Leukemia Involved in Cytoskeletal Proteins.	imatinib	30-38	EPH receptor B4	Homo sapiens	0-5
27161312-8	2016	Pretreatment of these cells with a c-kit kinase inhibitor (imatinib mesylate) also attenuated Flk-1 and CD31 expression.	imatinib	59-76	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	35-40
27161312-8	2016	Pretreatment of these cells with a c-kit kinase inhibitor (imatinib mesylate) also attenuated Flk-1 and CD31 expression.	imatinib	59-76	kinase insert domain protein receptor	Mus musculus	94-99
27161312-8	2016	Pretreatment of these cells with a c-kit kinase inhibitor (imatinib mesylate) also attenuated Flk-1 and CD31 expression.	imatinib	59-76	platelet/endothelial cell adhesion molecule 1	Mus musculus	104-108
27077705-2	2016	Clinically used c-KIT kinase inhibitors, i.e., Imatinib and Sunitinib, bear other important targets such as ABL or FLT3 kinases.	imatinib	47-55	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	16-21
27077705-2	2016	Clinically used c-KIT kinase inhibitors, i.e., Imatinib and Sunitinib, bear other important targets such as ABL or FLT3 kinases.	imatinib	47-55	fms related receptor tyrosine kinase 3	Homo sapiens	115-119
27551334-3	2016	Here we showed that the HSP90-HMWNC is present in leukemia cells from CML patients in blast stage, and in Imatinib (IM)-resistant 32Dp210 (T315I) leukemia cells.	imatinib	106-114	heat shock protein 90 alpha family class A member 1	Homo sapiens	24-29
27123048-9	2016	Imatinib, a tyrosine kinase inhibitor, may be an effective treatment against standard chemotherapy-resistant CNS germinoma patients exhibiting c-Kit mutations.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	143-148
26864341-5	2016	Conversely, allosteric stimulation of ABL1 kinase activity enhanced the antileukemia effect of ABL1 tyrosine kinase inhibitors (imatinib and ponatinib) in human and murine leukemias expressing BCR-ABL1, TEL-ABL1, and NUP214-ABL1.	imatinib	128-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-42
26864341-5	2016	Conversely, allosteric stimulation of ABL1 kinase activity enhanced the antileukemia effect of ABL1 tyrosine kinase inhibitors (imatinib and ponatinib) in human and murine leukemias expressing BCR-ABL1, TEL-ABL1, and NUP214-ABL1.	imatinib	128-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-99
26864341-5	2016	Conversely, allosteric stimulation of ABL1 kinase activity enhanced the antileukemia effect of ABL1 tyrosine kinase inhibitors (imatinib and ponatinib) in human and murine leukemias expressing BCR-ABL1, TEL-ABL1, and NUP214-ABL1.	imatinib	128-136	ets variant 6	Mus musculus	203-211
26864341-5	2016	Conversely, allosteric stimulation of ABL1 kinase activity enhanced the antileukemia effect of ABL1 tyrosine kinase inhibitors (imatinib and ponatinib) in human and murine leukemias expressing BCR-ABL1, TEL-ABL1, and NUP214-ABL1.	imatinib	128-136	nucleoporin 214	Mus musculus	217-223
26864341-5	2016	Conversely, allosteric stimulation of ABL1 kinase activity enhanced the antileukemia effect of ABL1 tyrosine kinase inhibitors (imatinib and ponatinib) in human and murine leukemias expressing BCR-ABL1, TEL-ABL1, and NUP214-ABL1.	imatinib	128-136	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	95-99
27226777-0	2016	EphB4/ephrinB2 Contributes to Imatinib Resistance in Chronic Myeloid Leukemia Involved in Cytoskeletal Proteins.	imatinib	30-38	ephrin B2	Homo sapiens	6-14
27226777-1	2016	INTRODUCTION: The mechanism of EphB4/ephrinB2 in the resistance of chronic myelogenous leukemia to imatinib keeps unknown.	imatinib	99-107	EPH receptor B4	Homo sapiens	31-36
27226777-1	2016	INTRODUCTION: The mechanism of EphB4/ephrinB2 in the resistance of chronic myelogenous leukemia to imatinib keeps unknown.	imatinib	99-107	ephrin B2	Homo sapiens	37-45
27226777-8	2016	EphB4 knockdown inhibited cell migration ability and restored sensitivity to imatinib in vitro and in vivo.	imatinib	77-85	EPH receptor B4	Homo sapiens	0-5
27226777-9	2016	Restored sensitivity to imatinib was observed in K562-R cells, along with increased levels of phospho-EphB4 and decreased phosphorylation levels of RhoA, Rac1, and Cdc42.	imatinib	24-32	EPH receptor B4	Homo sapiens	102-107
27226777-9	2016	Restored sensitivity to imatinib was observed in K562-R cells, along with increased levels of phospho-EphB4 and decreased phosphorylation levels of RhoA, Rac1, and Cdc42.	imatinib	24-32	ras homolog family member A	Homo sapiens	148-152
27226777-9	2016	Restored sensitivity to imatinib was observed in K562-R cells, along with increased levels of phospho-EphB4 and decreased phosphorylation levels of RhoA, Rac1, and Cdc42.	imatinib	24-32	Rac family small GTPase 1	Homo sapiens	154-158
27226777-9	2016	Restored sensitivity to imatinib was observed in K562-R cells, along with increased levels of phospho-EphB4 and decreased phosphorylation levels of RhoA, Rac1, and Cdc42.	imatinib	24-32	cell division cycle 42	Homo sapiens	164-169
27194977-1	2016	Nilotinib is a second-generation Bcr-Abl tyrosine kinase inhibitor (TKI) that is approved for the treatment of imatinib-resistant chronic myeloid leukaemia expressing the Bcr-Abl mutation.	imatinib	111-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
28197361-0	2017	NKp30 isoforms and NKp30 ligands are predictive biomarkers of response to imatinib mesylate in metastatic GIST patients.	imatinib	74-91	natural cytotoxicity triggering receptor 3	Homo sapiens	0-5
28197361-0	2017	NKp30 isoforms and NKp30 ligands are predictive biomarkers of response to imatinib mesylate in metastatic GIST patients.	imatinib	74-91	natural cytotoxicity triggering receptor 3	Homo sapiens	19-24
27027438-0	2016	BM microenvironmental protection of CML cells from imatinib through Stat5/NF-kappaB signaling and reversal by Wogonin.	imatinib	51-59	signal transducer and activator of transcription 5A	Homo sapiens	68-73
27027438-1	2016	Constitutive Stat5 activation enhanced cell survival and resistance to imatinib (IM) in chronic myelogenous leukemia (CML) cells.	imatinib	71-79	signal transducer and activator of transcription 5A	Homo sapiens	13-18
27092489-0	2016	Downregulation of Plasma miR-215 in Chronic Myeloid Leukemia Patients with Successful Discontinuation of Imatinib.	imatinib	105-113	microRNA 215	Homo sapiens	25-32
26980736-0	2016	Next-generation sequencing for sensitive detection of BCR-ABL1 mutations relevant to tyrosine kinase inhibitor choice in imatinib-resistant patients.	imatinib	121-129	BCR activator of RhoGEF and GTPase	Homo sapiens	54-62
27087366-5	2016	Here we combine various NMR experiments and surface plasmon resonance with enhanced sampling molecular dynamics simulations to shed light into the conformational dynamics associated with the binding of Imatinib to the proto-oncogene c-Src.	imatinib	202-210	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	218-238
25547508-0	2016	Imatinib-Sensitizing KIT Mutation in a Carney-Stratakis-Associated GI Stromal Tumor.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	21-24
26773037-3	2016	The type and number of low-level BCR-ABL1 mutations present after imatinib resistance has prognostic significance for subsequent treatment with nilotinib or dasatinib as second-line therapy.	imatinib	66-74	BCR activator of RhoGEF and GTPase	Homo sapiens	33-41
26967392-4	2016	Overexpression of RalA results in malignant transformation and progression, and induces resistance to imatinib (IM) in BaF3 and K562 cell lines.	imatinib	102-110	v-ral simian leukemia viral oncogene A (ras related)	Mus musculus	18-22
27194941-2	2016	While Bcr-Abl inhibitors including Imatinib showed antitumor efficacy on many CML patients, resistance was frequently reported in recent years.	imatinib	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-13
26942564-0	2016	Overexpression of RPS27a contributes to enhanced chemoresistance of CML cells to imatinib by the transactivated STAT3.	imatinib	81-89	ribosomal protein S27a	Homo sapiens	18-24
26919095-0	2016	Inhibition of protein kinase CK2 by CX-5011 counteracts imatinib-resistance preventing rpS6 phosphorylation in chronic myeloid leukaemia cells: new combined therapeutic strategies.	imatinib	56-64	ribosomal protein S6	Homo sapiens	87-91
26919095-2	2016	Although treatment with the Bcr-Abl-inhibitor imatinib represents the first-line therapy against CML, almost 20-30% of patients develop chemotherapeutic resistance and require alternative therapy.	imatinib	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
26919095-3	2016	Here we show that a strong hyper-phosphorylation/activation of ERK1/2, Akt Ser473, and 40S ribosomal protein S6 (rpS6) is detectable in imatinib-resistant KCL22 and K562 CML cells as compared to the -sensitive cell variants.	imatinib	136-144	mitogen-activated protein kinase 3	Homo sapiens	63-69
26919095-3	2016	Here we show that a strong hyper-phosphorylation/activation of ERK1/2, Akt Ser473, and 40S ribosomal protein S6 (rpS6) is detectable in imatinib-resistant KCL22 and K562 CML cells as compared to the -sensitive cell variants.	imatinib	136-144	AKT serine/threonine kinase 1	Homo sapiens	71-74
26919095-3	2016	Here we show that a strong hyper-phosphorylation/activation of ERK1/2, Akt Ser473, and 40S ribosomal protein S6 (rpS6) is detectable in imatinib-resistant KCL22 and K562 CML cells as compared to the -sensitive cell variants.	imatinib	136-144	ribosomal protein S6	Homo sapiens	87-111
26919095-3	2016	Here we show that a strong hyper-phosphorylation/activation of ERK1/2, Akt Ser473, and 40S ribosomal protein S6 (rpS6) is detectable in imatinib-resistant KCL22 and K562 CML cells as compared to the -sensitive cell variants.	imatinib	136-144	ribosomal protein S6	Homo sapiens	113-117
26919095-4	2016	In imatinib-resistant CML cells, high concentration of imatinib is required to strongly inhibit Bcr-Abl, ERK1/2 and Akt Ser473 phosphorylation, but under these conditions the phosphorylation of rpS6, a common downstream effector of MEK/ERK1/2 and PI3K/Akt/mTOR pathways is only slightly reduced.	imatinib	3-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
26896780-3	2016	In this study, protein-ligand interactions between FLT3 and kinase inhibitors (CEP701, PKC412, sunitinib, imatinib and dasatinib) were obtained through homology modelling and molecular docking.	imatinib	106-114	FMS-like tyrosine kinase 3	Mus musculus	51-55
26919095-4	2016	In imatinib-resistant CML cells, high concentration of imatinib is required to strongly inhibit Bcr-Abl, ERK1/2 and Akt Ser473 phosphorylation, but under these conditions the phosphorylation of rpS6, a common downstream effector of MEK/ERK1/2 and PI3K/Akt/mTOR pathways is only slightly reduced.	imatinib	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
26942564-0	2016	Overexpression of RPS27a contributes to enhanced chemoresistance of CML cells to imatinib by the transactivated STAT3.	imatinib	81-89	signal transducer and activator of transcription 3	Homo sapiens	112-117
26919095-4	2016	In imatinib-resistant CML cells, high concentration of imatinib is required to strongly inhibit Bcr-Abl, ERK1/2 and Akt Ser473 phosphorylation, but under these conditions the phosphorylation of rpS6, a common downstream effector of MEK/ERK1/2 and PI3K/Akt/mTOR pathways is only slightly reduced.	imatinib	55-63	mitogen-activated protein kinase 3	Homo sapiens	105-111
26919095-4	2016	In imatinib-resistant CML cells, high concentration of imatinib is required to strongly inhibit Bcr-Abl, ERK1/2 and Akt Ser473 phosphorylation, but under these conditions the phosphorylation of rpS6, a common downstream effector of MEK/ERK1/2 and PI3K/Akt/mTOR pathways is only slightly reduced.	imatinib	55-63	AKT serine/threonine kinase 1	Homo sapiens	116-119
26919095-4	2016	In imatinib-resistant CML cells, high concentration of imatinib is required to strongly inhibit Bcr-Abl, ERK1/2 and Akt Ser473 phosphorylation, but under these conditions the phosphorylation of rpS6, a common downstream effector of MEK/ERK1/2 and PI3K/Akt/mTOR pathways is only slightly reduced.	imatinib	55-63	ribosomal protein S6	Homo sapiens	194-198
26942564-2	2016	Phospho-STAT3 was overexpressed in imatinib-resistant CML patients as relative to imatinib responsive ones.	imatinib	35-43	signal transducer and activator of transcription 3	Homo sapiens	8-13
26919095-4	2016	In imatinib-resistant CML cells, high concentration of imatinib is required to strongly inhibit Bcr-Abl, ERK1/2 and Akt Ser473 phosphorylation, but under these conditions the phosphorylation of rpS6, a common downstream effector of MEK/ERK1/2 and PI3K/Akt/mTOR pathways is only slightly reduced.	imatinib	55-63	mitogen-activated protein kinase kinase 7	Homo sapiens	232-235
26942564-9	2016	Imatinib-resistant K562/G01 cells expressed significantly higher levels of STAT3 and RPS27a compared with those of K562 cells.	imatinib	0-8	signal transducer and activator of transcription 3	Homo sapiens	75-80
26919095-4	2016	In imatinib-resistant CML cells, high concentration of imatinib is required to strongly inhibit Bcr-Abl, ERK1/2 and Akt Ser473 phosphorylation, but under these conditions the phosphorylation of rpS6, a common downstream effector of MEK/ERK1/2 and PI3K/Akt/mTOR pathways is only slightly reduced.	imatinib	55-63	mitogen-activated protein kinase 3	Homo sapiens	236-242
26942564-9	2016	Imatinib-resistant K562/G01 cells expressed significantly higher levels of STAT3 and RPS27a compared with those of K562 cells.	imatinib	0-8	ribosomal protein S27a	Homo sapiens	85-91
26919095-4	2016	In imatinib-resistant CML cells, high concentration of imatinib is required to strongly inhibit Bcr-Abl, ERK1/2 and Akt Ser473 phosphorylation, but under these conditions the phosphorylation of rpS6, a common downstream effector of MEK/ERK1/2 and PI3K/Akt/mTOR pathways is only slightly reduced.	imatinib	55-63	AKT serine/threonine kinase 1	Homo sapiens	252-255
26942564-11	2016	The transactivated RPS27a could decrease the percentage of apoptotic CML cells induced by imatinib.	imatinib	90-98	ribosomal protein S27a	Homo sapiens	19-25
26919095-4	2016	In imatinib-resistant CML cells, high concentration of imatinib is required to strongly inhibit Bcr-Abl, ERK1/2 and Akt Ser473 phosphorylation, but under these conditions the phosphorylation of rpS6, a common downstream effector of MEK/ERK1/2 and PI3K/Akt/mTOR pathways is only slightly reduced.	imatinib	55-63	mechanistic target of rapamycin kinase	Homo sapiens	256-260
26130666-0	2016	Efficacy of Imatinib in Patients with Platelet-Derived Growth Factor Receptor Alpha-Mutated Gastrointestinal Stromal Tumors.	imatinib	12-20	platelet derived growth factor receptor alpha	Homo sapiens	38-83
26919095-6	2016	CK2-inhibition by CX-5011 induces cell death by apoptosis and acts synergistically with imatinib or the MEK-inhibitor U0126 in reducing the viability of imatinib-resistant CML cells.	imatinib	153-161	mitogen-activated protein kinase kinase 7	Homo sapiens	104-107
26919095-8	2016	These results disclose a novel CK2-mediated mechanism of acquired imatinib-resistance resulting in hyper-phosphorylation of rpS6.	imatinib	66-74	ribosomal protein S6	Homo sapiens	124-128
26919095-9	2016	We suggest that co-targeting CK2 and MEK protein kinases is a promising strategy to restore responsiveness of resistant CML cells to imatinib.	imatinib	133-141	mitogen-activated protein kinase kinase 7	Homo sapiens	37-40
26130666-3	2016	RESULTS: KIT and PDGFRA genotyping in 823 patients identified 18 patients (2%) with PDGFRA mutations who were treated with first-line imatinib.	imatinib	134-142	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	9-12
26130666-3	2016	RESULTS: KIT and PDGFRA genotyping in 823 patients identified 18 patients (2%) with PDGFRA mutations who were treated with first-line imatinib.	imatinib	134-142	platelet derived growth factor receptor alpha	Homo sapiens	17-23
26130666-3	2016	RESULTS: KIT and PDGFRA genotyping in 823 patients identified 18 patients (2%) with PDGFRA mutations who were treated with first-line imatinib.	imatinib	134-142	platelet derived growth factor receptor alpha	Homo sapiens	84-90
26130666-9	2016	CONCLUSION: Imatinib is active against non-D842V PDGFRA-mutant GISTs, whereas GISTs harboring the D842V mutation are primarily resistant to imatinib.	imatinib	12-20	platelet derived growth factor receptor alpha	Homo sapiens	49-55
26059983-0	2016	Gender and BCR-ABL transcript type are correlated with molecular response to imatinib treatment in patients with chronic myeloid leukemia.	imatinib	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-18
26885657-2	2016	Imatinib (IM) a selective inhibitor of C-KIT, is indicated for the treatment of KIT-positive unresectable and/or metastatic GIST, and has tripled the survival time of patients with metastatic GIST.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	39-44
27033238-7	2016	Transcriptome sequencing studies have identified a network of fusion genes involving kinase genes -ABL1,ABL2,PDGFRB,CSF1R,CRLF2,JAK2 and EPOR in-vitro and in-vivo studies along with emerging clinical observations indicate that patients with a kinase-activating aberration may respond to treatment with small molecular inhibitors like imatinib/dasatinib and ruxolitinib.	imatinib	334-342	erythropoietin receptor	Homo sapiens	137-141
26892093-0	2016	Hsp90 inhibitor, BIIB021, induces apoptosis and autophagy by regulating mTOR-Ulk1 pathway in imatinib-sensitive and -resistant chronic myeloid leukemia cells.	imatinib	93-101	heat shock protein 90 alpha family class A member 1	Homo sapiens	0-5
26892093-0	2016	Hsp90 inhibitor, BIIB021, induces apoptosis and autophagy by regulating mTOR-Ulk1 pathway in imatinib-sensitive and -resistant chronic myeloid leukemia cells.	imatinib	93-101	mechanistic target of rapamycin kinase	Homo sapiens	72-76
26892093-0	2016	Hsp90 inhibitor, BIIB021, induces apoptosis and autophagy by regulating mTOR-Ulk1 pathway in imatinib-sensitive and -resistant chronic myeloid leukemia cells.	imatinib	93-101	unc-51 like autophagy activating kinase 1	Homo sapiens	77-81
26582603-3	2016	The first-line treatment consists on BCR-ABL inhibitors such as Imatinib, Nilotinib and Dasatinib.	imatinib	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
25591869-4	2016	Imatinib mesylate, which was the first anti-BCR-ABL tyrosine kinase inhibitor, has demonstrated a high tolerance profile and efficacy in these patients for many years.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
27073655-4	2016	A patient with a c-kit mutation-positive thymic carcinoma received imatinib followed by sunitinib consecutively, which are both c-Kit inhibitors.	imatinib	67-75	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	17-22
27141462-3	2016	The purpose of the study was to determine cellular viability and the levels of, platelet derived growth factor (PDGF) and stem cell factor (SCF) in normal mouse leydig cells exposed to imatinib, and addressing the effect of imatinib on fertility potential.	imatinib	185-193	kit ligand	Mus musculus	140-143
27073655-4	2016	A patient with a c-kit mutation-positive thymic carcinoma received imatinib followed by sunitinib consecutively, which are both c-Kit inhibitors.	imatinib	67-75	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	128-133
26693810-0	2016	In Vivo Cytochrome P450 3A Isoenzyme Activity and Pharmacokinetics of Imatinib in Relation to Therapeutic Outcome in Patients With Chronic Myeloid Leukemia.	imatinib	70-78	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	8-26
26693810-1	2016	BACKGROUND: Cytochrome P450 3A (CYP3A) isoenzyme metabolic activity varies between individuals and is therefore a possible candidate of influence on the therapeutic outcome of the tyrosine kinase inhibitor imatinib in patients with chronic myeloid leukemia (CML).	imatinib	206-214	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	12-30
27161743-11	2016	Thrombin generation was not significantly affected by therapeutic levels of TKIs, whereas higher doses of dasatinib, bosutinib, ponatinib and imatinib significantly changed one or several of the thrombin generation parameters (n=7-8).	imatinib	142-150	coagulation factor II, thrombin	Homo sapiens	195-203
26693810-1	2016	BACKGROUND: Cytochrome P450 3A (CYP3A) isoenzyme metabolic activity varies between individuals and is therefore a possible candidate of influence on the therapeutic outcome of the tyrosine kinase inhibitor imatinib in patients with chronic myeloid leukemia (CML).	imatinib	206-214	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	32-37
26693810-2	2016	The aim of this study was to investigate the influence of CYP3A metabolic activity on the plasma concentration and outcome of imatinib in patients with CML.	imatinib	126-134	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	58-63
26693810-8	2016	These results indicate that although imatinib is metabolized by CYP3A enzymes, this activity is not the rate-limiting step in imatinib metabolism and excretion.	imatinib	37-45	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	64-69
26893362-0	2016	RACK1 overexpression is linked to acquired imatinib resistance in gastrointestinal stromal tumor.	imatinib	43-51	receptor for activated C kinase 1	Homo sapiens	0-5
27151023-3	2016	RESULTS: The expression level of PDGF-BB in bone marrow of ET patients was significantly higher than that in normal controls; the expression level of PDGFR-beta in bone marrow of ET patients was significantly higher than that in nornal controls; PDGF-BB could activate JAK2/STAT3 and PI3K/AKT pathway of megakaryocytes, while the imatinib could block the effect of PDGF-BB on megakaryocyte.	imatinib	330-338	platelet derived growth factor receptor beta	Homo sapiens	150-160
27151023-5	2016	Imatinib may have a therapeutical effect on ET via blocking of PDGFR.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	63-68
27009330-7	2016	CONCLUSIONS: The Fas/FasL signaling pathway may represent the major pathway that mediates apoptosis in CML treated with imatinib.	imatinib	120-128	Fas ligand	Homo sapiens	21-25
26893362-1	2016	Although treatment with imatinib, which inhibits KIT and PDGFR, controls advanced disease in about 80% of gastrointestinal stromal tumor (GIST) patients, resistance to imatinib often develops.	imatinib	24-32	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	49-52
26893362-1	2016	Although treatment with imatinib, which inhibits KIT and PDGFR, controls advanced disease in about 80% of gastrointestinal stromal tumor (GIST) patients, resistance to imatinib often develops.	imatinib	24-32	platelet derived growth factor receptor beta	Homo sapiens	57-62
26893362-4	2016	Imatinib treatment inhibits c-KIT activity and prevents RACK1 degradation, and RACK1 is upregulated in imatinib-resistant GIST cells compared to non-resistant parental cells.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	28-33
26893362-4	2016	Imatinib treatment inhibits c-KIT activity and prevents RACK1 degradation, and RACK1 is upregulated in imatinib-resistant GIST cells compared to non-resistant parental cells.	imatinib	0-8	receptor for activated C kinase 1	Homo sapiens	56-61
26893362-4	2016	Imatinib treatment inhibits c-KIT activity and prevents RACK1 degradation, and RACK1 is upregulated in imatinib-resistant GIST cells compared to non-resistant parental cells.	imatinib	103-111	receptor for activated C kinase 1	Homo sapiens	79-84
26893362-5	2016	Moreover, Erk and Akt signaling were reactivated by imatinib in resistant GIST cells.	imatinib	52-60	mitogen-activated protein kinase 1	Homo sapiens	10-13
26893362-5	2016	Moreover, Erk and Akt signaling were reactivated by imatinib in resistant GIST cells.	imatinib	52-60	AKT serine/threonine kinase 1	Homo sapiens	18-21
26893362-6	2016	RACK1 functioned as a scaffold protein and mediated Erk and Akt reactivation after imatinib treatment, thereby promoting GIST cell survival even in the presence of imatinib.	imatinib	83-91	receptor for activated C kinase 1	Homo sapiens	0-5
26893362-6	2016	RACK1 functioned as a scaffold protein and mediated Erk and Akt reactivation after imatinib treatment, thereby promoting GIST cell survival even in the presence of imatinib.	imatinib	164-172	receptor for activated C kinase 1	Homo sapiens	0-5
26893362-7	2016	Combined inhibition of KIT and RACK1 inhibited growth in imatinib-resistant GIST cell lines and reduced tumor relapse in GIST xenografts.	imatinib	57-65	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	23-26
26893362-7	2016	Combined inhibition of KIT and RACK1 inhibited growth in imatinib-resistant GIST cell lines and reduced tumor relapse in GIST xenografts.	imatinib	57-65	receptor for activated C kinase 1	Homo sapiens	31-36
26893362-8	2016	These findings provide new insight into the role of RACK1 in imatinib resistance in GIST.	imatinib	61-69	receptor for activated C kinase 1	Homo sapiens	52-57
26934052-1	2016	The most relevant therapeutic approaches to treat CML rely on the administration of tyrosine kinase inhibitors (TKIs) like Imatinib, which are able to counteract the activity of Bcr-Abl protein increasing patient"s life expectancy and survival.	imatinib	123-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185
26944912-0	2016	Cost-effectiveness of Tyrosine Kinase Inhibitor Treatment Strategies for Chronic Myeloid Leukemia in Chronic Phase After Generic Entry of Imatinib in the United States.	imatinib	138-146	TXK tyrosine kinase	Homo sapiens	22-37
26721204-0	2016	Blockade of the interaction between Bcr-Abl and PTB1B by small molecule SBF-1 to overcome imatinib-resistance of chronic myeloid leukemia cells.	imatinib	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
26937281-3	2016	Hyperactivation of Separase in human hematopoietic cells has been linked to a feedback mechanism that posttranslationally stimulates Separase proteolytic activity after imatinib therapy-induced reduction of Separase protein levels.	imatinib	169-177	extra spindle pole bodies like 1, separase	Homo sapiens	19-27
26937281-3	2016	Hyperactivation of Separase in human hematopoietic cells has been linked to a feedback mechanism that posttranslationally stimulates Separase proteolytic activity after imatinib therapy-induced reduction of Separase protein levels.	imatinib	169-177	extra spindle pole bodies like 1, separase	Homo sapiens	133-141
26937281-3	2016	Hyperactivation of Separase in human hematopoietic cells has been linked to a feedback mechanism that posttranslationally stimulates Separase proteolytic activity after imatinib therapy-induced reduction of Separase protein levels.	imatinib	169-177	extra spindle pole bodies like 1, separase	Homo sapiens	133-141
26937281-5	2016	Quantitative RT-PCR and Western blot immunostaining experiments revealed that c-MYB expression levels are decreased in an imatinib-dependent manner and positively correlate with Separase expression levels in cell lines and in clinical CML samples.	imatinib	122-130	extra spindle pole bodies like 1, separase	Homo sapiens	178-186
26898422-0	2016	Heme oxygenase-1 contributes to imatinib resistance by promoting autophagy in chronic myeloid leukemia through disrupting the mTOR signaling pathway.	imatinib	32-40	heme oxygenase 1	Homo sapiens	0-16
26898422-0	2016	Heme oxygenase-1 contributes to imatinib resistance by promoting autophagy in chronic myeloid leukemia through disrupting the mTOR signaling pathway.	imatinib	32-40	mechanistic target of rapamycin kinase	Homo sapiens	126-130
26898422-1	2016	Heme oxygenase-1 (HO-1) has been verified to play an important role in imatinib (IM)-resistant chronic myeloid leukemia (CML) cells, but the mechanism remains unclear.	imatinib	71-79	heme oxygenase 1	Homo sapiens	0-16
26898422-1	2016	Heme oxygenase-1 (HO-1) has been verified to play an important role in imatinib (IM)-resistant chronic myeloid leukemia (CML) cells, but the mechanism remains unclear.	imatinib	71-79	heme oxygenase 1	Homo sapiens	18-22
26721204-0	2016	Blockade of the interaction between Bcr-Abl and PTB1B by small molecule SBF-1 to overcome imatinib-resistance of chronic myeloid leukemia cells.	imatinib	90-98	SET binding factor 1	Homo sapiens	72-77
26721204-1	2016	In this study, a synthetic steroidal glycoside SBF-1 had strong and preferential antitumor effects on the human chronic myeloid leukemia (CML) cell line K562 and its imatinib-resistant form K562/G.	imatinib	166-174	SET binding factor 1	Homo sapiens	47-52
26721204-7	2016	Taking together these findings, this study, for the first time, suggests that the blockade of the interaction between Bcr-Abl and PTP1B may be a feasible strategy for the treatment of CML, especially CML with resistance to Bcr-Abl kinase inhibitor imatinib.	imatinib	248-256	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
26517532-4	2016	Conditional knockout of c-Abl in neurons or treatment of mice with STI571, a c-Abl family kinase inhibitor, reduced the loss of dopaminergic neurons and ameliorated the locomotive defects induced by short-term MPTP treatment.	imatinib	67-73	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	24-29
26721204-7	2016	Taking together these findings, this study, for the first time, suggests that the blockade of the interaction between Bcr-Abl and PTP1B may be a feasible strategy for the treatment of CML, especially CML with resistance to Bcr-Abl kinase inhibitor imatinib.	imatinib	248-256	protein tyrosine phosphatase non-receptor type 1	Homo sapiens	130-135
26517532-4	2016	Conditional knockout of c-Abl in neurons or treatment of mice with STI571, a c-Abl family kinase inhibitor, reduced the loss of dopaminergic neurons and ameliorated the locomotive defects induced by short-term MPTP treatment.	imatinib	67-73	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	77-82
26796526-3	2016	In this study, the mutational hotspot in the PIK3CA kinase domain encoded by exon 20 was evaluated in 529 imatinib-naive GISTs using PCR amplification and Sanger sequencing.	imatinib	106-114	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	45-51
26874514-9	2016	The results also showed that co-treatment with deferasirox and imatinib reduced the expression of BcrAbl, phosphorylated Bcr-Abl, nuclear factor-kappaB (NF-kappaB) and beta-catenin.	imatinib	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-104
26874514-9	2016	The results also showed that co-treatment with deferasirox and imatinib reduced the expression of BcrAbl, phosphorylated Bcr-Abl, nuclear factor-kappaB (NF-kappaB) and beta-catenin.	imatinib	63-71	nuclear factor kappa B subunit 1	Homo sapiens	130-151
26874514-9	2016	The results also showed that co-treatment with deferasirox and imatinib reduced the expression of BcrAbl, phosphorylated Bcr-Abl, nuclear factor-kappaB (NF-kappaB) and beta-catenin.	imatinib	63-71	nuclear factor kappa B subunit 1	Homo sapiens	153-162
26874514-9	2016	The results also showed that co-treatment with deferasirox and imatinib reduced the expression of BcrAbl, phosphorylated Bcr-Abl, nuclear factor-kappaB (NF-kappaB) and beta-catenin.	imatinib	63-71	catenin beta 1	Homo sapiens	168-180
26703895-9	2016	Importantly, the sensitivity of ATF7IP-PDGFRB-expressing Ba/F3 cells to imatinib is significantly higher than that of BCR-ABL1-transformed Ba/F3 cells, as assessed by the IC50.	imatinib	72-80	activating transcription factor 7 interacting protein	Mus musculus	32-38
26703895-9	2016	Importantly, the sensitivity of ATF7IP-PDGFRB-expressing Ba/F3 cells to imatinib is significantly higher than that of BCR-ABL1-transformed Ba/F3 cells, as assessed by the IC50.	imatinib	72-80	platelet derived growth factor receptor, beta polypeptide	Mus musculus	39-45
26818574-0	2016	Niemann-Pick disease type C1(NPC1) is involved in resistance against imatinib in the imatinib-resistant Ph+ acute lymphoblastic leukemia cell line SUP-B15/RI.	imatinib	69-77	NPC intracellular cholesterol transporter 1	Homo sapiens	0-33
26818574-0	2016	Niemann-Pick disease type C1(NPC1) is involved in resistance against imatinib in the imatinib-resistant Ph+ acute lymphoblastic leukemia cell line SUP-B15/RI.	imatinib	85-93	NPC intracellular cholesterol transporter 1	Homo sapiens	0-33
26818574-3	2016	In the present study, NPC1 was shown by microarray analysis to be more highly expressed in the Ph+ acute lymphoblastic leukemia cell line SUP-B15/RI, an imatinib-resistant variant of SUP-B15/S cells without bcr-abl gene mutation established in our lab.	imatinib	153-161	NPC intracellular cholesterol transporter 1	Homo sapiens	22-26
26818574-4	2016	Further investigation revealed a defect in the functional capacity of the NPC1 protein demonstrated by filipin staining accompanied by a lower intracellular imatinib mesylate(IM) concentration by high-performance liquid chromatography in SUP-B15/RI compared with SUP-B15/S cells.	imatinib	157-174	NPC intracellular cholesterol transporter 1	Homo sapiens	74-78
26839216-5	2016	A disruption of the SHP2-p85 complex took place after insulin/IGF1 stimulation or imatinib treatment, suggesting that the direct SHP2-p85 interaction was both independent of AKT activation and positively regulates the ERK signaling pathway.	imatinib	82-90	protein tyrosine phosphatase non-receptor type 11	Homo sapiens	20-24
26831065-3	2016	Aberrant platelet-derived growth factor receptor beta (PDGFRbeta) signaling in cancer has motivated the development of several antagonists currently in clinical use, including imatinib, sunitinib, and sorafenib.	imatinib	176-184	platelet derived growth factor receptor beta	Homo sapiens	9-53
26831065-3	2016	Aberrant platelet-derived growth factor receptor beta (PDGFRbeta) signaling in cancer has motivated the development of several antagonists currently in clinical use, including imatinib, sunitinib, and sorafenib.	imatinib	176-184	platelet derived growth factor receptor beta	Homo sapiens	55-64
26912052-2	2016	Bcr-Abl tyrosine kinase inhibitors (TKIs), such as imatinib mesylate (IM), revolutionized CML therapy.	imatinib	51-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
27366312-4	2016	The introduction of imatinib, a BCR-ABL1- targeting tyrosine kinase inhibitor (TKI) has revolutionized CML therapy.	imatinib	20-28	BCR activator of RhoGEF and GTPase	Homo sapiens	32-40
26839216-5	2016	A disruption of the SHP2-p85 complex took place after insulin/IGF1 stimulation or imatinib treatment, suggesting that the direct SHP2-p85 interaction was both independent of AKT activation and positively regulates the ERK signaling pathway.	imatinib	82-90	phosphoinositide-3-kinase regulatory subunit 2	Homo sapiens	25-28
26839216-5	2016	A disruption of the SHP2-p85 complex took place after insulin/IGF1 stimulation or imatinib treatment, suggesting that the direct SHP2-p85 interaction was both independent of AKT activation and positively regulates the ERK signaling pathway.	imatinib	82-90	protein tyrosine phosphatase non-receptor type 11	Homo sapiens	129-133
26839216-5	2016	A disruption of the SHP2-p85 complex took place after insulin/IGF1 stimulation or imatinib treatment, suggesting that the direct SHP2-p85 interaction was both independent of AKT activation and positively regulates the ERK signaling pathway.	imatinib	82-90	phosphoinositide-3-kinase regulatory subunit 2	Homo sapiens	134-137
26607903-0	2016	Perturbation of energy metabolism by fatty-acid derivative AIC-47 and imatinib in BCR-ABL-harboring leukemic cells.	imatinib	70-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
26607903-5	2016	Imatinib inhibited only the phosphorylation of BCR-ABL; whereas AIC-47 suppressed the expression of the protein itself.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
26607903-6	2016	Both AIC-47 and imatinib modulated the expression of pyruvate kinase M (PKM) isoforms from PKM2 to PKM1 through the down-regulation of polypyrimidine tract-binding protein 1 (PTBP1).	imatinib	16-24	pyruvate kinase M1/2	Homo sapiens	53-70
26607903-6	2016	Both AIC-47 and imatinib modulated the expression of pyruvate kinase M (PKM) isoforms from PKM2 to PKM1 through the down-regulation of polypyrimidine tract-binding protein 1 (PTBP1).	imatinib	16-24	pyruvate kinase M1/2	Homo sapiens	72-75
26607903-6	2016	Both AIC-47 and imatinib modulated the expression of pyruvate kinase M (PKM) isoforms from PKM2 to PKM1 through the down-regulation of polypyrimidine tract-binding protein 1 (PTBP1).	imatinib	16-24	pyruvate kinase M1/2	Homo sapiens	91-95
26607903-6	2016	Both AIC-47 and imatinib modulated the expression of pyruvate kinase M (PKM) isoforms from PKM2 to PKM1 through the down-regulation of polypyrimidine tract-binding protein 1 (PTBP1).	imatinib	16-24	polypyrimidine tract binding protein 1	Homo sapiens	135-173
26607903-6	2016	Both AIC-47 and imatinib modulated the expression of pyruvate kinase M (PKM) isoforms from PKM2 to PKM1 through the down-regulation of polypyrimidine tract-binding protein 1 (PTBP1).	imatinib	16-24	polypyrimidine tract binding protein 1	Homo sapiens	175-180
26607903-8	2016	Although inactivation of BCR-ABL by imatinib strongly suppressed glycolysis, compensatory fatty-acid oxidation (FAO) activation supported glucose-independent cell survival by up-regulating CPT1C, the rate-limiting FAO enzyme.	imatinib	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
26721343-0	2016	Imatinib reduces cholesterol uptake and matrix metalloproteinase activity in human THP-1 macrophages.	imatinib	0-8	GLI family zinc finger 2	Homo sapiens	83-88
25904380-3	2016	We found high levels of PKCE transcripts in Ph+ acute lymphoblastic leukemia (ALL) cells from patients and cell lines, and imatinib resistant chronic myeloid leukemia, which were also less responsive to imatinib-induced apoptosis than Ph+ cells with lower PKCE expression.	imatinib	203-211	protein kinase C epsilon	Homo sapiens	24-28
25904380-4	2016	Furthermore, the siRNA-mediated knockdown or peptide inhibition of PKCE in Ph+ cells increased imatinib-induced apoptosis while overexpression of PKCE reduced imatinib-induced apoptosis, with concomitant increase in the pro-survival factor AKT.	imatinib	95-103	protein kinase C epsilon	Homo sapiens	67-71
25904380-4	2016	Furthermore, the siRNA-mediated knockdown or peptide inhibition of PKCE in Ph+ cells increased imatinib-induced apoptosis while overexpression of PKCE reduced imatinib-induced apoptosis, with concomitant increase in the pro-survival factor AKT.	imatinib	159-167	protein kinase C epsilon	Homo sapiens	146-150
26708080-0	2016	Imatinib promotes apoptosis of giant cell tumor cells by targeting microRNA-30a-mediated runt-related transcription factor 2.	imatinib	0-8	microRNA 30a	Homo sapiens	67-79
26708080-0	2016	Imatinib promotes apoptosis of giant cell tumor cells by targeting microRNA-30a-mediated runt-related transcription factor 2.	imatinib	0-8	RUNX family transcription factor 2	Homo sapiens	89-124
26708080-7	2016	Results from the present study demonstrated that imatinib treatment inhibited cell viability, increased cell apoptosis, and significantly promoted caspase-3 and -9 activity in GCT.	imatinib	49-57	caspase 3	Homo sapiens	147-163
26708080-8	2016	In addition, imatinib treatment decreased the RunX2 protein expression level.	imatinib	13-21	RUNX family transcription factor 2	Homo sapiens	46-51
26708080-9	2016	Notably, imatinib was demonstrated to increase miR-30a expression.	imatinib	9-17	microRNA 30a	Homo sapiens	47-54
26708080-10	2016	However, upregulation of miR-30a expression reduced the RunX2 protein expression level, and downregulation of miR-30a expression reversed the anticancer effect of imatinib on GCT, increasing the expression level of RunX2 protein in GCT.	imatinib	163-171	microRNA 30a	Homo sapiens	110-117
26708080-10	2016	However, upregulation of miR-30a expression reduced the RunX2 protein expression level, and downregulation of miR-30a expression reversed the anticancer effect of imatinib on GCT, increasing the expression level of RunX2 protein in GCT.	imatinib	163-171	RUNX family transcription factor 2	Homo sapiens	215-220
26708080-11	2016	The results of the present study indicate that imatinib promotes apoptosis of GCT cells by targeting the miR-30a-mediated RunX2 signaling pathway.	imatinib	47-55	microRNA 30a	Homo sapiens	105-112
26708080-11	2016	The results of the present study indicate that imatinib promotes apoptosis of GCT cells by targeting the miR-30a-mediated RunX2 signaling pathway.	imatinib	47-55	RUNX family transcription factor 2	Homo sapiens	122-127
26721343-8	2016	Instead, we found that imatinib up-regulated microRNA 155 (miR155) by 43.8% and down-regulated ADAM metallopeptidase domain 28 (ADAM28) by 41.4%.	imatinib	23-31	microRNA 155	Homo sapiens	59-65
26721343-8	2016	Instead, we found that imatinib up-regulated microRNA 155 (miR155) by 43.8% and down-regulated ADAM metallopeptidase domain 28 (ADAM28) by 41.4%.	imatinib	23-31	ADAM metallopeptidase domain 28	Homo sapiens	95-126
26721343-8	2016	Instead, we found that imatinib up-regulated microRNA 155 (miR155) by 43.8% and down-regulated ADAM metallopeptidase domain 28 (ADAM28) by 41.4%.	imatinib	23-31	ADAM metallopeptidase domain 28	Homo sapiens	128-134
26721343-10	2016	CONCLUSION: Our results indicate that imatinib causes post-translational inhibition with respect to cholesterol uptake and regulation of MMP-2 and MMP-9.	imatinib	38-46	matrix metallopeptidase 2	Homo sapiens	137-142
26721343-10	2016	CONCLUSION: Our results indicate that imatinib causes post-translational inhibition with respect to cholesterol uptake and regulation of MMP-2 and MMP-9.	imatinib	38-46	matrix metallopeptidase 9	Homo sapiens	147-152
26758680-4	2016	Furthermore, we confirm that imatinib suppresses lung tumor growth in vivo, specifically in lung cancer cells harboring a gain-of-function (GOF) mutation in ABL1.	imatinib	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-161
26758680-7	2016	In summary, our results suggest that NSCLC patients with ABL1 mutations could be stratified for treatment with imatinib in combination with other therapies.	imatinib	111-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-61
26831735-0	2016	Secretion of IL-1beta from imatinib-resistant chronic myeloid leukemia cells contributes to BCR-ABL mutation-independent imatinib resistance.	imatinib	27-35	interleukin 1 beta	Homo sapiens	13-21
26831735-0	2016	Secretion of IL-1beta from imatinib-resistant chronic myeloid leukemia cells contributes to BCR-ABL mutation-independent imatinib resistance.	imatinib	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
26831735-0	2016	Secretion of IL-1beta from imatinib-resistant chronic myeloid leukemia cells contributes to BCR-ABL mutation-independent imatinib resistance.	imatinib	121-129	interleukin 1 beta	Homo sapiens	13-21
26831735-3	2016	Interleukin-1beta (IL-1beta) was more highly expressed in K562R than in the parental cell line K562S, and higher levels of IL-1beta contributed to the imatinib resistance of K562R.	imatinib	151-159	interleukin 1 beta	Homo sapiens	0-17
26831735-3	2016	Interleukin-1beta (IL-1beta) was more highly expressed in K562R than in the parental cell line K562S, and higher levels of IL-1beta contributed to the imatinib resistance of K562R.	imatinib	151-159	interleukin 1 beta	Homo sapiens	123-131
26721343-6	2016	Gel-based zymography showed that secretion and activity of MMP-2 and MMP-9 were inhibited by imatinib.	imatinib	93-101	matrix metallopeptidase 2	Homo sapiens	59-64
26721343-6	2016	Gel-based zymography showed that secretion and activity of MMP-2 and MMP-9 were inhibited by imatinib.	imatinib	93-101	matrix metallopeptidase 9	Homo sapiens	69-74
26815740-2	2016	Clinical resistance to the Bcr-Abl inhibitor imatinib is a critical problem in treating CML.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
26913392-0	2016	[Overexpression of SHP-1 Enhances the Sensitivity of K562 Cells to Imatinib].	imatinib	67-75	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	19-24
26913392-1	2016	OBJECTIVE: To explore the effect of overexpression of SH2-containing tyrosine phosphatase 1 (SHP-1) on sensitivity of chronic myelogenous 1eukemia (CML) K562 cell line to imatinib and its related mechamism.	imatinib	171-179	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	54-91
26913392-1	2016	OBJECTIVE: To explore the effect of overexpression of SH2-containing tyrosine phosphatase 1 (SHP-1) on sensitivity of chronic myelogenous 1eukemia (CML) K562 cell line to imatinib and its related mechamism.	imatinib	171-179	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	93-98
26913392-3	2016	The expression of SHP-1 in K562 cells treated with 0.2 micromol/L imatinib (IM) for 72 h was determined by Western blot.	imatinib	66-74	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	18-23
26371596-8	2016	The PDGF receptor tyrosine kinase inhibitor imatinib mesylate and a monoclonal antibody against PDGF receptor-alpha enhanced myocardial damage evidenced by serum cardiac troponin T release in the rat and mouse cardiac allografts 6 hours after reperfusion, respectively.	imatinib	44-61	platelet derived growth factor subunit B	Rattus norvegicus	4-8
26990482-4	2016	KIT is an established therapeutic target in cancers with activating mutations of KIT, such as gastrointestinal stromal tumors (GIST), and considerable efficacy has been achieved with various small molecule inhibitors of KIT including imatinib mesylate.	imatinib	234-251	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
26990482-4	2016	KIT is an established therapeutic target in cancers with activating mutations of KIT, such as gastrointestinal stromal tumors (GIST), and considerable efficacy has been achieved with various small molecule inhibitors of KIT including imatinib mesylate.	imatinib	234-251	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	81-84
26990482-4	2016	KIT is an established therapeutic target in cancers with activating mutations of KIT, such as gastrointestinal stromal tumors (GIST), and considerable efficacy has been achieved with various small molecule inhibitors of KIT including imatinib mesylate.	imatinib	234-251	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	81-84
26457546-2	2016	Imatinib mesylate is approved for the adjuvant treatment of KIT-positive gastrointestinal stromal tumor (GIST) following surgical resection.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	60-63
27467931-0	2016	BCR-ABL transcript variations in chronic phase chronic myelogenous leukemia patients on imatinib first-line: Possible role of the autologous immune system.	imatinib	88-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
26585829-1	2016	A convenient synthesis of imatinib, a potent inhibitor of ABL1 kinase and widely prescribed drug for the treatment of a variety of leukemias, was devised and applied to the construction of a series of novel imatinib analogues featuring a number of non-aromatic structural motifs in place of the parent molecule"s phenyl moiety.	imatinib	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-62
26585829-1	2016	A convenient synthesis of imatinib, a potent inhibitor of ABL1 kinase and widely prescribed drug for the treatment of a variety of leukemias, was devised and applied to the construction of a series of novel imatinib analogues featuring a number of non-aromatic structural motifs in place of the parent molecule"s phenyl moiety.	imatinib	207-215	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-62
27161125-8	2016	Additionally, imatinib enhanced the expression of C/EBPalpha in K562 cells compared with untreated cells (p < 0.05).	imatinib	14-22	CCAAT enhancer binding protein alpha	Homo sapiens	50-60
27161125-11	2016	Imatinib enhances the expression of C/EBPalpha in K562 cells, and the overexpression of C/EBPalpha inhibits cell proliferation and increases apoptosis via the Foxo3a-Bim pathway.	imatinib	0-8	CCAAT enhancer binding protein alpha	Homo sapiens	36-46
27161125-11	2016	Imatinib enhances the expression of C/EBPalpha in K562 cells, and the overexpression of C/EBPalpha inhibits cell proliferation and increases apoptosis via the Foxo3a-Bim pathway.	imatinib	0-8	forkhead box O3	Homo sapiens	159-165
26863882-0	2016	Cucurbitacin B Enhances the Anticancer Effect of Imatinib Mesylate Through Inhibition of MMP-2 Expression in MCF-7 and SW480 Tumor Cell Lines.	imatinib	49-66	matrix metallopeptidase 2	Homo sapiens	89-94
26587973-0	2016	KIT over-expression by p55PIK-PI3K leads to Imatinib-resistance in patients with gastrointestinal stromal tumors.	imatinib	44-52	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
26587973-0	2016	KIT over-expression by p55PIK-PI3K leads to Imatinib-resistance in patients with gastrointestinal stromal tumors.	imatinib	44-52	phosphoinositide-3-kinase regulatory subunit 3	Homo sapiens	23-29
26587973-1	2016	Imatinib is the first-line drug for gastrointestinal stromal tumors (GISTs), as mutated KIT is closely associated with the occurrence of GIST.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	88-91
26587973-5	2016	Furthermore, down-regulation of p55PIK significantly decreases KIT expression and re-sensitizes IMA-resistance-GIST cells to Imatinib in vitro and in vivo.	imatinib	125-133	phosphoinositide-3-kinase regulatory subunit 3	Homo sapiens	32-38
26757169-0	2016	Mitochondrial mutagenesis in BCR-ABL1-expressing cells sensitive and resistant to imatinib.	imatinib	82-90	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	33-37
26757169-1	2016	Imatinib revolutionized the treatment of chronic myeloid leukemia (CML) with the expression of the BCR-ABL1 tyrosine kinase, but imatinib resistance is an emerging problem.	imatinib	0-8	BCR activator of RhoGEF and GTPase	Mus musculus	99-107
26757169-2	2016	Imatinib can hinder the inhibitory effects of BCR-ABL1 on mitochondrial apoptotic pathway, so mitochondrial mutagenesis can be important for its action.	imatinib	0-8	BCR activator of RhoGEF and GTPase	Mus musculus	46-54
26757169-10	2016	In conclusion, some aspects of mtDNA mutagenesis, including sensitivity to oxidative stress and DNA repair can contribute to imatinib resistance in BCR-ABL1-expressing cells.	imatinib	125-133	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	152-156
27746819-0	2016	Myeloid Neoplasms with t(5;12) and ETV6-ACSL6 Gene Fusion, Potential Mimickers of Myeloid Neoplasm with PDGFRB Rearrangement: Case Report with Imatinib Therapy and Review of the Literature.	imatinib	143-151	ETS variant transcription factor 6	Homo sapiens	35-39
26428235-2	2016	Although targeted therapy involving tyrosine kinase inhibitors (TKIs) such as imatinib mesylate is highly effective for gastrointestinal stromal tumor carrying V560G c-kit mutation, it does not show much potential for targeting wild-type KIT (WT-KIT).	imatinib	78-95	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	166-171
26679828-0	2016	Knock-down of CIAPIN1 sensitizes K562 chronic myeloid leukemia cells to Imatinib by regulation of cell cycle and apoptosis-associated members via NF-kappaB and ERK5 signaling pathway.	imatinib	72-80	cytokine induced apoptosis inhibitor 1	Homo sapiens	14-21
26679828-0	2016	Knock-down of CIAPIN1 sensitizes K562 chronic myeloid leukemia cells to Imatinib by regulation of cell cycle and apoptosis-associated members via NF-kappaB and ERK5 signaling pathway.	imatinib	72-80	mitogen-activated protein kinase 7	Homo sapiens	160-164
26679828-3	2016	In this study, we found depletion of CIAPIN1 inhibited proliferation and triggered more apoptosis of K562CML (chronic myeloid leukemia) cells with or without Imatinib treatment.	imatinib	158-166	cytokine induced apoptosis inhibitor 1	Homo sapiens	37-44
26679828-5	2016	Importantly, treating CIAPIN1-depleted K562 cells with ERK5 signaling pathway specific inhibitor, XMD8-92, further inhibited proliferation and promoted apoptosis with or without Imatinib treatment.	imatinib	178-186	cytokine induced apoptosis inhibitor 1	Homo sapiens	22-29
26679828-8	2016	The nude mice transplantation model was also performed to confirm the enhanced sensitivity of CIAPIN1-depleted K562 cells to Imatinib.	imatinib	125-133	cytokine induced apoptosis inhibitor 1	Mus musculus	94-101
26679828-9	2016	Thus, our results provided a potential management by which CIAPIN1 knock-down might have a crucial impact on enhancing sensitivity of K562 cells to Imatinib in the therapeutic approaches, indicating that CIAPIN1 knock-down might serve as a combination with chemotherapeutical agents in leukemia diseases therapy.	imatinib	148-156	cytokine induced apoptosis inhibitor 1	Homo sapiens	59-66
26679828-9	2016	Thus, our results provided a potential management by which CIAPIN1 knock-down might have a crucial impact on enhancing sensitivity of K562 cells to Imatinib in the therapeutic approaches, indicating that CIAPIN1 knock-down might serve as a combination with chemotherapeutical agents in leukemia diseases therapy.	imatinib	148-156	cytokine induced apoptosis inhibitor 1	Homo sapiens	204-211
27648315-7	2016	This case, in conjunction with others in the literature, suggests a possible connection between t(4;5)(q21;q33) PRKG2/PDGFRB and systemic mastocytosis and highlights their favorable response to imatinib.	imatinib	194-202	protein kinase cGMP-dependent 2	Homo sapiens	112-117
27648315-7	2016	This case, in conjunction with others in the literature, suggests a possible connection between t(4;5)(q21;q33) PRKG2/PDGFRB and systemic mastocytosis and highlights their favorable response to imatinib.	imatinib	194-202	platelet derived growth factor receptor beta	Homo sapiens	118-124
27746819-0	2016	Myeloid Neoplasms with t(5;12) and ETV6-ACSL6 Gene Fusion, Potential Mimickers of Myeloid Neoplasm with PDGFRB Rearrangement: Case Report with Imatinib Therapy and Review of the Literature.	imatinib	143-151	acyl-CoA synthetase long chain family member 6	Homo sapiens	40-45
27746819-0	2016	Myeloid Neoplasms with t(5;12) and ETV6-ACSL6 Gene Fusion, Potential Mimickers of Myeloid Neoplasm with PDGFRB Rearrangement: Case Report with Imatinib Therapy and Review of the Literature.	imatinib	143-151	platelet derived growth factor receptor beta	Homo sapiens	104-110
27746819-1	2016	We report the second case of ETV6-ACSL6 associated myeloproliferative neoplasm that has received a full course of imatinib therapy.	imatinib	114-122	ETS variant transcription factor 6	Homo sapiens	29-33
27746819-1	2016	We report the second case of ETV6-ACSL6 associated myeloproliferative neoplasm that has received a full course of imatinib therapy.	imatinib	114-122	acyl-CoA synthetase long chain family member 6	Homo sapiens	34-39
26613118-8	2016	The average ICER per QALY for dasatinib- vs imatinib-initiating sequences is $100,000 for an imatinib-resistant population.	imatinib	44-52	cAMP responsive element modulator	Homo sapiens	12-16
27516199-10	2016	Considering that imatinib, a PDGF receptor inhibitor, entered the clinical trials for the treatment of pulmonary hypertension, the first patents were devoted to inhibitors of tyrosine kinase receptors, such as PDGFR and c-Kit.	imatinib	17-25	platelet derived growth factor receptor beta	Homo sapiens	210-215
27516199-10	2016	Considering that imatinib, a PDGF receptor inhibitor, entered the clinical trials for the treatment of pulmonary hypertension, the first patents were devoted to inhibitors of tyrosine kinase receptors, such as PDGFR and c-Kit.	imatinib	17-25	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	220-225
27580559-2	2016	Because specific rearrangements of the platelet-derived growth factor beta (PDGFB) locus by a novel fluorescence in situ hybridization method was detected, the patient was treated with imatinib mesylate at 400 mg/day.	imatinib	185-202	platelet derived growth factor subunit B	Homo sapiens	76-81
28253493-2	2016	The isoderivative chromosome 22, ider(22), and relative amplification or duplication of the BCR-ABL1 gene have been considered as one of the major reasons associated with the resistance to chemotherapy with imatinib mesylate, but the data remain unclear.	imatinib	207-224	BCR activator of RhoGEF and GTPase	Homo sapiens	92-100
26613118-8	2016	The average ICER per QALY for dasatinib- vs imatinib-initiating sequences is $100,000 for an imatinib-resistant population.	imatinib	93-101	cAMP responsive element modulator	Homo sapiens	12-16
26613118-9	2016	The average ICER per QALY for dasatinib- vs nilotinib-initiating sequences is $170,000 for an imatinib-resistant population, and $160,000 for an imatinib-intolerant population.	imatinib	94-102	cAMP responsive element modulator	Homo sapiens	12-16
26613118-9	2016	The average ICER per QALY for dasatinib- vs nilotinib-initiating sequences is $170,000 for an imatinib-resistant population, and $160,000 for an imatinib-intolerant population.	imatinib	145-153	cAMP responsive element modulator	Homo sapiens	12-16
26430910-0	2016	Imatinib discontinuation for hypereosinophilic syndrome harboring the FIP1L1-PDGFRA transcript.	imatinib	0-8	factor interacting with PAPOLA and CPSF1	Homo sapiens	70-76
26430910-0	2016	Imatinib discontinuation for hypereosinophilic syndrome harboring the FIP1L1-PDGFRA transcript.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	77-83
26765457-7	2016	The combination of WBC count at presentation and BCR-ABL(IS) at 3 months provides improved predictions of deep molecular response in imatinib-treated CML-CP patients.	imatinib	133-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
26510503-7	2016	c-Abl small interfering RNA (siRNA) and STI571 (c-Abl inhibitor) provided protection against Ang II-induced podocyte injury, suppressed the Ang II-induced c-Abl-SHIP2 interaction and SHIP2 phosphorylation, and maintained a stable level of nephrin phosphorylation.	imatinib	40-46	inositol polyphosphate phosphatase-like 1	Rattus norvegicus	161-166
27581134-3	2016	Tyrosine kinase inhibitors (TKIs), such as imatinib, are synthesized small molecules that primarily target BCR-ABL tyrosine kinases and have become a first-line treatment for CML.	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
26910070-2	2016	Imatinib mesylate (IM), a competitive inhibitor of BCR/ABL1 tyrosine kinase activity, is the current standard therapy for chronic myeloid leukaemia (CML) which is caused by the BCR/ABL1 gene fusion encoding a constitutively active tyrosine kinase.	imatinib	0-17	BCR activator of RhoGEF and GTPase	Homo sapiens	51-54
26910070-2	2016	Imatinib mesylate (IM), a competitive inhibitor of BCR/ABL1 tyrosine kinase activity, is the current standard therapy for chronic myeloid leukaemia (CML) which is caused by the BCR/ABL1 gene fusion encoding a constitutively active tyrosine kinase.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-59
26910070-2	2016	Imatinib mesylate (IM), a competitive inhibitor of BCR/ABL1 tyrosine kinase activity, is the current standard therapy for chronic myeloid leukaemia (CML) which is caused by the BCR/ABL1 gene fusion encoding a constitutively active tyrosine kinase.	imatinib	0-17	BCR activator of RhoGEF and GTPase	Homo sapiens	177-180
26910070-2	2016	Imatinib mesylate (IM), a competitive inhibitor of BCR/ABL1 tyrosine kinase activity, is the current standard therapy for chronic myeloid leukaemia (CML) which is caused by the BCR/ABL1 gene fusion encoding a constitutively active tyrosine kinase.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	181-185
26910070-2	2016	Imatinib mesylate (IM), a competitive inhibitor of BCR/ABL1 tyrosine kinase activity, is the current standard therapy for chronic myeloid leukaemia (CML) which is caused by the BCR/ABL1 gene fusion encoding a constitutively active tyrosine kinase.	imatinib	19-21	BCR activator of RhoGEF and GTPase	Homo sapiens	51-54
26910070-2	2016	Imatinib mesylate (IM), a competitive inhibitor of BCR/ABL1 tyrosine kinase activity, is the current standard therapy for chronic myeloid leukaemia (CML) which is caused by the BCR/ABL1 gene fusion encoding a constitutively active tyrosine kinase.	imatinib	19-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-59
26910070-2	2016	Imatinib mesylate (IM), a competitive inhibitor of BCR/ABL1 tyrosine kinase activity, is the current standard therapy for chronic myeloid leukaemia (CML) which is caused by the BCR/ABL1 gene fusion encoding a constitutively active tyrosine kinase.	imatinib	19-21	BCR activator of RhoGEF and GTPase	Homo sapiens	177-180
26910070-2	2016	Imatinib mesylate (IM), a competitive inhibitor of BCR/ABL1 tyrosine kinase activity, is the current standard therapy for chronic myeloid leukaemia (CML) which is caused by the BCR/ABL1 gene fusion encoding a constitutively active tyrosine kinase.	imatinib	19-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	181-185
26510503-7	2016	c-Abl small interfering RNA (siRNA) and STI571 (c-Abl inhibitor) provided protection against Ang II-induced podocyte injury, suppressed the Ang II-induced c-Abl-SHIP2 interaction and SHIP2 phosphorylation, and maintained a stable level of nephrin phosphorylation.	imatinib	40-46	angiotensinogen	Rattus norvegicus	93-99
26510503-7	2016	c-Abl small interfering RNA (siRNA) and STI571 (c-Abl inhibitor) provided protection against Ang II-induced podocyte injury, suppressed the Ang II-induced c-Abl-SHIP2 interaction and SHIP2 phosphorylation, and maintained a stable level of nephrin phosphorylation.	imatinib	40-46	angiotensinogen	Rattus norvegicus	140-146
26510503-7	2016	c-Abl small interfering RNA (siRNA) and STI571 (c-Abl inhibitor) provided protection against Ang II-induced podocyte injury, suppressed the Ang II-induced c-Abl-SHIP2 interaction and SHIP2 phosphorylation, and maintained a stable level of nephrin phosphorylation.	imatinib	40-46	inositol polyphosphate phosphatase-like 1	Rattus norvegicus	183-188
26510503-7	2016	c-Abl small interfering RNA (siRNA) and STI571 (c-Abl inhibitor) provided protection against Ang II-induced podocyte injury, suppressed the Ang II-induced c-Abl-SHIP2 interaction and SHIP2 phosphorylation, and maintained a stable level of nephrin phosphorylation.	imatinib	40-46	NPHS1 adhesion molecule, nephrin	Rattus norvegicus	239-246
26666578-10	2016	The presence of PDGFRA rearrangement in this case conferred a high sensitivity to imatinib treatment and a favorable clinical outcome.	imatinib	82-90	platelet derived growth factor receptor alpha	Homo sapiens	16-22
26779618-0	2016	Detecting Secondary C-KIT Mutations in the Peripheral Blood of Patients with Imatinib-Resistant Gastrointestinal Stromal Tumor.	imatinib	77-85	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	20-25
26779618-2	2016	Imatinib resistance is mostly caused by secondary mutations in C-KIT.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	63-68
26779618-9	2016	RESULTS: Imatinib-resistant lesions had single-nucleotide substitutions in C-KIT exon 13 in 3 patients and exon 18 in 1 patient.	imatinib	9-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	75-80
26779618-11	2016	One patient had growth of an imatinib-resistant tumor containing a C-KIT exon 13 mutation, and the fraction of ctDNA decreased after initiation of sunitinib.	imatinib	29-37	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	67-72
26721703-3	2016	CYP2C8 substrate drugs include amodiaquine, cerivastatin, dasabuvir, enzalutamide, imatinib, loperamide, montelukast, paclitaxel, pioglitazone, repaglinide, and rosiglitazone, and the number is increasing.	imatinib	83-91	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	0-6
26257279-0	2016	Imatinib Treatment in PDGFRA-Negative Childhood Hypereosinophilic Syndrome.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	22-28
26194865-8	2016	In order to provide another proof in favor of BIN1 and RIN1 endocytosis function in CML, we demonstrated that Imatinib induced, in K562 cell line, BIN1-RIN1 upregulation accompanied by a parallel AXL receptor internalization into cytoplasmic compartment.	imatinib	110-118	bridging integrator 1	Homo sapiens	46-50
26194865-8	2016	In order to provide another proof in favor of BIN1 and RIN1 endocytosis function in CML, we demonstrated that Imatinib induced, in K562 cell line, BIN1-RIN1 upregulation accompanied by a parallel AXL receptor internalization into cytoplasmic compartment.	imatinib	110-118	Ras and Rab interactor 1	Homo sapiens	55-59
26250462-0	2016	Concurrent effects of ABCB1 C3435T, ABCG2 C421A, and XRCC1 Arg194Trp genetic polymorphisms with risk of cancer, clinical output, and response to treatment with imatinib mesylate in patients with chronic myeloid leukemia.	imatinib	160-177	X-ray repair cross complementing 1	Homo sapiens	53-58
26194865-8	2016	In order to provide another proof in favor of BIN1 and RIN1 endocytosis function in CML, we demonstrated that Imatinib induced, in K562 cell line, BIN1-RIN1 upregulation accompanied by a parallel AXL receptor internalization into cytoplasmic compartment.	imatinib	110-118	bridging integrator 1	Homo sapiens	147-151
26250462-11	2016	Patients with CC421 ABCG2/TT3435 ABCB1 and CC421 ABCG2/TT27157 XRCC1 diplotypes might be at higher risk to rapid and severe development of CML and have weaker response to treatments with imatinib.	imatinib	187-195	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	20-25
26194865-8	2016	In order to provide another proof in favor of BIN1 and RIN1 endocytosis function in CML, we demonstrated that Imatinib induced, in K562 cell line, BIN1-RIN1 upregulation accompanied by a parallel AXL receptor internalization into cytoplasmic compartment.	imatinib	110-118	Ras and Rab interactor 1	Homo sapiens	152-156
26250462-11	2016	Patients with CC421 ABCG2/TT3435 ABCB1 and CC421 ABCG2/TT27157 XRCC1 diplotypes might be at higher risk to rapid and severe development of CML and have weaker response to treatments with imatinib.	imatinib	187-195	ATP binding cassette subfamily B member 1	Homo sapiens	33-38
26161459-0	2016	Impact of CYP2C8*3 polymorphism on in vitro metabolism of imatinib to N-desmethyl imatinib.	imatinib	58-66	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	10-16
26250462-11	2016	Patients with CC421 ABCG2/TT3435 ABCB1 and CC421 ABCG2/TT27157 XRCC1 diplotypes might be at higher risk to rapid and severe development of CML and have weaker response to treatments with imatinib.	imatinib	187-195	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	49-54
26250462-11	2016	Patients with CC421 ABCG2/TT3435 ABCB1 and CC421 ABCG2/TT27157 XRCC1 diplotypes might be at higher risk to rapid and severe development of CML and have weaker response to treatments with imatinib.	imatinib	187-195	X-ray repair cross complementing 1	Homo sapiens	63-68
26161459-15	2016	In conclusion, CYP2C8*3 is a gain-of-function polymorphism for imatinib N-demethylation, which appears to be mainly mediated by CYP2C8 and not CYP3A4 in vitro in HLM.	imatinib	63-71	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	15-21
26161459-15	2016	In conclusion, CYP2C8*3 is a gain-of-function polymorphism for imatinib N-demethylation, which appears to be mainly mediated by CYP2C8 and not CYP3A4 in vitro in HLM.	imatinib	63-71	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	128-134
26161459-15	2016	In conclusion, CYP2C8*3 is a gain-of-function polymorphism for imatinib N-demethylation, which appears to be mainly mediated by CYP2C8 and not CYP3A4 in vitro in HLM.	imatinib	63-71	oxysterol binding protein 2	Homo sapiens	162-165
26371140-2	2015	Imatinib, the first BCR-ABL1 TKI granted regulatory approval, has been surpassed in terms of molecular responses by the second-generation TKIs nilotinib, dasatinib, and bosutinib.	imatinib	0-8	BCR activator of RhoGEF and GTPase	Homo sapiens	20-28
26876246-0	2016	[Dasatinib treatment based on BCR- ABL mutation detection in imatinib- resistant patients with chronic myeloid leukemia].	imatinib	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-38
26705423-0	2015	Masked inv dup(22)(q11.23), tetrasomy 8 and trisomy 19 in a blast crisis-chronic myeloid leukemia after interrupted Imatinib-treatment.	imatinib	116-124	inversin	Homo sapiens	7-10
26500342-0	2015	KIR2DL5B genotype predicts outcomes in CML patients treated with response-directed sequential imatinib/nilotinib strategy.	imatinib	94-102	killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 5B	Homo sapiens	0-8
26415544-7	2015	Acidic extracellular pH greatly facilitated fluorescein uptake by all OATPs, and new molecular interactions were detected (between OATP2B1 and Imatinib, OATP3A1, 5A1 and 6A1 and estradiol 17-beta-d-glucuronide, and OATP1C1 and 4C1 and prostaglandin E2).	imatinib	143-151	solute carrier organic anion transporter family member 2B1	Homo sapiens	131-138
26408910-5	2015	Expression of BEX1 controls cell surface receptor signaling and restores imatinib response in resistant cells.	imatinib	73-81	brain expressed X-linked 1	Homo sapiens	14-18
26642944-3	2015	Inhibition kinetic profiles of a panel of UGT enzymes (UGT1A1, 1A3, 1A4, 1A6, 1A7, 1A8, 1A9, 1A10, 2B4, 2B7, 2B15, and 2B17) by four TKIs (axitinib, imatinib, lapatinib and vandetanib) were characterized by using hepatic microsomes and recombinant proteins.	imatinib	149-157	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	42-45
25791792-0	2015	Prognostic Relevance of p53 Overexpression in Gastrointestinal Stromal Tumors of the Small Intestine: Potential Implication for Adjuvant Treatment with Imatinib.	imatinib	152-160	tumor protein p53	Homo sapiens	24-27
26562217-1	2015	Despite the success of imatinib at inhibiting Bcr-Abl and treating chronic myelogenous leukemia (CML), resistance to the therapy occurs over time in patients.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
26562217-2	2015	In particular, the resistance to imatinib caused by the gatekeeper mutation T315I in Bcr-Abl remains a challenge in the clinic.	imatinib	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
26642944-5	2015	Imatinib was found to exhibit broad inhibition on several UGTs, particularly potent competitive inhibition against UGT2B17 with a Ki of 0.4 muM.	imatinib	0-8	UDP glucuronosyltransferase family 2 member B17	Homo sapiens	115-122
26642944-6	2015	The TKIs also exerted intermediate inhibition against several UGTs (i.e., UGT1A7 by lapatinib; UGT1A1 by imatinib; UGT1A4, 1A7 and 1A9 by axitinib; and UGT1A9 by vandetanib).	imatinib	105-113	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	95-101
26642944-7	2015	Results from modeling for the quantitative prediction of DDI risk indicated that the coadministration of lapatinib or imatinib at clinical doses could result in a significant increase in AUC of drugs primarily cleared by UGT1A1 or 2B17.	imatinib	118-126	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	221-227
26642944-8	2015	Lapatinib and imatinib may cause clinically significant DDIs when co-administered UGT1A1 or 2B17 substrates.	imatinib	14-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	82-88
26456889-0	2015	Inhibition of crosstalk between Bcr-Abl and PKC signaling by PEITC, augments imatinib sensitivity in chronic myelogenous leukemia cells.	imatinib	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
26456889-0	2015	Inhibition of crosstalk between Bcr-Abl and PKC signaling by PEITC, augments imatinib sensitivity in chronic myelogenous leukemia cells.	imatinib	77-85	protein kinase C alpha	Homo sapiens	44-47
26432864-5	2015	Imatinib significantly decreased bronchoalveolar lavage protein, total cells, neutrophils, and TNF-alpha levels in mice exposed to LPS plus VILI, indicating that it attenuates ALI in this clinically relevant model.	imatinib	0-8	tumor necrosis factor	Mus musculus	95-104
26779374-5	2015	In recent years, imatinib, a PDGFbetaR, ABL and KIT inhibitor, has revolutionized systemic therapy in DFSP.	imatinib	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-43
26460262-7	2015	Among genes linked to the inhibition of cellular proliferation by BCR-ABL inhibitor Imatinib, the FOS and STAT1 demonstrated significantly decreased expression in CML.	imatinib	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
26460262-7	2015	Among genes linked to the inhibition of cellular proliferation by BCR-ABL inhibitor Imatinib, the FOS and STAT1 demonstrated significantly decreased expression in CML.	imatinib	84-92	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	98-101
26460262-7	2015	Among genes linked to the inhibition of cellular proliferation by BCR-ABL inhibitor Imatinib, the FOS and STAT1 demonstrated significantly decreased expression in CML.	imatinib	84-92	signal transducer and activator of transcription 1	Homo sapiens	106-111
26546461-0	2015	A study to explore the correlation of ABCB1, ABCG2, OCT1 genetic polymorphisms and trough level concentration with imatinib mesylate-induced thrombocytopenia in chronic myeloid leukemia patients.	imatinib	115-132	ATP binding cassette subfamily B member 1	Homo sapiens	38-43
26546461-0	2015	A study to explore the correlation of ABCB1, ABCG2, OCT1 genetic polymorphisms and trough level concentration with imatinib mesylate-induced thrombocytopenia in chronic myeloid leukemia patients.	imatinib	115-132	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	45-50
26779374-5	2015	In recent years, imatinib, a PDGFbetaR, ABL and KIT inhibitor, has revolutionized systemic therapy in DFSP.	imatinib	17-25	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	48-51
26546461-0	2015	A study to explore the correlation of ABCB1, ABCG2, OCT1 genetic polymorphisms and trough level concentration with imatinib mesylate-induced thrombocytopenia in chronic myeloid leukemia patients.	imatinib	115-132	solute carrier family 22 member 1	Homo sapiens	52-56
26546461-3	2015	The present study was framed to explore the influence of common drug transporter gene polymorphisms of ABCB1, ABCG2, OCT1 and trough level concentration on commonly occurring adverse events in CML patients treated with imatinib mesylate.	imatinib	219-236	ATP binding cassette subfamily B member 1	Homo sapiens	103-108
26404639-2	2015	While myeloid/lymphoid neoplasms with eosinophilia and rearrangement of PDGFRA or PDGFRB exhibit exquisite responsiveness to imatinib, other eosinophilic disorders such as chronic eosinophilic leukemia--not otherwise specified (CEL-NOS) and idiopathic hypereosinophilic syndrome (HES) lack recurrent gene mutations or known druggable targets.	imatinib	125-133	platelet derived growth factor receptor alpha	Homo sapiens	72-78
26546461-3	2015	The present study was framed to explore the influence of common drug transporter gene polymorphisms of ABCB1, ABCG2, OCT1 and trough level concentration on commonly occurring adverse events in CML patients treated with imatinib mesylate.	imatinib	219-236	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	110-115
26546461-3	2015	The present study was framed to explore the influence of common drug transporter gene polymorphisms of ABCB1, ABCG2, OCT1 and trough level concentration on commonly occurring adverse events in CML patients treated with imatinib mesylate.	imatinib	219-236	solute carrier family 22 member 1	Homo sapiens	117-121
26321052-0	2015	ABL SH3 mutant inhibits BCR-ABL activity and increases imatinib sensitivity by targeting RIN1 protein in CML cell.	imatinib	55-63	Ras and Rab interactor 1	Homo sapiens	89-93
26404639-2	2015	While myeloid/lymphoid neoplasms with eosinophilia and rearrangement of PDGFRA or PDGFRB exhibit exquisite responsiveness to imatinib, other eosinophilic disorders such as chronic eosinophilic leukemia--not otherwise specified (CEL-NOS) and idiopathic hypereosinophilic syndrome (HES) lack recurrent gene mutations or known druggable targets.	imatinib	125-133	platelet derived growth factor receptor beta	Homo sapiens	82-88
26202934-3	2015	Upon imatinib inhibition of BCR-ABL1 kinase activity, beta-catenin expression was maintained in intrinsically resistant cells grown in suspension culture and sensitive cells cultured in direct contact (DC) with bone marrow (BM) stromal cells.	imatinib	5-13	BCR activator of RhoGEF and GTPase	Homo sapiens	28-36
26730054-27	2015	Tyrosine kinase receptor (KIT) inhibitor like imatinib is used for adjuvant treatment.	imatinib	46-54	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	26-29
26819809-4	2015	C-kit-negative GISTs could be treated by complete resection and/or imatinib, which is the same treatment for c-kit-positive GISTs.	imatinib	67-75	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-5
26644081-0	2015	Synergistic cytotoxicity from combination of imatinib and platinum-based anticancer drugs specifically in Bcr-Abl positive leukemia cells.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
26644081-1	2015	Imatinib, a multitargeted tyrosine kinase inhibitor, exhibits potent anticancer activity against leukemia harboring the Bcr-Abl oncogene and some solid tumors overexpressing c-kit and PDGFR.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
26644081-1	2015	Imatinib, a multitargeted tyrosine kinase inhibitor, exhibits potent anticancer activity against leukemia harboring the Bcr-Abl oncogene and some solid tumors overexpressing c-kit and PDGFR.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	174-179
26644081-1	2015	Imatinib, a multitargeted tyrosine kinase inhibitor, exhibits potent anticancer activity against leukemia harboring the Bcr-Abl oncogene and some solid tumors overexpressing c-kit and PDGFR.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	184-189
26644081-3	2015	In this study, we showed that combination of imatinib with platinum (Pt)-based anticancer agents, including cisplatin and oxaliplatin, exhibited synergistic cytotoxic effect specifically in Bcr-Abl+ human chronic myeloid leukemia cell line K562 but not in Bcr-Abl- RPMI8226 cells.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	190-197
26644081-3	2015	In this study, we showed that combination of imatinib with platinum (Pt)-based anticancer agents, including cisplatin and oxaliplatin, exhibited synergistic cytotoxic effect specifically in Bcr-Abl+ human chronic myeloid leukemia cell line K562 but not in Bcr-Abl- RPMI8226 cells.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	256-263
25684098-0	2015	Molecular changes associated with the development of resistance to imatinib in an imatinib-sensitive canine neoplastic mast cell line carrying a KIT c.1523A>T mutation.	imatinib	67-75	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	145-148
25684098-0	2015	Molecular changes associated with the development of resistance to imatinib in an imatinib-sensitive canine neoplastic mast cell line carrying a KIT c.1523A>T mutation.	imatinib	82-90	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	145-148
25684098-4	2015	Both sublines had a second KIT mutation c.2443G>C. Recombinant KIT with the second mutation was insensitive to 1 muM but sensitive to 10 muM imatinib.	imatinib	144-152	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	66-69
25684098-5	2015	The effect of imatinib on the phosphorylation of KIT and its downstream signalling proteins was then examined using these sublines.	imatinib	14-22	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	49-52
25684098-6	2015	KIT and ERK were constitutively phosphorylated in both sublines, and their phosphorylation was suppressed by 10 muM imatinib in rVI-MC1 cells.	imatinib	116-124	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	0-3
25684098-9	2015	This second mutation in KIT may play an important role in imatinib resistance in neoplastic mast cells.	imatinib	58-66	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	24-27
25684098-10	2015	Furthermore, KIT/SFK-independent activation of ERK would be involved in imatinib resistance when the neoplastic cells are exposed to higher concentrations of imatinib.	imatinib	72-80	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	13-16
25684098-10	2015	Furthermore, KIT/SFK-independent activation of ERK would be involved in imatinib resistance when the neoplastic cells are exposed to higher concentrations of imatinib.	imatinib	158-166	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	13-16
26072665-3	2015	As with indolent systemic mastocytosis (SM), treatment of MCAS focuses more against MC mediators than MC neoplasia, but some cases prove refractory even to the TK inhibitor (TKI) imatinib reported useful both in uncommon SM cases not bearing SM"s usual imatinib-resistant KIT-D816V mutation and in some cases of MCAS (which rarely bears KIT-D816V).	imatinib	179-187	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	272-275
26072665-3	2015	As with indolent systemic mastocytosis (SM), treatment of MCAS focuses more against MC mediators than MC neoplasia, but some cases prove refractory even to the TK inhibitor (TKI) imatinib reported useful both in uncommon SM cases not bearing SM"s usual imatinib-resistant KIT-D816V mutation and in some cases of MCAS (which rarely bears KIT-D816V).	imatinib	179-187	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	337-340
26202934-3	2015	Upon imatinib inhibition of BCR-ABL1 kinase activity, beta-catenin expression was maintained in intrinsically resistant cells grown in suspension culture and sensitive cells cultured in direct contact (DC) with bone marrow (BM) stromal cells.	imatinib	5-13	catenin beta 1	Homo sapiens	54-66
26576593-2	2015	BACKGROUND: Imatinib mesylate, a potent inhibitor of the KIT and PDGFR tyrosine kinases, is highly effective in the treatment of advanced gastrointestinal stromal tumors (GISTs).	imatinib	12-29	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	57-60
26576593-5	2015	We postulated combination therapy with imatinib plus bevacizumab would benefit patients with advanced GIST, particularly those reliant on VEGFA-dependent angiogenesis.	imatinib	39-47	vascular endothelial growth factor A	Homo sapiens	138-143
26695912-0	2015	Assessment of response to imatinib therapy in patients with chronic myeloid leukemia with e13a2 and e14a2 transcripts of BCR/ABL1 gene.	imatinib	26-34	BCR activator of RhoGEF and GTPase	Homo sapiens	121-124
26695912-0	2015	Assessment of response to imatinib therapy in patients with chronic myeloid leukemia with e13a2 and e14a2 transcripts of BCR/ABL1 gene.	imatinib	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-129
26695912-1	2015	OBJECTIVE: Assess the influence of e13a2 and e14a2 transcripts of BCR/ABL1 gene on the efficiency of imatinib ther apy in patients with chronic myeloid leukemia.	imatinib	101-109	BCR activator of RhoGEF and GTPase	Homo sapiens	66-69
26695912-1	2015	OBJECTIVE: Assess the influence of e13a2 and e14a2 transcripts of BCR/ABL1 gene on the efficiency of imatinib ther apy in patients with chronic myeloid leukemia.	imatinib	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-74
26571380-8	2015	The tyrosine kinase inhibitors, Imatinib Mesylate and Sorafenib showed significant inhibitory effects on proliferation of both mucin- and mixed-IHCCA.	imatinib	32-49	LOC100508689	Homo sapiens	127-132
26423566-0	2015	Characteristics of the TCR Vbeta repertoire in imatinib-resistant chronic myeloid leukemia patients with ABL mutations.	imatinib	47-55	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	23-26
26423566-0	2015	Characteristics of the TCR Vbeta repertoire in imatinib-resistant chronic myeloid leukemia patients with ABL mutations.	imatinib	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-108
26423566-4	2015	In this study, we investigated the distribution and clonality of the TCR Vbeta repertoire in 4 cases with imatinib-resistant CML in blast crisis (BC-CML) with abelson murine leukemia viral oncogene homolog 1 (ABL1) kinase domain mutations (KDMs).	imatinib	106-114	T cell receptor alpha variable 6-3	Mus musculus	69-72
26423566-4	2015	In this study, we investigated the distribution and clonality of the TCR Vbeta repertoire in 4 cases with imatinib-resistant CML in blast crisis (BC-CML) with abelson murine leukemia viral oncogene homolog 1 (ABL1) kinase domain mutations (KDMs).	imatinib	106-114	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	209-213
26634458-1	2015	Our study aimed to investigate the association between multidrug resistance (MDR1) gene polymorphisms and the response to imatinib (IM) in chronic myeloid leukemia (CML).	imatinib	122-130	ATP binding cassette subfamily B member 1	Homo sapiens	77-81
26501568-1	2015	The emergence of drug resistance of the BCR-ABL kinase inhibitor imatinib, especially toward the T315I gatekeeper mutation, poses a great challenge to targeted therapy in treating chronic myeloid leukemia (CML) patients.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-47
26706012-6	2015	Data driven from in vitro and animal studies on the merlin pathway allowed biologically targeted treatment strategies (employing Lapatinib, Erlotinib, Everolimus, Picropodophyllin, OSU.03012, Imatinib, Sorafenib, and Bevacizumab) aimed at multiple tumor shrinkage or regression or both and tumor arrest of progression with functional improvement.	imatinib	192-200	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	52-58
26606374-1	2015	Due to its inhibition of the Abl kinase domain in the BCR-ABL fusion protein, imatinib is strikingly effective in the initial stage of chronic myeloid leukemia with more than 90% of the patients showing complete remission.	imatinib	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-32
26606374-1	2015	Due to its inhibition of the Abl kinase domain in the BCR-ABL fusion protein, imatinib is strikingly effective in the initial stage of chronic myeloid leukemia with more than 90% of the patients showing complete remission.	imatinib	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
26447228-7	2015	In addition, Sos1- or Abl-silenced macrophages, or macrophages treated with the selective Abl inhibitor imatinib mesylate had a reduced capability to migrate into breast tumor spheroids, the majority of cells remaining at the margin and the outer layers of the spheroid itself.	imatinib	104-121	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	90-93
26434776-2	2015	From 11 880 phosphorylation sites, we confirm that H929 cells are primarily signaling through the BCR-ABL-ERK pathway, and we show that imatinib treatment not only downregulates phosphosites in this pathway but also upregulates phosphosites on proteins involved in RNA expression.	imatinib	136-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
26434776-2	2015	From 11 880 phosphorylation sites, we confirm that H929 cells are primarily signaling through the BCR-ABL-ERK pathway, and we show that imatinib treatment not only downregulates phosphosites in this pathway but also upregulates phosphosites on proteins involved in RNA expression.	imatinib	136-144	mitogen-activated protein kinase 1	Homo sapiens	106-109
26434776-3	2015	Metabolomics analyses reveal that BCR-ABL-ERK signaling in H929 cells drives the pentose phosphate pathway (PPP) and RNA biosynthesis, where pathway inhibition via imatinib results in marked PPP impairment and an accumulation of RNA nucleotides and negative regulation of mRNA.	imatinib	164-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
26434776-3	2015	Metabolomics analyses reveal that BCR-ABL-ERK signaling in H929 cells drives the pentose phosphate pathway (PPP) and RNA biosynthesis, where pathway inhibition via imatinib results in marked PPP impairment and an accumulation of RNA nucleotides and negative regulation of mRNA.	imatinib	164-172	mitogen-activated protein kinase 1	Homo sapiens	42-45
26178713-2	2015	HIV patients with chronic myeloid leukemia or gastrointestinal stromal tumour may need imatinib, a CYP3A4 substrate with known exposure response-relationships.	imatinib	87-95	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	99-105
26283036-3	2015	We now report on a retrospective series of PDGFB/PDGFRB positive advanced chordoma patients treated with imatinib as a single agent within a compassionate-use programme at Istituto Nazionale Tumori, Milan, Italy (INT) between August 2002 and November 2010, when the programme was closed.	imatinib	105-113	platelet derived growth factor subunit B	Homo sapiens	43-48
26283036-3	2015	We now report on a retrospective series of PDGFB/PDGFRB positive advanced chordoma patients treated with imatinib as a single agent within a compassionate-use programme at Istituto Nazionale Tumori, Milan, Italy (INT) between August 2002 and November 2010, when the programme was closed.	imatinib	105-113	platelet derived growth factor receptor beta	Homo sapiens	49-55
28031906-2	2015	Mutually exclusive KIT and PDGFRA mutations are central events in GIST pathogenesis, and their understanding is crucial because specific treatment targeting oncogenic KIT and PDGFRA activation (especially imatinib) has become available.	imatinib	205-213	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	19-22
25941032-0	2015	Novel fusion between the breakpoint cluster region and platelet-derived growth factor receptor-alpha genes in a patient with chronic myeloid leukemia-like neoplasm: undetectable residual disease after imatinib therapy.	imatinib	201-209	platelet derived growth factor receptor alpha	Homo sapiens	55-100
25941032-4	2015	The design of a specific quantitative PCR assay to monitor the molecular response during treatment with imatinib, a multitargeted tyrosine kinase inhibitor (TKI) with activity against ABL, c-Kit, and PDGFRA revealed an outstanding disease control with durably undetectable BCR-PDGFRA transcripts.	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	184-187
25941032-4	2015	The design of a specific quantitative PCR assay to monitor the molecular response during treatment with imatinib, a multitargeted tyrosine kinase inhibitor (TKI) with activity against ABL, c-Kit, and PDGFRA revealed an outstanding disease control with durably undetectable BCR-PDGFRA transcripts.	imatinib	104-112	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	189-194
25941032-4	2015	The design of a specific quantitative PCR assay to monitor the molecular response during treatment with imatinib, a multitargeted tyrosine kinase inhibitor (TKI) with activity against ABL, c-Kit, and PDGFRA revealed an outstanding disease control with durably undetectable BCR-PDGFRA transcripts.	imatinib	104-112	platelet derived growth factor receptor alpha	Homo sapiens	200-206
25941032-4	2015	The design of a specific quantitative PCR assay to monitor the molecular response during treatment with imatinib, a multitargeted tyrosine kinase inhibitor (TKI) with activity against ABL, c-Kit, and PDGFRA revealed an outstanding disease control with durably undetectable BCR-PDGFRA transcripts.	imatinib	104-112	BCR activator of RhoGEF and GTPase	Homo sapiens	273-276
25941032-4	2015	The design of a specific quantitative PCR assay to monitor the molecular response during treatment with imatinib, a multitargeted tyrosine kinase inhibitor (TKI) with activity against ABL, c-Kit, and PDGFRA revealed an outstanding disease control with durably undetectable BCR-PDGFRA transcripts.	imatinib	104-112	platelet derived growth factor receptor alpha	Homo sapiens	277-283
28031906-2	2015	Mutually exclusive KIT and PDGFRA mutations are central events in GIST pathogenesis, and their understanding is crucial because specific treatment targeting oncogenic KIT and PDGFRA activation (especially imatinib) has become available.	imatinib	205-213	platelet derived growth factor receptor alpha	Homo sapiens	27-33
28031906-2	2015	Mutually exclusive KIT and PDGFRA mutations are central events in GIST pathogenesis, and their understanding is crucial because specific treatment targeting oncogenic KIT and PDGFRA activation (especially imatinib) has become available.	imatinib	205-213	platelet derived growth factor receptor alpha	Homo sapiens	175-181
28031906-3	2015	The most frequent PDGFRA mutation (D842V) is associated with primary resistance to imatinib.	imatinib	83-91	platelet derived growth factor receptor alpha	Homo sapiens	18-24
26554155-2	2015	Specific inhibitors against BCR-ABL, such as Imatinib mesylate (IM), have greatly improved CML management; however, no single agent is a cure yet.	imatinib	45-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
26074249-0	2015	Imatinib mesylate treatment in a dog with gastrointestinal stromal tumors with a c-kit mutation.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	81-86
26355082-9	2015	The use of imatinib or dasatinib as a c-Kit inhibitor reduced the level of sphere-forming cells in culture.	imatinib	11-19	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	38-43
27294449-0	2015	C1236T polymorphism in MDR1 gene correlates with therapeutic response to imatinib mesylate in Indian patients with chronic myeloid leukaemia.	imatinib	73-90	ATP binding cassette subfamily B member 1	Homo sapiens	23-27
27294449-4	2015	We therefore studied three polymorphisms (C1236T, G2677T and C3435T) in the human multidrug-resistance gene (MDR1) in 86 patients with chronic myeloid leukaemia treated with imatinib.	imatinib	174-182	ATP binding cassette subfamily B member 1	Homo sapiens	109-113
27294449-7	2015	In conclusion, determination of C1236T MDR1 genotype may help to predict response to imatinib therapy in patients with chronic myeloid leukaemia.	imatinib	85-93	ATP binding cassette subfamily B member 1	Homo sapiens	39-43
26473951-4	2015	We found that KOSR protects CML cells from killing by BCR-ABL inhibitors--imatinib, dasatinib and nilotinib.	imatinib	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
26620257-0	2015	The tyrosine kinase inhibitor imatinib prevents lung injury and death after intravenous LPS in mice.	imatinib	30-38	toll-like receptor 4	Mus musculus	88-91
26620257-5	2015	In the present study, we tested the hypothesis that imatinib would protect against lung injury and systemic inflammation caused by intravenous LPS in an intact mouse model of endotoxemia mimicking early sepsis.	imatinib	52-60	toll-like receptor 4	Mus musculus	143-146
26620257-8	2015	However, pretreatment of mice with imatinib increased lung catalase activity and decreased intravenous LPS-induced lung oxidant injury as measured by gamma-H2AX, a marker of oxidant-induced DNA damage, lung apoptosis, and pulmonary edema.	imatinib	35-43	toll-like receptor 4	Mus musculus	103-106
26620257-8	2015	However, pretreatment of mice with imatinib increased lung catalase activity and decreased intravenous LPS-induced lung oxidant injury as measured by gamma-H2AX, a marker of oxidant-induced DNA damage, lung apoptosis, and pulmonary edema.	imatinib	35-43	H2A.X variant histone	Mus musculus	150-160
26620257-9	2015	Imatinib also attenuated systemic cytokine expression after intravenous LPS exposure.	imatinib	0-8	toll-like receptor 4	Mus musculus	72-75
26620257-10	2015	Finally, imatinib completely prevented mortality in an in vivo, intravenous LPS mouse model of endotoxemia and lung injury.	imatinib	9-17	toll-like receptor 4	Mus musculus	76-79
26375673-3	2015	Our data demonstrate that PIM inhibition enhances the effects of imatinib mesylate on Ph+ leukemia cells.	imatinib	65-82	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	26-29
26375673-4	2015	We also found that PIM inhibition results in suppression of leukemic cell proliferation and induction of apoptosis of Ph+ leukemia cells, including those resistant to imatinib mesylate.	imatinib	167-184	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	19-22
26474484-7	2015	Furthermore, the pro-survival and pro-migratory effects of SCF were augmented by c-kit overexpression and abrogated by c-kit inhibition with imatinib.	imatinib	141-149	KIT ligand	Homo sapiens	59-62
26474484-7	2015	Furthermore, the pro-survival and pro-migratory effects of SCF were augmented by c-kit overexpression and abrogated by c-kit inhibition with imatinib.	imatinib	141-149	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	119-124
26486351-8	2015	Identification of rearranged PDGFRA or PDGFRB is critical because of the exquisite responsiveness of these diseases to imatinib.	imatinib	119-127	platelet derived growth factor receptor alpha	Homo sapiens	29-35
26486351-8	2015	Identification of rearranged PDGFRA or PDGFRB is critical because of the exquisite responsiveness of these diseases to imatinib.	imatinib	119-127	platelet derived growth factor receptor beta	Homo sapiens	39-45
26473951-6	2015	In KOSR-protected CML cells, imatinib still inhibited the BCR-ABL tyrosine kinase, reduced the phosphorylation of STAT, ERK and AKT, down-regulated BCL2, BCLxL, MCL1 and up-regulated BIM.	imatinib	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
26473951-6	2015	In KOSR-protected CML cells, imatinib still inhibited the BCR-ABL tyrosine kinase, reduced the phosphorylation of STAT, ERK and AKT, down-regulated BCL2, BCLxL, MCL1 and up-regulated BIM.	imatinib	29-37	mitogen-activated protein kinase 1	Homo sapiens	120-123
26473951-6	2015	In KOSR-protected CML cells, imatinib still inhibited the BCR-ABL tyrosine kinase, reduced the phosphorylation of STAT, ERK and AKT, down-regulated BCL2, BCLxL, MCL1 and up-regulated BIM.	imatinib	29-37	AKT serine/threonine kinase 1	Homo sapiens	128-131
26473951-6	2015	In KOSR-protected CML cells, imatinib still inhibited the BCR-ABL tyrosine kinase, reduced the phosphorylation of STAT, ERK and AKT, down-regulated BCL2, BCLxL, MCL1 and up-regulated BIM.	imatinib	29-37	BCL2 apoptosis regulator	Homo sapiens	148-152
26473951-6	2015	In KOSR-protected CML cells, imatinib still inhibited the BCR-ABL tyrosine kinase, reduced the phosphorylation of STAT, ERK and AKT, down-regulated BCL2, BCLxL, MCL1 and up-regulated BIM.	imatinib	29-37	BCL2 like 1	Homo sapiens	154-159
26473951-6	2015	In KOSR-protected CML cells, imatinib still inhibited the BCR-ABL tyrosine kinase, reduced the phosphorylation of STAT, ERK and AKT, down-regulated BCL2, BCLxL, MCL1 and up-regulated BIM.	imatinib	29-37	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	161-165
26300393-0	2015	Genetic variations of hOCT1 gene and CYP3A4/A5 genes and their association with imatinib response in Chronic Myeloid Leukemia.	imatinib	80-88	solute carrier family 22 member 1	Homo sapiens	22-27
26500491-4	2015	In this study we examine the efficacy for the treatment of TBI of an FDA approved antagonist of the PDGFRalpha, Imatinib.	imatinib	112-120	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	100-110
26300393-0	2015	Genetic variations of hOCT1 gene and CYP3A4/A5 genes and their association with imatinib response in Chronic Myeloid Leukemia.	imatinib	80-88	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	37-43
26300393-1	2015	There is an increasing body of evidence demonstrating that mechanisms independent of BCR/ABL gene also contribute to imatinib resistance in Chronic Myeloid Leukemia (CML).	imatinib	117-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
26178642-7	2015	Patients losing molecular remission (two consecutive positive Q-RT-PCR with at least 1 BCR-ABL1/ABL1 value above 0.1%) resumed imatinib.	imatinib	127-135	BCR activator of RhoGEF and GTPase	Homo sapiens	87-95
26099262-1	2015	Imatinib has been identified as a tyrosine kinase inhibitor that selectively inhibits the Abl tyrosine kinases, including Bcr-Abl.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
26186064-2	2015	Our current studies have shown that metformin suppresses cell viability, induces apoptosis, and downregulates the mTORC1 signaling pathway both in the Ph+ALL cell line and primary blasts from Ph+ ALL patients, as well as the CML cell lines K562 (imatinib-sensitive) and K562R (imatinib-resistance).	imatinib	246-254	CREB regulated transcription coactivator 1	Mus musculus	114-120
26186064-2	2015	Our current studies have shown that metformin suppresses cell viability, induces apoptosis, and downregulates the mTORC1 signaling pathway both in the Ph+ALL cell line and primary blasts from Ph+ ALL patients, as well as the CML cell lines K562 (imatinib-sensitive) and K562R (imatinib-resistance).	imatinib	277-285	CREB regulated transcription coactivator 1	Mus musculus	114-120
26186064-3	2015	We have also shown that metformin activates the ERK pathway in Ph+ALL cells, SUP-B15, a side effect that can be overcome by U0126 (MEK1/2 inhibitor) or imatinib.	imatinib	152-160	mitogen-activated protein kinase 1	Homo sapiens	48-51
26298495-0	2015	Expanding the structural diversity of Bcr-Abl inhibitors: Hybrid molecules based on GNF-2 and Imatinib.	imatinib	94-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
26217035-9	2015	Recruitment of JunB to the p21 promoter was promoted by Adriamycin stimulation and was further enhanced by co-treatment with the c-Abl inhibitor imatinib.	imatinib	145-153	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	15-19
26217035-9	2015	Recruitment of JunB to the p21 promoter was promoted by Adriamycin stimulation and was further enhanced by co-treatment with the c-Abl inhibitor imatinib.	imatinib	145-153	H3 histone pseudogene 16	Homo sapiens	27-30
26217035-9	2015	Recruitment of JunB to the p21 promoter was promoted by Adriamycin stimulation and was further enhanced by co-treatment with the c-Abl inhibitor imatinib.	imatinib	145-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-134
25182956-0	2015	KIT and BRAF heterogeneous mutations in gastrointestinal stromal tumors after secondary imatinib resistance.	imatinib	88-96	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
26359456-0	2015	Implication of the Autologous Immune System in BCR-ABL Transcript Variations in Chronic Myelogenous Leukemia Patients Treated with Imatinib.	imatinib	131-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
26359456-3	2015	In analyzing our patients" data, we found that many patients who otherwise responded well to imatinib therapy still showed variations in their BCR-ABL transcripts.	imatinib	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-150
26359456-9	2015	Thus, the autologous immune response may explain the oscillations in BCR-ABL transcripts regularly observed in patients on imatinib.	imatinib	123-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
26428302-11	2015	Only in NESH/Abi-3-expressed cells did treatment with an Abl kinase inhibitor, imatinib mesylate, or siRNA-mediated knockdown of c-Abl promote the formation of invadopodia, which are ventral membrane protrusions with extracellular matrix degradation activity.	imatinib	79-96	ABI family member 3	Mus musculus	8-12
26428302-11	2015	Only in NESH/Abi-3-expressed cells did treatment with an Abl kinase inhibitor, imatinib mesylate, or siRNA-mediated knockdown of c-Abl promote the formation of invadopodia, which are ventral membrane protrusions with extracellular matrix degradation activity.	imatinib	79-96	ABI family member 3	Mus musculus	13-18
26622510-5	2015	The present study describes the case of a patient with imatinib-resistant CML who, following two months of treatment with nilotinib, no longer exhibited detectable BCR-ABL fusion genes or M244V mutations.	imatinib	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	164-171
26464823-0	2015	Association of The Common CYP1A1*2C Variant (Ile462Val Polymorphism) with Chronic Myeloid Leukemia (CML) in Patients Undergoing Imatinib Therapy.	imatinib	128-136	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	26-32
26464823-3	2015	The objective of this study was to investigate the risk factors associated with the CYP1A1*2C [rs1048943: A>G] polymorphism in CML patients and its role in therapeutic response to imatinib mesylate (IM) affecting clinico-pathological parameters, in the Indian population.	imatinib	183-200	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	84-90
26628884-5	2015	To our knowledge, this report is the first showing the value of imatinib in the management of ks in the context of long-lasting hiv control with adequate quantitative CD4 recovery.	imatinib	64-72	CD4 molecule	Homo sapiens	167-170
25182956-0	2015	KIT and BRAF heterogeneous mutations in gastrointestinal stromal tumors after secondary imatinib resistance.	imatinib	88-96	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	8-12
25182956-4	2015	The most frequent mechanism of imatinib resistance in GIST is the acquisition of secondary mutations in either KIT or PDGFRA.	imatinib	31-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	111-114
25182956-4	2015	The most frequent mechanism of imatinib resistance in GIST is the acquisition of secondary mutations in either KIT or PDGFRA.	imatinib	31-39	platelet derived growth factor receptor alpha	Homo sapiens	118-124
25182956-9	2015	RESULTS: The imatinib-resistant tumor showed not only heterogeneous mutations of KIT and BRAF besides the primary mutation, but also transdifferentiation into a rhabdomyosarcoma phenotype.	imatinib	13-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	81-84
25182956-9	2015	RESULTS: The imatinib-resistant tumor showed not only heterogeneous mutations of KIT and BRAF besides the primary mutation, but also transdifferentiation into a rhabdomyosarcoma phenotype.	imatinib	13-21	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	89-93
25182956-10	2015	According to Western blot analysis, in imatinib-resistant GIST with both KIT V559D and BRAF V600E mutations, the inhibition of KIT V559D by imatinib caused a strong decrease of AKT phosphorylation, while ERK1/2 phosphorylation was not affected.	imatinib	39-47	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
25182956-10	2015	According to Western blot analysis, in imatinib-resistant GIST with both KIT V559D and BRAF V600E mutations, the inhibition of KIT V559D by imatinib caused a strong decrease of AKT phosphorylation, while ERK1/2 phosphorylation was not affected.	imatinib	39-47	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	87-91
25182956-10	2015	According to Western blot analysis, in imatinib-resistant GIST with both KIT V559D and BRAF V600E mutations, the inhibition of KIT V559D by imatinib caused a strong decrease of AKT phosphorylation, while ERK1/2 phosphorylation was not affected.	imatinib	39-47	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	127-130
25182956-10	2015	According to Western blot analysis, in imatinib-resistant GIST with both KIT V559D and BRAF V600E mutations, the inhibition of KIT V559D by imatinib caused a strong decrease of AKT phosphorylation, while ERK1/2 phosphorylation was not affected.	imatinib	39-47	AKT serine/threonine kinase 1	Homo sapiens	177-180
25182956-10	2015	According to Western blot analysis, in imatinib-resistant GIST with both KIT V559D and BRAF V600E mutations, the inhibition of KIT V559D by imatinib caused a strong decrease of AKT phosphorylation, while ERK1/2 phosphorylation was not affected.	imatinib	39-47	mitogen-activated protein kinase 3	Homo sapiens	204-210
25182956-10	2015	According to Western blot analysis, in imatinib-resistant GIST with both KIT V559D and BRAF V600E mutations, the inhibition of KIT V559D by imatinib caused a strong decrease of AKT phosphorylation, while ERK1/2 phosphorylation was not affected.	imatinib	140-148	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
25182956-10	2015	According to Western blot analysis, in imatinib-resistant GIST with both KIT V559D and BRAF V600E mutations, the inhibition of KIT V559D by imatinib caused a strong decrease of AKT phosphorylation, while ERK1/2 phosphorylation was not affected.	imatinib	140-148	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	87-91
25182956-10	2015	According to Western blot analysis, in imatinib-resistant GIST with both KIT V559D and BRAF V600E mutations, the inhibition of KIT V559D by imatinib caused a strong decrease of AKT phosphorylation, while ERK1/2 phosphorylation was not affected.	imatinib	140-148	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	127-130
25182956-10	2015	According to Western blot analysis, in imatinib-resistant GIST with both KIT V559D and BRAF V600E mutations, the inhibition of KIT V559D by imatinib caused a strong decrease of AKT phosphorylation, while ERK1/2 phosphorylation was not affected.	imatinib	140-148	AKT serine/threonine kinase 1	Homo sapiens	177-180
25182956-10	2015	According to Western blot analysis, in imatinib-resistant GIST with both KIT V559D and BRAF V600E mutations, the inhibition of KIT V559D by imatinib caused a strong decrease of AKT phosphorylation, while ERK1/2 phosphorylation was not affected.	imatinib	140-148	mitogen-activated protein kinase 3	Homo sapiens	204-210
26722383-11	2015	IMC-G4 cells had an additional novel c-kit gene mutation of KIT-Tyr421Cys which is considered to induce neoplastic transformation of mouse mast cells and the mutation appeared to be resistant to a KIT inhibitor of imatinib but sensitive to another KIT inhibitor of nilotinib.	imatinib	214-222	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	37-42
26722383-11	2015	IMC-G4 cells had an additional novel c-kit gene mutation of KIT-Tyr421Cys which is considered to induce neoplastic transformation of mouse mast cells and the mutation appeared to be resistant to a KIT inhibitor of imatinib but sensitive to another KIT inhibitor of nilotinib.	imatinib	214-222	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	60-63
26716078-1	2015	In this case report, we describe a refractory CMML case without eosinophilia harboring a PDGFRB rearrangement leading to a favorable response with imatinib.	imatinib	147-155	platelet derived growth factor receptor beta	Homo sapiens	89-95
26072332-0	2015	Expression of the ETS transcription factor GABPalpha is positively correlated to the BCR-ABL1/ABL1 ratio in CML patients and affects imatinib sensitivity in vitro.	imatinib	133-141	GA binding protein transcription factor subunit alpha	Homo sapiens	43-52
26072332-0	2015	Expression of the ETS transcription factor GABPalpha is positively correlated to the BCR-ABL1/ABL1 ratio in CML patients and affects imatinib sensitivity in vitro.	imatinib	133-141	BCR activator of RhoGEF and GTPase	Homo sapiens	85-93
26072332-0	2015	Expression of the ETS transcription factor GABPalpha is positively correlated to the BCR-ABL1/ABL1 ratio in CML patients and affects imatinib sensitivity in vitro.	imatinib	133-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-93
26072332-1	2015	In Philadelphia-positive chronic myeloid leukemia (CML), imatinib resistance frequently emerges because of point mutations in the ABL1 kinase domain, but may also be the consequence of uncontrolled upstream signaling.	imatinib	57-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-134
26072332-5	2015	In functional studies, imatinib sensitivity is enhanced after GABPalpha knockdown in tyrosine kinase inhibitors (TKI)-sensitive K-562, as well as by overexpression of a deletion mutant in TKI-resistant NALM-1 cells.	imatinib	23-31	GA binding protein transcription factor subunit alpha	Homo sapiens	62-71
26122430-2	2015	The human organic cation transporter 1 (OCT1; SLC22A1) has been reported to be the main influx transporter involved in imatinib uptake into CML cells.	imatinib	119-127	solute carrier family 22 member 1	Homo sapiens	10-38
26122430-2	2015	The human organic cation transporter 1 (OCT1; SLC22A1) has been reported to be the main influx transporter involved in imatinib uptake into CML cells.	imatinib	119-127	solute carrier family 22 member 1	Homo sapiens	40-44
26122430-2	2015	The human organic cation transporter 1 (OCT1; SLC22A1) has been reported to be the main influx transporter involved in imatinib uptake into CML cells.	imatinib	119-127	solute carrier family 22 member 1	Homo sapiens	46-53
26122430-3	2015	Furthermore, variation in the efficiency of imatinib influx via OCT1 has been demonstrated to result in the inter-patient variation observed in primary response to imatinib.	imatinib	44-52	solute carrier family 22 member 1	Homo sapiens	64-68
26122430-3	2015	Furthermore, variation in the efficiency of imatinib influx via OCT1 has been demonstrated to result in the inter-patient variation observed in primary response to imatinib.	imatinib	164-172	solute carrier family 22 member 1	Homo sapiens	64-68
26122430-5	2015	Measuring both OCT1 mRNA levels and the functional activity of OCT1 in primary leukaemic cells has been demonstrated to predict molecular response and outcome in imatinib-treated CP-CML patients in several independent studies.	imatinib	162-170	solute carrier family 22 member 1	Homo sapiens	15-19
26122430-5	2015	Measuring both OCT1 mRNA levels and the functional activity of OCT1 in primary leukaemic cells has been demonstrated to predict molecular response and outcome in imatinib-treated CP-CML patients in several independent studies.	imatinib	162-170	solute carrier family 22 member 1	Homo sapiens	63-67
26458439-1	2015	The ABL tyrosine kinase inhibitor (TKI) imatinib mesylate has dramatically changed the treatment of chronic myeloid leukemia (CML).	imatinib	40-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
26458439-4	2015	Notably, point mutations within the ABL kinase domain are the most critical cause of imatinib resistance.	imatinib	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-39
26477768-0	2015	[Treatment of adult acute lymphoblastie leukemia with eosinophilia and abnormality of PDGFRA by autologous hematopoietic stem cell transplantation and imatinib: one case report and literatures review].	imatinib	151-159	platelet derived growth factor receptor alpha	Homo sapiens	86-92
26881646-5	2015	Deletion of the TP53 gene may be a major contributing factor in the development of resistance to imatinib and blast crisis.	imatinib	97-105	tumor protein p53	Homo sapiens	16-20
26248946-0	2015	Silencing of miR-21 sensitizes CML CD34+ stem/progenitor cells to imatinib-induced apoptosis by blocking PI3K/AKT pathway.	imatinib	66-74	microRNA 21	Homo sapiens	13-19
26248946-0	2015	Silencing of miR-21 sensitizes CML CD34+ stem/progenitor cells to imatinib-induced apoptosis by blocking PI3K/AKT pathway.	imatinib	66-74	CD34 molecule	Homo sapiens	35-39
26248946-0	2015	Silencing of miR-21 sensitizes CML CD34+ stem/progenitor cells to imatinib-induced apoptosis by blocking PI3K/AKT pathway.	imatinib	66-74	AKT serine/threonine kinase 1	Homo sapiens	110-113
26248946-2	2015	Here, we showed that transient inhibition of miR-21 by antagomiR-21 markedly increased imatinib-induced apoptosis in CML, but not normal CD34+ stem/progenitor cells.	imatinib	87-95	microRNA 21	Homo sapiens	45-51
26248946-3	2015	Furthermore, PI3K inhibitors also significantly sensitized CML CD34+ cells to imatinib-induced apoptosis.	imatinib	78-86	CD34 molecule	Homo sapiens	63-67
26248946-4	2015	MiR-21 or PI3K inhibitor in combination with imatinib treatment significantly decreased AKT phosphorylation and c-Myc expression than either agent did alone, but did not affect Bim and Bcl-6 expresssion.	imatinib	45-53	AKT serine/threonine kinase 1	Homo sapiens	88-91
26248946-4	2015	MiR-21 or PI3K inhibitor in combination with imatinib treatment significantly decreased AKT phosphorylation and c-Myc expression than either agent did alone, but did not affect Bim and Bcl-6 expresssion.	imatinib	45-53	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	112-117
26248946-5	2015	These findings indicate that miR-21 is required for maintaining the imatinib-resistant phenotype of CML CD34+ cells through PI3K/AKT signaling pathway, thus providing the basis for a promising therapeutic approach to eliminate CML LSCs.	imatinib	68-76	microRNA 21	Homo sapiens	29-35
26248946-5	2015	These findings indicate that miR-21 is required for maintaining the imatinib-resistant phenotype of CML CD34+ cells through PI3K/AKT signaling pathway, thus providing the basis for a promising therapeutic approach to eliminate CML LSCs.	imatinib	68-76	CD34 molecule	Homo sapiens	104-108
26248946-5	2015	These findings indicate that miR-21 is required for maintaining the imatinib-resistant phenotype of CML CD34+ cells through PI3K/AKT signaling pathway, thus providing the basis for a promising therapeutic approach to eliminate CML LSCs.	imatinib	68-76	AKT serine/threonine kinase 1	Homo sapiens	129-132
26320177-3	2015	Here we demonstrate that ZNF224 gene expression is down-regulated both in BCR-ABL positive cell lines and in primary CML samples and is restored after imatinib and second generation tyrosine kinase inhibitors treatment.	imatinib	151-159	zinc finger protein 224	Homo sapiens	25-31
26320177-5	2015	Finally, we report that ZNF224 is significantly down-regulated in patients with BCR-ABL positive chronic phase-CML showing poor response or resistance to imatinib treatment as compared to high-responder patients.	imatinib	154-162	zinc finger protein 224	Homo sapiens	24-30
26320177-5	2015	Finally, we report that ZNF224 is significantly down-regulated in patients with BCR-ABL positive chronic phase-CML showing poor response or resistance to imatinib treatment as compared to high-responder patients.	imatinib	154-162	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
26617858-9	2015	As compared with the control (GIST-R cells without any treatment), the expression levels of p-mTOR and Bcl-2 proteins of GIST-R cells in combination of Peg-IFNalpha-2b and imatinib group were decreased (P<0.01).	imatinib	172-180	mechanistic target of rapamycin kinase	Homo sapiens	94-98
26401097-2	2015	Initial developments in this field go back to the early 80s, but the success story really started with the selective BCR-ABL inhibitor, imatinib.	imatinib	136-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
26117541-0	2015	Integrative genomic analysis in K562 chronic myelogenous leukemia cells reveals that proximal NCOR1 binding positively regulates genes that govern erythroid differentiation and Imatinib sensitivity.	imatinib	177-185	nuclear receptor corepressor 1	Homo sapiens	94-99
26117541-5	2015	A matrix of gene and drug interactions built on NCI-60 data identified that Imatinib significantly targeted the NCOR1 governed transcriptome.	imatinib	76-84	nuclear receptor corepressor 1	Homo sapiens	112-117
26117541-6	2015	Stable knockdown of NCOR1 in K562 cells slowed growth and significantly repressed genes associated with NCOR1 cistrome, again, with the GO terms acetylation and ETS binding, and significantly dampened sensitivity to Imatinib-induced erythroid differentiation.	imatinib	216-224	nuclear receptor corepressor 1	Homo sapiens	20-25
26117541-7	2015	Mining public microarray data revealed that NCOR1-targeted genes were significantly enriched in Imatinib response gene signatures in cell lines and chronic myelogenous leukemia (CML) patients.	imatinib	96-104	nuclear receptor corepressor 1	Homo sapiens	44-49
26117541-8	2015	These approaches integrated cistrome, transcriptome and drug sensitivity relationships to reveal that NCOR1 function is surprisingly most associated with elevated gene expression, and that these targets, both in CML cell lines and patients, associate with sensitivity to Imatinib.	imatinib	271-279	nuclear receptor corepressor 1	Homo sapiens	102-107
26562280-3	2015	The advent of new treatment options for NF1 such as topical vitamin D3 analogues, lovastatin, rapamycin (or sirolimus), and imatinib mesylate has added new dimensions that require further investigation to provide the greatest benefit to patients.	imatinib	124-141	neurofibromin 1	Homo sapiens	40-43
26331539-7	2015	Imatinib mesylate and other tyrosine kinase inhibitors (TKIs) that target the kinase activity of BCR-ABL have improved patient survival markedly.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
26026391-7	2015	Some mice were given the RTK inhibitor imatinib after injection of cancer cells; tumor growth was measured based on bioluminescence.	imatinib	39-47	ret proto-oncogene	Homo sapiens	25-28
26026391-15	2015	Imatinib inhibited growth of KIT(+) colon cancer organoids in culture and growth of xenograft tumors in mice.	imatinib	0-8	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	29-32
26067856-5	2015	RESULTS: Sunitinib, which targets the imatinib-inhibited tyrosine kinases of VEGFR, KIT, PDGFR, and FLT-3, was without effect in COV434 and KGN cell lines.	imatinib	38-46	kinase insert domain receptor	Homo sapiens	77-82
26067856-5	2015	RESULTS: Sunitinib, which targets the imatinib-inhibited tyrosine kinases of VEGFR, KIT, PDGFR, and FLT-3, was without effect in COV434 and KGN cell lines.	imatinib	38-46	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	84-87
26067856-5	2015	RESULTS: Sunitinib, which targets the imatinib-inhibited tyrosine kinases of VEGFR, KIT, PDGFR, and FLT-3, was without effect in COV434 and KGN cell lines.	imatinib	38-46	platelet derived growth factor receptor beta	Homo sapiens	89-94
26067856-5	2015	RESULTS: Sunitinib, which targets the imatinib-inhibited tyrosine kinases of VEGFR, KIT, PDGFR, and FLT-3, was without effect in COV434 and KGN cell lines.	imatinib	38-46	fms related receptor tyrosine kinase 3	Homo sapiens	100-105
26617858-9	2015	As compared with the control (GIST-R cells without any treatment), the expression levels of p-mTOR and Bcl-2 proteins of GIST-R cells in combination of Peg-IFNalpha-2b and imatinib group were decreased (P<0.01).	imatinib	172-180	BCL2 apoptosis regulator	Homo sapiens	103-108
26118315-0	2015	BCR-ABL1 mutation development during first-line treatment with dasatinib or imatinib for chronic myeloid leukemia in chronic phase.	imatinib	76-84	BCR activator of RhoGEF and GTPase	Homo sapiens	0-8
25985771-0	2015	Predicting Effectiveness of Imatinib Mesylate in Tumors Expressing Platelet-Derived Growth Factors (PDGF-AA, PDGF-BB), Stem Cell Factor Ligands and Their Respective Receptors (PDGFR-alpha, PDGFR-beta, and c-kit).	imatinib	28-45	platelet derived growth factor receptor alpha	Homo sapiens	176-187
25985771-0	2015	Predicting Effectiveness of Imatinib Mesylate in Tumors Expressing Platelet-Derived Growth Factors (PDGF-AA, PDGF-BB), Stem Cell Factor Ligands and Their Respective Receptors (PDGFR-alpha, PDGFR-beta, and c-kit).	imatinib	28-45	platelet derived growth factor receptor beta	Homo sapiens	189-199
25985771-0	2015	Predicting Effectiveness of Imatinib Mesylate in Tumors Expressing Platelet-Derived Growth Factors (PDGF-AA, PDGF-BB), Stem Cell Factor Ligands and Their Respective Receptors (PDGFR-alpha, PDGFR-beta, and c-kit).	imatinib	28-45	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	205-210
25985771-1	2015	INTRODUCTION: This research aims to optimize and predict the effectiveness of imatinib mesylate (imatinib) in tumors expressing platelet-derived growth factors (PDGF-AA, BB), kit/stem cell factor (SCF) ligands and their respective receptors (PDGFR-alpha, PDGFR-beta, and c-kit).	imatinib	78-95	KIT ligand	Homo sapiens	179-195
25985771-1	2015	INTRODUCTION: This research aims to optimize and predict the effectiveness of imatinib mesylate (imatinib) in tumors expressing platelet-derived growth factors (PDGF-AA, BB), kit/stem cell factor (SCF) ligands and their respective receptors (PDGFR-alpha, PDGFR-beta, and c-kit).	imatinib	78-95	KIT ligand	Homo sapiens	197-200
25985771-1	2015	INTRODUCTION: This research aims to optimize and predict the effectiveness of imatinib mesylate (imatinib) in tumors expressing platelet-derived growth factors (PDGF-AA, BB), kit/stem cell factor (SCF) ligands and their respective receptors (PDGFR-alpha, PDGFR-beta, and c-kit).	imatinib	78-95	platelet derived growth factor receptor alpha	Homo sapiens	242-253
25985771-1	2015	INTRODUCTION: This research aims to optimize and predict the effectiveness of imatinib mesylate (imatinib) in tumors expressing platelet-derived growth factors (PDGF-AA, BB), kit/stem cell factor (SCF) ligands and their respective receptors (PDGFR-alpha, PDGFR-beta, and c-kit).	imatinib	78-95	platelet derived growth factor receptor beta	Homo sapiens	255-265
25985771-1	2015	INTRODUCTION: This research aims to optimize and predict the effectiveness of imatinib mesylate (imatinib) in tumors expressing platelet-derived growth factors (PDGF-AA, BB), kit/stem cell factor (SCF) ligands and their respective receptors (PDGFR-alpha, PDGFR-beta, and c-kit).	imatinib	78-95	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	271-276
25985771-1	2015	INTRODUCTION: This research aims to optimize and predict the effectiveness of imatinib mesylate (imatinib) in tumors expressing platelet-derived growth factors (PDGF-AA, BB), kit/stem cell factor (SCF) ligands and their respective receptors (PDGFR-alpha, PDGFR-beta, and c-kit).	imatinib	78-86	KIT ligand	Homo sapiens	179-195
25985771-1	2015	INTRODUCTION: This research aims to optimize and predict the effectiveness of imatinib mesylate (imatinib) in tumors expressing platelet-derived growth factors (PDGF-AA, BB), kit/stem cell factor (SCF) ligands and their respective receptors (PDGFR-alpha, PDGFR-beta, and c-kit).	imatinib	78-86	KIT ligand	Homo sapiens	197-200
25985771-1	2015	INTRODUCTION: This research aims to optimize and predict the effectiveness of imatinib mesylate (imatinib) in tumors expressing platelet-derived growth factors (PDGF-AA, BB), kit/stem cell factor (SCF) ligands and their respective receptors (PDGFR-alpha, PDGFR-beta, and c-kit).	imatinib	78-86	platelet derived growth factor receptor alpha	Homo sapiens	242-253
25985771-1	2015	INTRODUCTION: This research aims to optimize and predict the effectiveness of imatinib mesylate (imatinib) in tumors expressing platelet-derived growth factors (PDGF-AA, BB), kit/stem cell factor (SCF) ligands and their respective receptors (PDGFR-alpha, PDGFR-beta, and c-kit).	imatinib	78-86	platelet derived growth factor receptor beta	Homo sapiens	255-265
25985771-1	2015	INTRODUCTION: This research aims to optimize and predict the effectiveness of imatinib mesylate (imatinib) in tumors expressing platelet-derived growth factors (PDGF-AA, BB), kit/stem cell factor (SCF) ligands and their respective receptors (PDGFR-alpha, PDGFR-beta, and c-kit).	imatinib	78-86	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	271-276
25985771-9	2015	CONCLUSION: The effect of imatinib is transient and reversible, reduces tyrosine phosphorylation of tumor-derived PDGFR-alpha, PDGFR-beta, and c-kit without affecting their levels of expression.	imatinib	26-34	platelet derived growth factor receptor alpha	Homo sapiens	114-125
25985771-9	2015	CONCLUSION: The effect of imatinib is transient and reversible, reduces tyrosine phosphorylation of tumor-derived PDGFR-alpha, PDGFR-beta, and c-kit without affecting their levels of expression.	imatinib	26-34	platelet derived growth factor receptor beta	Homo sapiens	127-137
25985771-9	2015	CONCLUSION: The effect of imatinib is transient and reversible, reduces tyrosine phosphorylation of tumor-derived PDGFR-alpha, PDGFR-beta, and c-kit without affecting their levels of expression.	imatinib	26-34	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	143-148
25985771-11	2015	Tumors of PDGF-AA/PDGFR-alpha exhibit significant resistance to imatinib which requires administering imatinib three times a day, whereas resistance of tumors of PDGF-BB/PDGFR-beta or KIT-positive is relatively lower which requires administering imatinib two times a day only to produce an actual inhibition 100 % identical to that predicted for tumor growth.	imatinib	64-72	platelet derived growth factor receptor alpha	Homo sapiens	18-29
25985771-11	2015	Tumors of PDGF-AA/PDGFR-alpha exhibit significant resistance to imatinib which requires administering imatinib three times a day, whereas resistance of tumors of PDGF-BB/PDGFR-beta or KIT-positive is relatively lower which requires administering imatinib two times a day only to produce an actual inhibition 100 % identical to that predicted for tumor growth.	imatinib	102-110	platelet derived growth factor receptor alpha	Homo sapiens	18-29
25985771-11	2015	Tumors of PDGF-AA/PDGFR-alpha exhibit significant resistance to imatinib which requires administering imatinib three times a day, whereas resistance of tumors of PDGF-BB/PDGFR-beta or KIT-positive is relatively lower which requires administering imatinib two times a day only to produce an actual inhibition 100 % identical to that predicted for tumor growth.	imatinib	102-110	platelet derived growth factor receptor alpha	Homo sapiens	18-29
26118315-1	2015	BCR-ABL1 mutations are a common, well-characterized mechanism of resistance to imatinib as first-line treatment of chronic myeloid leukemia in chronic phase (CML-CP).	imatinib	79-87	BCR activator of RhoGEF and GTPase	Homo sapiens	0-8
26108972-1	2015	The intracellular uptake and retention (IUR) of imatinib is reported to be controlled by the influx transporter SLC22A1 (organic cation transporter 1).	imatinib	48-56	solute carrier family 22 member 1	Homo sapiens	112-119
26108972-1	2015	The intracellular uptake and retention (IUR) of imatinib is reported to be controlled by the influx transporter SLC22A1 (organic cation transporter 1).	imatinib	48-56	solute carrier family 22 member 1	Homo sapiens	121-149
25953263-0	2015	Revealing genome-wide mRNA and microRNA expression patterns in leukemic cells highlighted "hsa-miR-2278" as a tumor suppressor for regain of chemotherapeutic imatinib response due to targeting STAT5A.	imatinib	158-166	microRNA 2278	Homo sapiens	95-103
25953263-3	2015	In this study, we aimed to determine differing genome-wide microRNA (miRNA) and messenger RNA (mRNA) expression profiles in imatinib resistant (K562/IMA-3 muM) and parental cells by targeting STAT5A via small interfering RNA (siRNA) applications.	imatinib	124-132	signal transducer and activator of transcription 5A	Homo sapiens	192-198
25953263-0	2015	Revealing genome-wide mRNA and microRNA expression patterns in leukemic cells highlighted "hsa-miR-2278" as a tumor suppressor for regain of chemotherapeutic imatinib response due to targeting STAT5A.	imatinib	158-166	signal transducer and activator of transcription 5A	Homo sapiens	193-199
25953263-8	2015	This study provides new insights in discovering the mechanism of imatinib resistance due to upregulating the tumor-suppressor hsa-miR-2278 which stands for a functional therapeutic approach, inhibited leukemic cell proliferation, induced apoptosis, and regain of chemotherapeutic drug response in CML therapy.	imatinib	65-73	microRNA 2278	Homo sapiens	130-138
26317515-0	2015	Ribavirin Inhibits the Activity of mTOR/eIF4E, ERK/Mnk1/eIF4E Signaling Pathway and Synergizes with Tyrosine Kinase Inhibitor Imatinib to Impair Bcr-Abl Mediated Proliferation and Apoptosis in Ph+ Leukemia.	imatinib	126-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-152
26316776-0	2015	Inactivity of imatinib in gastrointestinal stromal tumors (GISTs) harboring a KIT activation-loop domain mutation (exon 17 mutation pN822K).	imatinib	14-22	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	78-81
26290562-11	2015	On evaluation, he was found to be BCR-ABL positive and responded well to imatinib treatment.	imatinib	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
26316776-2	2015	Imatinib mesylate is an oral small molecular tyrosine kinase inhibitor that mainly targets abl, c-KIT, and PDGFRalpha.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-94
26316776-2	2015	Imatinib mesylate is an oral small molecular tyrosine kinase inhibitor that mainly targets abl, c-KIT, and PDGFRalpha.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	96-101
26316776-2	2015	Imatinib mesylate is an oral small molecular tyrosine kinase inhibitor that mainly targets abl, c-KIT, and PDGFRalpha.	imatinib	0-17	platelet derived growth factor receptor alpha	Homo sapiens	107-117
26316776-7	2015	In this article, we focus on a case of a patient suffering from GIST, harboring an extremely rare KIT activation-loop domain mutation (exon 17 mutation pN822K) treated with imatinib.	imatinib	173-181	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	98-101
25417705-7	2015	In CML, Cks1 expression was increased, and treatment with the Abl kinase inhibitor, imatinib, reduced Cks1 expression.	imatinib	84-92	CDC28 protein kinase regulatory subunit 1B pseudogene 7	Homo sapiens	102-106
26279306-1	2015	This is the largest Latin American study of BCR-ABL mutations in chronic myeloid leukemia (CML) patients, resistant to imatinib (IM).	imatinib	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
26147296-0	2015	Adiponectin enhances Imatinib anti-tumour activity in human chronic myeloid leukaemia cells with serum levels associated with Imatinib efficacy in early chronic phase patients.	imatinib	21-29	adiponectin, C1Q and collagen domain containing	Homo sapiens	0-11
26251899-0	2015	UV Differentially Induces Oxidative Stress, DNA Damage and Apoptosis in BCR-ABL1-Positive Cells Sensitive and Resistant to Imatinib.	imatinib	123-131	BCR activator of RhoGEF and GTPase	Homo sapiens	72-80
26251899-1	2015	Chronic myeloid leukemia (CML) cells express the active BCR-ABL1 protein, which has been targeted by imatinib in CML therapy, but resistance to this drug is an emerging problem.	imatinib	101-109	BCR activator of RhoGEF and GTPase	Homo sapiens	56-64
26251899-2	2015	BCR-ABL1 induces endogenous oxidative stress promoting genomic instability and imatinib resistance.	imatinib	79-87	BCR activator of RhoGEF and GTPase	Homo sapiens	0-8
26251899-3	2015	In the present work, we investigated the extent of oxidative stress, DNA damage, apoptosis and expression of apoptosis-related genes in BCR-ABL1 cells sensitive and resistant to imatinib.	imatinib	178-186	BCR activator of RhoGEF and GTPase	Homo sapiens	136-144
26251899-5	2015	UV irradiation at a dose rate of 0.12 J/(m2   s) induced more DNA damage detected by the T4 pyrimidine dimers glycosylase and hOGG1, recognizing oxidative modifications to DNA bases in imatinib-resistant than -sensitive cells.	imatinib	185-193	8-oxoguanine DNA glycosylase	Homo sapiens	126-131
25790472-0	2015	Imatinib inhibits inactivation of the ATM/ATR signaling pathway and recovery from adriamycin/doxorubicin-induced DNA damage checkpoint arrest.	imatinib	0-8	ATM serine/threonine kinase	Homo sapiens	38-41
25790472-0	2015	Imatinib inhibits inactivation of the ATM/ATR signaling pathway and recovery from adriamycin/doxorubicin-induced DNA damage checkpoint arrest.	imatinib	0-8	ATR serine/threonine kinase	Homo sapiens	42-45
25790472-5	2015	Here we show that imatinib inhibits inactivation of ATM/ATR signaling pathway to suppress recovery from Adriamycin/doxorubicin-induced DNA damage checkpoint arrest.	imatinib	18-26	ATM serine/threonine kinase	Homo sapiens	52-55
25790472-5	2015	Here we show that imatinib inhibits inactivation of ATM/ATR signaling pathway to suppress recovery from Adriamycin/doxorubicin-induced DNA damage checkpoint arrest.	imatinib	18-26	ATR serine/threonine kinase	Homo sapiens	56-59
25790472-8	2015	Consistently, imatinib induced a persistent activation of ATR-Chk1 signaling.	imatinib	14-22	ATR serine/threonine kinase	Homo sapiens	58-61
25790472-8	2015	Consistently, imatinib induced a persistent activation of ATR-Chk1 signaling.	imatinib	14-22	checkpoint kinase 1	Homo sapiens	62-66
25790472-11	2015	Furthermore, imatinib induced a persistent activation of ATM-KAP1 signaling, and a possible involvement of imatinib in an ATM-dependent DNA damage response is suggested.	imatinib	13-21	ATM serine/threonine kinase	Homo sapiens	57-60
26147296-0	2015	Adiponectin enhances Imatinib anti-tumour activity in human chronic myeloid leukaemia cells with serum levels associated with Imatinib efficacy in early chronic phase patients.	imatinib	126-134	adiponectin, C1Q and collagen domain containing	Homo sapiens	0-11
25790472-11	2015	Furthermore, imatinib induced a persistent activation of ATM-KAP1 signaling, and a possible involvement of imatinib in an ATM-dependent DNA damage response is suggested.	imatinib	13-21	tripartite motif containing 28	Homo sapiens	61-65
26147296-5	2015	MATERIALS AND METHODS: Effects of recombinant adiponectin protein, in enhancing Imatinib anti-tumour activities, in K562 and MEG-01 CML cells, were examined in vitro and in vivo.	imatinib	80-88	adiponectin, C1Q and collagen domain containing	Homo sapiens	46-57
25790472-11	2015	Furthermore, imatinib induced a persistent activation of ATM-KAP1 signaling, and a possible involvement of imatinib in an ATM-dependent DNA damage response is suggested.	imatinib	107-115	ATM serine/threonine kinase	Homo sapiens	122-125
25790472-12	2015	These results reveal that imatinib inhibits recovery from Adriamycin-induced DNA damage checkpoint arrest in an ATM/ATR-dependent manner and raise the possibility that imatinib may inhibit resumption of tumor proliferation after chemo- and radiotherapy.	imatinib	26-34	ATM serine/threonine kinase	Homo sapiens	112-115
26147296-8	2015	RESULTS: Data presented here indicate that adiponectin enhanced Imatinib efficacy in vitro and in vivo.	imatinib	64-72	adiponectin, C1Q and collagen domain containing	Homo sapiens	43-54
25790472-12	2015	These results reveal that imatinib inhibits recovery from Adriamycin-induced DNA damage checkpoint arrest in an ATM/ATR-dependent manner and raise the possibility that imatinib may inhibit resumption of tumor proliferation after chemo- and radiotherapy.	imatinib	26-34	ATR serine/threonine kinase	Homo sapiens	116-119
25790472-12	2015	These results reveal that imatinib inhibits recovery from Adriamycin-induced DNA damage checkpoint arrest in an ATM/ATR-dependent manner and raise the possibility that imatinib may inhibit resumption of tumor proliferation after chemo- and radiotherapy.	imatinib	168-176	ATM serine/threonine kinase	Homo sapiens	112-115
26147296-10	2015	Most importantly, additional clinical data revealed that adiponectin plasma levels in CML ECP patients, correlated with Imatinib efficacy.	imatinib	120-128	adiponectin, C1Q and collagen domain containing	Homo sapiens	57-68
26147296-11	2015	CONCLUSIONS: Adiponectin enhanced Imatinib anti-tumour activity in human chronic myeloid leukaemia cells and its serum levels were associated with Imatinib efficacy, in early chronic phase patients.	imatinib	34-42	adiponectin, C1Q and collagen domain containing	Homo sapiens	13-24
26147296-11	2015	CONCLUSIONS: Adiponectin enhanced Imatinib anti-tumour activity in human chronic myeloid leukaemia cells and its serum levels were associated with Imatinib efficacy, in early chronic phase patients.	imatinib	147-155	adiponectin, C1Q and collagen domain containing	Homo sapiens	13-24
26343356-4	2015	We have shown that transmembrane transporter hOCT1 genotyping predicts imatinib activity.	imatinib	71-79	solute carrier family 22 member 1	Homo sapiens	45-50
26240289-1	2015	In the June 1, 2005, issue of Clinical Cancer Research, Antonescu and colleagues defined second-site KIT mutations in gastrointestinal stromal tumor (GIST) as the leading mechanism of acquired resistance to imatinib.	imatinib	207-215	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	101-104
26343356-7	2015	RESULTS: BMI1, PHC3, CBX6 and CBX7 expression was significantly increased during imatinib treatment.	imatinib	81-89	BMI1 proto-oncogene, polycomb ring finger	Homo sapiens	9-13
26343356-7	2015	RESULTS: BMI1, PHC3, CBX6 and CBX7 expression was significantly increased during imatinib treatment.	imatinib	81-89	polyhomeotic homolog 3	Homo sapiens	15-19
26343356-7	2015	RESULTS: BMI1, PHC3, CBX6 and CBX7 expression was significantly increased during imatinib treatment.	imatinib	81-89	chromobox 6	Homo sapiens	21-25
25913326-0	2015	A thirty-five nucleotides BCR-ABL1 insertion mutation of controversial significance confers resistance to imatinib in a patient with chronic myeloid leukemia (CML).	imatinib	106-114	BCR activator of RhoGEF and GTPase	Homo sapiens	26-34
26343356-7	2015	RESULTS: BMI1, PHC3, CBX6 and CBX7 expression was significantly increased during imatinib treatment.	imatinib	81-89	chromobox 7	Homo sapiens	30-34
25913326-4	2015	Although deletion or insertion of nucleotides in BCR-ABL1 has rarely been described, we identified a CML patient with an already described 35 nucleotides insertion (BCR-ABL1(35INS)) of controversial significance, that confers resistance to imatinib but sensitivity to dasatinib.	imatinib	240-248	BCR activator of RhoGEF and GTPase	Homo sapiens	49-57
25913326-4	2015	Although deletion or insertion of nucleotides in BCR-ABL1 has rarely been described, we identified a CML patient with an already described 35 nucleotides insertion (BCR-ABL1(35INS)) of controversial significance, that confers resistance to imatinib but sensitivity to dasatinib.	imatinib	240-248	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-57
25761934-2	2015	Imatinib is clinically active in FIP1L1-PDGFRA-positive diseases.	imatinib	0-8	factor interacting with PAPOLA and CPSF1	Homo sapiens	33-39
25865047-6	2015	In human GIST cells carrying imatinib-sensitive and imatinib-resistant mutations in KIT, PDGFRA was reduced by RNA interference (knockdown) or inhibited with crenolanib besylate (a selective inhibitor of PDGFRA and PDGFRB).	imatinib	29-37	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	84-87
25865047-6	2015	In human GIST cells carrying imatinib-sensitive and imatinib-resistant mutations in KIT, PDGFRA was reduced by RNA interference (knockdown) or inhibited with crenolanib besylate (a selective inhibitor of PDGFRA and PDGFRB).	imatinib	29-37	platelet derived growth factor receptor alpha	Homo sapiens	89-95
25865047-6	2015	In human GIST cells carrying imatinib-sensitive and imatinib-resistant mutations in KIT, PDGFRA was reduced by RNA interference (knockdown) or inhibited with crenolanib besylate (a selective inhibitor of PDGFRA and PDGFRB).	imatinib	52-60	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	84-87
25865047-6	2015	In human GIST cells carrying imatinib-sensitive and imatinib-resistant mutations in KIT, PDGFRA was reduced by RNA interference (knockdown) or inhibited with crenolanib besylate (a selective inhibitor of PDGFRA and PDGFRB).	imatinib	52-60	platelet derived growth factor receptor alpha	Homo sapiens	89-95
25865047-12	2015	PDGFRA knockdown or inhibition with crenolanib efficiently reduced proliferation of imatinib-sensitive and imatinib-resistant KIT(+)ETV1(+)PDGFRA(+) GIST cells (50% maximal inhibitory concentration = 5-32 nM), but not of cells lacking KIT, ETV1, or PDGFRA (50% maximal inhibitory concentration >230 nM).	imatinib	84-92	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	0-6
25979368-0	2015	Curcumin potentiates the anti-leukemia effects of imatinib by downregulation of the AKT/mTOR pathway and BCR/ABL gene expression in Ph+ acute lymphoblastic leukemia.	imatinib	50-58	AKT serine/threonine kinase 1	Homo sapiens	84-87
25979368-0	2015	Curcumin potentiates the anti-leukemia effects of imatinib by downregulation of the AKT/mTOR pathway and BCR/ABL gene expression in Ph+ acute lymphoblastic leukemia.	imatinib	50-58	mechanistic target of rapamycin kinase	Homo sapiens	88-92
25979368-0	2015	Curcumin potentiates the anti-leukemia effects of imatinib by downregulation of the AKT/mTOR pathway and BCR/ABL gene expression in Ph+ acute lymphoblastic leukemia.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-112
25979368-7	2015	Curcumin exerted synergetic anti-leukemia effects with imatinib by inhibition of the imatinib-mediated overactivation of AKT/mTOR signaling and down-regulation of BCR/ABL gene expression.	imatinib	55-63	AKT serine/threonine kinase 1	Homo sapiens	121-124
25979368-7	2015	Curcumin exerted synergetic anti-leukemia effects with imatinib by inhibition of the imatinib-mediated overactivation of AKT/mTOR signaling and down-regulation of BCR/ABL gene expression.	imatinib	55-63	mechanistic target of rapamycin kinase	Homo sapiens	125-129
25865047-12	2015	PDGFRA knockdown or inhibition with crenolanib efficiently reduced proliferation of imatinib-sensitive and imatinib-resistant KIT(+)ETV1(+)PDGFRA(+) GIST cells (50% maximal inhibitory concentration = 5-32 nM), but not of cells lacking KIT, ETV1, or PDGFRA (50% maximal inhibitory concentration >230 nM).	imatinib	107-115	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	0-6
25865047-18	2015	The PDGFRA inhibitor crenolanib might be used to treat patients with imatinib-resistant, KIT-mutant GIST.	imatinib	69-77	platelet derived growth factor receptor alpha	Homo sapiens	4-10
25979368-7	2015	Curcumin exerted synergetic anti-leukemia effects with imatinib by inhibition of the imatinib-mediated overactivation of AKT/mTOR signaling and down-regulation of BCR/ABL gene expression.	imatinib	85-93	AKT serine/threonine kinase 1	Homo sapiens	121-124
25979368-7	2015	Curcumin exerted synergetic anti-leukemia effects with imatinib by inhibition of the imatinib-mediated overactivation of AKT/mTOR signaling and down-regulation of BCR/ABL gene expression.	imatinib	85-93	mechanistic target of rapamycin kinase	Homo sapiens	125-129
25810235-2	2015	Imatinib is an inhibitor of the proto-oncogene tyrosine kinase (c-kit) and the first-line agent in patients with locally advanced and metastatic GIST.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	64-69
25920395-0	2015	Correlation of C/EBPalpha expression with response and resistance to imatinib in chronic myeloid leukaemia.	imatinib	69-77	CCAAT enhancer binding protein alpha	Homo sapiens	15-25
25920395-4	2015	METHODS: We quantified the expression of C/EBPalpha gene in 126 chronic myeloid leukaemia samples (82 from newly diagnosed and 44 from imatinib-resistant patients) and 20 control samples.	imatinib	135-143	CCAAT enhancer binding protein alpha	Homo sapiens	41-51
25920395-6	2015	RESULTS: C/EBPalpha expression level was significantly lower in the imatinib-resistant group than in the pretreatment and control group (P = 0.0398).	imatinib	68-76	CCAAT enhancer binding protein alpha	Homo sapiens	9-19
25920395-7	2015	Low CAAT/enhancer binding protein alpha levels in the imatinib-resistant group were significantly associated with advanced phase (P = 0.04), with more peripheral blasts (P = 0.0001), high BCR-ABL levels (P = 0.018) and T315I and P-loop mutations (P = 0.0002).	imatinib	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	188-195
25761934-2	2015	Imatinib is clinically active in FIP1L1-PDGFRA-positive diseases.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	40-46
25761934-3	2015	Using in vitro screening to identify imatinib-resistant mutations, we frequently detected a Phe to Ser exchange at position 604 (F604S) of FIP1L1-PDGFRA alone or in combination with other exchanges.	imatinib	37-45	factor interacting with PAPOLA and CPSF1	Homo sapiens	139-145
25761934-3	2015	Using in vitro screening to identify imatinib-resistant mutations, we frequently detected a Phe to Ser exchange at position 604 (F604S) of FIP1L1-PDGFRA alone or in combination with other exchanges.	imatinib	37-45	platelet derived growth factor receptor alpha	Homo sapiens	146-152
25761934-10	2015	Interestingly, FIP1L1-PDGFRA/L629P, a recently identified mutation in an imatinib-resistant CEL patient, also showed protein stabilization similar to that observed with FIP1L1-PDGFRA/F604S.	imatinib	73-81	factor interacting with PAPOLA and CPSF1	Homo sapiens	15-21
25761934-10	2015	Interestingly, FIP1L1-PDGFRA/L629P, a recently identified mutation in an imatinib-resistant CEL patient, also showed protein stabilization similar to that observed with FIP1L1-PDGFRA/F604S.	imatinib	73-81	platelet derived growth factor receptor alpha	Homo sapiens	22-28
25761934-10	2015	Interestingly, FIP1L1-PDGFRA/L629P, a recently identified mutation in an imatinib-resistant CEL patient, also showed protein stabilization similar to that observed with FIP1L1-PDGFRA/F604S.	imatinib	73-81	platelet derived growth factor receptor alpha	Homo sapiens	176-182
26314429-0	2015	[Effect of Recombinant Adenovirus AdE-SH2-Caspase 8 on the Apoptosis of Imatinib-resistant K562/G01 Cell Line].	imatinib	72-80	caspase 8	Homo sapiens	42-51
25592261-1	2015	Imatinib inhibits the activity of several tyrosine kinases, including BCR-ABL, KIT and platelet-derived growth factor receptor (PDGFR).	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	79-82
26314429-1	2015	OBJECTIVE: To investigate the effect of SH2-Caspase 8 fusion protein expressed by recombinant adenovirus AdE-SH2-Caspase8-HA-GFP (SC) on the apoptosis of K562/G01 cell line, which is a BCR/ABL positive chronic myeloid leukemia cell line and resistant to imatinib.	imatinib	254-262	caspase 8	Homo sapiens	44-53
25592261-7	2015	Anti-tumour activity of imatinib has also been demonstrated in canine GISTs with a KIT mutation and in feline hypereosinophilic syndrome; however, to date only one of each of these cases has been reported.	imatinib	24-32	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	83-86
25592261-8	2015	In conclusion, analysis of KIT mutations appears to provide valuable data for individual treatment with imatinib in dogs and cats.	imatinib	104-112	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	27-30
25980323-1	2015	The aim of this study was to evaluate the capacity of BR55, an ultrasound contrast agent specifically targeting vascular endothelial growth factor receptor 2 (VEGFR2), to distinguish the specific anti-VEGFR2 therapy effect of sunitinib from other anti-angiogenic effects of a therapy (imatinib) that does not directly inhibit VEGFR2.	imatinib	285-293	kinase insert domain protein receptor	Mus musculus	159-165
25980323-1	2015	The aim of this study was to evaluate the capacity of BR55, an ultrasound contrast agent specifically targeting vascular endothelial growth factor receptor 2 (VEGFR2), to distinguish the specific anti-VEGFR2 therapy effect of sunitinib from other anti-angiogenic effects of a therapy (imatinib) that does not directly inhibit VEGFR2.	imatinib	285-293	kinase insert domain protein receptor	Mus musculus	201-207
25980323-1	2015	The aim of this study was to evaluate the capacity of BR55, an ultrasound contrast agent specifically targeting vascular endothelial growth factor receptor 2 (VEGFR2), to distinguish the specific anti-VEGFR2 therapy effect of sunitinib from other anti-angiogenic effects of a therapy (imatinib) that does not directly inhibit VEGFR2.	imatinib	285-293	kinase insert domain protein receptor	Mus musculus	201-207
25756742-0	2015	Switching to second-generation tyrosine kinase inhibitor improves the response and outcome of frontline imatinib-treated patients with chronic myeloid leukemia with more than 10% of BCR-ABL/ABL ratio at 3 months.	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-189
26276287-1	2015	OBJECTIVE: To study the effects of PDGF-Rb antagonists imatinib on endometrial injury repairing in the mouse model.	imatinib	55-63	platelet derived growth factor receptor, beta polypeptide	Mus musculus	35-42
26276287-2	2015	METHODS: The cultured MSCs cells from male mice were marked with BrdU in vitro, and then transplanted to the female mice which suffered from radiation injury through tail vein, PDGF-Rb antagonists imatinib was injected through abdominal cavity.	imatinib	197-205	platelet derived growth factor receptor, beta polypeptide	Mus musculus	177-184
26276287-6	2015	SRY gene presented positive in radiation transplantation group and imatinib intervention group; BrdU incorporation showed negative in radiation control group and normal control group which died in the early stage in mice; the incorporation of BrdU was higher in radiation transplantation group compared with imatinib intervention group; CD34 was positive on the uterus of all the four groups, which showed highest in radiation control group and lowest in radiation control group; The MVD in imatinib intervention group was lower than radiation control group; the difference of MVD was significantly compared with normal control group (P < 0.05).	imatinib	67-75	sex determining region of Chr Y	Mus musculus	0-3
26276287-6	2015	SRY gene presented positive in radiation transplantation group and imatinib intervention group; BrdU incorporation showed negative in radiation control group and normal control group which died in the early stage in mice; the incorporation of BrdU was higher in radiation transplantation group compared with imatinib intervention group; CD34 was positive on the uterus of all the four groups, which showed highest in radiation control group and lowest in radiation control group; The MVD in imatinib intervention group was lower than radiation control group; the difference of MVD was significantly compared with normal control group (P < 0.05).	imatinib	308-316	sex determining region of Chr Y	Mus musculus	0-3
26276287-6	2015	SRY gene presented positive in radiation transplantation group and imatinib intervention group; BrdU incorporation showed negative in radiation control group and normal control group which died in the early stage in mice; the incorporation of BrdU was higher in radiation transplantation group compared with imatinib intervention group; CD34 was positive on the uterus of all the four groups, which showed highest in radiation control group and lowest in radiation control group; The MVD in imatinib intervention group was lower than radiation control group; the difference of MVD was significantly compared with normal control group (P < 0.05).	imatinib	308-316	sex determining region of Chr Y	Mus musculus	0-3
26309809-0	2015	Reactive Oxygen Species and Mitochondrial DNA Damage and Repair in BCR-ABL1 Cells Resistant to Imatinib.	imatinib	95-103	BCR activator of RhoGEF and GTPase	Homo sapiens	67-70
26309809-2	2015	We reported previously that CML cells expressing the BCR/ABL1 fusion gene, accumulated a high level of reactive oxygen species (ROS) due to deregulated mitochondrial electron transport chain, which in turn led to genomic instability, resulting in imatinib resistance.	imatinib	247-255	BCR activator of RhoGEF and GTPase	Homo sapiens	53-61
26208715-7	2015	Imatinib treatment was resumed in the patients" posttransplantation following detection of BCR-ABL transcripts.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
26185540-6	2015	The C-Kit inhibitor, imatinib mesylate, was administrated to confirm the effect of stromal cells on the tumorigenesis.	imatinib	21-38	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	4-9
25808917-0	2015	Combination of EUTOS score and 3-month BCR-ABL transcript level identifies a group of good-risk chronic myeloid leukemia patients with favorable response to frontline imatinib therapy.	imatinib	167-175	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
25970686-0	2015	KIT, PDGFRA, and BRAF mutational spectrum impacts on the natural history of imatinib-naive localized GIST: a population-based study.	imatinib	76-84	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
25970686-0	2015	KIT, PDGFRA, and BRAF mutational spectrum impacts on the natural history of imatinib-naive localized GIST: a population-based study.	imatinib	76-84	platelet derived growth factor receptor alpha	Homo sapiens	5-11
25970686-0	2015	KIT, PDGFRA, and BRAF mutational spectrum impacts on the natural history of imatinib-naive localized GIST: a population-based study.	imatinib	76-84	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	17-21
26276287-7	2015	CONCLUSIONS: PDGF-Rb antagonists imatinib could inhibit the repairing function of MSCs in the endometrial lesions in mice.	imatinib	33-41	platelet derived growth factor receptor, beta polypeptide	Mus musculus	13-20
25756742-0	2015	Switching to second-generation tyrosine kinase inhibitor improves the response and outcome of frontline imatinib-treated patients with chronic myeloid leukemia with more than 10% of BCR-ABL/ABL ratio at 3 months.	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-189
25963192-0	2015	CD-200 induces apoptosis and inhibits Bcr-Abl signaling in imatinib-resistant chronic myeloid leukemia with T315I mutation.	imatinib	59-67	CD200 antigen	Mus musculus	0-6
25940371-0	2015	Synergistic antiproliferative effect of imatinib and adriamycin in platelet-derived growth factor receptor-expressing osteosarcoma cells.	imatinib	40-48	receptor-like tyrosine kinase	Mus musculus	84-106
25940371-5	2015	Platelet-derived growth factor-BB induced activation of both MEK-ERK and phosphatidylinositol 3-kinase-protein kinase B signaling pathways and promoted survival in OS cells deprived of serum, and these effects were blocked by the PDGF receptor inhibitor imatinib.	imatinib	254-262	midkine	Mus musculus	61-64
26905120-2	2015	AIMS: This study aimed to compare the hematologic, breakpoint cluster region-abelson (BCR-ABL) and liver function enzymes changes during treatment period of Imatinib.	imatinib	157-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-84
26905120-2	2015	AIMS: This study aimed to compare the hematologic, breakpoint cluster region-abelson (BCR-ABL) and liver function enzymes changes during treatment period of Imatinib.	imatinib	157-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
26905120-9	2015	Iranian made and Indian-made Imatinib has a same effect on improvement of hematologic, BCR-ABL, electrolytes in CML patients.	imatinib	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
25963192-0	2015	CD-200 induces apoptosis and inhibits Bcr-Abl signaling in imatinib-resistant chronic myeloid leukemia with T315I mutation.	imatinib	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
25963192-6	2015	CD-200 inhibited cell proliferation in the BaF3/WT cells, and also in the BaF3/T315I cells with Imatinib resistance.	imatinib	96-104	CD200 antigen	Mus musculus	0-6
25963192-11	2015	Taken together, our study demonstrates that CD-200 exhibits apoptosis induction and anti-proliferative effect by blocking the Bcr-Abl signaling pathways in the Bcr-Abl/T315I with resistance to Imatinib.	imatinib	193-201	CD200 antigen	Mus musculus	44-50
25963192-12	2015	We suggest that CD-200 may be a natural product to target Bcr-Abl and overcome Imatinib resistance in CML patients.	imatinib	79-87	CD200 molecule	Homo sapiens	16-22
26417552-7	2015	Here, we report a case of CML (BCR-ABL rearrangement positive) who presented with large haematoma in the anterior as well as posterior compartment of left thigh and treated successfully with hydroxyurea and imatinib.	imatinib	207-215	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
26458641-4	2015	All of them had the BCR-ABL fusion gene and responded well to treatment with imatinib mesylate.	imatinib	77-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
25765543-5	2015	The transcription factor E2F1 is elevated in high CIP2A patients and following 1 month of in vivo treatment 2G TKIs suppress E2F1 and reduce CIP2A; these effects are not seen with imatinib.	imatinib	180-188	E2F transcription factor 1	Homo sapiens	25-29
25330443-6	2015	Additionally, Hsps, DJ-1 and thioredoxin, which were also shown to decrease in primary cells from imatinib-resistant patients, may be promising potential targets for mechanistic research and new clinical treatments.	imatinib	98-106	Parkinsonism associated deglycase	Homo sapiens	20-40
25765543-10	2015	The data supports the view that CIP2A inhibits PP2Ac, stabilising E2F1, creating a CIP2A/c-Myc/E2F1 positive feedback loop, which imatinib cannot overcome.	imatinib	130-138	cellular inhibitor of PP2A	Homo sapiens	32-37
25765543-1	2015	High cancerous inhibitor of PP2A (CIP2A) protein levels at diagnosis of chronic myeloid leukaemia (CML) are predictive of disease progression in imatinib-treated patients.	imatinib	145-153	cellular inhibitor of PP2A	Homo sapiens	5-32
25765543-10	2015	The data supports the view that CIP2A inhibits PP2Ac, stabilising E2F1, creating a CIP2A/c-Myc/E2F1 positive feedback loop, which imatinib cannot overcome.	imatinib	130-138	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	89-94
25765543-1	2015	High cancerous inhibitor of PP2A (CIP2A) protein levels at diagnosis of chronic myeloid leukaemia (CML) are predictive of disease progression in imatinib-treated patients.	imatinib	145-153	cellular inhibitor of PP2A	Homo sapiens	34-39
25916699-0	2015	Celecoxib sensitizes imatinib-resistant K562 cells to imatinib by inhibiting MRP1-5, ABCA2 and ABCG2 transporters via Wnt and Ras signaling pathways.	imatinib	21-29	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	95-100
25765543-10	2015	The data supports the view that CIP2A inhibits PP2Ac, stabilising E2F1, creating a CIP2A/c-Myc/E2F1 positive feedback loop, which imatinib cannot overcome.	imatinib	130-138	E2F transcription factor 1	Homo sapiens	95-99
25964201-7	2015	Interestingly, cross-resistance to imatinib and enzastaurin (selective inhibitors of c-Kit and PKC-beta, respectively), was observed and the use of YK-4-279 with enzastaurin in vitro led to marked drug synergy, suggesting a potential role for combination therapies in the future.	imatinib	35-43	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	85-90
25916699-0	2015	Celecoxib sensitizes imatinib-resistant K562 cells to imatinib by inhibiting MRP1-5, ABCA2 and ABCG2 transporters via Wnt and Ras signaling pathways.	imatinib	54-62	ATP binding cassette subfamily C member 1	Homo sapiens	77-83
25916699-0	2015	Celecoxib sensitizes imatinib-resistant K562 cells to imatinib by inhibiting MRP1-5, ABCA2 and ABCG2 transporters via Wnt and Ras signaling pathways.	imatinib	54-62	ATP binding cassette subfamily A member 2	Homo sapiens	85-90
25916699-0	2015	Celecoxib sensitizes imatinib-resistant K562 cells to imatinib by inhibiting MRP1-5, ABCA2 and ABCG2 transporters via Wnt and Ras signaling pathways.	imatinib	54-62	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	95-100
25916699-3	2015	Our previous studies have highlighted the role of cyclooxygenase-2 (COX-2) in regulating the expression of multidrug resistant protein-1 (MDR1), P-gp, in imatinib-resistant K562 cells (IR-K562) via PGE2-cAMP-PKC-NF-kappaB pathway and inhibition of COX-2 by celecoxib, a COX-2 specific inhibitor, inhibits this pathway and reverses the drug resistance.	imatinib	154-162	prostaglandin-endoperoxide synthase 2	Homo sapiens	50-66
25916699-3	2015	Our previous studies have highlighted the role of cyclooxygenase-2 (COX-2) in regulating the expression of multidrug resistant protein-1 (MDR1), P-gp, in imatinib-resistant K562 cells (IR-K562) via PGE2-cAMP-PKC-NF-kappaB pathway and inhibition of COX-2 by celecoxib, a COX-2 specific inhibitor, inhibits this pathway and reverses the drug resistance.	imatinib	154-162	prostaglandin-endoperoxide synthase 2	Homo sapiens	68-73
25916699-3	2015	Our previous studies have highlighted the role of cyclooxygenase-2 (COX-2) in regulating the expression of multidrug resistant protein-1 (MDR1), P-gp, in imatinib-resistant K562 cells (IR-K562) via PGE2-cAMP-PKC-NF-kappaB pathway and inhibition of COX-2 by celecoxib, a COX-2 specific inhibitor, inhibits this pathway and reverses the drug resistance.	imatinib	154-162	ATP binding cassette subfamily B member 1	Homo sapiens	107-136
25916699-3	2015	Our previous studies have highlighted the role of cyclooxygenase-2 (COX-2) in regulating the expression of multidrug resistant protein-1 (MDR1), P-gp, in imatinib-resistant K562 cells (IR-K562) via PGE2-cAMP-PKC-NF-kappaB pathway and inhibition of COX-2 by celecoxib, a COX-2 specific inhibitor, inhibits this pathway and reverses the drug resistance.	imatinib	154-162	ATP binding cassette subfamily B member 1	Homo sapiens	138-142
25916699-3	2015	Our previous studies have highlighted the role of cyclooxygenase-2 (COX-2) in regulating the expression of multidrug resistant protein-1 (MDR1), P-gp, in imatinib-resistant K562 cells (IR-K562) via PGE2-cAMP-PKC-NF-kappaB pathway and inhibition of COX-2 by celecoxib, a COX-2 specific inhibitor, inhibits this pathway and reverses the drug resistance.	imatinib	154-162	phosphoglycolate phosphatase	Homo sapiens	145-149
25916699-3	2015	Our previous studies have highlighted the role of cyclooxygenase-2 (COX-2) in regulating the expression of multidrug resistant protein-1 (MDR1), P-gp, in imatinib-resistant K562 cells (IR-K562) via PGE2-cAMP-PKC-NF-kappaB pathway and inhibition of COX-2 by celecoxib, a COX-2 specific inhibitor, inhibits this pathway and reverses the drug resistance.	imatinib	154-162	prostaglandin-endoperoxide synthase 2	Homo sapiens	248-253
25916699-3	2015	Our previous studies have highlighted the role of cyclooxygenase-2 (COX-2) in regulating the expression of multidrug resistant protein-1 (MDR1), P-gp, in imatinib-resistant K562 cells (IR-K562) via PGE2-cAMP-PKC-NF-kappaB pathway and inhibition of COX-2 by celecoxib, a COX-2 specific inhibitor, inhibits this pathway and reverses the drug resistance.	imatinib	154-162	prostaglandin-endoperoxide synthase 2	Homo sapiens	248-253
25916699-4	2015	Studies have identified that not only MDR1 but other ATP-binding cassette transport proteins (ABC transporters) are involved in the development of imatinib resistance.	imatinib	147-155	ATP binding cassette subfamily B member 1	Homo sapiens	38-42
25916699-5	2015	Here, we tried to study the role of COX-2 in the regulation of other ABC transporters such as MRP1, MRP2, MRP3, ABCA2 and ABCG2 that have been already implicated in imatinib resistance development.	imatinib	165-173	prostaglandin-endoperoxide synthase 2	Homo sapiens	36-41
25916699-5	2015	Here, we tried to study the role of COX-2 in the regulation of other ABC transporters such as MRP1, MRP2, MRP3, ABCA2 and ABCG2 that have been already implicated in imatinib resistance development.	imatinib	165-173	ATP binding cassette subfamily C member 1	Homo sapiens	94-98
25916699-5	2015	Here, we tried to study the role of COX-2 in the regulation of other ABC transporters such as MRP1, MRP2, MRP3, ABCA2 and ABCG2 that have been already implicated in imatinib resistance development.	imatinib	165-173	ATP binding cassette subfamily C member 2	Homo sapiens	100-104
25916699-5	2015	Here, we tried to study the role of COX-2 in the regulation of other ABC transporters such as MRP1, MRP2, MRP3, ABCA2 and ABCG2 that have been already implicated in imatinib resistance development.	imatinib	165-173	ATP binding cassette subfamily C member 3	Homo sapiens	106-110
25916699-5	2015	Here, we tried to study the role of COX-2 in the regulation of other ABC transporters such as MRP1, MRP2, MRP3, ABCA2 and ABCG2 that have been already implicated in imatinib resistance development.	imatinib	165-173	ATP binding cassette subfamily A member 2	Homo sapiens	112-117
25916699-5	2015	Here, we tried to study the role of COX-2 in the regulation of other ABC transporters such as MRP1, MRP2, MRP3, ABCA2 and ABCG2 that have been already implicated in imatinib resistance development.	imatinib	165-173	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	122-127
25964201-7	2015	Interestingly, cross-resistance to imatinib and enzastaurin (selective inhibitors of c-Kit and PKC-beta, respectively), was observed and the use of YK-4-279 with enzastaurin in vitro led to marked drug synergy, suggesting a potential role for combination therapies in the future.	imatinib	35-43	protein kinase C beta	Homo sapiens	95-103
25996455-3	2015	In this work, molecular dynamics simulations of the Abl kinase complexes with cancer drugs (Imatinib and Dasatinib) were combined with structure-based network modeling to characterize dynamics of the residue interaction networks in these systems.	imatinib	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-55
25996455-5	2015	Our data have indicated that specific Imatinib binding to a small number of highly connected residues could lead to network-bridging effects and allow for efficient allosteric communication, which is mediated by a dominant pathway sensitive to the unphosphorylated Abl state.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	265-268
26304076-0	2015	[The prognostic value of early BCR-ABL transcripts level in 251 patients with chronic myeloid leukemia after treatment with imatinib].	imatinib	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
25857479-0	2015	Korean Red Ginseng Extract Enhances the Anticancer Effects of Imatinib Mesylate Through Abrogation p38 and STAT5 Activation in KBM-5 Cells.	imatinib	62-79	mitogen-activated protein kinase 14	Homo sapiens	99-102
25737405-3	2015	The essential role of PDGFR signaling on restenosis post-angioplasty or atherosclerosis has been demonstrated by using blocking antibodies to PDGF or the tyrosine kinase inhibitor imatinib.	imatinib	180-188	platelet derived growth factor receptor beta	Homo sapiens	22-27
25934947-3	2015	The introduction of molecularly targeted therapy (e.g., with imatinib mesylate) following the discovery of the role of oncogenic mutations in the receptor tyrosine kinases KIT and platelet-derived growth factor alpha (PDGFRA) significantly increased patient survival.	imatinib	61-78	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	172-175
25934947-3	2015	The introduction of molecularly targeted therapy (e.g., with imatinib mesylate) following the discovery of the role of oncogenic mutations in the receptor tyrosine kinases KIT and platelet-derived growth factor alpha (PDGFRA) significantly increased patient survival.	imatinib	61-78	platelet derived growth factor receptor alpha	Homo sapiens	218-224
26304076-1	2015	OBJECTIVE: To understand the prognostic value of early monitoring BCR-ABL transcripts in patients with chronic myeloid leukemia (CML) after treatment with imatinib, and to provide the information for early assessment of prognosis and treatment options.	imatinib	155-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
26304076-4	2015	RESULTS: At 3 months after imatinib treatment BCR-ABL transcriptional levels>10%, >1%-<= 10% and <= 1% were found in 92, 94 and 64 patients, their PFS were 53.3%, 71.3% and 86.2%, respectively.	imatinib	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
26304076-7	2015	When 182 patients received imatinib treatment at 6 months, 22 patients with BCR-ABL transcriptional levels>10%, 50>1% -<= 10% and 110 <= 1%, their PFS were 27.3% vs 66.0% vs 82.7% (P<0.05), the OS of three groups were 86.4% vs 94.0% vs 100%.	imatinib	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
26304076-9	2015	Logistic regression confirmed that the level of BCR-ABL transcriptional level at 3 and 6 months after imatinib treatment was independent factor to influence the progress of disease.	imatinib	102-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
26304076-10	2015	CONCLUSION: It is important for the prognosis evaluation of CML patients to monitor BCR-ABL transcriptional level at 3 and 6 months after imatinib treatment.	imatinib	138-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
25786656-1	2015	BACKGROUND: Imatinib mesylate is a chemotherapeutic drug that inhibits the tyrosine kinase activity of c-KIT and has been successfully used to treat leukemias and some solid tumors.	imatinib	12-29	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	103-108
26107505-1	2015	The tyrosine kinase (TK) inhibitor imatinib provides a highly effective therapy for chronic myeloid leukemia (CML) via inhibition of the oncogenic TK BCR-ABL1.	imatinib	35-43	BCR activator of RhoGEF and GTPase	Rattus norvegicus	150-158
26087013-0	2015	Clonal Evolution and Blast Crisis Correlate with Enhanced Proteolytic Activity of Separase in BCR-ABL b3a2 Fusion Type CML under Imatinib Therapy.	imatinib	129-137	extra spindle pole bodies like 1, separase	Homo sapiens	82-90
26087013-0	2015	Clonal Evolution and Blast Crisis Correlate with Enhanced Proteolytic Activity of Separase in BCR-ABL b3a2 Fusion Type CML under Imatinib Therapy.	imatinib	129-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
26087013-7	2015	We investigated the influence of p210BCR-ABL breakpoint variants and imatinib treatment on expression and proteolytic activity of Separase as measured with a specific fluorogenic assay on CML cell lines (b2a2: KCL-22, BV-173; b3a2: K562, LAMA-84).	imatinib	69-77	extra spindle pole bodies like 1, separase	Homo sapiens	130-138
26087013-8	2015	Despite a drop in Separase protein levels an up to 5.4-fold increase of Separase activity under imatinib treatment was observed exclusively in b3a2 but not in b2a2 cell lines.	imatinib	96-104	extra spindle pole bodies 1, separase	Mus musculus	18-26
26087013-8	2015	Despite a drop in Separase protein levels an up to 5.4-fold increase of Separase activity under imatinib treatment was observed exclusively in b3a2 but not in b2a2 cell lines.	imatinib	96-104	extra spindle pole bodies 1, separase	Mus musculus	72-80
26087013-9	2015	Mimicking the influence of imatinib on BV-173 and LAMA-84 cells by ESPL1 silencing stimulated Separase proteolytic activity in both b3a2 and b2a2 cell lines.	imatinib	27-35	extra spindle pole bodies like 1, separase	Homo sapiens	67-72
26087013-9	2015	Mimicking the influence of imatinib on BV-173 and LAMA-84 cells by ESPL1 silencing stimulated Separase proteolytic activity in both b3a2 and b2a2 cell lines.	imatinib	27-35	extra spindle pole bodies like 1, separase	Homo sapiens	94-102
25786656-13	2015	CONCLUSION: DU145 and PC3 cells displayed a contradictory behavior in response to imatinib, which was underpinned by a distinct expression pattern (or activity) of target regulators of cell-cycle, apoptosis, and angiogenesis.	imatinib	82-90	chromobox 8	Homo sapiens	22-25
25786656-14	2015	The paradoxical effect of imatinib in PC3 cells may be related with the differential expression of c-KIT protein variants.	imatinib	26-34	chromobox 8	Homo sapiens	38-41
25786656-14	2015	The paradoxical effect of imatinib in PC3 cells may be related with the differential expression of c-KIT protein variants.	imatinib	26-34	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	99-104
25786656-4	2015	METHODS: Two cell line models of HRPC (DU145 and PC3) were exposed to 20 muM of imatinib for 6-72 hr.	imatinib	80-88	chromobox 8	Homo sapiens	49-52
25786656-8	2015	RESULTS: Imatinib significantly decreased the viability of DU145 cells but paradoxically augmented the viability of PC3 cells.	imatinib	9-17	chromobox 8	Homo sapiens	116-119
25786656-9	2015	DU145 cells displayed diminished expression of anti-apoptotic Bcl-2 protein and augmented levels of caspase-8 and -9, as well as, increased enzymatic activity of caspase-3 in response to imatinib.	imatinib	187-195	caspase 3	Homo sapiens	162-171
26106294-4	2015	We show that ACM-hSOD1(G93A), but not ACM-hSOD1(WT), increases c-Abl activity in motoneurons, interneurons and glial cells, starting at 60 min; the c-Abl inhibitor STI571 (imatinib) prevents this ACM-hSOD1(G93A)-mediated motoneuron death.	imatinib	164-170	superoxide dismutase 1	Homo sapiens	17-22
26106294-4	2015	We show that ACM-hSOD1(G93A), but not ACM-hSOD1(WT), increases c-Abl activity in motoneurons, interneurons and glial cells, starting at 60 min; the c-Abl inhibitor STI571 (imatinib) prevents this ACM-hSOD1(G93A)-mediated motoneuron death.	imatinib	172-180	superoxide dismutase 1	Homo sapiens	17-22
25802333-0	2015	Induction of heme oxygenase-1 by Na+-H+ exchanger 1 protein plays a crucial role in imatinib-resistant chronic myeloid leukemia cells.	imatinib	84-92	heme oxygenase 1	Homo sapiens	13-29
25915587-8	2015	Treatment of mice with the c-KIT inhibitor imatinib mesylate limited effusion precipitation by mouse and human adenocarcinoma cells.	imatinib	43-60	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	27-32
25712735-8	2015	In conclusion, an IFN/imatinib induction treatment followed by a temporary IFN maintenance therapy may enable a high rate of treatment discontinuation in CML patients in at least MMR when stopping imatinib.	imatinib	197-205	interferon alpha 1	Homo sapiens	18-21
25712735-8	2015	In conclusion, an IFN/imatinib induction treatment followed by a temporary IFN maintenance therapy may enable a high rate of treatment discontinuation in CML patients in at least MMR when stopping imatinib.	imatinib	197-205	interferon alpha 1	Homo sapiens	75-78
25852058-0	2015	CDKN2A/p16 Loss Implicates CDK4 as a Therapeutic Target in Imatinib-Resistant Dermatofibrosarcoma Protuberans.	imatinib	59-67	cyclin dependent kinase inhibitor 2A	Homo sapiens	0-6
25852058-0	2015	CDKN2A/p16 Loss Implicates CDK4 as a Therapeutic Target in Imatinib-Resistant Dermatofibrosarcoma Protuberans.	imatinib	59-67	cyclin dependent kinase inhibitor 2A	Homo sapiens	7-10
25852058-0	2015	CDKN2A/p16 Loss Implicates CDK4 as a Therapeutic Target in Imatinib-Resistant Dermatofibrosarcoma Protuberans.	imatinib	59-67	cyclin dependent kinase 4	Homo sapiens	27-31
25852058-14	2015	CDK4/6 inhibition is a preclinically effective treatment against p16-negative, imatinib-resistant FS-DFSP, and should be evaluated as a therapeutic strategy in patients with unresectable or metastatic imatinib-resistant DFSP.	imatinib	79-87	cyclin dependent kinase 4	Homo sapiens	0-6
25852058-14	2015	CDK4/6 inhibition is a preclinically effective treatment against p16-negative, imatinib-resistant FS-DFSP, and should be evaluated as a therapeutic strategy in patients with unresectable or metastatic imatinib-resistant DFSP.	imatinib	201-209	cyclin dependent kinase 4	Homo sapiens	0-6
25631405-0	2015	Ph-negative isolated myeloid sarcoma with NPM1 gene mutation in adolescent with Ph-positive chronic myeloid leukemia in remission after treatment with allogeneic bone marrow transplantation and imatinib mesylate.	imatinib	194-202	nucleophosmin 1	Homo sapiens	42-46
26316486-1	2015	Imatinib mesylate is a small-molecule tyrosine kinase inhibitor (TKi) designed to target c-ABL and BCR-ABL, approved for the treatment of chronic myeloid leukemia and gastrointestinal stromal tumors.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-94
26316486-1	2015	Imatinib mesylate is a small-molecule tyrosine kinase inhibitor (TKi) designed to target c-ABL and BCR-ABL, approved for the treatment of chronic myeloid leukemia and gastrointestinal stromal tumors.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
26316486-3	2015	The aim of this work was to investigate the possible contribution of interleukin (IL)-33 and IL-31, cytokines involved in disorders associated with itching, in the pathogenesis of pruritus in a patient undergoing imatinib mesylate treatment.	imatinib	213-230	interleukin 31	Homo sapiens	93-98
26316486-5	2015	In light of these findings, imatinib mesylate-related symptoms of dermatologic toxicities might be related to the release of IL-31 and IL-33.	imatinib	28-45	interleukin 31	Homo sapiens	125-130
26316486-5	2015	In light of these findings, imatinib mesylate-related symptoms of dermatologic toxicities might be related to the release of IL-31 and IL-33.	imatinib	28-45	interleukin 33	Homo sapiens	135-140
26316486-7	2015	This report, to the best of our knowledge, is the first work describing the possible involvement of the IL-31/IL-33 axis in the pathogenesis of skin side effects related to imatinib mesylate treatment.	imatinib	173-190	interleukin 31	Homo sapiens	104-109
26316486-7	2015	This report, to the best of our knowledge, is the first work describing the possible involvement of the IL-31/IL-33 axis in the pathogenesis of skin side effects related to imatinib mesylate treatment.	imatinib	173-190	interleukin 33	Homo sapiens	110-115
25695690-1	2015	PURPOSE: Although durable responses can be achieved with tyrosine kinase inhibitors such as imatinib in melanomas harboring KIT mutations, the efficacy of alternative inhibitors after progression to imatinib and the activity of these agents on brain metastases are unknown.	imatinib	92-100	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	124-127
26029664-6	2015	Imatinib therapy decreases both MDSCs and arginase 1 levels to normal ones.	imatinib	0-8	arginase 1	Homo sapiens	42-52
25683919-1	2015	GNF-2 and GNF-5 are members of a new class of non-receptor tyrosine kinases inhibitors that possess excellent selectivity towards imatinib-resistant mutations found in chronic myeloid leukemia patients.	imatinib	130-138	growth and fatness 2	Mus musculus	0-5
25311496-7	2015	These findings confirm the strong predictive value of 3-month and 6-month BCR-ABL(IS) levels in imatinib-resistant patients.	imatinib	96-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
26316486-0	2015	Possible Role of Interleukin-31/33 Axis in Imatinib Mesylate-Associated Skin Toxicity.	imatinib	43-60	interleukin 31	Homo sapiens	17-31
25697481-9	2015	Overexpression of miR-424 was shown to suppress proliferation and induce apoptosis of K562 cells as well as sensitize these cells to imatinib treatment.	imatinib	133-141	microRNA 424	Homo sapiens	18-25
25883211-3	2015	Here we show that co-treatment with clinically validated inhibitors of c-ABL (imatinib) and EGFR (lapatinib) results in synergistic growth inhibition in TNBC cells.	imatinib	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-76
25697481-0	2015	Restoration of miR-424 suppresses BCR-ABL activity and sensitizes CML cells to imatinib treatment.	imatinib	79-87	microRNA 424	Homo sapiens	15-22
25707497-5	2015	Time to progression after discontinuation of imatinib was longer in group B than in group A. Fifteen miRNAs were highly statistically differentially expressed between groups A and B, targeting more than 3000 genes, including AGO1, BCL2, CDK6, SMAD4, PTEN, CCND1, VEGFA, and RB1.	imatinib	45-53	argonaute RISC component 1	Homo sapiens	225-229
25707497-5	2015	Time to progression after discontinuation of imatinib was longer in group B than in group A. Fifteen miRNAs were highly statistically differentially expressed between groups A and B, targeting more than 3000 genes, including AGO1, BCL2, CDK6, SMAD4, PTEN, CCND1, VEGFA, and RB1.	imatinib	45-53	cyclin dependent kinase 6	Homo sapiens	237-241
25908454-6	2015	Moreover, leukemia cell lines overexpressing ABCB1 have also been shown to be more resistant to the tyrosine kinase inhibitor imatinib mesylate.	imatinib	126-143	ATP binding cassette subfamily B member 1	Homo sapiens	45-50
24706111-0	2015	microRNA-218 increase the sensitivity of gastrointestinal stromal tumor to imatinib through PI3K/AKT pathway.	imatinib	75-83	AKT serine/threonine kinase 1	Homo sapiens	97-100
24706111-6	2015	The effects of miR-218 ectopic expression on the apoptosis of imatinib mesylate-induce GIST cells were determined by Annexin V/PI double staining method and flow cytometry.	imatinib	62-79	annexin A5	Homo sapiens	117-126
24706111-7	2015	The effects of miR-218 ectopic expression on the AKT and phospho-AKT (p-AKT) expressions of imatinib mesylate-induce GIST cells were determined by Western blot and flow cytometry with the PI3K pathway inhibitor Wortmannin.	imatinib	92-109	AKT serine/threonine kinase 1	Homo sapiens	65-68
24706111-7	2015	The effects of miR-218 ectopic expression on the AKT and phospho-AKT (p-AKT) expressions of imatinib mesylate-induce GIST cells were determined by Western blot and flow cytometry with the PI3K pathway inhibitor Wortmannin.	imatinib	92-109	AKT serine/threonine kinase 1	Homo sapiens	65-68
26191303-1	2015	The myeloid and lymphoid neoplasms with eosinophilia and PDGFRA gene rearrangements usually show a good response to Imatinib and are typically associated with a normal karyotype, occasionally exhibiting a secondary chromosomal abnormality associated with clonal evolution.	imatinib	116-124	platelet derived growth factor receptor alpha	Homo sapiens	57-63
25623274-2	2015	Inhibition of platelet derived growth factor receptor (PDGFR) kinases has been suggested to provide an additional therapeutic modality, and clinical studies with the non-selective PDGFR inhibitor imatinib appear to validate this hypothesis.	imatinib	196-204	platelet derived growth factor receptor beta	Homo sapiens	180-185
25761894-6	2015	Both imatinib and dasatinib decreased the presence of CD11b(+)CD14(-)CD33(+) myeloid cells as well as the inhibitory molecules and the remaining myeloid suppressor cells had an increased CD40 expression.	imatinib	5-13	integrin subunit alpha M	Homo sapiens	54-59
25761894-6	2015	Both imatinib and dasatinib decreased the presence of CD11b(+)CD14(-)CD33(+) myeloid cells as well as the inhibitory molecules and the remaining myeloid suppressor cells had an increased CD40 expression.	imatinib	5-13	CD14 molecule	Homo sapiens	62-66
25761894-6	2015	Both imatinib and dasatinib decreased the presence of CD11b(+)CD14(-)CD33(+) myeloid cells as well as the inhibitory molecules and the remaining myeloid suppressor cells had an increased CD40 expression.	imatinib	5-13	CD33 molecule	Homo sapiens	69-73
25761894-6	2015	Both imatinib and dasatinib decreased the presence of CD11b(+)CD14(-)CD33(+) myeloid cells as well as the inhibitory molecules and the remaining myeloid suppressor cells had an increased CD40 expression.	imatinib	5-13	CD40 molecule	Homo sapiens	187-191
25897414-0	2015	Coexistence of P190 and P210 BCR/ABL transcripts in chronic myeloid leukemia blast crisis resistant to imatinib.	imatinib	103-111	contactin associated protein 1	Homo sapiens	15-36
25897414-6	2015	Imatinib resistance was confirmed by a screening for ABL kinase domain E255K mutations, and dasatinib was administered.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
25897414-13	2015	Thus monitoring the resistance of imatinib in CML patients, especially for advanced phase CML and BCR-ABL ALL, may be meaningful to guide clinical treatment and predict the prognosis.	imatinib	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
25844926-8	2015	Analysis of CYP2W1 expression in the colon adenocarcinoma cell line HCC2998 revealed that the gene expression can be induced by e.g. the antitumor agent imatinib, linoleic acid and its derivatives.	imatinib	153-161	cytochrome P450 family 2 subfamily W member 1	Homo sapiens	12-18
25844926-9	2015	The imatinib mediated induction of CYP2W1 suggests an adjuvant therapy to treatment with duocarmycins that thus would involve induction of tumor CYP2W1 levels followed by the CYP2W1 activated duocarmycin prodrugs.	imatinib	4-12	cytochrome P450 family 2 subfamily W member 1	Homo sapiens	35-41
25844926-9	2015	The imatinib mediated induction of CYP2W1 suggests an adjuvant therapy to treatment with duocarmycins that thus would involve induction of tumor CYP2W1 levels followed by the CYP2W1 activated duocarmycin prodrugs.	imatinib	4-12	cytochrome P450 family 2 subfamily W member 1	Homo sapiens	145-151
25844926-9	2015	The imatinib mediated induction of CYP2W1 suggests an adjuvant therapy to treatment with duocarmycins that thus would involve induction of tumor CYP2W1 levels followed by the CYP2W1 activated duocarmycin prodrugs.	imatinib	4-12	cytochrome P450 family 2 subfamily W member 1	Homo sapiens	145-151
26413254-0	2015	Characterizing of Four Common BCR-ABL Kinase Domain Mutations (T315I, Y253H, M351T and E255K) in Iranian Chronic Myelogenous Leukemia Patients With Imatinib Resistance.	imatinib	148-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
26413254-3	2015	One of the most considerable causes of resistance against Imatinib as the first line of therapy, are BCR-ABL kinase domain mutations.	imatinib	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
26413254-4	2015	OBJECTIVES: One of the most considerable causes of resistance against Imatinib as the first line of therapy, are BCR-ABL kinase domain mutations.	imatinib	70-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
26413254-15	2015	CONCLUSIONS: Identification of ABL kinase domain mutations may be used as a proper and useful method for improving therapeutic strategies, avoiding delay in treatment and excessive expenditure in CML patients with Imatinib resistance.	imatinib	214-222	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-34
25740611-0	2015	Incidence and clinical importance of BCR-ABL1 mutations in Iranian patients with chronic myeloid leukemia on imatinib.	imatinib	109-117	BCR activator of RhoGEF and GTPase	Homo sapiens	37-45
25740611-1	2015	Mutations of the BCR-ABL1 kinase domain seem to be the most common cause of imatinib mesylate resistance in chronic myeloid leukemia (CML).	imatinib	76-93	BCR activator of RhoGEF and GTPase	Homo sapiens	17-20
25740611-1	2015	Mutations of the BCR-ABL1 kinase domain seem to be the most common cause of imatinib mesylate resistance in chronic myeloid leukemia (CML).	imatinib	76-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-25
25740611-9	2015	We conclude that BCR- ABL1 mutations are associated with the clinical resistance, but may not be considered the only cause of resistance to imatinib.	imatinib	140-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-26
25060390-2	2015	The results indicated that the fluorescence intensity of CuInS2 /ZnS/TGA could be quenched by imatinib, dasatinib, nilotinib, gefitinib and erlotinib, which hinted that CuInS2 /ZnS/TGA QDs could be used in the detection of TKI in active pharmaceutical ingredients (API).	imatinib	94-102	T-box transcription factor 1	Homo sapiens	69-72
25060390-2	2015	The results indicated that the fluorescence intensity of CuInS2 /ZnS/TGA could be quenched by imatinib, dasatinib, nilotinib, gefitinib and erlotinib, which hinted that CuInS2 /ZnS/TGA QDs could be used in the detection of TKI in active pharmaceutical ingredients (API).	imatinib	94-102	T-box transcription factor 1	Homo sapiens	181-184
25849484-7	2015	Our data revealed that Imatinib (IM) induced BCR-ABL inhibition results in significant (p<0.05) upregulation of Notch activity, assessed by Hes1 expression.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
25849484-7	2015	Our data revealed that Imatinib (IM) induced BCR-ABL inhibition results in significant (p<0.05) upregulation of Notch activity, assessed by Hes1 expression.	imatinib	23-31	notch receptor 1	Homo sapiens	115-120
25849484-7	2015	Our data revealed that Imatinib (IM) induced BCR-ABL inhibition results in significant (p<0.05) upregulation of Notch activity, assessed by Hes1 expression.	imatinib	23-31	hes family bHLH transcription factor 1	Homo sapiens	143-147
25849484-11	2015	Finally, we also confirmed the potential antagonism between Notch and BCR/ABL in In Vivo, using publically available GSE-database, by analysing gene expression profile of paired samples from chronic-phase CML patients pre- and post-Imatinib therapy.	imatinib	232-240	notch receptor 1	Homo sapiens	60-65
25849484-11	2015	Finally, we also confirmed the potential antagonism between Notch and BCR/ABL in In Vivo, using publically available GSE-database, by analysing gene expression profile of paired samples from chronic-phase CML patients pre- and post-Imatinib therapy.	imatinib	232-240	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
25678499-4	2015	Morgana is also underexpressed in the BM of a portion of patients affected by Philadelphia-positive CML (Ph(+) CML) caused by the BCR-ABL oncogene, and in this condition, morgana underexpression predicts a worse response to imatinib, the standard treatment for Ph(+) CML.	imatinib	224-232	cysteine and histidine rich domain containing 1	Homo sapiens	0-7
25678499-4	2015	Morgana is also underexpressed in the BM of a portion of patients affected by Philadelphia-positive CML (Ph(+) CML) caused by the BCR-ABL oncogene, and in this condition, morgana underexpression predicts a worse response to imatinib, the standard treatment for Ph(+) CML.	imatinib	224-232	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
25678499-4	2015	Morgana is also underexpressed in the BM of a portion of patients affected by Philadelphia-positive CML (Ph(+) CML) caused by the BCR-ABL oncogene, and in this condition, morgana underexpression predicts a worse response to imatinib, the standard treatment for Ph(+) CML.	imatinib	224-232	cysteine and histidine rich domain containing 1	Homo sapiens	171-178
25678499-5	2015	Thus, morgana acts as an oncosuppressor with different modalities: (1) Morgana underexpression induces centrosome amplification and cytogenetic abnormalities, and (2) in Ph(+) CML, it synergizes with BCR-ABL signaling, reducing the efficacy of imatinib treatment.	imatinib	244-252	cysteine and histidine rich domain containing 1	Homo sapiens	6-13
25678499-6	2015	Importantly, ROCK inhibition in the BM of patients underexpressing morgana restored the efficacy of imatinib to induce apoptosis, suggesting that ROCK inhibitors, combined with imatinib treatment, can overcome suboptimal responses in patients in which morgana is underexpressed.	imatinib	100-108	cysteine and histidine rich domain containing 1	Homo sapiens	67-74
25678499-6	2015	Importantly, ROCK inhibition in the BM of patients underexpressing morgana restored the efficacy of imatinib to induce apoptosis, suggesting that ROCK inhibitors, combined with imatinib treatment, can overcome suboptimal responses in patients in which morgana is underexpressed.	imatinib	100-108	cysteine and histidine rich domain containing 1	Homo sapiens	252-259
25678499-6	2015	Importantly, ROCK inhibition in the BM of patients underexpressing morgana restored the efficacy of imatinib to induce apoptosis, suggesting that ROCK inhibitors, combined with imatinib treatment, can overcome suboptimal responses in patients in which morgana is underexpressed.	imatinib	177-185	cysteine and histidine rich domain containing 1	Homo sapiens	67-74
25814086-5	2015	Today, BCR-ABL tyrosine kinase inhibitors (TKIs), such as imatinib, induce remarkable responses in CML patients and have become the mainstay of CML therapy.	imatinib	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	7-14
25814086-7	2015	Some of the clinical trials testing IFNalpha plus imatinib combination therapy suggest that addition of IFNalpha increases the speed and rate of responses with imatinib therapy.	imatinib	50-58	interferon alpha 1	Homo sapiens	104-112
25814086-7	2015	Some of the clinical trials testing IFNalpha plus imatinib combination therapy suggest that addition of IFNalpha increases the speed and rate of responses with imatinib therapy.	imatinib	160-168	interferon alpha 1	Homo sapiens	36-44
25814086-7	2015	Some of the clinical trials testing IFNalpha plus imatinib combination therapy suggest that addition of IFNalpha increases the speed and rate of responses with imatinib therapy.	imatinib	160-168	interferon alpha 1	Homo sapiens	104-112
25673643-0	2015	FGFR-Mediated Reactivation of MAPK Signaling Attenuates Antitumor Effects of Imatinib in Gastrointestinal Stromal Tumors.	imatinib	77-85	mitogen-activated protein kinase 1	Homo sapiens	30-34
25673643-2	2015	Although treatment with the KIT and PDGFR inhibitor imatinib can control advanced disease in about 80% of GIST patients, the beneficial effect is not durable.	imatinib	52-60	platelet derived growth factor receptor beta	Homo sapiens	36-41
25673643-3	2015	Here, we report that ligands from the FGF family reduced the effectiveness of imatinib in GIST cells, and FGF2 and FGFR1 are highly expressed in all primary GIST samples examined.	imatinib	78-86	fibroblast growth factor 2	Homo sapiens	38-41
25673643-4	2015	The combination of KIT and FGFR inhibition showed increased growth inhibition in imatinib-sensitive GIST cell lines and improved efficacy in patient-derived GIST xenografts.	imatinib	81-89	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	19-22
25673643-5	2015	In addition, inhibition of MAPK signaling by imatinib was not sustained in GIST cells.	imatinib	45-53	mitogen-activated protein kinase 1	Homo sapiens	27-31
25673643-7	2015	Downregulation of Sprouty proteins played a role in the imatinib-induced feedback activation of FGF signaling in GIST cells.	imatinib	56-64	fibroblast growth factor 2	Homo sapiens	96-99
25673643-8	2015	SIGNIFICANCE: We here show that FGFR-mediated reactivation of the MAPK pathway attenuates the antiproliferation effects of imatinib in GISTs.	imatinib	123-131	mitogen-activated protein kinase 1	Homo sapiens	66-70
25673643-9	2015	The imatinib-induced ERK rebound can be repressed by the FGFR inhibitor BGJ398, and combined KIT and FGFR inhibition leads to increased efficacy in vitro and in patient-derived xenografts.	imatinib	4-12	mitogen-activated protein kinase 1	Homo sapiens	21-24
25673643-9	2015	The imatinib-induced ERK rebound can be repressed by the FGFR inhibitor BGJ398, and combined KIT and FGFR inhibition leads to increased efficacy in vitro and in patient-derived xenografts.	imatinib	4-12	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	93-96
25039350-0	2015	Exposure of chronic myelogenous leukemia cells to imatinib results in the post-transcriptional induction of manganese superoxide dismutase.	imatinib	50-58	superoxide dismutase 2	Homo sapiens	108-138
25056761-0	2015	Relationship between SLCO1B3 and ABCA3 polymorphisms and imatinib response in chronic myeloid leukemia patients.	imatinib	57-65	solute carrier organic anion transporter family member 1B3	Homo sapiens	21-28
25056761-0	2015	Relationship between SLCO1B3 and ABCA3 polymorphisms and imatinib response in chronic myeloid leukemia patients.	imatinib	57-65	ATP binding cassette subfamily A member 3	Homo sapiens	33-38
25389112-3	2015	Moreover, CBY1 transcriptional induction proceeding from promoter de-methylation is a component of BCR-ABL1+ cell response to Imatinib (IM).	imatinib	126-134	chibby family member 1, beta catenin antagonist	Homo sapiens	10-14
25389112-3	2015	Moreover, CBY1 transcriptional induction proceeding from promoter de-methylation is a component of BCR-ABL1+ cell response to Imatinib (IM).	imatinib	126-134	BCR activator of RhoGEF and GTPase	Homo sapiens	99-107
25635590-12	2015	Using this receptor-focused approach, it is possible to capture the observed fold change in binding affinities between the wild-type and disease-centric mutations in ABL kinase for Imatinib and the second-generation ABL drugs.	imatinib	181-189	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-169
25039350-2	2015	In order to investigate the biological consequences of treating CML cells with such drugs, we previously reported that the antioxidant selenoprotein glutathione peroxidase-1 (GPx-1) was induced by imatinib in both patient samples and cultured cells.	imatinib	197-205	glutathione peroxidase 1	Homo sapiens	175-180
25501030-6	2015	Based on interaction studies of imatinib with the cytochrome P450 (CYP450) inhibitors VID400 and ketoconazole, it is proposed that imatinib may interfere with the vitamin D3 cascade due to its metabolism by CYP27B1, which is involved in vitamin D3 metabolism.	imatinib	131-139	cytochrome P450 family 27 subfamily B member 1	Homo sapiens	207-214
25757539-0	2015	PI3K/AKT/mTOR pathway is activated after imatinib secondary resistance in gastrointestinal stromal tumors (GISTs).	imatinib	41-49	AKT serine/threonine kinase 1	Homo sapiens	5-8
25757539-0	2015	PI3K/AKT/mTOR pathway is activated after imatinib secondary resistance in gastrointestinal stromal tumors (GISTs).	imatinib	41-49	mechanistic target of rapamycin kinase	Homo sapiens	9-13
25757539-1	2015	Phosphatidylinositol-3-kinase (PI3K)/AKT/mammalian target of the rapamycin (mTOR) pathway activation may be related to imatinib resistance; however, no study has focused on whether signal conduction of this pathway will change after imatinib resistance.	imatinib	119-127	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	0-29
25757539-1	2015	Phosphatidylinositol-3-kinase (PI3K)/AKT/mammalian target of the rapamycin (mTOR) pathway activation may be related to imatinib resistance; however, no study has focused on whether signal conduction of this pathway will change after imatinib resistance.	imatinib	119-127	AKT serine/threonine kinase 1	Homo sapiens	37-40
25757539-1	2015	Phosphatidylinositol-3-kinase (PI3K)/AKT/mammalian target of the rapamycin (mTOR) pathway activation may be related to imatinib resistance; however, no study has focused on whether signal conduction of this pathway will change after imatinib resistance.	imatinib	119-127	mechanistic target of rapamycin kinase	Homo sapiens	76-80
25757539-1	2015	Phosphatidylinositol-3-kinase (PI3K)/AKT/mammalian target of the rapamycin (mTOR) pathway activation may be related to imatinib resistance; however, no study has focused on whether signal conduction of this pathway will change after imatinib resistance.	imatinib	233-241	AKT serine/threonine kinase 1	Homo sapiens	37-40
25757539-1	2015	Phosphatidylinositol-3-kinase (PI3K)/AKT/mammalian target of the rapamycin (mTOR) pathway activation may be related to imatinib resistance; however, no study has focused on whether signal conduction of this pathway will change after imatinib resistance.	imatinib	233-241	mechanistic target of rapamycin kinase	Homo sapiens	76-80
25757539-4	2015	The activation of AKT/mTOR was significantly higher in imatinib secondary resistant GIST (53.1 %) than in imatinib-sensitive (27.1 %) and primary resistant GIST (33.3 %) (P = 0.049).	imatinib	55-63	AKT serine/threonine kinase 1	Homo sapiens	18-21
25757539-4	2015	The activation of AKT/mTOR was significantly higher in imatinib secondary resistant GIST (53.1 %) than in imatinib-sensitive (27.1 %) and primary resistant GIST (33.3 %) (P = 0.049).	imatinib	55-63	mechanistic target of rapamycin kinase	Homo sapiens	22-26
25757539-4	2015	The activation of AKT/mTOR was significantly higher in imatinib secondary resistant GIST (53.1 %) than in imatinib-sensitive (27.1 %) and primary resistant GIST (33.3 %) (P = 0.049).	imatinib	106-114	AKT serine/threonine kinase 1	Homo sapiens	18-21
25757539-4	2015	The activation of AKT/mTOR was significantly higher in imatinib secondary resistant GIST (53.1 %) than in imatinib-sensitive (27.1 %) and primary resistant GIST (33.3 %) (P = 0.049).	imatinib	106-114	mechanistic target of rapamycin kinase	Homo sapiens	22-26
25757539-6	2015	AKT/mTOR status was inactivated in pre-imatinib and on-treatment samples in eight patients with effective imatinib; however, the status of six patients was changed from inactivated to activated in 12 patients at the time of tumor progression.	imatinib	39-47	AKT serine/threonine kinase 1	Homo sapiens	0-3
25757539-6	2015	AKT/mTOR status was inactivated in pre-imatinib and on-treatment samples in eight patients with effective imatinib; however, the status of six patients was changed from inactivated to activated in 12 patients at the time of tumor progression.	imatinib	39-47	mechanistic target of rapamycin kinase	Homo sapiens	4-8
25757539-6	2015	AKT/mTOR status was inactivated in pre-imatinib and on-treatment samples in eight patients with effective imatinib; however, the status of six patients was changed from inactivated to activated in 12 patients at the time of tumor progression.	imatinib	106-114	AKT serine/threonine kinase 1	Homo sapiens	0-3
29147425-0	2015	Polymorphism T81C in H-RAS Oncogene Is Associated With Disease Progression in Imatinib (TKI) Treated Chronic Myeloid Leukemia Patients.	imatinib	78-86	HRas proto-oncogene, GTPase	Homo sapiens	21-26
25757539-6	2015	AKT/mTOR status was inactivated in pre-imatinib and on-treatment samples in eight patients with effective imatinib; however, the status of six patients was changed from inactivated to activated in 12 patients at the time of tumor progression.	imatinib	106-114	mechanistic target of rapamycin kinase	Homo sapiens	4-8
25757539-8	2015	PI3K/AKT/mTOR pathway can be partly activated after imatinib secondary resistance in GIST.	imatinib	52-60	AKT serine/threonine kinase 1	Homo sapiens	5-8
25757539-8	2015	PI3K/AKT/mTOR pathway can be partly activated after imatinib secondary resistance in GIST.	imatinib	52-60	mechanistic target of rapamycin kinase	Homo sapiens	9-13
25245580-0	2015	ABCB1 polymorphisms predict imatinib response in chronic myeloid leukemia patients: a systematic review and meta-analysis.	imatinib	28-36	ATP binding cassette subfamily B member 1	Homo sapiens	0-5
25822986-1	2015	Imatinib mesylate (Gleevec) inhibits Abl1, c-Kit, and related protein tyrosine kinases (PTKs) and serves as a therapeutic for chronic myelogenous leukemia and gastrointestinal stromal tumors.	imatinib	0-17	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	37-41
25822986-4	2015	Whereas progenitor differentiation relies on partial inhibition of c-Kit by imatinib, lineage commitment depends upon inhibition of other PTKs.	imatinib	76-84	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	67-72
25822986-1	2015	Imatinib mesylate (Gleevec) inhibits Abl1, c-Kit, and related protein tyrosine kinases (PTKs) and serves as a therapeutic for chronic myelogenous leukemia and gastrointestinal stromal tumors.	imatinib	0-17	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	43-48
25822986-1	2015	Imatinib mesylate (Gleevec) inhibits Abl1, c-Kit, and related protein tyrosine kinases (PTKs) and serves as a therapeutic for chronic myelogenous leukemia and gastrointestinal stromal tumors.	imatinib	19-26	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	37-41
25822986-1	2015	Imatinib mesylate (Gleevec) inhibits Abl1, c-Kit, and related protein tyrosine kinases (PTKs) and serves as a therapeutic for chronic myelogenous leukemia and gastrointestinal stromal tumors.	imatinib	19-26	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	43-48
25889792-4	2015	Interestingly, its expression on human monocyte-derived dendritic cells (moDC) is dramatically upregulated upon treatment with IL-10 but also by the BCR-ABL tyrosine kinase inhibitors (TKI) imatinib, nilotinib or dasatinib used for the treatment of chronic myeloid leukemia (CML).	imatinib	190-198	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
25781619-2	2015	Dramatic metabolic responses following imatinib treatment indicate a high, KIT-dependent glucose turnover which has been particularly helpful for predicting tumor response to imatinib.	imatinib	39-47	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	75-78
25889792-6	2015	RESULTS: The immunosuppressive cytokine IL-10 and the BCR-ABL TKI imatinib or nilotinib, that were examined here, concordantly inhibit the PI3K/Akt signaling pathway, thereby activating the downstream serine/threonine protein kinase GSK3ss, and subsequently the microphthalmia-associated transcription factor (MITF) that is phosphorylated and translocated into the nucleus.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
25889792-6	2015	RESULTS: The immunosuppressive cytokine IL-10 and the BCR-ABL TKI imatinib or nilotinib, that were examined here, concordantly inhibit the PI3K/Akt signaling pathway, thereby activating the downstream serine/threonine protein kinase GSK3ss, and subsequently the microphthalmia-associated transcription factor (MITF) that is phosphorylated and translocated into the nucleus.	imatinib	66-74	AKT serine/threonine kinase 1	Homo sapiens	144-147
25889792-6	2015	RESULTS: The immunosuppressive cytokine IL-10 and the BCR-ABL TKI imatinib or nilotinib, that were examined here, concordantly inhibit the PI3K/Akt signaling pathway, thereby activating the downstream serine/threonine protein kinase GSK3ss, and subsequently the microphthalmia-associated transcription factor (MITF) that is phosphorylated and translocated into the nucleus.	imatinib	66-74	melanocyte inducing transcription factor	Homo sapiens	262-308
25889792-6	2015	RESULTS: The immunosuppressive cytokine IL-10 and the BCR-ABL TKI imatinib or nilotinib, that were examined here, concordantly inhibit the PI3K/Akt signaling pathway, thereby activating the downstream serine/threonine protein kinase GSK3ss, and subsequently the microphthalmia-associated transcription factor (MITF) that is phosphorylated and translocated into the nucleus.	imatinib	66-74	melanocyte inducing transcription factor	Homo sapiens	310-314
25889792-9	2015	CONCLUSIONS: In summary, imatinib, nilotinib or IL-10 congruently inhibit the PI3K/Akt signaling pathway thereby activating MITF in moDC, resulting in a tolerogenic phenotype.	imatinib	25-33	AKT serine/threonine kinase 1	Homo sapiens	83-86
25889792-9	2015	CONCLUSIONS: In summary, imatinib, nilotinib or IL-10 congruently inhibit the PI3K/Akt signaling pathway thereby activating MITF in moDC, resulting in a tolerogenic phenotype.	imatinib	25-33	melanocyte inducing transcription factor	Homo sapiens	124-128
25781619-2	2015	Dramatic metabolic responses following imatinib treatment indicate a high, KIT-dependent glucose turnover which has been particularly helpful for predicting tumor response to imatinib.	imatinib	175-183	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	75-78
25686603-2	2015	Introduction of ABL1 kinase inhibitors (for example, imatinib) has markedly improved patient survival, but acquired drug resistance remains a challenge.	imatinib	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-20
25573989-5	2015	shRNA-mediated RAN inhibition or treatment of cells with the XPO1 inhibitor, KPT-330 (Selinexor), increased the imatinib sensitivity of CML cell lines with kinase-independent TKI resistance.	imatinib	112-120	RAN, member RAS oncogene family	Homo sapiens	15-18
25573989-5	2015	shRNA-mediated RAN inhibition or treatment of cells with the XPO1 inhibitor, KPT-330 (Selinexor), increased the imatinib sensitivity of CML cell lines with kinase-independent TKI resistance.	imatinib	112-120	exportin 1	Homo sapiens	61-65
25573989-6	2015	Inhibition of either RAN or XPO1 impaired colony formation of CD34(+) cells from newly diagnosed and TKI-resistant CML patients in the presence of imatinib, without effects on CD34(+) cells from normal cord blood or from a patient harboring the BCR-ABL1(T315I) mutant.	imatinib	147-155	RAN, member RAS oncogene family	Homo sapiens	21-24
25573989-6	2015	Inhibition of either RAN or XPO1 impaired colony formation of CD34(+) cells from newly diagnosed and TKI-resistant CML patients in the presence of imatinib, without effects on CD34(+) cells from normal cord blood or from a patient harboring the BCR-ABL1(T315I) mutant.	imatinib	147-155	exportin 1	Homo sapiens	28-32
25573989-7	2015	These data implicate RAN in BCR-ABL1 kinase-independent imatinib resistance and show that shRNA library screens are useful to identify alternative pathways critical to drug resistance in CML.	imatinib	56-64	RAN, member RAS oncogene family	Homo sapiens	21-24
25573989-7	2015	These data implicate RAN in BCR-ABL1 kinase-independent imatinib resistance and show that shRNA library screens are useful to identify alternative pathways critical to drug resistance in CML.	imatinib	56-64	BCR activator of RhoGEF and GTPase	Homo sapiens	28-36
24638008-0	2015	In vivo imatinib sensitivity in a patient with GI stromal tumor bearing a PDGFRA deletion DIM842-844.	imatinib	8-16	platelet derived growth factor receptor alpha	Homo sapiens	74-80
25042176-6	2015	c-KIT mutations are more common than in other types of melanoma and this has led to significant advances in the use of imatinib for the treatment of metastatic mucosal melanoma.	imatinib	119-127	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-5
25873877-8	2015	Structurally, it is similar to imatinib (the older tyrosine kinase inhibitor), but it is much more potent in inhibiting BCR-ABL due to its much increased affinity for its binding site.	imatinib	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
25410137-1	2015	Imatinib was the first BCR-ABL1 tyrosine kinase inhibitor (TKI) developed for the treatment of patients with chronic myeloid leukemia (CML); subsequently, the introduction of more potent BCR-ABL1 TKIs has raised expectations regarding the speed and depth of response.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
25410137-1	2015	Imatinib was the first BCR-ABL1 tyrosine kinase inhibitor (TKI) developed for the treatment of patients with chronic myeloid leukemia (CML); subsequently, the introduction of more potent BCR-ABL1 TKIs has raised expectations regarding the speed and depth of response.	imatinib	0-8	BCR activator of RhoGEF and GTPase	Homo sapiens	23-31
25432174-4	2015	Addition of the FGFR3 ligand FGF2 to GIST cells restored KIT phosphorylation during imatinib treatment, allowing sensitive cells to proliferate in the presence of the drug.	imatinib	84-92	fibroblast growth factor receptor 3	Homo sapiens	16-21
25688753-10	2015	Imatinib has a therapeutic role in the presence of an imatinib-sensitive KIT mutation or in KITD816-unmutated patients.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
25688753-10	2015	Imatinib has a therapeutic role in the presence of an imatinib-sensitive KIT mutation or in KITD816-unmutated patients.	imatinib	54-62	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
25432174-9	2015	Our findings provide a mechanistic rationale to evaluate existing FGFR inhibitors and multikinase inhibitors that target FGFR3 as promising strategies to improve treatment of patients with GIST with de novo or acquired resistance to imatinib.	imatinib	233-241	fibroblast growth factor receptor 3	Homo sapiens	121-126
25432174-4	2015	Addition of the FGFR3 ligand FGF2 to GIST cells restored KIT phosphorylation during imatinib treatment, allowing sensitive cells to proliferate in the presence of the drug.	imatinib	84-92	fibroblast growth factor 2	Homo sapiens	29-33
25572173-2	2015	Despite the clinical success of imatinib, which targets KIT, most patients with advanced GIST develop resistance and eventually die of the disease.	imatinib	32-40	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	56-59
25432174-4	2015	Addition of the FGFR3 ligand FGF2 to GIST cells restored KIT phosphorylation during imatinib treatment, allowing sensitive cells to proliferate in the presence of the drug.	imatinib	84-92	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	57-60
25432174-5	2015	FGF2 expression was increased in imatinib-resistant GIST cells, the growth of which was blocked by RNAi-mediated silencing of FGFR3.	imatinib	33-41	fibroblast growth factor 2	Homo sapiens	0-4
25572173-6	2015	Combined targeting of ETV1 stability by imatinib and MEK162 resulted in increased growth suppression in vitro and complete tumor regression in vivo.	imatinib	40-48	ETS variant transcription factor 1	Homo sapiens	22-26
25432174-5	2015	FGF2 expression was increased in imatinib-resistant GIST cells, the growth of which was blocked by RNAi-mediated silencing of FGFR3.	imatinib	33-41	fibroblast growth factor receptor 3	Homo sapiens	126-131
25432174-6	2015	Moreover, combining KIT and FGFR3 inhibitors synergized to block the growth of imatinib-resistant cells.	imatinib	79-87	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	20-23
25432174-6	2015	Moreover, combining KIT and FGFR3 inhibitors synergized to block the growth of imatinib-resistant cells.	imatinib	79-87	fibroblast growth factor receptor 3	Homo sapiens	28-33
25432174-7	2015	Signaling crosstalk between KIT and FGFR3 activated the MAPK pathway to promote resistance to imatinib.	imatinib	94-102	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	28-31
25432174-7	2015	Signaling crosstalk between KIT and FGFR3 activated the MAPK pathway to promote resistance to imatinib.	imatinib	94-102	fibroblast growth factor receptor 3	Homo sapiens	36-41
25432174-8	2015	Clinically, an IHC analysis of tumor specimens from imatinib-resistant GIST patients revealed a relative increase in FGF2 levels, with a trend toward increased expression in imatinib-naive samples consistent with possible involvement in drug resistance.	imatinib	52-60	fibroblast growth factor 2	Homo sapiens	117-121
24844361-7	2015	Among 10 evaluable patients, rapid loss of phospho-CRKL occurred during the imatinib window in seven patients (all achieved CR) and incomplete inhibition in three patients (none with CR).	imatinib	76-84	CRK like proto-oncogene, adaptor protein	Homo sapiens	51-55
25804236-0	2015	Functional activity of CD34-positive cells in chronic myeloid leukemia patients with different response to imatinib therapy.	imatinib	107-115	CD34 molecule	Homo sapiens	23-27
25804236-4	2015	AIM: to determine the CD34 antigen expression in bone marrow and peripheral blood cells in CML patients with different response to imatinib therapy using the results of hematopoietic cells culturing and the data of flow cytometry.	imatinib	131-139	CD34 molecule	Homo sapiens	22-26
25804236-8	2015	The results of cytometric studies have shown that the number of CD34(+) cells in bone marrow was significantly higher compared to the number of CD34(+) cells in peripheral blood cells and increased with the acquisition of leukemic cells the resistance to imatinib.	imatinib	255-263	CD34 molecule	Homo sapiens	64-68
25427437-8	2015	One case had a KRAS G12V (c.35G>T) mutation in both the primary gastric tumor and a post-imatinib recurrence.	imatinib	92-100	KRAS proto-oncogene, GTPase	Homo sapiens	15-19
24975316-0	2015	Imatinib non-responsive chronic eosinophilic leukemia with ETV6-PDGFRA fusion gene.	imatinib	0-8	ETS variant transcription factor 6	Homo sapiens	59-63
24975316-0	2015	Imatinib non-responsive chronic eosinophilic leukemia with ETV6-PDGFRA fusion gene.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	64-70
24884318-6	2015	Furthermore, CPT in combination with imatinib dramatically decreased the activity of the Bcr/Abl pathway in both K562 and K562-R cells.	imatinib	37-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
25575688-1	2015	Imatinib resistance has been associated with BCR-ABL alterations, but other mechanisms might be involved, like drug transporters.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
25575688-6	2015	By exploring P-gP expression of resistant cells, we observed the potential of P-gP inhibitor in circumventing Imatinib resistance.	imatinib	110-118	phosphoglycolate phosphatase	Homo sapiens	13-17
25575688-6	2015	By exploring P-gP expression of resistant cells, we observed the potential of P-gP inhibitor in circumventing Imatinib resistance.	imatinib	110-118	phosphoglycolate phosphatase	Homo sapiens	78-82
24884318-7	2015	Our results demonstrated that CPT increased imatinib-induced apoptosis in a Bcr/Abl dependent manner, suggesting a novel strategy for the treatment of CML.	imatinib	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
27308396-0	2015	Imatinib may be ABL to improve anti-angiogenic therapy.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-19
25818829-0	2015	Is the BCR-ABL/GUSB transcript level at diagnosis an early predictive marker for chronic myeloid leukemia patients treated with imatinib?	imatinib	128-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	7-14
25818829-0	2015	Is the BCR-ABL/GUSB transcript level at diagnosis an early predictive marker for chronic myeloid leukemia patients treated with imatinib?	imatinib	128-136	glucuronidase beta	Homo sapiens	15-19
25501124-0	2015	Dual inhibition of Bcr-Abl and Hsp90 by C086 potently inhibits the proliferation of imatinib-resistant CML cells.	imatinib	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
25605011-4	2015	We examined the in vitro- and in vivo effects of the KIT-targeting drug imatinib on growth and development of human MC.	imatinib	72-80	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	53-56
25605011-5	2015	Imatinib was found to inhibit stem cell factor (SCF)-induced differentiation of MC in long-term suspension cultures (IC50: 0.01 microM).	imatinib	0-8	KIT ligand	Homo sapiens	30-46
25605011-5	2015	Imatinib was found to inhibit stem cell factor (SCF)-induced differentiation of MC in long-term suspension cultures (IC50: 0.01 microM).	imatinib	0-8	KIT ligand	Homo sapiens	48-51
25688862-0	2015	Spred2 modulates the erythroid differentiation induced by imatinib in chronic myeloid leukemia cells.	imatinib	58-66	sprouty related EVH1 domain containing 2	Homo sapiens	0-6
25688862-2	2015	Our previous work has demonstrated that Sprouty-related EVH1 domainprotein2 (Spred2) was involved in imatinib mediated cytotoxicity in CML cells.	imatinib	101-109	sprouty related EVH1 domain containing 2	Homo sapiens	40-75
25688862-2	2015	Our previous work has demonstrated that Sprouty-related EVH1 domainprotein2 (Spred2) was involved in imatinib mediated cytotoxicity in CML cells.	imatinib	101-109	sprouty related EVH1 domain containing 2	Homo sapiens	77-83
25688862-5	2015	Imatinib could induce Spred2 expression and enhance erythroid differentiation in K562 cells.	imatinib	0-8	sprouty related EVH1 domain containing 2	Homo sapiens	22-28
25688862-6	2015	However, the imatinib induced erythroid differentiation could be blocked by Spred2 silence using lentiviral vector PLKO.1-shSpred2.	imatinib	13-21	sprouty related EVH1 domain containing 2	Homo sapiens	76-82
25688862-8	2015	Furthermore, Spred2 interference partly restored p-ERK level leading to inhibition of erythroid differentiation in imatinib treated K562 cells.	imatinib	115-123	sprouty related EVH1 domain containing 2	Homo sapiens	13-19
25688862-9	2015	In conclusion, Spred2 was involved in erythroid differentiation of CML cells and participated in imatinib induced erythroid differentiation partly through ERK signaling.	imatinib	97-105	sprouty related EVH1 domain containing 2	Homo sapiens	15-21
25688862-9	2015	In conclusion, Spred2 was involved in erythroid differentiation of CML cells and participated in imatinib induced erythroid differentiation partly through ERK signaling.	imatinib	97-105	mitogen-activated protein kinase 1	Homo sapiens	155-158
25554490-2	2015	Imatinib, a targeted anticancer drug, exerts a therapeutic effect against GISTs by repressing the kinase activity of KIT.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	117-120
25554490-8	2015	Treatment of GIST882-R with imatinib in combination with gefitinib, an EGFR inhibitor, partially prevented cell growth, implying that EGFR may be involved in acquisition of secondary imatinib resistance in GIST.	imatinib	28-36	epidermal growth factor receptor	Homo sapiens	71-75
25554490-8	2015	Treatment of GIST882-R with imatinib in combination with gefitinib, an EGFR inhibitor, partially prevented cell growth, implying that EGFR may be involved in acquisition of secondary imatinib resistance in GIST.	imatinib	28-36	epidermal growth factor receptor	Homo sapiens	134-138
25554490-8	2015	Treatment of GIST882-R with imatinib in combination with gefitinib, an EGFR inhibitor, partially prevented cell growth, implying that EGFR may be involved in acquisition of secondary imatinib resistance in GIST.	imatinib	183-191	epidermal growth factor receptor	Homo sapiens	134-138
25554490-10	2015	The goal of the study was to investigate the mechanism of acquired resistance in GISTs against imatinib, a molecularly targeted drug that inhibits kinase activity of the KIT protein and that has been approved for the treatment of GISTs.	imatinib	95-103	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	170-173
25554490-11	2015	In imatinib-resistant GIST cells, we observed elevated expression of KIT and restoration of its kinase activity, as well as activation of multiple proliferative signaling pathways.	imatinib	3-11	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	69-72
25557174-2	2015	METHODS: RTK expression (c-Kit, c-Met, AXL, HER-1, HER-2, IGF-1R) in pre-/post-imatinib (IM) GIST patient samples (n=16) and 4 GIST cell lines were examined for RTK inhibitor activity.	imatinib	79-87	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	25-30
25658984-0	2015	Comprehensive genomic profiling identifies a novel TNKS2-PDGFRA fusion that defines a myeloid neoplasm with eosinophilia that responded dramatically to imatinib therapy.	imatinib	152-160	tankyrase 2	Homo sapiens	51-56
25658984-0	2015	Comprehensive genomic profiling identifies a novel TNKS2-PDGFRA fusion that defines a myeloid neoplasm with eosinophilia that responded dramatically to imatinib therapy.	imatinib	152-160	platelet derived growth factor receptor alpha	Homo sapiens	57-63
25730044-3	2015	In the present study, we used quantitative real-time reverse transcription-polymerase chain reaction (RT-qPCR) to monitor BCR-ABL expression in Moroccan CML patients undergoing imatinib treatment, and compared the results with those of conventional PCR and fluorescence in situ hybridization (FISH).	imatinib	177-185	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
25501124-0	2015	Dual inhibition of Bcr-Abl and Hsp90 by C086 potently inhibits the proliferation of imatinib-resistant CML cells.	imatinib	84-92	heat shock protein 90 alpha family class A member 1	Homo sapiens	31-36
25501124-1	2015	PURPOSE: Although tyrosine kinase inhibitors (TKI) such as imatinib provide an effective treatment against Bcr-Abl kinase activity in the mature cells of patients with chronic myelogenous leukemia (CML), TKIs probably cannot eradicate the leukemia stem cell (LSC) population.	imatinib	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
26155391-12	2015	In conclusion, PDL1 expression refines the prediction of metastatic relapse in localized GIST and might improve our ability to better tailor adjuvant imatinib.	imatinib	150-158	CD274 molecule	Homo sapiens	15-19
25647305-13	2015	Taken together, our results clearly suggested that NC promoted erythroid differentiation and apoptosis through c-Myc-miRNAs regulatory axis, providing potential possibility to overcome imatinib resistance.	imatinib	185-193	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	111-116
25450971-0	2015	Imatinib restores VASP activity and its interaction with Zyxin in BCR-ABL leukemic cells.	imatinib	0-8	vasodilator stimulated phosphoprotein	Homo sapiens	18-22
25480336-2	2015	Recent work has identified the Abl family kinases (c-Abl and Arg) as important regulators of endothelial cell (EC) barrier function and suggests that their inhibition by currently available pharmaceutical agents such as imatinib may be EC protective.	imatinib	220-228	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	31-34
25480336-2	2015	Recent work has identified the Abl family kinases (c-Abl and Arg) as important regulators of endothelial cell (EC) barrier function and suggests that their inhibition by currently available pharmaceutical agents such as imatinib may be EC protective.	imatinib	220-228	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	51-64
25480336-6	2015	Imatinib attenuates LPS-induced lung EC permeability, restores VE-cadherin junctions, and reduces inflammation by suppressing VCAM-1 expression and inflammatory cytokine (IL-8 and IL-6) secretion.	imatinib	0-8	cadherin 5	Mus musculus	63-74
25480336-6	2015	Imatinib attenuates LPS-induced lung EC permeability, restores VE-cadherin junctions, and reduces inflammation by suppressing VCAM-1 expression and inflammatory cytokine (IL-8 and IL-6) secretion.	imatinib	0-8	vascular cell adhesion molecule 1	Mus musculus	126-132
25480336-6	2015	Imatinib attenuates LPS-induced lung EC permeability, restores VE-cadherin junctions, and reduces inflammation by suppressing VCAM-1 expression and inflammatory cytokine (IL-8 and IL-6) secretion.	imatinib	0-8	chemokine (C-X-C motif) ligand 15	Mus musculus	171-175
25480336-6	2015	Imatinib attenuates LPS-induced lung EC permeability, restores VE-cadherin junctions, and reduces inflammation by suppressing VCAM-1 expression and inflammatory cytokine (IL-8 and IL-6) secretion.	imatinib	0-8	interleukin 6	Mus musculus	180-184
25480336-7	2015	Conversely, in EC exposed to pathological 18% cyclic stretch (CS) (in vitro model of VILI), imatinib decreases VE-cadherin expression, disrupts cell-cell junctions, and increases IL-8 levels.	imatinib	92-100	cadherin 5	Mus musculus	111-122
25480336-7	2015	Conversely, in EC exposed to pathological 18% cyclic stretch (CS) (in vitro model of VILI), imatinib decreases VE-cadherin expression, disrupts cell-cell junctions, and increases IL-8 levels.	imatinib	92-100	chemokine (C-X-C motif) ligand 15	Mus musculus	179-183
25450971-0	2015	Imatinib restores VASP activity and its interaction with Zyxin in BCR-ABL leukemic cells.	imatinib	0-8	zyxin	Homo sapiens	57-62
25450971-0	2015	Imatinib restores VASP activity and its interaction with Zyxin in BCR-ABL leukemic cells.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
25450971-8	2015	Imatinib induced an increase in phosphorylation at Ser157 of VASP and decreased VASP and BCR-ABL interaction.	imatinib	0-8	vasodilator stimulated phosphoprotein	Homo sapiens	61-65
25450971-8	2015	Imatinib induced an increase in phosphorylation at Ser157 of VASP and decreased VASP and BCR-ABL interaction.	imatinib	0-8	vasodilator stimulated phosphoprotein	Homo sapiens	80-84
25450971-8	2015	Imatinib induced an increase in phosphorylation at Ser157 of VASP and decreased VASP and BCR-ABL interaction.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
25450971-9	2015	VASP did not interact with Zyxin in K562 cells; however, after Imatinib treatment, this interaction was restored.	imatinib	63-71	vasodilator stimulated phosphoprotein	Homo sapiens	0-4
25450971-11	2015	Phosphorylation of VASP on Ser157 was restored in Imatinib responsive patients though not in the resistant patients.	imatinib	50-58	vasodilator stimulated phosphoprotein	Homo sapiens	19-23
25579165-0	2015	Molecular response to imatinib in chronic myeloid leukaemia with a variant e13a3 BCR-ABL1 fusion.	imatinib	22-30	BCR activator of RhoGEF and GTPase	Homo sapiens	81-89
25594139-2	2015	The c-kit inhibitor STI571 represents one of the most important treatments for patients with mastocytosis.	imatinib	20-26	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	4-9
25594139-5	2015	STI571 activates PKCdelta isoform resulting in HMC-1(560) apoptosis.	imatinib	0-6	protein kinase C delta	Homo sapiens	17-25
25594139-6	2015	The apoptosis observed is PKCdelta-dependent, since PKCdelta-silencing avoids STI571 effect.	imatinib	78-84	protein kinase C delta	Homo sapiens	26-34
25594139-6	2015	The apoptosis observed is PKCdelta-dependent, since PKCdelta-silencing avoids STI571 effect.	imatinib	78-84	protein kinase C delta	Homo sapiens	52-60
25594139-8	2015	Therefore, PKCdelta modulations can lead to a serious decrease in STI571 treatment-effectiveness.	imatinib	66-72	protein kinase C delta	Homo sapiens	11-19
26218127-0	2015	Coupled delivery of imatinib mesylate and doxorubicin with nanoscaled polymeric vectors for a sustained downregulation of BCR-ABL in chronic myeloid leukemia.	imatinib	20-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
25615000-11	2015	CONCLUSIONS: Lack of response to TKIs associated with mutation in the BCR-ABL gene was significantly higher in imatinib-treated patients, and all mutations arose after treatment.	imatinib	111-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
25765803-0	2015	[Treatment-free molecular remission achieved by combination therapy with imatinib and IFNalpha in CML with BIM deletion polymorphism relapsed after stop imatinib].	imatinib	153-161	interferon alpha 1	Homo sapiens	86-94
25831762-0	2015	[Inhibitors for ABL, KIT and PDGFR tyrosine kinases--imatinib, nitotinib, and dasatinib].	imatinib	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-19
25560572-0	2015	HMG-COA reductase inhibitors: An opportunity for the improvement of imatinib safety.	imatinib	68-76	3-hydroxy-3-methylglutaryl-CoA reductase	Rattus norvegicus	0-17
29147422-5	2015	The presence of activating mutations of C-KIT has prompted use of C-KIT inhibitors such as imatinib and sunitini.	imatinib	91-99	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	40-45
29147422-5	2015	The presence of activating mutations of C-KIT has prompted use of C-KIT inhibitors such as imatinib and sunitini.	imatinib	91-99	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	66-71
25475722-0	2015	Adiponectin signals through Adiponectin Receptor 1 to reverse imatinib resistance in K562 human chronic myeloid leukemia cells.	imatinib	62-70	adiponectin, C1Q and collagen domain containing	Homo sapiens	0-11
25589240-4	2015	Tyrosine kinase inhibitor STI-571, protein kinase C inhibitor K252B, and cyclin-dependent kinase inhibitor olomoucine attenuated PrP106-126-induced altered MDM functions.	imatinib	26-33	prion protein	Homo sapiens	129-132
25483100-2	2015	Bcr-Abl/T315I is the predominant mutation that causes resistance to Imatinib.	imatinib	68-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
25305453-0	2015	MiR-30e induces apoptosis and sensitizes K562 cells to imatinib treatment via regulation of the BCR-ABL protein.	imatinib	55-63	microRNA 30e	Homo sapiens	0-7
25305453-0	2015	MiR-30e induces apoptosis and sensitizes K562 cells to imatinib treatment via regulation of the BCR-ABL protein.	imatinib	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
25305453-9	2015	Enforced expression of miR-30e in K562 cells suppressed proliferation and induced apoptosis of these cells and sensitized them to imatinib treatment.	imatinib	130-138	microRNA 30e	Homo sapiens	23-30
25475722-0	2015	Adiponectin signals through Adiponectin Receptor 1 to reverse imatinib resistance in K562 human chronic myeloid leukemia cells.	imatinib	62-70	adiponectin receptor 1	Homo sapiens	28-50
25475722-3	2015	In this study, we first established imatinib-resistant K562 CML cells, and then evaluated the effect of Adiponectin in reversing imatinib resistance.	imatinib	129-137	adiponectin, C1Q and collagen domain containing	Homo sapiens	104-115
25475722-4	2015	The data presented here demonstrated that Adiponectin was able to reverse K562 resistance to imatinib in vitro and in vivo.	imatinib	93-101	adiponectin, C1Q and collagen domain containing	Homo sapiens	42-53
25449787-0	2015	Divalproex sodium enhances the anti-leukemic effects of imatinib in chronic myeloid leukemia cells partly through SIRT1.	imatinib	56-64	sirtuin 1	Homo sapiens	114-119
25449787-1	2015	Imatinib (IM) represents a breakthrough in the treatment of chronic myeloid leukemia (CML) by inhibiting the activity of Bcr-Abl tyrosine kinase.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
25629972-1	2015	BACKGROUND: Mutations in the ABL kinase domain and SH3-SH2 domain of the BCR/ABL gene and amplification of the Philadelphia chromosome are the two important BCR/ABL dependent mechanisms of imatinib resistance.	imatinib	189-197	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-32
25629972-1	2015	BACKGROUND: Mutations in the ABL kinase domain and SH3-SH2 domain of the BCR/ABL gene and amplification of the Philadelphia chromosome are the two important BCR/ABL dependent mechanisms of imatinib resistance.	imatinib	189-197	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
25629972-1	2015	BACKGROUND: Mutations in the ABL kinase domain and SH3-SH2 domain of the BCR/ABL gene and amplification of the Philadelphia chromosome are the two important BCR/ABL dependent mechanisms of imatinib resistance.	imatinib	189-197	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-164
25629972-4	2015	RESULTS: Among the different mechanisms of imatinib resistance, kinase domain mutations (39%) of the BCR/ABL gene were seen to be more prevalent, followed by mutations in the SH3-SH2 domain (4%) and then BCR/ABL amplification with the least frequency (1%).	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
25629972-4	2015	RESULTS: Among the different mechanisms of imatinib resistance, kinase domain mutations (39%) of the BCR/ABL gene were seen to be more prevalent, followed by mutations in the SH3-SH2 domain (4%) and then BCR/ABL amplification with the least frequency (1%).	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	204-211
25475722-5	2015	Additional data with molecular approaches suggested that the reversion of Adiponectin in imatinib resistance signals through AdipoR1 but not AdipoR2 to downregulate Bcr-Abl expression and effect in imatinib-resistant K562 CML cells.	imatinib	89-97	adiponectin, C1Q and collagen domain containing	Homo sapiens	74-85
25475722-5	2015	Additional data with molecular approaches suggested that the reversion of Adiponectin in imatinib resistance signals through AdipoR1 but not AdipoR2 to downregulate Bcr-Abl expression and effect in imatinib-resistant K562 CML cells.	imatinib	89-97	adiponectin receptor 1	Homo sapiens	125-132
25475722-5	2015	Additional data with molecular approaches suggested that the reversion of Adiponectin in imatinib resistance signals through AdipoR1 but not AdipoR2 to downregulate Bcr-Abl expression and effect in imatinib-resistant K562 CML cells.	imatinib	89-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	165-172
25475722-5	2015	Additional data with molecular approaches suggested that the reversion of Adiponectin in imatinib resistance signals through AdipoR1 but not AdipoR2 to downregulate Bcr-Abl expression and effect in imatinib-resistant K562 CML cells.	imatinib	198-206	adiponectin, C1Q and collagen domain containing	Homo sapiens	74-85
25475722-5	2015	Additional data with molecular approaches suggested that the reversion of Adiponectin in imatinib resistance signals through AdipoR1 but not AdipoR2 to downregulate Bcr-Abl expression and effect in imatinib-resistant K562 CML cells.	imatinib	198-206	adiponectin receptor 1	Homo sapiens	125-132
25475722-6	2015	Taken together, our data showed that Adiponectin can reverse imatinib resistance in CML, and to a certain extent elucidate the mechanism of Adiponectin reversing imatinib resistance that may provide a new and promising approach in imatinib resistance management in CML therapy.	imatinib	61-69	adiponectin, C1Q and collagen domain containing	Homo sapiens	37-48
25475722-6	2015	Taken together, our data showed that Adiponectin can reverse imatinib resistance in CML, and to a certain extent elucidate the mechanism of Adiponectin reversing imatinib resistance that may provide a new and promising approach in imatinib resistance management in CML therapy.	imatinib	162-170	adiponectin, C1Q and collagen domain containing	Homo sapiens	140-151
25358338-0	2015	Human organic cation transporter 1 protein levels of granulocytes can optimize imatinib therapy in patients with chronic myeloid leukemia.	imatinib	79-87	solute carrier family 22 member 1	Homo sapiens	6-34
25475722-6	2015	Taken together, our data showed that Adiponectin can reverse imatinib resistance in CML, and to a certain extent elucidate the mechanism of Adiponectin reversing imatinib resistance that may provide a new and promising approach in imatinib resistance management in CML therapy.	imatinib	162-170	adiponectin, C1Q and collagen domain containing	Homo sapiens	140-151
25358338-1	2015	The human organic cation transporter 1 (hOCT1) is the major active influx protein responsible for the transport of imatinib mesylate (IM) into cells.	imatinib	115-132	solute carrier family 22 member 1	Homo sapiens	10-38
25358338-1	2015	The human organic cation transporter 1 (hOCT1) is the major active influx protein responsible for the transport of imatinib mesylate (IM) into cells.	imatinib	115-132	solute carrier family 22 member 1	Homo sapiens	40-45
26658996-3	2015	Molecular studies on GIST have improved our understanding of the biology of the disease and have led to the use of targeted therapy approach, such as imatinib for KIT/PDGFRA-mutated GIST.	imatinib	150-158	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	163-166
25366602-2	2015	This study assessed whether inhibition of TNC upregulation in brain by imatinib mesylate (imatinib), an inhibitor of the tyrosine kinases of platelet-derived growth factor receptors, prevents EBI after experimental SAH.	imatinib	71-88	tenascin C	Rattus norvegicus	42-45
25366602-2	2015	This study assessed whether inhibition of TNC upregulation in brain by imatinib mesylate (imatinib), an inhibitor of the tyrosine kinases of platelet-derived growth factor receptors, prevents EBI after experimental SAH.	imatinib	71-79	tenascin C	Rattus norvegicus	42-45
25366602-5	2015	Imatinib-treated SAH rats were also treated by a cisternal injection of recombinant TNC.	imatinib	0-8	tenascin C	Rattus norvegicus	84-87
25366602-7	2015	Imatinib treatment suppressed both TNC upregulation and EBI at 24 h. Recombinant TNC reinduced EBI in imatinib-treated SAH rats.	imatinib	0-8	tenascin C	Rattus norvegicus	35-38
25366602-7	2015	Imatinib treatment suppressed both TNC upregulation and EBI at 24 h. Recombinant TNC reinduced EBI in imatinib-treated SAH rats.	imatinib	0-8	tenascin C	Rattus norvegicus	81-84
25366602-7	2015	Imatinib treatment suppressed both TNC upregulation and EBI at 24 h. Recombinant TNC reinduced EBI in imatinib-treated SAH rats.	imatinib	102-110	tenascin C	Rattus norvegicus	81-84
26159458-0	2015	BCR-ABL1 Transcript Levels at 3 and 6 Months Are Better for Identifying Chronic Myeloid Leukemia Patients with Poor Outcome in Response to Second-Line Second-Generation Tyrosine Kinase Inhibitors after Imatinib Failure: A Report from a Single Institution.	imatinib	202-210	BCR activator of RhoGEF and GTPase	Homo sapiens	0-8
26658996-3	2015	Molecular studies on GIST have improved our understanding of the biology of the disease and have led to the use of targeted therapy approach, such as imatinib for KIT/PDGFRA-mutated GIST.	imatinib	150-158	platelet derived growth factor receptor alpha	Homo sapiens	167-173
25250944-0	2015	PTCH1 expression at diagnosis predicts imatinib failure in chronic myeloid leukaemia patients in chronic phase.	imatinib	39-47	patched 1	Homo sapiens	0-5
25250944-10	2015	Given the different treatments available for CML, measuring PTCH1 expression at diagnosis may help establish who will benefit best from imatinib and who is better selected for second generation TKI.	imatinib	136-144	patched 1	Homo sapiens	60-65
25417047-0	2015	Association of ABCG2 polymorphism with clinical efficacy of imatinib in patients with gastrointestinal stromal tumor.	imatinib	60-68	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	15-20
25964959-1	2015	Chronic myeloid leukemia (CML), a myeloproliferative disorder characterized by the BCR-ABL oncoprotein, presents its treatment based on tyrosine kinase inhibitors (TKIs), mainly imatinib.	imatinib	178-186	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
26291129-1	2015	A reciprocal translocation of the ABL1 gene to the BCR gene results in the expression of the oncogenic BCR-ABL1 fusion protein, which characterizes human chronic myeloid leukemia (CML), a myeloproliferative disorder considered invariably fatal until the introduction of the imatinib family of tyrosine kinase inhibitors (TKI).	imatinib	274-282	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-38
26291129-1	2015	A reciprocal translocation of the ABL1 gene to the BCR gene results in the expression of the oncogenic BCR-ABL1 fusion protein, which characterizes human chronic myeloid leukemia (CML), a myeloproliferative disorder considered invariably fatal until the introduction of the imatinib family of tyrosine kinase inhibitors (TKI).	imatinib	274-282	BCR activator of RhoGEF and GTPase	Homo sapiens	51-54
26291129-1	2015	A reciprocal translocation of the ABL1 gene to the BCR gene results in the expression of the oncogenic BCR-ABL1 fusion protein, which characterizes human chronic myeloid leukemia (CML), a myeloproliferative disorder considered invariably fatal until the introduction of the imatinib family of tyrosine kinase inhibitors (TKI).	imatinib	274-282	BCR activator of RhoGEF and GTPase	Homo sapiens	103-111
25701353-7	2015	Based on the above findings, our study demonstrated that simultaneously inhibiting the Hh pathway and autophagy could markedly reduce cell viability and induce apoptosis of imatinib-sensitive or -resistant BCR-ABL(+) cells.	imatinib	173-181	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	206-213
25701353-10	2015	In conclusion, this study indicated that simultaneously inhibiting the Hh pathway and autophagy could potently kill imatinib-sensitive or -resistant BCR-ABL(+) cells, providing a novel concept that simultaneously inhibiting the Hh pathway and autophagy might be a potent new strategy to overcome CML drug resistance.	imatinib	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
24930392-11	2015	Supranutritional dose of selenite when combined with imatinib induced apoptotic machinery by decreasing Bcl-2 expression, increasing caspase-3 activity and subsequently fragmenting DNA and blunted cytoprotective autophagy by decreasing Beclin-1 expression and autophagosomes formation.	imatinib	53-61	BCL2 apoptosis regulator	Homo sapiens	104-109
24930392-11	2015	Supranutritional dose of selenite when combined with imatinib induced apoptotic machinery by decreasing Bcl-2 expression, increasing caspase-3 activity and subsequently fragmenting DNA and blunted cytoprotective autophagy by decreasing Beclin-1 expression and autophagosomes formation.	imatinib	53-61	caspase 3	Homo sapiens	133-142
24930392-11	2015	Supranutritional dose of selenite when combined with imatinib induced apoptotic machinery by decreasing Bcl-2 expression, increasing caspase-3 activity and subsequently fragmenting DNA and blunted cytoprotective autophagy by decreasing Beclin-1 expression and autophagosomes formation.	imatinib	53-61	beclin 1	Homo sapiens	236-244
25482933-2	2015	In the present study, we determined the effect of dasatinib which was approved for imatinib resistant chronic myelogenous leukemia (CML) and (Ph(+)) acute lymphoblastic leukemia (ALL) treatment on P-gp-mediated MDR.	imatinib	83-91	ATP binding cassette subfamily B member 1	Homo sapiens	197-201
25417047-1	2015	PURPOSE: Imatinib is a substrate of drug transporters and metabolizing enzymes, including members of the cytochrome P450 (CYP) system.	imatinib	9-17	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	105-120
25417047-1	2015	PURPOSE: Imatinib is a substrate of drug transporters and metabolizing enzymes, including members of the cytochrome P450 (CYP) system.	imatinib	9-17	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	122-125
25417047-10	2015	CONCLUSIONS: The ABCG2 421C>A genetic variation could influence clinical efficacy in terms of PFS in patients with advanced GIST undergoing imatinib therapy.	imatinib	143-151	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	17-22
24865476-0	2015	Imatinib mesylate stimulates low-density lipoprotein receptor-related protein 1-mediated ERK phosphorylation in insulin-producing cells.	imatinib	0-17	LDL receptor related protein 1	Rattus norvegicus	29-79
24997326-1	2015	Gastric gastrointestinal stromal tumors (GISTs) usually contain the mast/stem cell growth factor receptor Kit gene (KIT) or platelet-derived growth factor receptor A (PDGFRA) mutations that can be targeted by, or mediate resistance to, imatinib.	imatinib	236-244	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	106-109
24997326-1	2015	Gastric gastrointestinal stromal tumors (GISTs) usually contain the mast/stem cell growth factor receptor Kit gene (KIT) or platelet-derived growth factor receptor A (PDGFRA) mutations that can be targeted by, or mediate resistance to, imatinib.	imatinib	236-244	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	116-119
24997326-1	2015	Gastric gastrointestinal stromal tumors (GISTs) usually contain the mast/stem cell growth factor receptor Kit gene (KIT) or platelet-derived growth factor receptor A (PDGFRA) mutations that can be targeted by, or mediate resistance to, imatinib.	imatinib	236-244	platelet derived growth factor receptor alpha	Homo sapiens	124-165
24997326-1	2015	Gastric gastrointestinal stromal tumors (GISTs) usually contain the mast/stem cell growth factor receptor Kit gene (KIT) or platelet-derived growth factor receptor A (PDGFRA) mutations that can be targeted by, or mediate resistance to, imatinib.	imatinib	236-244	platelet derived growth factor receptor alpha	Homo sapiens	167-173
24997326-7	2015	We predicted that 32% of patients would have primary resistance to imatinib, based on mutations in exon 17 of KIT, exon 18 of PDGFRA (D842V), or no mutation in either gene.	imatinib	67-75	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	110-113
24997326-7	2015	We predicted that 32% of patients would have primary resistance to imatinib, based on mutations in exon 17 of KIT, exon 18 of PDGFRA (D842V), or no mutation in either gene.	imatinib	67-75	platelet derived growth factor receptor alpha	Homo sapiens	126-132
26288116-1	2015	This is the largest Latin American study of BCR-ABL mutations in chronic myeloid leukemia (CML) patients, resistant to imatinib (IM).	imatinib	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
25807654-5	2015	RESULTS: This patient developed an acquired resistance associated with two p-BCR/ABL1 mutations (E255K and G250E) during treatment with imatinib.	imatinib	136-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-85
25807654-7	2015	The mu-BCR/ABL1 mutation should be investigated after imatinib treatment failure.	imatinib	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-15
24865476-0	2015	Imatinib mesylate stimulates low-density lipoprotein receptor-related protein 1-mediated ERK phosphorylation in insulin-producing cells.	imatinib	0-17	Eph receptor B1	Rattus norvegicus	89-92
24865476-2	2015	The tyrosine kinase inhibitor imatinib, which inhibits PDGFR and c-Abl, and which has previously been reported to counteract beta-cell death and diabetes, has been suggested to reduce atherosclerosis by inhibiting PDGFR-induced LRP1 phosphorylation.	imatinib	30-38	LDL receptor related protein 1	Rattus norvegicus	228-232
24865476-3	2015	The aim of the present study was to study LRP1 function in beta-cells and to what extent imatinib modulates LRP1 activity.	imatinib	89-97	LDL receptor related protein 1	Rattus norvegicus	108-112
24865476-11	2015	Imatinib blocked phosphorylation of LRP1 by PDGFR activation but induced phosphorylation of ERK.	imatinib	0-8	LDL receptor related protein 1	Rattus norvegicus	36-40
24865476-11	2015	Imatinib blocked phosphorylation of LRP1 by PDGFR activation but induced phosphorylation of ERK.	imatinib	0-8	Eph receptor B1	Rattus norvegicus	92-95
24865476-12	2015	LRP1 silencing blocked imatinib-induced phosphorylation of ERK.	imatinib	23-31	LDL receptor related protein 1	Rattus norvegicus	0-4
24865476-12	2015	LRP1 silencing blocked imatinib-induced phosphorylation of ERK.	imatinib	23-31	Eph receptor B1	Rattus norvegicus	59-62
24865476-14	2015	siRNA-mediated knockdown of the imatinib target c-Abl resulted in an increased ERK phosphorylation at basal conditions, with no further increase in response to imatinib.	imatinib	32-40	Eph receptor B1	Rattus norvegicus	79-82
24865476-15	2015	Imatinib-induced cell survival of tunicamycin-treated cells was partially mediated by ERK activation.	imatinib	0-8	Eph receptor B1	Rattus norvegicus	86-89
24865476-16	2015	We have concluded that imatinib promotes LRP1-dependent ERK activation, possibly via inhibition of c-Abl, and that this could contribute to the pro-survival effects of imatinib on beta-cells.	imatinib	23-31	LDL receptor related protein 1	Rattus norvegicus	41-45
24865476-16	2015	We have concluded that imatinib promotes LRP1-dependent ERK activation, possibly via inhibition of c-Abl, and that this could contribute to the pro-survival effects of imatinib on beta-cells.	imatinib	23-31	Eph receptor B1	Rattus norvegicus	56-59
24865476-16	2015	We have concluded that imatinib promotes LRP1-dependent ERK activation, possibly via inhibition of c-Abl, and that this could contribute to the pro-survival effects of imatinib on beta-cells.	imatinib	168-176	LDL receptor related protein 1	Rattus norvegicus	41-45
31388478-2	2015	Bosutinib is active against leukemia cells expressing imatinib-resistant BCR-ABL1 mutations.	imatinib	54-62	BCR activator of RhoGEF and GTPase	Homo sapiens	73-81
25039279-1	2015	The expression and activity of the uptake transporter human organic cation transporter 1 (hOCT1; SLC22A1) is an independent predictor of response to imatinib treatment in patients with chronic myeloid leukaemia (CML).	imatinib	149-157	solute carrier family 22 member 1	Homo sapiens	60-88
25039279-1	2015	The expression and activity of the uptake transporter human organic cation transporter 1 (hOCT1; SLC22A1) is an independent predictor of response to imatinib treatment in patients with chronic myeloid leukaemia (CML).	imatinib	149-157	solute carrier family 22 member 1	Homo sapiens	90-95
25039279-1	2015	The expression and activity of the uptake transporter human organic cation transporter 1 (hOCT1; SLC22A1) is an independent predictor of response to imatinib treatment in patients with chronic myeloid leukaemia (CML).	imatinib	149-157	solute carrier family 22 member 1	Homo sapiens	97-104
25039279-2	2015	We have recently shown that peroxisome proliferator-activated receptor (PPAR) activation can increase the killing effect of imatinib in CML cells, due to upregulated hOCT1 gene expression and increased imatinib uptake.	imatinib	124-132	peroxisome proliferator activated receptor alpha	Homo sapiens	28-70
25039279-2	2015	We have recently shown that peroxisome proliferator-activated receptor (PPAR) activation can increase the killing effect of imatinib in CML cells, due to upregulated hOCT1 gene expression and increased imatinib uptake.	imatinib	124-132	peroxisome proliferator activated receptor alpha	Homo sapiens	72-76
25039279-2	2015	We have recently shown that peroxisome proliferator-activated receptor (PPAR) activation can increase the killing effect of imatinib in CML cells, due to upregulated hOCT1 gene expression and increased imatinib uptake.	imatinib	124-132	solute carrier family 22 member 1	Homo sapiens	166-171
25039279-2	2015	We have recently shown that peroxisome proliferator-activated receptor (PPAR) activation can increase the killing effect of imatinib in CML cells, due to upregulated hOCT1 gene expression and increased imatinib uptake.	imatinib	202-210	peroxisome proliferator activated receptor alpha	Homo sapiens	28-70
25039279-2	2015	We have recently shown that peroxisome proliferator-activated receptor (PPAR) activation can increase the killing effect of imatinib in CML cells, due to upregulated hOCT1 gene expression and increased imatinib uptake.	imatinib	202-210	peroxisome proliferator activated receptor alpha	Homo sapiens	72-76
25039279-5	2015	Hence, agonists for PXR, RAR and RXR may be potentially used to improve the efficacy of imatinib in patients with CML.	imatinib	88-96	nuclear receptor subfamily 1 group I member 2	Homo sapiens	20-23
25039279-5	2015	Hence, agonists for PXR, RAR and RXR may be potentially used to improve the efficacy of imatinib in patients with CML.	imatinib	88-96	retinoic acid receptor alpha	Homo sapiens	25-28
25039279-5	2015	Hence, agonists for PXR, RAR and RXR may be potentially used to improve the efficacy of imatinib in patients with CML.	imatinib	88-96	retinoid X receptor alpha	Homo sapiens	33-36
26636412-7	2015	However, after 6 months of imatinib therapy, she had to be considered as warning (Ph+ 26.5%, BCR-ABL1 >1%) according to the European LeukemiaNet 2013 recommendations.	imatinib	27-35	BCR activator of RhoGEF and GTPase	Homo sapiens	93-101
27274622-5	2015	The dysregulated migration initiates, in part, through phosphorylation events signaled through the unstimulated PDGF receptor via focal adhesion kinase (FAK) whose total basal expression and phosphorylation at tyrosine 391 is markedly increased in the PAH cells and is inhibited by a motif mimicking cell-permeable peptide (MMCPP) targeting the Tyr751 region of the PDGF receptor and by imatinib.	imatinib	387-395	protein tyrosine kinase 2	Homo sapiens	130-151
27274622-5	2015	The dysregulated migration initiates, in part, through phosphorylation events signaled through the unstimulated PDGF receptor via focal adhesion kinase (FAK) whose total basal expression and phosphorylation at tyrosine 391 is markedly increased in the PAH cells and is inhibited by a motif mimicking cell-permeable peptide (MMCPP) targeting the Tyr751 region of the PDGF receptor and by imatinib.	imatinib	387-395	protein tyrosine kinase 2	Homo sapiens	153-156
27274622-9	2015	The upstream inhibitors FAK (PF-573228) and imatinib block this activation of JNK and p38 at the edge of the site of injury and correspondingly inhibit migration.	imatinib	44-52	mitogen-activated protein kinase 8	Homo sapiens	78-81
27274622-9	2015	The upstream inhibitors FAK (PF-573228) and imatinib block this activation of JNK and p38 at the edge of the site of injury and correspondingly inhibit migration.	imatinib	44-52	mitogen-activated protein kinase 14	Homo sapiens	86-89
25599554-10	2015	Initially the patient was treated with a 100 mg daily dose of imatinib mesylate, a specific inhibitor of the tyrosine-kinase domain of PDGFR.	imatinib	62-79	platelet derived growth factor receptor beta	Homo sapiens	135-140
26098203-3	2015	Despite the successful clinical use of imatinib mesylate, a selective receptor tyrosine kinase (RTK) inhibitor that targets KIT, PDGFRA and BCR-ABL, we still do not have treatment for the long-term control of advanced GIST.	imatinib	39-56	ret proto-oncogene	Homo sapiens	70-94
26098203-3	2015	Despite the successful clinical use of imatinib mesylate, a selective receptor tyrosine kinase (RTK) inhibitor that targets KIT, PDGFRA and BCR-ABL, we still do not have treatment for the long-term control of advanced GIST.	imatinib	39-56	ret proto-oncogene	Homo sapiens	96-99
26098203-3	2015	Despite the successful clinical use of imatinib mesylate, a selective receptor tyrosine kinase (RTK) inhibitor that targets KIT, PDGFRA and BCR-ABL, we still do not have treatment for the long-term control of advanced GIST.	imatinib	39-56	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	124-127
26098203-3	2015	Despite the successful clinical use of imatinib mesylate, a selective receptor tyrosine kinase (RTK) inhibitor that targets KIT, PDGFRA and BCR-ABL, we still do not have treatment for the long-term control of advanced GIST.	imatinib	39-56	platelet derived growth factor receptor alpha	Homo sapiens	129-135
26098203-3	2015	Despite the successful clinical use of imatinib mesylate, a selective receptor tyrosine kinase (RTK) inhibitor that targets KIT, PDGFRA and BCR-ABL, we still do not have treatment for the long-term control of advanced GIST.	imatinib	39-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
26372795-1	2015	INTRODUCTION: The Bcr-Abl inhibitor imatinib was approved in 2001 for chronic myeloid leukemia therapy, and dramatically changed the lives of patients affected by this disease.	imatinib	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
26372795-2	2015	Since it also inhibits platelet derived growth factor receptor (PDGFR) and c-Kit, imatinib is used for various other tumors caused by abnormalities of one or both these two enzymes.	imatinib	82-90	platelet derived growth factor receptor beta	Homo sapiens	23-62
26372795-2	2015	Since it also inhibits platelet derived growth factor receptor (PDGFR) and c-Kit, imatinib is used for various other tumors caused by abnormalities of one or both these two enzymes.	imatinib	82-90	platelet derived growth factor receptor beta	Homo sapiens	64-69
26372795-2	2015	Since it also inhibits platelet derived growth factor receptor (PDGFR) and c-Kit, imatinib is used for various other tumors caused by abnormalities of one or both these two enzymes.	imatinib	82-90	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	75-80
25682460-3	2015	Recently, Imatinib mesylate has shown a significantly prolonged progression-free survival and overall survival in metastatic and locally advanced c-Kit positive gastro-intestinal stromal tumors (GISTs) and more recently a prolonged disease-free survival in operated high risk GIST.	imatinib	10-27	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	146-151
25821558-2	2015	We evaluated the inhibitory effects of the HSP90 ATPase inhibitor AUY922 on 32D mouse hematopoietic cells expressing wild-type Bcr-Abl (b3a2, 32Dp210) and mutant Bcr-Abl imatinib (IM)-resistant cell lines.	imatinib	170-178	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-169
25882020-1	2015	Imatinib mesylate is a competitive inhibitor of BCR/ ABL tyrosine kinase and inhibits also several receptor tyrosin kinases.	imatinib	0-17	BCR activator of RhoGEF and GTPase	Homo sapiens	48-51
25786456-2	2015	Platelet-derived growth factor receptor alpha-related disorders were first specified in 2008 as a distinct group of clonal eosinophilic disorders with exceptional responsiveness to imatinib.	imatinib	181-189	platelet derived growth factor receptor alpha	Homo sapiens	0-45
25872528-0	2015	A novel compound against oncogenic Aurora kinase A overcomes imatinib resistance in chronic myeloid leukemia cells.	imatinib	61-69	aurora kinase A	Homo sapiens	35-50
25872528-2	2015	Here, we evaluated a novel compound AKI603 against oncogenic Aurora kinase A (Aur-A) in imatinib-resistant CML cells.	imatinib	88-96	aurora kinase A	Homo sapiens	61-76
25872528-2	2015	Here, we evaluated a novel compound AKI603 against oncogenic Aurora kinase A (Aur-A) in imatinib-resistant CML cells.	imatinib	88-96	aurora kinase A	Homo sapiens	78-83
25872528-3	2015	We found that Aur-A was highly activated in imatinib-resistant KBM5-T315I cells.	imatinib	44-52	aurora kinase A	Homo sapiens	14-19
25882020-1	2015	Imatinib mesylate is a competitive inhibitor of BCR/ ABL tyrosine kinase and inhibits also several receptor tyrosin kinases.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
25882020-2	2015	Since its launch to the market, imatinib has proven to be very valuable in the treatment of Philadelphia chromosome (BCR/ ABL) -  positive (Ph+) chronic myeloid leukemia and Kit (CD117) positive gastrointestinal stromal tumors.	imatinib	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-125
25882020-2	2015	Since its launch to the market, imatinib has proven to be very valuable in the treatment of Philadelphia chromosome (BCR/ ABL) -  positive (Ph+) chronic myeloid leukemia and Kit (CD117) positive gastrointestinal stromal tumors.	imatinib	32-40	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	174-177
25882020-2	2015	Since its launch to the market, imatinib has proven to be very valuable in the treatment of Philadelphia chromosome (BCR/ ABL) -  positive (Ph+) chronic myeloid leukemia and Kit (CD117) positive gastrointestinal stromal tumors.	imatinib	32-40	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	179-184
25481675-1	2015	KIT and PDGFRA gene mutations are the major genetic alterations seen in gastrointestinal stromal tumors (GISTs) and are being used clinically for predicting response to imatinib therapy.	imatinib	169-177	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
25465126-0	2015	Synergism between bosutinib (SKI-606) and the Chk1 inhibitor (PF-00477736) in highly imatinib-resistant BCR/ABL+ leukemia cells.	imatinib	85-93	checkpoint kinase 1	Homo sapiens	46-50
25465126-0	2015	Synergism between bosutinib (SKI-606) and the Chk1 inhibitor (PF-00477736) in highly imatinib-resistant BCR/ABL+ leukemia cells.	imatinib	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
25962435-6	2015	BCR-ABL transcripts were undetectable in cases after 2, 3 and 4 treated with imatinib after 6, 6 and 3 months, respectively, and in one patient who had undergone allogeneic hematopoietic stem cell transplantation after 4 months.	imatinib	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
25481675-1	2015	KIT and PDGFRA gene mutations are the major genetic alterations seen in gastrointestinal stromal tumors (GISTs) and are being used clinically for predicting response to imatinib therapy.	imatinib	169-177	platelet derived growth factor receptor alpha	Homo sapiens	8-14
25319658-0	2015	Targeting bcr-abl transcripts with siRNAs in an imatinib-resistant chronic myeloid leukemia patient: challenges and future directions.	imatinib	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
25319658-4	2015	This chapter describes the in vivo application of targeted non-virally delivered synthetic bcr-abl siRNA in a female patient with recurrent Philadelphia chromosome positive chronic myeloid leukemia (CML) resistant to imatinib (Y253F mutation) and chemotherapy after allogeneic hematopoietic stem cell transplantation.	imatinib	217-225	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
25112370-5	2015	Evodiamine-exerted stimulatory effects were blocked by c-kit receptor tyrosine kinase inhibitor imatinib.	imatinib	96-104	KIT proto-oncogene receptor tyrosine kinase	Rattus norvegicus	55-85
25435999-0	2015	Methylation analysis of the DAPK1 gene in imatinib-resistant chronic myeloid leukemia patients.	imatinib	42-50	death associated protein kinase 1	Homo sapiens	28-33
26458312-3	2015	The current study assesses and validates expression profiles of selected oncogenic and tumor suppressing miRNAs that are associated with different imatinib mesylate (IM) response in CML patients carrying rare BCR-ABL variants.	imatinib	147-164	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-216
25435999-6	2015	The present study included a number of patients who were identified to be resistant to the common chemotherapeutic agent imatinib (STI571, Gleevec , Glivec ), exhibiting at least one mutation in the breakpoint cluster region-Abelson murine leukemia (BCR-ABL) gene.	imatinib	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	199-248
25435999-6	2015	The present study included a number of patients who were identified to be resistant to the common chemotherapeutic agent imatinib (STI571, Gleevec , Glivec ), exhibiting at least one mutation in the breakpoint cluster region-Abelson murine leukemia (BCR-ABL) gene.	imatinib	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	250-257
25435999-10	2015	These findings indicate that DAPK1 methylation may be associated with a signaling pathway for imatinib resistance in chronic myeloid leukemia.	imatinib	94-102	death associated protein kinase 1	Homo sapiens	29-34
26429162-9	2015	Efficient Imatinib therapy may contribute to low WT1 levels in CP patients.	imatinib	10-18	WT1 transcription factor	Homo sapiens	49-52
25621775-6	2015	Imatinib mesilate is a selective inhibitor of KIT and PDGFRA with an antityrosine kinase activity (TKI) used in advanced or metastatic GIST as well as in adjuvant setting after complete resection of neoplasm.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	46-49
25621775-6	2015	Imatinib mesilate is a selective inhibitor of KIT and PDGFRA with an antityrosine kinase activity (TKI) used in advanced or metastatic GIST as well as in adjuvant setting after complete resection of neoplasm.	imatinib	0-17	platelet derived growth factor receptor alpha	Homo sapiens	54-60
25025538-1	2015	Dasatinib, which is an inhibitor of BCR-ABL and SRC family tyrosine kinases, is used for the treatment of patients with Philadelphia chromosome (Ph) positive leukemia, especially for those who develop resistance or who are intolerant to imatinib.	imatinib	237-245	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
25727702-2	2015	The poster child for this alternative approach to the treatment of cancer is imatinib, a small-molecule kinase inhibitor designed to target chronic myeloid leukaemia driven by the BCR-ABL translocation in a defined patient population.	imatinib	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	180-187
25506832-9	2014	Using PCR we confirmed the significant up-regulation and down-regulation of miR-493-5p and IL8 by imatinib treatment, respectively in K562 cells.	imatinib	98-106	C-X-C motif chemokine ligand 8	Homo sapiens	91-94
25755909-0	2014	Long-lasting complete response to imatinib in a patient with systemic mastocytosis exhibiting wild type KIT.	imatinib	34-42	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	104-107
25755909-3	2014	In adult patients the transforming KIT mutation D816V is usually present and confers resistance against imatinib.	imatinib	104-112	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	35-38
25755909-5	2014	Nonetheless, imatinib may work in patients with SM lacking KIT D816V.	imatinib	13-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	59-62
25755909-13	2014	This case-study confirms the long-term efficacy and safety of imatinib in patients with SM lacking activating KIT mutations.	imatinib	62-70	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	110-113
25755909-14	2014	Imatinib should be considered in select cases of SM in whom MCs exhibit wild-type KIT.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	82-85
25527332-1	2015	BACKGROUND: Treatment of chronic myelogenous leukemia (CML) with the BCR-ABL tyrosine kinase inhibitor (TKI) imatinib significantly improves patient outcomes.	imatinib	109-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
25527332-2	2015	As some patients are unresponsive to imatinib, next generation BCR-ABL inhibitors such as nilotinib have been developed to treat patients with imatinib-resistant CML.	imatinib	143-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
25506832-12	2014	The IL8 inhibition also further sensitized K562 cells to imatinib cytotoxicity (p < 0.0001).	imatinib	57-65	C-X-C motif chemokine ligand 8	Homo sapiens	4-7
24885373-2	2014	In contrast, we report that imatinib mesylate prevented bleomycin (BLM)-induced pulmonary fibrosis in mice by inhibiting platelet-derived growth factor receptor (PDGFR), even when it was administered only in the early phase.	imatinib	28-45	platelet derived growth factor receptor, beta polypeptide	Mus musculus	121-160
25488584-11	2014	Systemic treatment with imatinib for unresectable or recurrent tumors with positive c-KIT could be the best therapeutic option.	imatinib	24-32	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	84-89
25549138-1	2014	The discovery of BCR/ABL as a driver oncogene in chronic myeloid leukemia (CML) resulted in the development of Imatinib, which, in fact, demonstrated the potential of targeting the kinase in cancers by effectively treating the CML patients.	imatinib	111-119	BCR activator of RhoGEF and GTPase	Mus musculus	17-20
25549138-1	2014	The discovery of BCR/ABL as a driver oncogene in chronic myeloid leukemia (CML) resulted in the development of Imatinib, which, in fact, demonstrated the potential of targeting the kinase in cancers by effectively treating the CML patients.	imatinib	111-119	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	21-24
24885373-2	2014	In contrast, we report that imatinib mesylate prevented bleomycin (BLM)-induced pulmonary fibrosis in mice by inhibiting platelet-derived growth factor receptor (PDGFR), even when it was administered only in the early phase.	imatinib	28-45	platelet derived growth factor receptor, beta polypeptide	Mus musculus	162-167
24885373-9	2014	PDGFR inhibitors (imatinib, PDGFR-blocking antibodies) suppressed fibrocyte migration in vitro, and reduced the number of fibrocytes in the lungs of BLM-treated mice.	imatinib	18-26	platelet derived growth factor receptor, beta polypeptide	Mus musculus	0-5
25331939-1	2014	Despite the clinical efficacy achieved with frontline therapies for BCR-ABL-positive disease, such as imatinib and second-generation ABL inhibitors like nilotinib or dasatinib that were originally designed to override insensitivity to imatinib, drug resistance still remains a challenge, especially for patients with advanced-stage chronic myeloid leukemia or Philadelphia chromosome-positive acute lymphoblastic leukemia.	imatinib	102-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
25432281-0	2014	Role of glutathione-S-transferase M1 (GSTM1) and T1 (GSTT1) genes in the development and progress of chronic myeloid leukemia and in the formation of response to imatinib therapy.	imatinib	162-170	glutathione S-transferase mu 1	Homo sapiens	8-36
25300860-8	2014	Imatinib inhibition of c-Abl kinase activity also enhanced ADCC-phenocopying ABL1 knockdown-against several EGFR-expressing head-and-neck squamous cell carcinoma cell lines by ex vivo primary natural killer cells.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-28
25300860-8	2014	Imatinib inhibition of c-Abl kinase activity also enhanced ADCC-phenocopying ABL1 knockdown-against several EGFR-expressing head-and-neck squamous cell carcinoma cell lines by ex vivo primary natural killer cells.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-81
25300860-8	2014	Imatinib inhibition of c-Abl kinase activity also enhanced ADCC-phenocopying ABL1 knockdown-against several EGFR-expressing head-and-neck squamous cell carcinoma cell lines by ex vivo primary natural killer cells.	imatinib	0-8	epidermal growth factor receptor	Homo sapiens	108-112
25387678-6	2014	Overexpression of p15INK4B together with STI571 (imatinib) or BCR-ABL1 small interfering RNA (siRNA) also enhanced growth inhibition and apoptosis induction of K562 cells.	imatinib	41-47	cyclin dependent kinase inhibitor 2B	Homo sapiens	18-26
25387678-6	2014	Overexpression of p15INK4B together with STI571 (imatinib) or BCR-ABL1 small interfering RNA (siRNA) also enhanced growth inhibition and apoptosis induction of K562 cells.	imatinib	49-57	cyclin dependent kinase inhibitor 2B	Homo sapiens	18-26
25432281-0	2014	Role of glutathione-S-transferase M1 (GSTM1) and T1 (GSTT1) genes in the development and progress of chronic myeloid leukemia and in the formation of response to imatinib therapy.	imatinib	162-170	glutathione S-transferase mu 1	Homo sapiens	38-43
25432281-0	2014	Role of glutathione-S-transferase M1 (GSTM1) and T1 (GSTT1) genes in the development and progress of chronic myeloid leukemia and in the formation of response to imatinib therapy.	imatinib	162-170	glutathione S-transferase theta 1	Homo sapiens	53-58
25432281-3	2014	Combinations of the "zero" GSTM1 and GSTT1 genotypes were risk factors indicating the probable disease progress and failure of high cytogenetic response after 12 months of imatinib therapy (400 mg daily).	imatinib	172-180	glutathione S-transferase mu 1	Homo sapiens	27-32
25432281-3	2014	Combinations of the "zero" GSTM1 and GSTT1 genotypes were risk factors indicating the probable disease progress and failure of high cytogenetic response after 12 months of imatinib therapy (400 mg daily).	imatinib	172-180	glutathione S-transferase theta 1	Homo sapiens	37-42
25568846-11	2014	Patients with higher ABCG2 expression in imatinib-exposed samples showed poor treatment outcome with dasatinib.	imatinib	41-49	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	21-26
25568846-12	2014	On the other hand, a higher expression level of ABCB1 in imatinib-exposed samples did not affect second-generation TKI responses but was correlated with poor imatinib responses.	imatinib	57-65	ATP binding cassette subfamily B member 1	Homo sapiens	48-53
25568846-0	2014	OCT-1, ABCB1, and ABCG2 Expression in Imatinib-Resistant Chronic Myeloid Leukemia Treated with Dasatinib or Nilotinib.	imatinib	38-46	solute carrier family 22 member 1	Homo sapiens	0-5
25568846-12	2014	On the other hand, a higher expression level of ABCB1 in imatinib-exposed samples did not affect second-generation TKI responses but was correlated with poor imatinib responses.	imatinib	158-166	ATP binding cassette subfamily B member 1	Homo sapiens	48-53
25568846-0	2014	OCT-1, ABCB1, and ABCG2 Expression in Imatinib-Resistant Chronic Myeloid Leukemia Treated with Dasatinib or Nilotinib.	imatinib	38-46	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	18-23
25188725-0	2014	Dual glutathione-S-transferase-theta1 and -mu1 gene deletions determine imatinib failure in chronic myeloid leukemia.	imatinib	72-80	glutathione S-transferase theta 1	Homo sapiens	5-46
25239662-4	2014	In silico molecular docking studies revealed that mostly SFR can be attached to Bcr-Abl protein, positioned inside the protein"s binding cavity at the same place with the drug used in the treatment of CML, imatinib mesylate (IM).	imatinib	206-223	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
25188725-2	2014	There is an increased risk of CML in subjects with (i) deletions of genes encoding glutathione-S-transferase (GST)-theta1 (GSTT1) and -mu1, (GSTM1) and (ii) the GST-pi1 (GSTP1) single-nucleotide polymorphism (SNP) Ile105Val (GSTP1*B; rs1695); however, their effects on imatinib treatment outcome are not known.	imatinib	269-277	glutathione S-transferase pi 1	Homo sapiens	161-168
25188725-3	2014	Here, we assess the role of these GSTs in relation to imatinib treatment outcome in 193 CML patients.	imatinib	54-62	glutathione S-transferase mu 1	Homo sapiens	34-38
25188725-4	2014	Deletion of GSTT1 alone, or in combination with deletion of the GSTM1 gene, significantly increased the likelihood of imatinib failure (P = 0.021 and P < 0.001, respectively).	imatinib	118-126	glutathione S-transferase theta 1	Homo sapiens	12-17
25188725-4	2014	Deletion of GSTT1 alone, or in combination with deletion of the GSTM1 gene, significantly increased the likelihood of imatinib failure (P = 0.021 and P < 0.001, respectively).	imatinib	118-126	glutathione S-transferase mu 1	Homo sapiens	64-69
25188725-6	2014	Losses of the GSTT1 and GSTM1 genes are therefore important determinants of imatinib failure in CML.	imatinib	76-84	glutathione S-transferase theta 1	Homo sapiens	14-19
25188725-6	2014	Losses of the GSTT1 and GSTM1 genes are therefore important determinants of imatinib failure in CML.	imatinib	76-84	glutathione S-transferase mu 1	Homo sapiens	24-29
25568846-3	2014	The mRNA expression of the OCT-1, ABCG2, and ABCB1 genes was quantified by using paired bone marrow samples obtained before administering imatinib and at the point of detecting imatinib resistance (just before starting second-generation TKIs).	imatinib	138-146	solute carrier family 22 member 1	Homo sapiens	27-32
25568846-3	2014	The mRNA expression of the OCT-1, ABCG2, and ABCB1 genes was quantified by using paired bone marrow samples obtained before administering imatinib and at the point of detecting imatinib resistance (just before starting second-generation TKIs).	imatinib	177-185	solute carrier family 22 member 1	Homo sapiens	27-32
25568846-4	2014	The expression levels of OCT-1 and ABCG2 were lower in follow-up than in imatinib-naive samples.	imatinib	73-81	solute carrier family 22 member 1	Homo sapiens	25-30
25568846-4	2014	The expression levels of OCT-1 and ABCG2 were lower in follow-up than in imatinib-naive samples.	imatinib	73-81	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	35-40
25568846-5	2014	ABCB1 revealed highly variable expression levels before and after imatinib treatment.	imatinib	66-74	ATP binding cassette subfamily B member 1	Homo sapiens	0-5
25568846-6	2014	In addition, median ABCB1 expression in follow-up samples was lower in patients achieving complete cytogenetic response or major molecular response during imatinib treatment than in failed patients.	imatinib	155-163	ATP binding cassette subfamily B member 1	Homo sapiens	20-25
25568846-7	2014	Higher ABCG2 expression in imatinib-exposed samples showed a negative impact on optimal response to dasatinib.	imatinib	27-35	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	7-12
25568846-8	2014	Patients with higher ABCG2 expression in imatinib-exposed samples also had shorter progression- free survival with dasatinib treatment.	imatinib	41-49	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	21-26
25568846-10	2014	In imatinib-resistant CML, OCT-1 and ABCG2 mRNA expression decreased after imatinib treatment.	imatinib	3-11	solute carrier family 22 member 1	Homo sapiens	27-32
25568846-10	2014	In imatinib-resistant CML, OCT-1 and ABCG2 mRNA expression decreased after imatinib treatment.	imatinib	3-11	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	37-42
25568846-10	2014	In imatinib-resistant CML, OCT-1 and ABCG2 mRNA expression decreased after imatinib treatment.	imatinib	75-83	solute carrier family 22 member 1	Homo sapiens	27-32
25568846-10	2014	In imatinib-resistant CML, OCT-1 and ABCG2 mRNA expression decreased after imatinib treatment.	imatinib	75-83	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	37-42
25435722-3	2014	The development of the BCR-ABL-targeted imatinib mesylate represents a paradigm shift in the treatment of CML.	imatinib	40-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
25435722-6	2014	This study designed to assess the behavior of IL-1beta through newly diagnosed patients, different responders groups (optimal, suboptimal and failure cytogenetic response) and advanced stages (acceleration and crisis groups) of CML Iraqi patients whom receiving Imatinib mesylate (tyrosine kinase inhibitor), trying to elucidate the role of immunity in pathophysiology of CML disease development and treatments.	imatinib	262-279	interleukin 1 beta	Homo sapiens	46-54
25435722-7	2014	In this study 96 Iraqi CML patients under imatinib mesylate treatment categorized by complete blood picture and fluorescent in situ hybridization analysis into different response groups and stages, then used an enzyme linked immunosorbent assay technique to assess serum level of IL-1beta in each response group and advance stage (acceleration and transformed) of CML patients, in comparison to level in 32 healthy control subjects and 32 newly diagnosed CML.	imatinib	42-59	interleukin 1 beta	Homo sapiens	280-288
25151958-0	2014	AKT-induced reactive oxygen species generate imatinib-resistant clones emerging from chronic myeloid leukemia progenitor cells.	imatinib	45-53	AKT serine/threonine kinase 1	Homo sapiens	0-3
25060527-0	2014	Clinical impact of ABCC1 and ABCC2 genotypes and haplotypes in mediating imatinib resistance among chronic myeloid leukaemia patients.	imatinib	73-81	ATP binding cassette subfamily C member 1	Homo sapiens	19-24
25060527-0	2014	Clinical impact of ABCC1 and ABCC2 genotypes and haplotypes in mediating imatinib resistance among chronic myeloid leukaemia patients.	imatinib	73-81	ATP binding cassette subfamily C member 2	Homo sapiens	29-34
25060527-11	2014	WHAT IS NEW AND CONCLUSION: Our results suggest the ABCC2 T-24 G1249 T3972 haplotype was associated with imatinib resistance.	imatinib	105-113	ATP binding cassette subfamily C member 2	Homo sapiens	52-57
25317746-6	2014	Furthermore,we evaluated the sensitivity of the mutant to imatinib and dasatinib.CONCLUSIONS AND RELEVANCE We report a novel KIT gain-of-function mutation with S628N substitution (exon 13) and show that it is sensitive to imatinib in vitro.	imatinib	58-66	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	125-128
25317746-6	2014	Furthermore,we evaluated the sensitivity of the mutant to imatinib and dasatinib.CONCLUSIONS AND RELEVANCE We report a novel KIT gain-of-function mutation with S628N substitution (exon 13) and show that it is sensitive to imatinib in vitro.	imatinib	222-230	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	125-128
25281405-1	2014	Imatinib resistance in chronic myeloid leukemia (CML) is commonly due to BCR-ABL kinase domain mutations (KDMs).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
23818300-2	2014	Two functional single nucleotide polymorphisms (SNPs), p53 R72P and MDM2 SNP309, are associated with alternation of p53 activity, however the association regarding CML susceptibility and BP transformation under imatinib treatment is unclear.	imatinib	211-219	tumor protein p53	Homo sapiens	116-119
25443888-0	2014	Stromal cells attenuate the cytotoxicity of imatinib on Philadelphia chromosome-positive leukemia cells by up-regulating the VE-cadherin/beta-catenin signal.	imatinib	44-52	cadherin 5	Homo sapiens	125-136
25443888-0	2014	Stromal cells attenuate the cytotoxicity of imatinib on Philadelphia chromosome-positive leukemia cells by up-regulating the VE-cadherin/beta-catenin signal.	imatinib	44-52	catenin beta 1	Homo sapiens	137-149
25443888-2	2014	Herein, we investigated the protective effects of the stromal cell-mediated VE-cadherin-beta-catenin signal on Ph+ leukemia cells during imatinib treatment.	imatinib	137-145	cadherin 5	Homo sapiens	76-87
25443888-2	2014	Herein, we investigated the protective effects of the stromal cell-mediated VE-cadherin-beta-catenin signal on Ph+ leukemia cells during imatinib treatment.	imatinib	137-145	catenin beta 1	Homo sapiens	88-100
25443888-4	2014	Knockdown of VE-cadherin with shRNA diminished the beta-catenin protein and partly resensitized Ph+ leukemia cells to imatinib despite the presence of stromal cells, suggesting VE-cadherin is a potential target in the treatment of Ph+ leukemia.	imatinib	118-126	cadherin 5	Homo sapiens	13-24
25443888-4	2014	Knockdown of VE-cadherin with shRNA diminished the beta-catenin protein and partly resensitized Ph+ leukemia cells to imatinib despite the presence of stromal cells, suggesting VE-cadherin is a potential target in the treatment of Ph+ leukemia.	imatinib	118-126	cadherin 5	Homo sapiens	177-188
23818300-1	2014	The genetic or functional inactivation of the p53 pathway plays an important role with regards to disease progression from the chronic phase (CP) to blast phase (BP) and imatinib treatment response in chronic myeloid leukemia (CML).	imatinib	170-178	tumor protein p53	Homo sapiens	46-49
23818300-2	2014	Two functional single nucleotide polymorphisms (SNPs), p53 R72P and MDM2 SNP309, are associated with alternation of p53 activity, however the association regarding CML susceptibility and BP transformation under imatinib treatment is unclear.	imatinib	211-219	tumor protein p53	Homo sapiens	55-58
25175494-0	2014	Relapse of myeloid neoplasm with eosinophilia and PDGFRA rearrangement after imatinib discontinuation in a pediatric patient.	imatinib	77-85	platelet derived growth factor receptor alpha	Homo sapiens	50-56
23818300-2	2014	Two functional single nucleotide polymorphisms (SNPs), p53 R72P and MDM2 SNP309, are associated with alternation of p53 activity, however the association regarding CML susceptibility and BP transformation under imatinib treatment is unclear.	imatinib	211-219	MDM2 proto-oncogene	Homo sapiens	68-72
25375091-0	2014	MTOR inhibition enhances NVP-AUY922-induced autophagy-mediated KIT degradation and cytotoxicity in imatinib-resistant gastrointestinal stromal tumors.	imatinib	99-107	mechanistic target of rapamycin kinase	Homo sapiens	0-4
25393253-5	2014	Finally, co-culture experiments of K562 CML cells with CXCL12 expressing mesenchymal cells (OP9 cells or human CXCL12 transfected 3T3 cells) revealed enhanced mRNA levels for MDR1 in a CXCL12 rich environment.These results suggest that imatinib treatment restores the bone marrow microenvironment in CML with the presence of CXCL12 expressing reticular cells but in turn induces the overexpression of MDR1 in haematopoietic cells due to up-regulated expression of CXCL12.	imatinib	236-244	C-X-C motif chemokine ligand 12	Homo sapiens	55-61
25393253-5	2014	Finally, co-culture experiments of K562 CML cells with CXCL12 expressing mesenchymal cells (OP9 cells or human CXCL12 transfected 3T3 cells) revealed enhanced mRNA levels for MDR1 in a CXCL12 rich environment.These results suggest that imatinib treatment restores the bone marrow microenvironment in CML with the presence of CXCL12 expressing reticular cells but in turn induces the overexpression of MDR1 in haematopoietic cells due to up-regulated expression of CXCL12.	imatinib	236-244	C-X-C motif chemokine ligand 12	Homo sapiens	111-117
25393253-5	2014	Finally, co-culture experiments of K562 CML cells with CXCL12 expressing mesenchymal cells (OP9 cells or human CXCL12 transfected 3T3 cells) revealed enhanced mRNA levels for MDR1 in a CXCL12 rich environment.These results suggest that imatinib treatment restores the bone marrow microenvironment in CML with the presence of CXCL12 expressing reticular cells but in turn induces the overexpression of MDR1 in haematopoietic cells due to up-regulated expression of CXCL12.	imatinib	236-244	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	175-179
25393253-5	2014	Finally, co-culture experiments of K562 CML cells with CXCL12 expressing mesenchymal cells (OP9 cells or human CXCL12 transfected 3T3 cells) revealed enhanced mRNA levels for MDR1 in a CXCL12 rich environment.These results suggest that imatinib treatment restores the bone marrow microenvironment in CML with the presence of CXCL12 expressing reticular cells but in turn induces the overexpression of MDR1 in haematopoietic cells due to up-regulated expression of CXCL12.	imatinib	236-244	chemokine (C-X-C motif) ligand 12	Mus musculus	111-117
25393253-5	2014	Finally, co-culture experiments of K562 CML cells with CXCL12 expressing mesenchymal cells (OP9 cells or human CXCL12 transfected 3T3 cells) revealed enhanced mRNA levels for MDR1 in a CXCL12 rich environment.These results suggest that imatinib treatment restores the bone marrow microenvironment in CML with the presence of CXCL12 expressing reticular cells but in turn induces the overexpression of MDR1 in haematopoietic cells due to up-regulated expression of CXCL12.	imatinib	236-244	chemokine (C-X-C motif) ligand 12	Mus musculus	111-117
25393253-5	2014	Finally, co-culture experiments of K562 CML cells with CXCL12 expressing mesenchymal cells (OP9 cells or human CXCL12 transfected 3T3 cells) revealed enhanced mRNA levels for MDR1 in a CXCL12 rich environment.These results suggest that imatinib treatment restores the bone marrow microenvironment in CML with the presence of CXCL12 expressing reticular cells but in turn induces the overexpression of MDR1 in haematopoietic cells due to up-regulated expression of CXCL12.	imatinib	236-244	chemokine (C-X-C motif) ligand 12	Mus musculus	111-117
24739665-1	2014	BACKGROUND: Previous reports have suggested that imatinib may increase cyclosporine exposure by CYP3A4 inhibition.	imatinib	49-57	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	96-102
24739665-6	2014	In addition, a validated model-based approach was used to derive quantitative predictions of CYP3A4-mediated drug interactions with imatinib as a victim or precipitant drug.	imatinib	132-140	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	93-99
24739665-8	2014	The modeling approach predicted weak-to-moderate effect of major CYP3A4 inhibitors on imatinib exposure.	imatinib	86-94	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	65-71
24739665-9	2014	However, the inhibitory potency of imatinib was found to be similar to that of verapamil, suggesting significant influence of imatinib on the pharmacokinetics of drugs highly metabolized by CYP3A4.	imatinib	35-43	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	190-196
24739665-9	2014	However, the inhibitory potency of imatinib was found to be similar to that of verapamil, suggesting significant influence of imatinib on the pharmacokinetics of drugs highly metabolized by CYP3A4.	imatinib	126-134	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	190-196
25526032-10	2014	Furthermore, inhibition of c-Abl with STI571 also abrogated the effect on apoptosis caused by MLH1.	imatinib	38-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-32
25526032-10	2014	Furthermore, inhibition of c-Abl with STI571 also abrogated the effect on apoptosis caused by MLH1.	imatinib	38-44	mutL homolog 1	Homo sapiens	94-98
25375091-2	2014	Herein, we showed rapamycin, a MTOR inhibitor and autophagy inducer, could reduce total and phospho-KIT expression levels and enhance apoptosis in imatinib-resistant GIST cells.	imatinib	147-155	mechanistic target of rapamycin kinase	Homo sapiens	31-35
25426931-1	2014	ABL tyrosine kinase inhibitors (TKI) like Imatinib, Dasatinib and Nilotinib are the gold standard in conventional treatment of CML.	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
25621010-5	2014	Our case revealed the presence of hyperdiploidy including multiple copies of the Ph chromosome, presence of b3a2 fusion transcript,T315I mutation in BCR-ABL KD in pre imatinib mesylate (IM) treatment.	imatinib	167-184	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
25349971-7	2014	RESULTS: We showed that overexpression levels of miR-125a-5p and miR-107 were associated with imatinib resistance in GIST specimens.	imatinib	94-102	microRNA 107	Homo sapiens	65-72
25349971-8	2014	Functionally, miR-125a-5p expression modulated imatinib sensitivity in GIST882 cells with a homozygous KIT mutation but not in GIST48 cells with double KIT mutations.	imatinib	47-55	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	103-106
25473890-0	2014	AMACR amplification and overexpression in primary imatinib-naive gastrointestinal stromal tumors: a driver of cell proliferation indicating adverse prognosis.	imatinib	50-58	alpha-methylacyl-CoA racemase	Homo sapiens	0-5
25451263-0	2014	Targeting miR-21 sensitizes Ph+ ALL Sup-b15 cells to imatinib-induced apoptosis through upregulation of PTEN.	imatinib	53-61	microRNA 21	Homo sapiens	10-16
25417721-0	2014	Inhibition of STAT3-interacting protein 1 (STATIP1) promotes STAT3 transcriptional up-regulation and imatinib mesylate resistance in the chronic myeloid leukemia.	imatinib	101-118	elongator acetyltransferase complex subunit 2	Homo sapiens	14-41
25349971-9	2014	Overexpression of miR-125a-5p suppressed PTPN18 expression, and silencing of PTPN18 expression increased cell viability in GIST882 cells upon imatinib treatment.	imatinib	142-150	protein tyrosine phosphatase non-receptor type 18	Homo sapiens	77-83
25349971-10	2014	PTPN18 protein levels were significantly lower in the imatinib-resistant GISTs and inversely correlated with miR-125a-5p.	imatinib	54-62	protein tyrosine phosphatase non-receptor type 18	Homo sapiens	0-6
25349971-12	2014	CONCLUSIONS: Our findings highlight a novel functional role of miR-125a-5p on imatinib response through PTPN18 regulation in GIST.	imatinib	78-86	protein tyrosine phosphatase non-receptor type 18	Homo sapiens	104-110
25451263-0	2014	Targeting miR-21 sensitizes Ph+ ALL Sup-b15 cells to imatinib-induced apoptosis through upregulation of PTEN.	imatinib	53-61	phosphatase and tensin homolog	Homo sapiens	104-108
25417721-0	2014	Inhibition of STAT3-interacting protein 1 (STATIP1) promotes STAT3 transcriptional up-regulation and imatinib mesylate resistance in the chronic myeloid leukemia.	imatinib	101-118	elongator acetyltransferase complex subunit 2	Homo sapiens	43-50
25417721-0	2014	Inhibition of STAT3-interacting protein 1 (STATIP1) promotes STAT3 transcriptional up-regulation and imatinib mesylate resistance in the chronic myeloid leukemia.	imatinib	101-118	signal transducer and activator of transcription 3	Homo sapiens	14-19
25417721-7	2014	Furthermore, we demonstrated that Lucena, an Imatinib (IM)-resistant cell line, exhibits lower STATIP1 mRNA levels and undergoes apoptosis/cell cycle arrest in response to STAT3 inhibition together with IM treatment.	imatinib	45-53	elongator acetyltransferase complex subunit 2	Homo sapiens	95-102
25451263-2	2014	Here, we showed that imatinib treatment induced significant upregulation of miR-21 and downregulation of PTEN in Ph+ ALL cell line Sup-b15.	imatinib	21-29	microRNA 21	Homo sapiens	76-82
25417721-7	2014	Furthermore, we demonstrated that Lucena, an Imatinib (IM)-resistant cell line, exhibits lower STATIP1 mRNA levels and undergoes apoptosis/cell cycle arrest in response to STAT3 inhibition together with IM treatment.	imatinib	45-53	signal transducer and activator of transcription 3	Homo sapiens	172-177
25451263-2	2014	Here, we showed that imatinib treatment induced significant upregulation of miR-21 and downregulation of PTEN in Ph+ ALL cell line Sup-b15.	imatinib	21-29	phosphatase and tensin homolog	Homo sapiens	105-109
25451263-3	2014	Transient inhibition of miR-21 resulted in increased apoptosis, PTEN upregulation and AKT dephosphorylation, whereas ectopic overexpression of miR-21 further conferred imatinib resistance.	imatinib	168-176	microRNA 21	Homo sapiens	143-149
25451263-4	2014	Furthermore, knockdown of PTEN protected the cells from imatinib-induced apoptosis achieved by inhibition of miR-21.	imatinib	56-64	phosphatase and tensin homolog	Homo sapiens	26-30
25451263-4	2014	Furthermore, knockdown of PTEN protected the cells from imatinib-induced apoptosis achieved by inhibition of miR-21.	imatinib	56-64	microRNA 21	Homo sapiens	109-115
25451263-6	2014	Therefore, miR-21 contributes to imatinib resistance in Ph+ ALL cells and antagonizing miR-21 demonstrates therapeutic potential by sensitizing the malignancy to imatinib therapy.	imatinib	33-41	microRNA 21	Homo sapiens	11-17
25451263-6	2014	Therefore, miR-21 contributes to imatinib resistance in Ph+ ALL cells and antagonizing miR-21 demonstrates therapeutic potential by sensitizing the malignancy to imatinib therapy.	imatinib	162-170	microRNA 21	Homo sapiens	87-93
25264277-0	2014	Exposure of neuroblastoma cell lines to imatinib results in the upregulation of the CDK inhibitor p27(KIP1) as a consequence of c-Abl inhibition.	imatinib	40-48	interferon alpha inducible protein 27	Homo sapiens	98-101
25520872-6	2014	In high-risk GISTs with or without imatinib adjuvant therapy, EGFR negative expression are associated with decreased RFS when compared to positive cases.	imatinib	35-43	epidermal growth factor receptor	Homo sapiens	62-66
25520872-10	2014	In our study, detection of EGFR expression helps to precisely subdivide high-risk GISTs for different prognosis and probably predict outcomes for imatinib treatment.	imatinib	146-154	epidermal growth factor receptor	Homo sapiens	27-31
25264277-0	2014	Exposure of neuroblastoma cell lines to imatinib results in the upregulation of the CDK inhibitor p27(KIP1) as a consequence of c-Abl inhibition.	imatinib	40-48	cyclin dependent kinase inhibitor 1B	Homo sapiens	102-106
25264277-0	2014	Exposure of neuroblastoma cell lines to imatinib results in the upregulation of the CDK inhibitor p27(KIP1) as a consequence of c-Abl inhibition.	imatinib	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-133
25264277-1	2014	Imatinib mesylate is a tyrosine kinase inhibitor with selectivity for abelson tyrosine-protein kinase 1 (c-Abl), breakpoint cluster region (Bcr)-Abl fusion protein (Bcr-Abl), mast/stem cell growth factor receptor Kit (c-Kit), and platelet-derived growth factor receptor (PDGFR).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-110
25264277-1	2014	Imatinib mesylate is a tyrosine kinase inhibitor with selectivity for abelson tyrosine-protein kinase 1 (c-Abl), breakpoint cluster region (Bcr)-Abl fusion protein (Bcr-Abl), mast/stem cell growth factor receptor Kit (c-Kit), and platelet-derived growth factor receptor (PDGFR).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-148
25239608-2	2014	Imatinib, sunitinib, and regorafenib are approved therapies; however, efficacy is often limited by the acquisition of polyclonal secondary resistance mutations in KIT, with those located in the activation (A) loop (exons 17/18) being particularly problematic.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	163-166
25264277-1	2014	Imatinib mesylate is a tyrosine kinase inhibitor with selectivity for abelson tyrosine-protein kinase 1 (c-Abl), breakpoint cluster region (Bcr)-Abl fusion protein (Bcr-Abl), mast/stem cell growth factor receptor Kit (c-Kit), and platelet-derived growth factor receptor (PDGFR).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	165-172
25239608-4	2014	EXPERIMENTAL DESIGN: The cellular and in vivo activities of ponatinib, imatinib, sunitinib, and regorafenib against mutant KIT were evaluated using an accelerated mutagenesis assay and a panel of engineered and GIST-derived cell lines.	imatinib	71-79	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	123-126
25264277-1	2014	Imatinib mesylate is a tyrosine kinase inhibitor with selectivity for abelson tyrosine-protein kinase 1 (c-Abl), breakpoint cluster region (Bcr)-Abl fusion protein (Bcr-Abl), mast/stem cell growth factor receptor Kit (c-Kit), and platelet-derived growth factor receptor (PDGFR).	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	218-223
25264277-1	2014	Imatinib mesylate is a tyrosine kinase inhibitor with selectivity for abelson tyrosine-protein kinase 1 (c-Abl), breakpoint cluster region (Bcr)-Abl fusion protein (Bcr-Abl), mast/stem cell growth factor receptor Kit (c-Kit), and platelet-derived growth factor receptor (PDGFR).	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	230-269
25264277-1	2014	Imatinib mesylate is a tyrosine kinase inhibitor with selectivity for abelson tyrosine-protein kinase 1 (c-Abl), breakpoint cluster region (Bcr)-Abl fusion protein (Bcr-Abl), mast/stem cell growth factor receptor Kit (c-Kit), and platelet-derived growth factor receptor (PDGFR).	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	271-276
25264277-3	2014	However, although neuroblastoma cells express c-Kit and PDGFR, the imatinib concentrations required to achieve significant growth inhibitory effects (>= 10 muM) are substantially higher than those required for inhibition of ligand-induced phosphorylation of wild type c-Kit and PDGFR (<= 1 muM), suggesting that additional mechanisms are responsible for the antitumor activity of imatinib on these cells.	imatinib	67-75	latexin	Homo sapiens	159-162
25264277-3	2014	However, although neuroblastoma cells express c-Kit and PDGFR, the imatinib concentrations required to achieve significant growth inhibitory effects (>= 10 muM) are substantially higher than those required for inhibition of ligand-induced phosphorylation of wild type c-Kit and PDGFR (<= 1 muM), suggesting that additional mechanisms are responsible for the antitumor activity of imatinib on these cells.	imatinib	67-75	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	271-276
25264277-3	2014	However, although neuroblastoma cells express c-Kit and PDGFR, the imatinib concentrations required to achieve significant growth inhibitory effects (>= 10 muM) are substantially higher than those required for inhibition of ligand-induced phosphorylation of wild type c-Kit and PDGFR (<= 1 muM), suggesting that additional mechanisms are responsible for the antitumor activity of imatinib on these cells.	imatinib	67-75	platelet derived growth factor receptor beta	Homo sapiens	281-286
25264277-3	2014	However, although neuroblastoma cells express c-Kit and PDGFR, the imatinib concentrations required to achieve significant growth inhibitory effects (>= 10 muM) are substantially higher than those required for inhibition of ligand-induced phosphorylation of wild type c-Kit and PDGFR (<= 1 muM), suggesting that additional mechanisms are responsible for the antitumor activity of imatinib on these cells.	imatinib	67-75	latexin	Homo sapiens	296-299
25264277-4	2014	In this study, we show that treatment of neuroblastoma cell lines with 1-15 muM imatinib resulted in a dose dependent inhibition of 5-bromo-2"-deoxyuridine (BrdU) incorporation into newly synthesized DNA.	imatinib	80-88	latexin	Homo sapiens	76-79
25264277-5	2014	The antiproliferative effect of imatinib was dependent on the upregulation of the cyclin-dependent kinase (CDK) inhibitor p27(KIP1) in the nuclear compartment as a result of increased p27(KIP1) protein stability.	imatinib	32-40	interferon alpha inducible protein 27	Homo sapiens	122-125
25264277-5	2014	The antiproliferative effect of imatinib was dependent on the upregulation of the cyclin-dependent kinase (CDK) inhibitor p27(KIP1) in the nuclear compartment as a result of increased p27(KIP1) protein stability.	imatinib	32-40	cyclin dependent kinase inhibitor 1B	Homo sapiens	126-130
25264277-5	2014	The antiproliferative effect of imatinib was dependent on the upregulation of the cyclin-dependent kinase (CDK) inhibitor p27(KIP1) in the nuclear compartment as a result of increased p27(KIP1) protein stability.	imatinib	32-40	interferon alpha inducible protein 27	Homo sapiens	184-187
25264277-5	2014	The antiproliferative effect of imatinib was dependent on the upregulation of the cyclin-dependent kinase (CDK) inhibitor p27(KIP1) in the nuclear compartment as a result of increased p27(KIP1) protein stability.	imatinib	32-40	cyclin dependent kinase inhibitor 1B	Homo sapiens	188-192
25264277-9	2014	Given the low affinity of active c-Abl for imatinib, these data provide a molecular explanation for the relatively high imatinib concentrations required to inhibit neuroblastoma cell proliferation.	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-38
25264277-9	2014	Given the low affinity of active c-Abl for imatinib, these data provide a molecular explanation for the relatively high imatinib concentrations required to inhibit neuroblastoma cell proliferation.	imatinib	120-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-38
24240679-3	2014	We used a model of MPN, which is induced by co-expression of the oncoproteins HIP1/PDGFbetaR (H/P) and AML1/ETO from their endogenous loci, to examine the mechanisms of disease development and recurrence following imatinib withdrawal.	imatinib	214-222	protease, serine 27	Mus musculus	19-22
25431951-0	2014	Antitumor activity of S116836, a novel tyrosine kinase inhibitor, against imatinib-resistant FIP1L1-PDGFRalpha-expressing cells.	imatinib	74-82	factor interacting with PAPOLA and CPSF1	Homo sapiens	93-99
25431951-0	2014	Antitumor activity of S116836, a novel tyrosine kinase inhibitor, against imatinib-resistant FIP1L1-PDGFRalpha-expressing cells.	imatinib	74-82	platelet derived growth factor receptor alpha	Homo sapiens	100-110
25431951-2	2014	Most FIP1L1-PDGFRalpha-positive patients respond well to the tyrosine kinase inhibitor (TKI) imatinib.	imatinib	93-101	factor interacting with PAPOLA and CPSF1	Homo sapiens	5-11
25431951-2	2014	Most FIP1L1-PDGFRalpha-positive patients respond well to the tyrosine kinase inhibitor (TKI) imatinib.	imatinib	93-101	platelet derived growth factor receptor alpha	Homo sapiens	12-22
25431951-3	2014	Resistance to imatinib in HES/CEL has been described mainly due to the T674I mutation in FIP1L1-PDGFRalpha, which is homologous to the imatinib-resistant T315I mutation in BCR-ABL.	imatinib	14-22	factor interacting with PAPOLA and CPSF1	Homo sapiens	89-95
25431951-3	2014	Resistance to imatinib in HES/CEL has been described mainly due to the T674I mutation in FIP1L1-PDGFRalpha, which is homologous to the imatinib-resistant T315I mutation in BCR-ABL.	imatinib	14-22	platelet derived growth factor receptor alpha	Homo sapiens	96-106
25431951-3	2014	Resistance to imatinib in HES/CEL has been described mainly due to the T674I mutation in FIP1L1-PDGFRalpha, which is homologous to the imatinib-resistant T315I mutation in BCR-ABL.	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-179
25431951-3	2014	Resistance to imatinib in HES/CEL has been described mainly due to the T674I mutation in FIP1L1-PDGFRalpha, which is homologous to the imatinib-resistant T315I mutation in BCR-ABL.	imatinib	135-143	factor interacting with PAPOLA and CPSF1	Homo sapiens	89-95
25431951-3	2014	Resistance to imatinib in HES/CEL has been described mainly due to the T674I mutation in FIP1L1-PDGFRalpha, which is homologous to the imatinib-resistant T315I mutation in BCR-ABL.	imatinib	135-143	platelet derived growth factor receptor alpha	Homo sapiens	96-106
25431951-3	2014	Resistance to imatinib in HES/CEL has been described mainly due to the T674I mutation in FIP1L1-PDGFRalpha, which is homologous to the imatinib-resistant T315I mutation in BCR-ABL.	imatinib	135-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-179
24240679-4	2014	Although the MPN displayed a full hematologic response to imatinib, 100% of the diseased mice relapsed upon drug withdrawal.	imatinib	58-66	protease, serine 27	Mus musculus	13-16
24240679-7	2014	Supplementation of imatinib with granulocyte colony-stimulating factor or arsenic trioxide reduced MPN-initiating cell frequencies and the combination of imatinib with arsenic trioxide cured a large fraction of mice with MPNs.	imatinib	19-27	protease, serine 27	Mus musculus	99-102
24240679-9	2014	These data suggest that treatment with a combination of arsenic trioxide and imatinib can eliminate refractory MPN-initiating cells and reduce disease relapse.	imatinib	77-85	protease, serine 27	Mus musculus	111-114
25301112-0	2014	ABCB1 haplotypes but not individual SNPs predict for optimal response/failure in Egyptian patients with chronic-phase chronic myeloid leukemia receiving imatinib mesylate.	imatinib	153-170	ATP binding cassette subfamily B member 1	Homo sapiens	0-5
25609545-0	2014	Metabolic response by FDG-PET to imatinib correlates with exon 11 KIT mutation and predicts outcome in patients with mucosal melanoma.	imatinib	33-41	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	66-69
25609545-1	2014	BACKGROUND: In patients with metastatic melanoma and KIT amplifications and/or mutations, therapy with imatinib mesylate may prolong survival.	imatinib	103-120	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	53-56
25995993-1	2014	Patients with chronic myeloid leukemia (CML) are commonly treated with a specific inhibitor of BCR-ABL tyrosine kinase, imatinib mesylate (IM).	imatinib	120-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
25995993-3	2014	Somatic mutations, especially T315I mutation, in BCR-ABL kinase domain represent the most common mechanism underlying drug resistance to tyrosine kinase inhibitors (TKI), including imatinib.	imatinib	181-189	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
25216683-9	2014	The dynamics of BCR-ABL1 clearance observed in our study suggest that the use of standard or high-dose imatinib or a second-generation tyrosine kinase inhibitor such as nilotinib or dasatinib elicits similar responses when administered as front-line therapy for patients with chronic myeloid leukemia in chronic phase.	imatinib	103-111	BCR activator of RhoGEF and GTPase	Homo sapiens	16-24
25584281-1	2014	Dasatinib is a second-generation multi-target tyrosine kinase inhibitor (TKI) that has activity against many imatinib-resistant BCR-ABL mutant forms, Src, and c-Kit tyrosine kinases.	imatinib	109-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
24699303-4	2014	This inverse correlation between Abi-1 and alpha4 integrin expression, as well as linkage to elevated phospho-Akt and phospho-Erk signaling, was confirmed in imatinib mesylate -resistant leukemic cells.	imatinib	158-175	abl interactor 1	Homo sapiens	33-38
25057771-0	2014	Imatinib binding to human serum albumin modulates heme association and reactivity.	imatinib	0-8	albumin	Homo sapiens	26-39
24699303-4	2014	This inverse correlation between Abi-1 and alpha4 integrin expression, as well as linkage to elevated phospho-Akt and phospho-Erk signaling, was confirmed in imatinib mesylate -resistant leukemic cells.	imatinib	158-175	AKT serine/threonine kinase 1	Homo sapiens	110-113
24743220-0	2014	Frequent mono-allelic loss associated with deficient PTEN expression in imatinib-resistant gastrointestinal stromal tumors.	imatinib	72-80	phosphatase and tensin homolog	Homo sapiens	53-57
24743220-2	2014	In this study, we have performed a comprehensive molecular and immunohistochemical characterization of PTEN in 58 imatinib-naive and 54 imatinib-treated gastrointestinal stromal tumors (GISTs).	imatinib	114-122	phosphatase and tensin homolog	Homo sapiens	103-107
24743220-4	2014	At the genomic level, PTEN was affected mainly by mono-allelic loss, which was significantly less frequent in imatinib-naive vs imatinib-resistant tumors (9% vs 39%, P<0.001).	imatinib	110-118	phosphatase and tensin homolog	Homo sapiens	22-26
24743220-4	2014	At the genomic level, PTEN was affected mainly by mono-allelic loss, which was significantly less frequent in imatinib-naive vs imatinib-resistant tumors (9% vs 39%, P<0.001).	imatinib	128-136	phosphatase and tensin homolog	Homo sapiens	22-26
24743220-7	2014	Low PTEN protein expression was common (50%) and often paralleled with total immunonegativity in imatinib-resistant tumors.	imatinib	97-105	phosphatase and tensin homolog	Homo sapiens	4-8
24743220-13	2014	In conclusion, depleted PTEN expression associated with mono-allelic PTEN loss occurs frequently in imatinib-resistant GIST and might serve as a biomarker for stratifying patients for optimal treatment.	imatinib	100-108	phosphatase and tensin homolog	Homo sapiens	24-28
24743220-13	2014	In conclusion, depleted PTEN expression associated with mono-allelic PTEN loss occurs frequently in imatinib-resistant GIST and might serve as a biomarker for stratifying patients for optimal treatment.	imatinib	100-108	phosphatase and tensin homolog	Homo sapiens	69-73
24743220-15	2014	Novel therapies targeting multiple components of the integrated KIT receptor signaling pathways in imatinib-resistant GIST warrant further studies.	imatinib	99-107	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	64-67
25360622-7	2014	In contrast, depletion of CDKN3 expression conferred resistance to imatinib-induced apoptosis in the leukemic cells and accelerated the growth of xenograph leukemia in mice.	imatinib	67-75	cyclin-dependent kinase inhibitor 3	Mus musculus	26-31
25057771-5	2014	All data were obtained at pH 7.0, and 20.0  C and 37.0  C. Imatinib binding to the FA7 site of HSA and trHSA inhibits allosterically heme-Fe(III) association to the FA1 site and vice versa, according to linked functions.	imatinib	59-67	FA complementation group A	Homo sapiens	165-168
25057771-6	2014	Moreover, imatinib binding to the secondary FA2 site of HSA-heme-Fe(III) inhibits allosterically peroxynitrite detoxification.	imatinib	10-18	FA complementation group B	Homo sapiens	44-47
25057771-7	2014	Docking simulations and local structural comparison with other imatinib-binding proteins support functional data indicating the preferential binding of imatinib to the FA1 and FA7 sites of HSA, and to the FA2 and FA7 sites of HSA-heme-Fe(III).	imatinib	63-71	FA complementation group A	Homo sapiens	168-171
25057771-7	2014	Docking simulations and local structural comparison with other imatinib-binding proteins support functional data indicating the preferential binding of imatinib to the FA1 and FA7 sites of HSA, and to the FA2 and FA7 sites of HSA-heme-Fe(III).	imatinib	63-71	FA complementation group B	Homo sapiens	205-208
25057771-7	2014	Docking simulations and local structural comparison with other imatinib-binding proteins support functional data indicating the preferential binding of imatinib to the FA1 and FA7 sites of HSA, and to the FA2 and FA7 sites of HSA-heme-Fe(III).	imatinib	152-160	FA complementation group A	Homo sapiens	168-171
25057771-2	2014	However, human serum albumin (HSA) may represent the secondary carrier of imatinib in pathological states characterized by low AGP levels, such as pancreatic cancer, hepatic cirrhosis, hepatitis, hyperthyroidism, nephrotic syndrome, malnutrition, and cachexia.	imatinib	74-82	albumin	Homo sapiens	15-28
25057771-3	2014	Here, thermodynamics of imatinib binding to full-length HSA and its recombinant Asp1-Glu382 truncated form (containing only the FA1, FA2, FA6, and FA7 binding sites; trHSA), in the absence and presence of ferric heme (heme-Fe(III)), and the thermodynamics of heme-Fe(III) binding to HSA and trHSA, in the absence and presence of imatinib, has been investigated.	imatinib	24-32	beta-secretase 2	Homo sapiens	80-84
25436260-0	2014	Coexistent BCR-ABL1 and JAK2 V617F:  converting CML dwarves to ET staghorns with  imatinib therapy.	imatinib	82-90	BCR activator of RhoGEF and GTPase	Homo sapiens	11-19
25333252-0	2014	The BCL2 inhibitor ABT-199 significantly enhances imatinib-induced cell death in chronic myeloid leukemia progenitors.	imatinib	50-58	BCL2 apoptosis regulator	Homo sapiens	4-8
25170123-3	2014	Children with a BCR-ABL1/ABL ratio higher than 10% at 3 months after the start of imatinib had a larger spleen size and a higher white blood cell count compared with those with BCR-ABL1/ABL <=10%.	imatinib	82-90	BCR activator of RhoGEF and GTPase	Homo sapiens	16-24
25170123-3	2014	Children with a BCR-ABL1/ABL ratio higher than 10% at 3 months after the start of imatinib had a larger spleen size and a higher white blood cell count compared with those with BCR-ABL1/ABL <=10%.	imatinib	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-23
25170123-3	2014	Children with a BCR-ABL1/ABL ratio higher than 10% at 3 months after the start of imatinib had a larger spleen size and a higher white blood cell count compared with those with BCR-ABL1/ABL <=10%.	imatinib	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-28
25170123-4	2014	Children with BCR-ABL1/ABL <=10% 3 months after starting imatinib had higher rates of complete cytogenetic response and major molecular response at 12 months compared with those with BCR-ABL1/ABL >10%.	imatinib	60-68	BCR activator of RhoGEF and GTPase	Homo sapiens	14-22
25170123-4	2014	Children with BCR-ABL1/ABL <=10% 3 months after starting imatinib had higher rates of complete cytogenetic response and major molecular response at 12 months compared with those with BCR-ABL1/ABL >10%.	imatinib	60-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-21
25170123-4	2014	Children with BCR-ABL1/ABL <=10% 3 months after starting imatinib had higher rates of complete cytogenetic response and major molecular response at 12 months compared with those with BCR-ABL1/ABL >10%.	imatinib	60-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-26
25550846-12	2014	Since the exon 8 mutations appeared to be really sensitive to imatinib as shown in the present case study, accurate genotyping including exon 8 of the c-kit gene is necessary in GISTs to predict response to imatinib in both the unresectable/metastatic and adjuvant settings.	imatinib	62-70	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	151-156
25550846-12	2014	Since the exon 8 mutations appeared to be really sensitive to imatinib as shown in the present case study, accurate genotyping including exon 8 of the c-kit gene is necessary in GISTs to predict response to imatinib in both the unresectable/metastatic and adjuvant settings.	imatinib	207-215	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	151-156
25088577-2	2014	D816V KIT mutation, found in ~80% of SM, is resistant to the currently available tyrosine kinase inhibitors (TKIs) (e.g. imatinib mesylate).	imatinib	121-138	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	6-9
25436260-0	2014	Coexistent BCR-ABL1 and JAK2 V617F:  converting CML dwarves to ET staghorns with  imatinib therapy.	imatinib	82-90	Janus kinase 2	Homo sapiens	24-28
25201268-7	2014	The inhibition of ABL1 by imatinib mesylate and danusertib was also electrochemically investigated and IC50 values of 0.53 and 0.08 muM determined.	imatinib	26-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-22
25153794-3	2014	Using P-EIM, we measured binding kinetics and affinity between small molecule drugs (imatinib and SB202190) and their target proteins (kinases Abl1 and p38-alpha).	imatinib	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-147
25153794-3	2014	Using P-EIM, we measured binding kinetics and affinity between small molecule drugs (imatinib and SB202190) and their target proteins (kinases Abl1 and p38-alpha).	imatinib	85-93	mitogen-activated protein kinase 14	Homo sapiens	152-161
25092176-8	2014	In vivo, imatinib impaired tumor angiogenesis and lymphoma growth in SOX11-positive MCL xenograft tumors.	imatinib	9-17	SRY-box transcription factor 11	Homo sapiens	69-74
25002122-0	2014	Niche anchorage and signaling through membrane-bound Kit-ligand/c-kit receptor are kinase independent and imatinib insensitive.	imatinib	106-114	kit ligand	Mus musculus	53-63
24931551-8	2014	We expressed AdNFATc3-green fluorescent protein in NRVMs and showed imatinib treatment significantly increased nuclear factor of activated T cells translocation that was inhibited by the calcineurin inhibitor FK506 or CaMKII inhibitors.	imatinib	68-76	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	218-224
25280212-1	2014	SIRT1 inhibition facilitates elimination of CML stem cells by Imatinib, in part via p53 activation.	imatinib	62-70	sirtuin 1	Homo sapiens	0-5
25274034-16	2014	We speculate that stroma-directed therapies, including anti-PDGFR agents like Imatinib, may be useful in combination with other therapies for treatment of luminal cancers.	imatinib	78-86	platelet derived growth factor receptor beta	Homo sapiens	60-65
25002122-0	2014	Niche anchorage and signaling through membrane-bound Kit-ligand/c-kit receptor are kinase independent and imatinib insensitive.	imatinib	106-114	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	64-69
25002122-7	2014	Kinase inhibition of c-kit by imatinib reduced cluster coalescence, but allowed cluster phosphorylation and F-actin polymerization, which required PI3K recruitment and a newly identified juxtamembrane residue.	imatinib	30-38	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	21-26
24798484-0	2014	Velocity of early BCR-ABL transcript elimination as an optimized predictor of outcome in chronic myeloid leukemia (CML) patients in chronic phase on treatment with imatinib.	imatinib	164-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
24612223-6	2014	Nilotinib, sunitinib, and imatinib were found to be potent CYP1A2 inhibitor.	imatinib	26-34	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	59-65
24697802-4	2014	Imatinib, a tyrosine kinase inhibitor, interferes with both transforming growth factor beta and platelet-derived growth factor signaling pathways.	imatinib	0-8	transforming growth factor beta 1	Homo sapiens	60-91
24913304-7	2014	Furthermore, p53(mut_c) cells exhibited a pronounced side population that could be suppressed by RNAi knockdown of ABCG2 as well as treatment with the ATP-binding-cassette transporter inhibitors imatinib, MK571 and tariquidar.	imatinib	195-203	tumor protein p53	Homo sapiens	13-16
24390454-8	2014	Imatinib is a useful adjuvant drug even in PDGRFA/FIP1L1-negative HES.	imatinib	0-8	factor interacting with PAPOLA and CPSF1	Homo sapiens	50-56
25139846-0	2014	Familial systemic mastocytosis with germline KIT K509I mutation is sensitive to treatment with imatinib, dasatinib and PKC412.	imatinib	95-103	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	45-48
25139846-3	2014	In vitro treatment with imatinib, dasatinib and PKC412 reduced cell viability of primary mast cells harboring KIT K509I mutation.	imatinib	24-32	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	110-113
25139846-5	2014	Both patients with familial systemic mastocytosis had remarkable hematological and skin improvement after three months of imatinib treatment, suggesting that it may be an effective front line therapy for patients harboring KIT K509I mutation.	imatinib	122-130	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	223-226
25115808-0	2014	Outcome prediction by the transcript level of BCR-ABL at 3 months in patients with chronic myeloid leukemia treated with imatinib--a single institution historical experience.	imatinib	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
25056090-1	2014	An imatinib intermediate, 6-methyl-N-[4-(pyridin-3-yl)pyrimidin-2-yl]benzene-1,3-diaminepyridopyrimidotoluidine (PPT-1), was developed for the colorimetric sensing of Cu(2+) ions in aqueous solution.	imatinib	3-11	palmitoyl-protein thioesterase 1	Homo sapiens	113-118
25003536-0	2014	Novel somatic KIT exon 8 mutation with dramatic response to imatinib in a patient with mucosal melanoma: a case report.	imatinib	60-68	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-17
25003536-4	2014	Tumor response to imatinib mesylate has been reported in about half of the patients with tumors harboring KIT mutations.	imatinib	18-35	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	106-109
25003536-10	2014	This biology may explain the successful application of imatinib in animals with tumors harboring exon 8 KIT mutations and in our patient with mucosal melanoma.	imatinib	55-63	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	104-107
25003536-11	2014	This report expands the population of patients with melanoma who might benefit from imatinib to those with somatic exon 8 KIT mutations.	imatinib	84-92	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	122-125
24850877-8	2014	RESULTS: After 6 months of imatinib treatment, plasma levels of soluble vascular cell adhesion molecule 1 decreased significantly (P < 0.001), while tissue levels of soluble intercellular adhesion molecule 1 increased (P < 0.01).	imatinib	27-35	vascular cell adhesion molecule 1	Homo sapiens	72-105
24850877-8	2014	RESULTS: After 6 months of imatinib treatment, plasma levels of soluble vascular cell adhesion molecule 1 decreased significantly (P < 0.001), while tissue levels of soluble intercellular adhesion molecule 1 increased (P < 0.01).	imatinib	27-35	intercellular adhesion molecule 1	Homo sapiens	177-210
25338569-7	2014	The expression level of calcineurin in S4C2 cells was higher than that in S9 cells.When CsA inhibited the calcineurin activity, the expression of DNA damage marker gamma-H2AX in S9 cells was significantly lower than that in S4C2 cells,while the expression level of gamma-H2AX between the two cell lines was no significantly different after treatment with imatinib, the expression level of gamma-H2AX in S9 cells was lower than that in S4C2 cells when the two drugs were combined.	imatinib	355-363	H2A.X variant histone	Mus musculus	164-174
25324906-7	2014	Imatinib may be effective for patients with with c-Kit gene mutations.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	49-54
25255859-5	2014	Imatinib or trehalose improves metabolic parameters of Atg7(+/-)-ob/ob mice and enhances autophagic flux.	imatinib	0-8	autophagy related 7	Mus musculus	55-59
25243742-7	2014	In wildtype mice, defective sprouting angiogenesis could be mimicked by blocking PDGFRbeta signalling using the tyrosine kinase inhibitor Imatinib mesylate.	imatinib	138-155	platelet derived growth factor receptor, beta polypeptide	Mus musculus	81-90
25132497-3	2014	We found that clinically reported BCR-ABL1 compound mutants center on 12 key positions and confer varying resistance to imatinib, nilotinib, dasatinib, ponatinib, rebastinib, and bosutinib.	imatinib	120-128	BCR activator of RhoGEF and GTPase	Homo sapiens	34-42
25198091-0	2014	Real-time analysis of imatinib- and dasatinib-induced effects on chronic myelogenous leukemia cell interaction with fibronectin.	imatinib	22-30	fibronectin 1	Homo sapiens	116-127
25186176-0	2014	A therapeutically targetable mechanism of BCR-ABL-independent imatinib resistance in chronic myeloid leukemia.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
25186176-1	2014	Resistance to the BCR-ABL inhibitor imatinib mesylate (IM) poses a major problem for the treatment of chronic myeloid leukemia (CML).	imatinib	36-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
25253994-3	2014	METHODS: PDGFR signaling was inhibited using Sunitinib malate, Imatinib mesylate or Regorafenib in murine and human luminal-like and claudin-low mammary tumor cell lines or Masitinib in only the human cell lines.	imatinib	63-80	platelet derived growth factor receptor, beta polypeptide	Mus musculus	9-14
25183062-1	2014	BACKGROUND: The extraordinary success of imatinib in the treatment of BCR-ABL1 associated cancers underscores the need to identify novel functional gene fusions in cancer.	imatinib	41-49	BCR activator of RhoGEF and GTPase	Homo sapiens	70-78
23642471-1	2014	Imatinib mesylate is a tyrosine kinase inhibitor that targets the BCR-ABL, c-kit, and PDGF (platelet-derived growth factor) receptors.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
23642471-1	2014	Imatinib mesylate is a tyrosine kinase inhibitor that targets the BCR-ABL, c-kit, and PDGF (platelet-derived growth factor) receptors.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	75-80
25198091-4	2014	The effect of two clinically used kinase inhibitors, imatinib (a relatively specific c-ABL inhibitor) and dasatinib (dual ABL/SRC family kinase inhibitor), on cell binding to fibronectin is described.	imatinib	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-90
25198091-4	2014	The effect of two clinically used kinase inhibitors, imatinib (a relatively specific c-ABL inhibitor) and dasatinib (dual ABL/SRC family kinase inhibitor), on cell binding to fibronectin is described.	imatinib	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-90
25198091-4	2014	The effect of two clinically used kinase inhibitors, imatinib (a relatively specific c-ABL inhibitor) and dasatinib (dual ABL/SRC family kinase inhibitor), on cell binding to fibronectin is described.	imatinib	53-61	fibronectin 1	Homo sapiens	175-186
25198091-5	2014	Both imatinib and low-dose (several nM) dasatinib reinforced CML cell interaction with fibronectin while no significant change was induced in BCR-ABL-negative cells.	imatinib	5-13	fibronectin 1	Homo sapiens	87-98
25198091-9	2014	In the intracellular context, EC50 for BCR-ABL inhibition was in subnanomolar range for dasatinib and in submicromolar one for imatinib.	imatinib	127-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
25198091-10	2014	EC50 for direct inhibition of LYN kinase was found to be about 20 nM for dasatinib and more than 10 microM for imatinib.	imatinib	111-119	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	30-33
24939418-3	2014	In this study, interactions between As2O3 and BTZ were examined in imatinib-resistant Bcr/Abl+ (K562r) cells.	imatinib	67-75	BCR activator of RhoGEF and GTPase	Homo sapiens	86-89
24981766-8	2014	Intraperitoneal administration of imatinib, a potent inhibitor of PDGFRbeta, and transduction of PDGFRbeta/Fc chimeric protein by an adenoviral system both reduced inflammatory lymphangiogenesis induced by thioglycollate in mice.	imatinib	34-42	platelet derived growth factor receptor, beta polypeptide	Mus musculus	66-75
25841461-5	2014	KIT inhibitors, most notably imatinib, have shown promising clinical activity in KIT-mutant advanced melanoma, including mucosal melanoma, with clinical response rates exceeding 35% in patients with hot-spot mutations in exon 11 or 13 and/or a high mutant/wild-type allelic ratio.	imatinib	29-37	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
25841461-5	2014	KIT inhibitors, most notably imatinib, have shown promising clinical activity in KIT-mutant advanced melanoma, including mucosal melanoma, with clinical response rates exceeding 35% in patients with hot-spot mutations in exon 11 or 13 and/or a high mutant/wild-type allelic ratio.	imatinib	29-37	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	81-84
25621158-0	2014	Imatinib in pulmonary arterial hypertension: c-Kit inhibition.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	45-50
25621158-4	2014	Imatinib, a tyrosine kinase inhibitor that targets c-Kit, has been shown to be beneficial for patients with PAH.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	51-56
25621158-5	2014	Here we hypothesize that the clinical benefit of imatinib in PAH could be related to c-Kit inhibition of progenitor cell mobilization and maturation into mast cells.	imatinib	49-57	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	85-90
25621158-9	2014	Circulating CD34(+)CD133(+) and c-Kit(+) progenitor cells as well as c-Kit(+)/CD34(+)CD133(+) decreased with imatinib therapy (all P < 0.05).	imatinib	109-117	CD34 molecule	Homo sapiens	12-16
25621158-9	2014	Circulating CD34(+)CD133(+) and c-Kit(+) progenitor cells as well as c-Kit(+)/CD34(+)CD133(+) decreased with imatinib therapy (all P < 0.05).	imatinib	109-117	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	32-37
25621158-9	2014	Circulating CD34(+)CD133(+) and c-Kit(+) progenitor cells as well as c-Kit(+)/CD34(+)CD133(+) decreased with imatinib therapy (all P < 0.05).	imatinib	109-117	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	69-74
25621158-9	2014	Circulating CD34(+)CD133(+) and c-Kit(+) progenitor cells as well as c-Kit(+)/CD34(+)CD133(+) decreased with imatinib therapy (all P < 0.05).	imatinib	109-117	CD34 molecule	Homo sapiens	78-82
25621158-11	2014	The findings support c-Kit inhibition as a potential mechanism of action of imatinib in PAH and suggest that tryptase is a potential biomarker of response to therapy.	imatinib	76-84	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	21-26
25202073-1	2014	BACKGROUND/AIM: BCR-ABL-positive (BCR-ABL(+)) leukemia is very difficult to treat although much improvement has been achieved due to the clinical application of imatinib and the second-generation tyrosine kinase inhibitors (TKIs).	imatinib	161-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
25202073-1	2014	BACKGROUND/AIM: BCR-ABL-positive (BCR-ABL(+)) leukemia is very difficult to treat although much improvement has been achieved due to the clinical application of imatinib and the second-generation tyrosine kinase inhibitors (TKIs).	imatinib	161-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
25202073-5	2014	RESULTS: This drug showed treatment efficacy in naive and imatinib-resistant BCR-ABL(+) leukemia cells, particularly in cells harboring T315I-mutated BCR-ABL, for which no effective inhibitor is available to date.	imatinib	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
24837466-0	2014	Distinct characteristics of e13a2 versus e14a2 BCR-ABL1 driven chronic myeloid leukemia under first-line therapy with imatinib.	imatinib	118-126	BCR activator of RhoGEF and GTPase	Homo sapiens	47-55
24939418-8	2014	Therefore, further studies are required to assess the potential of BTZ and As2O3 combinatory treatment of chronic myeloid leukemia, particularly using imatinib-resistant Bcr/Abl+ clones.	imatinib	151-159	BCR activator of RhoGEF and GTPase	Homo sapiens	170-173
25187697-0	2014	Downregulated microRNA-148b in circulating PBMCs in chronic myeloid leukemia patients with undetectable minimal residual disease: a possible biomarker to discontinue imatinib safely.	imatinib	166-174	microRNA 148b	Homo sapiens	14-27
25148385-2	2014	We studied the effect of inhibition of c-Abl kinase activity by imatinib with chemotherapy drugs and found a striking difference in cell survival after combined mitoxantrone (MX) and imatinib treatment compared to a panel of other chemotherapy drugs.	imatinib	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-44
25148385-2	2014	We studied the effect of inhibition of c-Abl kinase activity by imatinib with chemotherapy drugs and found a striking difference in cell survival after combined mitoxantrone (MX) and imatinib treatment compared to a panel of other chemotherapy drugs.	imatinib	183-191	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-44
25148385-9	2014	The effect of imatinib was decreased by c-Abl siRNA suggesting a role for catalytically inactive c-Abl in the death cascade.	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-45
25148385-9	2014	The effect of imatinib was decreased by c-Abl siRNA suggesting a role for catalytically inactive c-Abl in the death cascade.	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-102
24825187-5	2014	Confocal microscopy identified different subcellular localizations of DOG1 in imatinib-sensitive and imatinib-resistant cells.	imatinib	78-86	anoctamin 1	Homo sapiens	70-74
25133686-7	2014	As a specific inhibitor of tyrosine kinases, imatinib blocked the activity of tyrosine kinases and the expression of phospho-Crkl, induced by the de novo BCR/ABL protein caused by K562 EVs bearing BCR/ABL DNA.	imatinib	45-53	v-crk avian sarcoma virus CT10 oncogene homolog-like	Mus musculus	125-129
25133686-7	2014	As a specific inhibitor of tyrosine kinases, imatinib blocked the activity of tyrosine kinases and the expression of phospho-Crkl, induced by the de novo BCR/ABL protein caused by K562 EVs bearing BCR/ABL DNA.	imatinib	45-53	BCR activator of RhoGEF and GTPase	Mus musculus	154-161
25133686-7	2014	As a specific inhibitor of tyrosine kinases, imatinib blocked the activity of tyrosine kinases and the expression of phospho-Crkl, induced by the de novo BCR/ABL protein caused by K562 EVs bearing BCR/ABL DNA.	imatinib	45-53	BCR activator of RhoGEF and GTPase	Mus musculus	197-204
24825187-5	2014	Confocal microscopy identified different subcellular localizations of DOG1 in imatinib-sensitive and imatinib-resistant cells.	imatinib	101-109	anoctamin 1	Homo sapiens	70-74
24825187-8	2014	However, inhibition of DOG1 conveyed pro-apoptotic effects among early apoptotic imatinib-resistant cells.	imatinib	81-89	anoctamin 1	Homo sapiens	23-27
24954033-5	2014	We observed that the resistance to DRN and imatinib was proportional to the expression level of ABCB1.	imatinib	43-51	ATP binding cassette subfamily B member 1	Homo sapiens	96-101
25276339-3	2014	Cytogenetically, most tumors are characterized by translocation 17:22 leading to overexpression of tyrosine kinase PDGFB which can be targeted with tyrosine kinase inhibitor, Imatinib.	imatinib	175-183	platelet derived growth factor subunit B	Homo sapiens	115-120
24954033-0	2014	Resistance to daunorubicin, imatinib, or nilotinib depends on expression levels of ABCB1 and ABCG2 in human leukemia cells.	imatinib	28-36	ATP binding cassette subfamily B member 1	Homo sapiens	83-88
24954033-0	2014	Resistance to daunorubicin, imatinib, or nilotinib depends on expression levels of ABCB1 and ABCG2 in human leukemia cells.	imatinib	28-36	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	93-98
24954033-6	2014	Similarly, the resistance to nilotinib and imatinib was proportional to the expression level of ABCG2.	imatinib	43-51	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	96-101
24954033-9	2014	Only cells which expression of ABCB1 or ABCG2 exceeded a certain level exhibited a significantly decreased intracellular level of imatinib, and this effect was accompanied by a significantly increased resistance to this drug.	imatinib	130-138	ATP binding cassette subfamily B member 1	Homo sapiens	31-36
24954033-9	2014	Only cells which expression of ABCB1 or ABCG2 exceeded a certain level exhibited a significantly decreased intracellular level of imatinib, and this effect was accompanied by a significantly increased resistance to this drug.	imatinib	130-138	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	40-45
24830786-0	2014	H2AX phosphorylation regulated by p38 is involved in Bim expression and apoptosis in chronic myelogenous leukemia cells induced by imatinib.	imatinib	131-139	H2A.X variant histone	Homo sapiens	0-4
24830786-5	2014	Overexpression of H2AX increased apoptotic sensitivity of CML cells (K562) induced by imatinib.	imatinib	86-94	H2A.X variant histone	Homo sapiens	18-22
24830786-0	2014	H2AX phosphorylation regulated by p38 is involved in Bim expression and apoptosis in chronic myelogenous leukemia cells induced by imatinib.	imatinib	131-139	mitogen-activated protein kinase 14	Homo sapiens	34-37
24830786-9	2014	Our data further indicated that imatinib may stimulate mitogen-activated protein kinase (MAPK) family member p38, and H2AX phosphorylation followed a similar time course, suggesting a parallel response.	imatinib	32-40	mitogen-activated protein kinase 14	Homo sapiens	109-112
24830786-0	2014	H2AX phosphorylation regulated by p38 is involved in Bim expression and apoptosis in chronic myelogenous leukemia cells induced by imatinib.	imatinib	131-139	BCL2 like 11	Homo sapiens	53-56
24830786-15	2014	Taken together, these data demonstrated that H2AX phosphorylation regulated by p38 is involved in Bim expression and apoptosis in CML cells induced by imatinib.	imatinib	151-159	H2A.X variant histone	Homo sapiens	45-49
24830786-15	2014	Taken together, these data demonstrated that H2AX phosphorylation regulated by p38 is involved in Bim expression and apoptosis in CML cells induced by imatinib.	imatinib	151-159	mitogen-activated protein kinase 14	Homo sapiens	79-82
24747551-0	2014	A calpain-cleaved fragment of beta-catenin promotes BCRABL1+ cell survival evoked by autophagy induction in response to imatinib.	imatinib	120-128	catenin beta 1	Homo sapiens	30-42
24830786-15	2014	Taken together, these data demonstrated that H2AX phosphorylation regulated by p38 is involved in Bim expression and apoptosis in CML cells induced by imatinib.	imatinib	151-159	BCL2 like 11	Homo sapiens	98-101
24747551-5	2014	Here we proved that the cytoplasmic accumulation of beta-catenin driven by up-regulation of its antagonist Chibby1 is a component of autophagy induction in response to imatinib in BCR-ABL1+ cells opposing the apoptotic death.	imatinib	168-176	catenin beta 1	Homo sapiens	52-64
24747551-5	2014	Here we proved that the cytoplasmic accumulation of beta-catenin driven by up-regulation of its antagonist Chibby1 is a component of autophagy induction in response to imatinib in BCR-ABL1+ cells opposing the apoptotic death.	imatinib	168-176	BCR activator of RhoGEF and GTPase	Homo sapiens	180-188
24528201-7	2014	Cell treatment with the tyrosine kinase inhibitor Gleevec (imatinib) or with the alkalizing agent NH4 Cl causes an accumulation of "functional" AICD capable of up-regulating both TTR and NEP, leading to a reduction in total cellular Abeta levels.	imatinib	59-67	transthyretin	Homo sapiens	179-182
25089713-1	2014	One of the potential mechanisms of imatinib mesylate (IM) resistance in chronic myeloid leukemia (CML) is increased level of P-glycoprotein (Pgp).	imatinib	35-52	ATP binding cassette subfamily B member 1	Homo sapiens	125-139
25089713-1	2014	One of the potential mechanisms of imatinib mesylate (IM) resistance in chronic myeloid leukemia (CML) is increased level of P-glycoprotein (Pgp).	imatinib	35-52	ATP binding cassette subfamily B member 1	Homo sapiens	141-144
24528201-7	2014	Cell treatment with the tyrosine kinase inhibitor Gleevec (imatinib) or with the alkalizing agent NH4 Cl causes an accumulation of "functional" AICD capable of up-regulating both TTR and NEP, leading to a reduction in total cellular Abeta levels.	imatinib	59-67	membrane metalloendopeptidase	Homo sapiens	187-190
25098340-4	2014	Constitutive activation of STAT5 and STAT3 are associated with imatinib resistance on leukemia cells.	imatinib	63-71	signal transducer and activator of transcription 5A	Homo sapiens	27-32
25174682-0	2014	Impact of KIT exon 10 M541L allelic variant on the response to imatinib in aggressive fibromatosis: analysis of the desminib series by competitive allele specific Taqman PCR technology.	imatinib	63-71	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	10-13
25098340-4	2014	Constitutive activation of STAT5 and STAT3 are associated with imatinib resistance on leukemia cells.	imatinib	63-71	signal transducer and activator of transcription 3	Homo sapiens	37-42
25098340-5	2014	Development of drugs targeting SH2 domains of STAT5 and STAT3 provides a novel strategy for the treatment of the imatinib-resistant CML.	imatinib	113-121	signal transducer and activator of transcription 5A	Homo sapiens	46-51
25098340-5	2014	Development of drugs targeting SH2 domains of STAT5 and STAT3 provides a novel strategy for the treatment of the imatinib-resistant CML.	imatinib	113-121	signal transducer and activator of transcription 3	Homo sapiens	56-61
24890748-9	2014	With imatinib in particular, we found a reliable trend towards decreased MMP-2 and MMP-14 expression levels in p16-positive and p16-negative SCC tumour cell lines in addition to an induced apoptotic effect.	imatinib	5-13	matrix metallopeptidase 2	Homo sapiens	73-78
23966360-0	2014	Effect of imatinib on male reproductive hormones in BCR-ABL positive CML patients: A preliminary report.	imatinib	10-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
24923444-7	2014	Treatment of IL-3 and serum-starved 32D cells with 1 muM imatinib mysylate inhibited IL-3 stimulated kinase activities of both c-Abl and Jak2.	imatinib	57-65	interleukin 3	Mus musculus	13-17
24923444-7	2014	Treatment of IL-3 and serum-starved 32D cells with 1 muM imatinib mysylate inhibited IL-3 stimulated kinase activities of both c-Abl and Jak2.	imatinib	57-65	interleukin 3	Mus musculus	85-89
24923444-7	2014	Treatment of IL-3 and serum-starved 32D cells with 1 muM imatinib mysylate inhibited IL-3 stimulated kinase activities of both c-Abl and Jak2.	imatinib	57-65	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	127-132
24923444-7	2014	Treatment of IL-3 and serum-starved 32D cells with 1 muM imatinib mysylate inhibited IL-3 stimulated kinase activities of both c-Abl and Jak2.	imatinib	57-65	Janus kinase 2	Mus musculus	137-141
24923444-9	2014	IL-3 efficiently inhibited apoptosis of 32Dp210K/R+Abl cells induced by imatinib mysylate but not Jak2 kinase inhibitor TG101209.	imatinib	72-80	interleukin 3	Mus musculus	0-4
24923444-9	2014	IL-3 efficiently inhibited apoptosis of 32Dp210K/R+Abl cells induced by imatinib mysylate but not Jak2 kinase inhibitor TG101209.	imatinib	72-80	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	51-54
25023053-7	2014	Suppressing BCR-ABL by imatinib mesylate (IM) significantly decreased CIP2A expression.	imatinib	23-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
25023053-7	2014	Suppressing BCR-ABL by imatinib mesylate (IM) significantly decreased CIP2A expression.	imatinib	23-40	cellular inhibitor of PP2A	Homo sapiens	70-75
24890748-0	2014	Imatinib-associated matrix metalloproteinase suppression in p16-positive squamous cell carcinoma compared to HPV-negative HNSCC cells in vitro.	imatinib	0-8	cyclin dependent kinase inhibitor 2A	Homo sapiens	60-63
24890748-6	2014	Imatinib blocks the PTK receptor c-kit and forestalls its PTK activity.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	33-38
24890748-7	2014	The aim of the present study was to investigate the expression pattern of MMP-14 and MMP-2 in human papilloma virus (HPV)-negative and p16-positive SCC and to evaluate the chemosensitivity of the tumour cells to the chemotherapeutic agents, imatinib and 5-fluorouracil (5-FU).	imatinib	241-249	matrix metallopeptidase 14	Homo sapiens	74-80
24890748-9	2014	With imatinib in particular, we found a reliable trend towards decreased MMP-2 and MMP-14 expression levels in p16-positive and p16-negative SCC tumour cell lines in addition to an induced apoptotic effect.	imatinib	5-13	matrix metallopeptidase 14	Homo sapiens	83-89
24890748-9	2014	With imatinib in particular, we found a reliable trend towards decreased MMP-2 and MMP-14 expression levels in p16-positive and p16-negative SCC tumour cell lines in addition to an induced apoptotic effect.	imatinib	5-13	cyclin dependent kinase inhibitor 2A	Homo sapiens	111-114
24890748-9	2014	With imatinib in particular, we found a reliable trend towards decreased MMP-2 and MMP-14 expression levels in p16-positive and p16-negative SCC tumour cell lines in addition to an induced apoptotic effect.	imatinib	5-13	cyclin dependent kinase inhibitor 2A	Homo sapiens	128-131
24890748-10	2014	We found statistically significant imatinib-induced suppression of MMP-2- and MMP-14, dependent on the incubation time and the cell line.	imatinib	35-43	matrix metallopeptidase 2	Homo sapiens	67-84
24890748-11	2014	We detected a significant suppression of MMP-2 and MMP-14 especially in p16-negative HNSCC14C cells after prolonged treatment time with imatinib.	imatinib	136-144	matrix metallopeptidase 2	Homo sapiens	41-46
24890748-11	2014	We detected a significant suppression of MMP-2 and MMP-14 especially in p16-negative HNSCC14C cells after prolonged treatment time with imatinib.	imatinib	136-144	matrix metallopeptidase 14	Homo sapiens	51-57
24890748-11	2014	We detected a significant suppression of MMP-2 and MMP-14 especially in p16-negative HNSCC14C cells after prolonged treatment time with imatinib.	imatinib	136-144	cyclin dependent kinase inhibitor 2A	Homo sapiens	72-75
24890748-14	2014	We detected a significant suppression of MMP-2 and MMP-14 in all the incubated SCC cell lines, partially after treatment with imatinib.	imatinib	126-134	matrix metallopeptidase 2	Homo sapiens	41-46
24589908-1	2014	The aim of the study was to investigate any possible influence of polymorphisms of transmembrane transporters human organic cation transporter 1 (hOCT1), ABCB1, ABCG2 on imatinib pharmacokinetics in 33 men and 27 women (median age and range, 56 and 27-79 years, respectively) affected by chronic myeloid leukemia.	imatinib	170-178	ATP binding cassette subfamily B member 1	Homo sapiens	154-159
24589908-0	2014	The c.480C>G polymorphism of hOCT1 influences imatinib clearance in patients affected by chronic myeloid leukemia.	imatinib	49-57	solute carrier family 22 member 1	Homo sapiens	32-37
24890748-14	2014	We detected a significant suppression of MMP-2 and MMP-14 in all the incubated SCC cell lines, partially after treatment with imatinib.	imatinib	126-134	matrix metallopeptidase 14	Homo sapiens	51-57
24589908-1	2014	The aim of the study was to investigate any possible influence of polymorphisms of transmembrane transporters human organic cation transporter 1 (hOCT1), ABCB1, ABCG2 on imatinib pharmacokinetics in 33 men and 27 women (median age and range, 56 and 27-79 years, respectively) affected by chronic myeloid leukemia.	imatinib	170-178	solute carrier family 22 member 1	Homo sapiens	146-151
24589908-1	2014	The aim of the study was to investigate any possible influence of polymorphisms of transmembrane transporters human organic cation transporter 1 (hOCT1), ABCB1, ABCG2 on imatinib pharmacokinetics in 33 men and 27 women (median age and range, 56 and 27-79 years, respectively) affected by chronic myeloid leukemia.	imatinib	170-178	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	161-166
24890748-15	2014	We found higher suppression of MMP-2 in the CERV196 cells after incubation with imatinib.	imatinib	80-88	matrix metallopeptidase 2	Homo sapiens	31-36
24589908-5	2014	In conclusion, the hOCT1 c.480C>G SNP may significantly influence imatinib pharmacokinetics, supporting further analyses in larger groups of patients.	imatinib	69-77	solute carrier family 22 member 1	Homo sapiens	19-24
24890748-16	2014	We detected a reliable trend towards increased chemosensitivity of p16-positive tumour cells in vitro after treatment with imatinib.	imatinib	123-131	cyclin dependent kinase inhibitor 2A	Homo sapiens	67-70
25322553-5	2014	In addition, Gleevec activated caspase-3 and its downstream substrates PARP, and the caspase pan inhibitor Z-VAD-FMK (50 micromol x L(-1)) markedly reduced Gleevec-induced apoptosis from 47.97% +/- 10.56% to 31.05% +/- 9.206% (P < 0.05).	imatinib	13-20	caspase 3	Homo sapiens	31-40
25360237-1	2014	Five BCR-ABL1 tyrosine kinase inhibitors (TKIs), imatinib, nilotinib, dasatinib, bosutinib, and ponatinib, are currently approved for the treatment of chronic myeloid leukemia (CML).	imatinib	49-57	BCR activator of RhoGEF and GTPase	Homo sapiens	5-13
25322553-5	2014	In addition, Gleevec activated caspase-3 and its downstream substrates PARP, and the caspase pan inhibitor Z-VAD-FMK (50 micromol x L(-1)) markedly reduced Gleevec-induced apoptosis from 47.97% +/- 10.56% to 31.05% +/- 9.206% (P < 0.05).	imatinib	13-20	poly(ADP-ribose) polymerase 1	Homo sapiens	71-75
25322553-8	2014	In summary, Gleevec induced apoptosis in K562 cells via caspase-3 activation.	imatinib	12-19	caspase 3	Homo sapiens	56-65
25085003-5	2014	We show its ability to increase the inactivation of a stably inserted reporter gene in a chicken cell line that lacks any other AID/APOBEC proteins, and to increase the number of imatinib-resistant clones in a human cellular model for chronic myeloid leukemia through induction of mutations in the BCR-ABL1 fusion gene.	imatinib	179-187	BCR activator of RhoGEF and GTPase	Homo sapiens	298-306
25152116-1	2014	OBJECTIVE: To analyze the association of different types of ABL tyrosine point mutations and imatinib resistance to probe the relation between ABL tyrosine point mutations and the prognosis of patients with chronic myeloid leukemia (CML).	imatinib	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-63
24848114-8	2014	Furthermore, inhibition of ABL and PDGFR with imatinib protected against infection of mice with modest loads of C. rodentium, whereas the kinases were dispensable for high inocula or late after infection.	imatinib	46-54	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	27-30
25079219-3	2014	RESULTS: We report the application of EHMT1 and EHMT2 specific chemical inhibitors to sensitize CML cell lines to interferon and imatinib treatments.	imatinib	129-137	euchromatic histone lysine methyltransferase 1	Homo sapiens	38-43
25079219-3	2014	RESULTS: We report the application of EHMT1 and EHMT2 specific chemical inhibitors to sensitize CML cell lines to interferon and imatinib treatments.	imatinib	129-137	euchromatic histone lysine methyltransferase 2	Homo sapiens	48-53
28250386-1	2014	Imatinib mesylate is the leading compound to treat chronic myeloid leukemia (CML) and other cancers, through its inhibition of Bcr-Abl tyrosine kinases.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
28250386-2	2014	However, resistance to imatinib develops frequently, particularly in late-stage disease and has necessitated the development of new Bcr-Abl inhibitors.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
24859364-0	2014	Prognosis for patients with CML and >10% BCR-ABL1 after 3 months of imatinib depends on the rate of BCR-ABL1 decline.	imatinib	71-79	BCR activator of RhoGEF and GTPase	Homo sapiens	44-52
24859364-0	2014	Prognosis for patients with CML and >10% BCR-ABL1 after 3 months of imatinib depends on the rate of BCR-ABL1 decline.	imatinib	71-79	BCR activator of RhoGEF and GTPase	Homo sapiens	103-111
24848114-8	2014	Furthermore, inhibition of ABL and PDGFR with imatinib protected against infection of mice with modest loads of C. rodentium, whereas the kinases were dispensable for high inocula or late after infection.	imatinib	46-54	platelet derived growth factor receptor, beta polypeptide	Mus musculus	35-40
24658813-6	2014	GRe-exerted BR was abolished in the presence of neurotoxin tetrodotoxin or Ca2+ channel blocker verapamil or c-Kit receptor tyrosine kinase inhibitor imatinib.	imatinib	150-158	KIT proto-oncogene receptor tyrosine kinase	Rattus norvegicus	109-139
24711084-6	2014	Notably, the dramatic antitumor activity of certain targeted therapeutics such as imatinib (Gleevec) in gastrointestinal stromal tumors has been traced in part to IDO downregulation.	imatinib	82-90	indoleamine 2,3-dioxygenase 1	Homo sapiens	163-166
24840522-0	2014	The DREAM complex in antitumor activity of imatinib mesylate in gastrointestinal stromal tumors.	imatinib	43-60	potassium voltage-gated channel interacting protein 3	Homo sapiens	4-9
24840522-7	2014	Interfering with DREAM complex formation either by siRNA-mediated knockdown or by pharmacological inhibition of the regulatory kinase dual-specificity tyrosine phosphorylation-regulated kinase 1A was shown to enhance imatinib-induced gastrointestinal stromal tumor cell death.	imatinib	217-225	potassium voltage-gated channel interacting protein 3	Homo sapiens	17-22
24840522-7	2014	Interfering with DREAM complex formation either by siRNA-mediated knockdown or by pharmacological inhibition of the regulatory kinase dual-specificity tyrosine phosphorylation-regulated kinase 1A was shown to enhance imatinib-induced gastrointestinal stromal tumor cell death.	imatinib	217-225	dual specificity tyrosine phosphorylation regulated kinase 1A	Homo sapiens	134-195
24840522-8	2014	SUMMARY: Targeting the DREAM complex and imatinib-induced quiescence could provide opportunities for future therapeutic interventions toward more efficient imatinib responses.	imatinib	156-164	potassium voltage-gated channel interacting protein 3	Homo sapiens	23-28
24848770-1	2014	PURPOSE OF REVIEW: The presence of the Philadelphia chromosome causing the fusion between BCR to ABL1 in B cell precursor acute lymphoblastic leukemias (ALLs) was associated with a particularly bad prognosis, which has been markedly improved with the addition of imatinib to chemotherapy.	imatinib	263-271	BCR activator of RhoGEF and GTPase	Homo sapiens	90-93
24848770-1	2014	PURPOSE OF REVIEW: The presence of the Philadelphia chromosome causing the fusion between BCR to ABL1 in B cell precursor acute lymphoblastic leukemias (ALLs) was associated with a particularly bad prognosis, which has been markedly improved with the addition of imatinib to chemotherapy.	imatinib	263-271	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-101
25313780-2	2014	Tyrosine kinase inhibitors (TKIs), such as imatinibmesylate, have been used for the adjuvant treatment of KIT-positive GISTs.	imatinib	43-59	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	106-109
25029499-0	2014	Identification of drug combinations containing imatinib for treatment of BCR-ABL+ leukemias.	imatinib	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
25015329-0	2014	Identification of kit(M541L) somatic mutation in chronic eosinophilic leukemia, not otherwise specified and its implication in low-dose imatinib response.	imatinib	136-144	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	18-21
25015329-2	2014	The M541L KIT substitution (KIT(M541L)) has been described to be associated with pediatric mastocytosis, to enhance growth rate of the affected cells and to confer higher sensitivity to imatinib therapy.	imatinib	186-194	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	10-13
25015329-2	2014	The M541L KIT substitution (KIT(M541L)) has been described to be associated with pediatric mastocytosis, to enhance growth rate of the affected cells and to confer higher sensitivity to imatinib therapy.	imatinib	186-194	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	28-31
25015329-8	2014	Our study strongly suggests to search for the KIT(M541L) in patients with CEL, NOS, negative for PDGFRalpha and PDGFRbeta abnormalities, to identify a subgroup of cases who may benefit from low dose imatinib therapy.	imatinib	199-207	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	46-49
24982339-0	2014	PKC potentiates tyrosine kinase inhibitors STI571 and dasatinib cytotoxic effect.	imatinib	43-49	protein kinase C delta	Homo sapiens	0-3
24982339-5	2014	Moreover, PKC activation potentiates STI571 and dasatinib cytotoxic effects in HMC-1(560) and HMC-1(560,816) cells, respectively, by increasing necrotic populations.	imatinib	37-43	protein kinase C delta	Homo sapiens	10-13
24982339-7	2014	The results obtained evidence that either STI571 or dasatinib apoptotic cell death are PKCdelta-dependent.	imatinib	42-48	protein kinase C delta	Homo sapiens	87-95
24982339-9	2014	CONCLUSION: PKCdelta modulation is essential and determines mastocytosis treatment effectiveness, since STI571 and dasatinib effects are PKCdelta-dependent.	imatinib	104-110	protein kinase C delta	Homo sapiens	12-20
24982339-9	2014	CONCLUSION: PKCdelta modulation is essential and determines mastocytosis treatment effectiveness, since STI571 and dasatinib effects are PKCdelta-dependent.	imatinib	104-110	protein kinase C delta	Homo sapiens	137-145
24913811-4	2014	The present study aimed to examine the impact of GSTT1 and GSTM1 polymorphisms on the response to imatinib in patients with CML.	imatinib	98-106	glutathione S-transferase theta 1	Homo sapiens	49-54
24472814-0	2014	MDR1 expression predicts outcome of Ph+ chronic phase CML patients on second-line nilotinib therapy after imatinib failure.	imatinib	106-114	ATP binding cassette subfamily B member 1	Homo sapiens	0-4
24472814-6	2014	(v) Nilotinib was able to impede proliferation of MDR1-overexpressing imatinib-resistant cells.	imatinib	70-78	ATP binding cassette subfamily B member 1	Homo sapiens	50-54
24472814-7	2014	High MDR1 gene expression might identify patients whose mode of imatinib resistance is essentially determined by increased efflux activity of MDR1 and therefore can be overcome by second-line nilotinib treatment.	imatinib	64-72	ATP binding cassette subfamily B member 1	Homo sapiens	5-9
24472814-7	2014	High MDR1 gene expression might identify patients whose mode of imatinib resistance is essentially determined by increased efflux activity of MDR1 and therefore can be overcome by second-line nilotinib treatment.	imatinib	64-72	ATP binding cassette subfamily B member 1	Homo sapiens	142-146
24844604-5	2014	Low imatinib levels were predicted in young male patients and those receiving P-gp/CYP3A4 inducers.	imatinib	4-12	phosphoglycolate phosphatase	Homo sapiens	78-82
24844604-5	2014	Low imatinib levels were predicted in young male patients and those receiving P-gp/CYP3A4 inducers.	imatinib	4-12	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	83-89
24913811-4	2014	The present study aimed to examine the impact of GSTT1 and GSTM1 polymorphisms on the response to imatinib in patients with CML.	imatinib	98-106	glutathione S-transferase mu 1	Homo sapiens	59-64
24913811-10	2014	Moreover, the GSTT1 present/GSTM1 present appeared to be associated with a final dose of 600 or 800 mg of imatinib, but not significantly.	imatinib	106-114	glutathione S-transferase theta 1	Homo sapiens	14-19
24913811-10	2014	Moreover, the GSTT1 present/GSTM1 present appeared to be associated with a final dose of 600 or 800 mg of imatinib, but not significantly.	imatinib	106-114	glutathione S-transferase mu 1	Homo sapiens	28-33
24947165-8	2014	A significant anti-apoptotic effect of OPN on imatinib-induced apoptosis was identified.	imatinib	46-54	secreted phosphoprotein 1	Homo sapiens	39-42
25669042-10	2014	Most gastrointestinal stromal tumors (GISTs) have KIT or platelet-derived growth factor receptor a mutations, related to the effectiveness of imatinib.	imatinib	142-150	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	50-53
24763825-0	2014	Incidence of Bcr-Abl kinase domain mutations in imatinib refractory chronic myeloid leukemia patients from South India.	imatinib	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
24763825-1	2014	Mutations in the Bcr-Abl kinase domain (KD) are a major cause for acquired resistance to imatinib (IM) treatment and have been associated with progression and poor prognosis in chronic myeloid leukemia patients.	imatinib	89-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
24364873-0	2014	Uptake of imatinib-loaded polyelectrolyte complexes by BCR-ABL(+) cells: a long-acting drug-delivery strategy for targeting oncoprotein activity.	imatinib	10-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
24364873-1	2014	RATIONALE & AIM: Imatinib mesylate (IM), a selective tyrosine kinase inhibitor of the oncoprotein BCR-ABL, is the "gold standard" for patients with chronic myeloid leukemia (CML) but the drug does not eliminate CML stem cells, leading to disease relapse on drug discontinuation.	imatinib	21-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
24662807-4	2014	We hypothesized that subjects treated with Imatinib or Nilotinib, potent inhibitors of tyrosine kinases including c-Kit but also Abl1, PDFGFRalpha, and PDFGFRbeta, that are used to treat chronic myeloid leukemia (CML), would experience changes in thermal pain sensitivity.	imatinib	43-51	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	114-119
24662807-4	2014	We hypothesized that subjects treated with Imatinib or Nilotinib, potent inhibitors of tyrosine kinases including c-Kit but also Abl1, PDFGFRalpha, and PDFGFRbeta, that are used to treat chronic myeloid leukemia (CML), would experience changes in thermal pain sensitivity.	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-133
25222580-12	2014	CONCLUSIONS: The ratio of overall survival of patients with advanced GIST with a mutation other than exon 11 KIT mutation treated with imatinib is similar to the ratio of overall survival of patients with GIST with exon 11 KIT mutation.	imatinib	135-143	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	109-112
24727039-4	2014	The results of estrogenic activity, detected by E-screen and expressed as EC50, showed a high potential of imatinib (10(-7) muM) followed by cisplatin and 5-fluorouracil.	imatinib	107-115	latexin	Homo sapiens	124-127
24657654-0	2014	HS-438, a new inhibitor of imatinib-resistant BCR-ABL T315I mutation in chronic myeloid leukemia.	imatinib	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
24657654-1	2014	Imatinib is a selective breakpoint cluster region-Abelson (BCR-ABL) tyrosine kinase inhibitor (TKI) that has significantly improved the prognosis of patients with chronic myeloid leukemia (CML).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-57
24657654-1	2014	Imatinib is a selective breakpoint cluster region-Abelson (BCR-ABL) tyrosine kinase inhibitor (TKI) that has significantly improved the prognosis of patients with chronic myeloid leukemia (CML).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
24657654-2	2014	However, T315I gene mutations of the BCR-ABL kinase domain have been shown to confer resistance to imatinib.	imatinib	99-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
24657654-4	2014	We found that HS-438 strongly inhibited the expression of BCR-ABL signaling pathways in wild-type BCR-ABL (BaF3/WT) cells as well as T315I-mutated BCR-ABL (BaF3/T315I) cells with resistance to imatinib.	imatinib	193-201	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
25068103-4	2014	We herein report a case of T-PLL with a novel SEPT9-ABL1 fusion gene which induced strong resistance to tyrosine kinase inhibitors such as imatinib and dasatinib.	imatinib	139-147	septin 9	Homo sapiens	46-51
25068103-4	2014	We herein report a case of T-PLL with a novel SEPT9-ABL1 fusion gene which induced strong resistance to tyrosine kinase inhibitors such as imatinib and dasatinib.	imatinib	139-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-56
24778155-6	2014	Correspondingly, CD26(+) LSC decreased to low or undetectable levels during successful treatment with imatinib.	imatinib	102-110	dipeptidyl peptidase 4	Homo sapiens	17-21
24947165-10	2014	CONCLUSIONS: Our study identifies anti-apoptotic effects of OPN that, through beta-catenin-mediated Mcl-1 up-regulation, significantly antagonized imatinib-induced apoptosis in GISTs.	imatinib	147-155	secreted phosphoprotein 1	Homo sapiens	60-63
24947165-10	2014	CONCLUSIONS: Our study identifies anti-apoptotic effects of OPN that, through beta-catenin-mediated Mcl-1 up-regulation, significantly antagonized imatinib-induced apoptosis in GISTs.	imatinib	147-155	catenin beta 1	Homo sapiens	78-90
24947165-10	2014	CONCLUSIONS: Our study identifies anti-apoptotic effects of OPN that, through beta-catenin-mediated Mcl-1 up-regulation, significantly antagonized imatinib-induced apoptosis in GISTs.	imatinib	147-155	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	100-105
24947165-11	2014	These results provide a potential rationale for therapeutic strategies targeting both OPN and Mcl-1 of the same anti-apoptotic signaling pathway, which may account for resistance to imatinib in GISTs.	imatinib	182-190	secreted phosphoprotein 1	Homo sapiens	86-89
24947165-11	2014	These results provide a potential rationale for therapeutic strategies targeting both OPN and Mcl-1 of the same anti-apoptotic signaling pathway, which may account for resistance to imatinib in GISTs.	imatinib	182-190	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	94-99
24680616-0	2014	Guggulsterone of Commiphora mukul resin reverses drug resistance in imatinib-resistant leukemic cells by inhibiting cyclooxygenase-2 and P-glycoprotein.	imatinib	68-76	prostaglandin-endoperoxide synthase 2	Homo sapiens	116-132
24680616-1	2014	The purpose of this study was to investigate the effects of guggulsterone on cyclooxygenase-2 and P-glycoprotein mediated drug resistance in imatinib-resistant K562 cells (K562/IMA).	imatinib	141-149	prostaglandin-endoperoxide synthase 2	Homo sapiens	77-93
24680616-5	2014	When imatinib (1 muM) was combined with guggulsterone (60, 120 muM), the mean apoptotic population of K562/IMA cells was 15.47% and 24.91%.	imatinib	5-13	latexin	Homo sapiens	17-20
24680616-5	2014	When imatinib (1 muM) was combined with guggulsterone (60, 120 muM), the mean apoptotic population of K562/IMA cells was 15.47% and 24.91%.	imatinib	5-13	latexin	Homo sapiens	63-66
24680616-6	2014	It was increased by 3.82 and 6.79 times, compared with imatinib (1 muM) treatment alone.	imatinib	55-63	latexin	Homo sapiens	67-70
24863063-0	2014	Imatinib inhibits VEGF-independent angiogenesis by targeting neuropilin 1-dependent ABL1 activation in endothelial cells.	imatinib	0-8	neuropilin 1	Homo sapiens	61-73
24913355-1	2014	BACKGROUND: The Abelson tyrosine kinase (c-Abl) inhibitor STI571 (Glivec ) has been shown to effectively inhibit colorectal cancer cell migration and invasion.	imatinib	58-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-46
24913355-8	2014	Importantly, treatment with STI571 did abolish Abi1 Y435-phosphorylation, suppressed the matrix dissolution, decreased fibronectin attachment, and suppressed cell invasion through reconstituted extracellular matrix.	imatinib	28-34	abl interactor 1	Homo sapiens	47-51
24913355-8	2014	Importantly, treatment with STI571 did abolish Abi1 Y435-phosphorylation, suppressed the matrix dissolution, decreased fibronectin attachment, and suppressed cell invasion through reconstituted extracellular matrix.	imatinib	28-34	fibronectin 1	Homo sapiens	119-130
25120810-6	2014	C-kit expression is a frequent finding in triple negative breast cancers; 1 activating mutation which was also found in gastrointestinal stromal tumors was detected; a few cases might benefit from imatinib.	imatinib	197-205	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-5
24687085-0	2014	Patients with myeloid malignancies bearing PDGFRB fusion genes achieve durable long-term remissions with imatinib.	imatinib	105-113	platelet derived growth factor receptor beta	Homo sapiens	43-49
24687085-3	2014	Reciprocal translocations involving PDGFRB result in fusion genes with constitutively activated receptor tyrosine kinase sensitive to inhibition with imatinib.	imatinib	150-158	platelet derived growth factor receptor beta	Homo sapiens	36-42
24687085-7	2014	Imatinib is well-tolerated and achieves excellent long-term responses in patients with PDGFRB rearrangements.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	87-93
24863063-0	2014	Imatinib inhibits VEGF-independent angiogenesis by targeting neuropilin 1-dependent ABL1 activation in endothelial cells.	imatinib	0-8	vascular endothelial growth factor A	Homo sapiens	18-22
24863063-0	2014	Imatinib inhibits VEGF-independent angiogenesis by targeting neuropilin 1-dependent ABL1 activation in endothelial cells.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-88
24863063-6	2014	Accordingly, both physiological and pathological angiogenesis in the retina were inhibited by treatment with Imatinib, a small molecule inhibitor of ABL1 which is widely used to prevent the proliferation of tumor cells that express BCR-ABL fusion proteins.	imatinib	109-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-153
24629639-0	2014	ApoptomiRs expression modulated by BCR-ABL is linked to CML progression and imatinib resistance.	imatinib	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
24553398-2	2014	METHODS: We present a single-center report of a series of 12 imatinib-refractory patients in advanced phases, 9 of whom harbored BCR-ABL1 mutations.	imatinib	61-69	BCR activator of RhoGEF and GTPase	Homo sapiens	129-137
24619861-0	2014	BCR/ABL level at 6 months identifies good risk CML subgroup after failing early molecular response at 3 months following imatinib therapy for CML in chronic phase.	imatinib	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
24619861-1	2014	It is unclear if patients with CML treated with imatinib who fail to achieve BCR/ABL transcript levels <10%(IS) at 3 months i.e. an early molecular response (EMR) have a better prognosis if they achieve a response by 6 months.	imatinib	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
24619861-7	2014	A BCR/ABL transcript level at 6 months can identify a "good-risk" subgroup among patients who fail to achieve an EMR on Imatinib therapy for CML.	imatinib	120-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	2-9
24392933-10	2014	Treatment with the c-Abl pharmacological inhibitors, imatinib and GNF-5, had similar effects.	imatinib	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-24
24615985-4	2014	Our docking studies showed that the N-morpholino derivative fits and blocks the oncogenic tyrosine kinases bcr/abl and epidermal growth factor receptor (EGFR) in a similar fashion to that of the potent anticancer agent imatinib.	imatinib	219-227	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
24615985-4	2014	Our docking studies showed that the N-morpholino derivative fits and blocks the oncogenic tyrosine kinases bcr/abl and epidermal growth factor receptor (EGFR) in a similar fashion to that of the potent anticancer agent imatinib.	imatinib	219-227	epidermal growth factor receptor	Homo sapiens	119-151
24615985-4	2014	Our docking studies showed that the N-morpholino derivative fits and blocks the oncogenic tyrosine kinases bcr/abl and epidermal growth factor receptor (EGFR) in a similar fashion to that of the potent anticancer agent imatinib.	imatinib	219-227	epidermal growth factor receptor	Homo sapiens	153-157
24456122-0	2014	Complete response of monoblastic myeloid sarcoma with FIP1L1- PDGFRA rearrangement to imatinib monotherapy.	imatinib	86-94	factor interacting with PAPOLA and CPSF1	Homo sapiens	54-60
24456122-0	2014	Complete response of monoblastic myeloid sarcoma with FIP1L1- PDGFRA rearrangement to imatinib monotherapy.	imatinib	86-94	platelet derived growth factor receptor alpha	Homo sapiens	62-68
24667683-0	2014	Statins inhibit ABCB1 and ABCG2 drug transporter activity in chronic myeloid leukemia cells and potentiate antileukemic effects of imatinib.	imatinib	131-139	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	26-31
24652072-0	2014	Mechanisms of resistance to imatinib mesylate in KIT-positive metastatic uveal melanoma.	imatinib	28-45	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	49-52
24652072-1	2014	Imatinib mesylate is used in targeted therapy of cancer to inhibit type III tyrosine kinase receptors, such as KIT and platelet-derived growth factor receptors (PDGFRs).	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	111-114
24652072-2	2014	Expression of KIT in uveal melanoma (UM) suggests that this receptor may be the target of imatinib mesylate therapy.	imatinib	90-98	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-17
24652072-11	2014	This study provides evidence that tumor microenvironment cytokines such as SCF may promote resistance to imatinib mesylate in metastatic UM.	imatinib	105-122	KIT ligand	Homo sapiens	75-78
24460680-0	2014	Complete and long-lasting cytologic and molecular remission of FIP1L1-PDGFRA-positive acute eosinophil myeloid leukaemia, treated with low-dose imatinib monotherapy.	imatinib	144-152	factor interacting with PAPOLA and CPSF1	Homo sapiens	63-69
24460680-0	2014	Complete and long-lasting cytologic and molecular remission of FIP1L1-PDGFRA-positive acute eosinophil myeloid leukaemia, treated with low-dose imatinib monotherapy.	imatinib	144-152	platelet derived growth factor receptor alpha	Homo sapiens	70-76
24460680-2	2014	The fusion product of such genes is a tyrosine kinase oncoprotein sensitive to imatinib, which to date results to be the standard of care for FIP1L1-PDGFRA-positive chronic myeloproliferative disorders with eosinophilia.	imatinib	79-87	factor interacting with PAPOLA and CPSF1	Homo sapiens	142-148
24460680-2	2014	The fusion product of such genes is a tyrosine kinase oncoprotein sensitive to imatinib, which to date results to be the standard of care for FIP1L1-PDGFRA-positive chronic myeloproliferative disorders with eosinophilia.	imatinib	79-87	platelet derived growth factor receptor alpha	Homo sapiens	149-155
24460680-4	2014	Here, we report a rare case of FIP1L1-PDGFRA-positive acute myeloid leukaemia, with marked peripheral blood and bone marrow eosinophilia, treated with low dose of imatinib monotherapy, achieving a rapid and long-lasting complete cytologic and molecular remission, without need for intensive chemotherapy.	imatinib	163-171	factor interacting with PAPOLA and CPSF1	Homo sapiens	31-37
24460680-4	2014	Here, we report a rare case of FIP1L1-PDGFRA-positive acute myeloid leukaemia, with marked peripheral blood and bone marrow eosinophilia, treated with low dose of imatinib monotherapy, achieving a rapid and long-lasting complete cytologic and molecular remission, without need for intensive chemotherapy.	imatinib	163-171	platelet derived growth factor receptor alpha	Homo sapiens	38-44
24726617-0	2014	Imatinib inhibits the expression of SCO2 and FRATAXIN genes that encode mitochondrial proteins in human Bcr-Abl+ leukemia cells.	imatinib	0-8	synthesis of cytochrome C oxidase 2	Homo sapiens	36-40
24726617-0	2014	Imatinib inhibits the expression of SCO2 and FRATAXIN genes that encode mitochondrial proteins in human Bcr-Abl+ leukemia cells.	imatinib	0-8	frataxin	Homo sapiens	45-53
24726617-0	2014	Imatinib inhibits the expression of SCO2 and FRATAXIN genes that encode mitochondrial proteins in human Bcr-Abl+ leukemia cells.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
24726617-1	2014	Imatinib mesylate (IM/Gleevec ), a selective inhibitor of chimeric Bcr-Abl tyrosine kinase, was developed as a first line drug to treat CML and ALL Ph(+) patients.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
24667683-6	2014	This effect is related to increased intracellular concentration of imatinib in CD34+ CML cells and cell lines measured using uptake of (14)C-labeled imatinib.	imatinib	67-75	CD34 molecule	Homo sapiens	79-83
24667683-6	2014	This effect is related to increased intracellular concentration of imatinib in CD34+ CML cells and cell lines measured using uptake of (14)C-labeled imatinib.	imatinib	149-157	CD34 molecule	Homo sapiens	79-83
24667683-7	2014	Lovastatin does not influence influx but significantly inhibits efflux of imatinib mediated by ATP-binding cassette (ABC) transporters: ABCB1 and ABCG2.	imatinib	74-82	ATP binding cassette subfamily B member 1	Homo sapiens	136-141
24667683-7	2014	Lovastatin does not influence influx but significantly inhibits efflux of imatinib mediated by ATP-binding cassette (ABC) transporters: ABCB1 and ABCG2.	imatinib	74-82	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	146-151
24591339-10	2014	Also, imatinib significantly reduced the mRNA expression of collagen type I, III, and platelet-derived growth factor receptor-beta phosphorylation in the hearts of SHR.	imatinib	6-14	platelet derived growth factor receptor beta	Rattus norvegicus	60-130
24680705-0	2014	Down-regulation of miR-199b associated with imatinib drug resistance in 9q34.1 deleted BCR/ABL positive CML patients.	imatinib	44-52	microRNA 199b	Homo sapiens	19-27
24680705-0	2014	Down-regulation of miR-199b associated with imatinib drug resistance in 9q34.1 deleted BCR/ABL positive CML patients.	imatinib	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
24680705-4	2014	We have designed a study to determine miR-219-2 and miR-199b expression levels which would help to understand the prognosis of imatinib therapy.	imatinib	127-135	microRNA 219a-2	Homo sapiens	38-47
24680705-4	2014	We have designed a study to determine miR-219-2 and miR-199b expression levels which would help to understand the prognosis of imatinib therapy.	imatinib	127-135	microRNA 199b	Homo sapiens	52-60
24680705-12	2014	The follow-up study showed that the miR-199b was found to be strongly associated with imatinib resistance, as 44.11% patients showed resistance to imatinib therapy.	imatinib	86-94	microRNA 199b	Homo sapiens	36-44
24680705-12	2014	The follow-up study showed that the miR-199b was found to be strongly associated with imatinib resistance, as 44.11% patients showed resistance to imatinib therapy.	imatinib	147-155	microRNA 199b	Homo sapiens	36-44
24659124-7	2014	In vitro, imatinib inhibited cell proliferation, MMP-2 expression and activity and also attenuated the production of proinflammatory cytokines.	imatinib	10-18	matrix metallopeptidase 2	Mus musculus	49-54
24674454-4	2014	Different CD117 expression patterns could be related to different KIT mutational status in the two lesions: gastric GIST showed a dot-like pattern and lacked KIT mutations; duodenal GIST had a strong membranous expression pattern, likely due to KIT exon 9 duplication, which is associated with lower response to imatinib.	imatinib	312-320	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	10-15
24925195-0	2014	Successful imatinib therapy for neuroendocrine carcinoma with activating Kit mutation: a case study.	imatinib	11-19	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
24925195-8	2014	Despite previously reported KIT expression in NET, this is the first documented case of an activating KIT mutation in NET and of successful treatment with both a KIF11 inhibitor and imatinib, each of which was elucidated through molecular profiling of the patient"s tumor.	imatinib	182-190	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	28-31
24925195-8	2014	Despite previously reported KIT expression in NET, this is the first documented case of an activating KIT mutation in NET and of successful treatment with both a KIF11 inhibitor and imatinib, each of which was elucidated through molecular profiling of the patient"s tumor.	imatinib	182-190	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	102-105
24925195-9	2014	Imatinib may be a valuable therapy in NET harboring activating KIT mutations.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	63-66
24553365-0	2014	Interferon decreases VEGF levels in patients with chronic myeloid leukemia treated with imatinib.	imatinib	88-96	vascular endothelial growth factor A	Homo sapiens	21-25
24553365-4	2014	Under treatment, significant lowest levels were observed in imatinib+IFN arm.	imatinib	60-68	interferon alpha 1	Homo sapiens	69-72
24726782-0	2014	VEGF in chronic myeloid leukemia treated with interferon and imatinib.	imatinib	61-69	vascular endothelial growth factor A	Homo sapiens	0-4
24753251-1	2014	Tyrosine kinase inhibitors such as imatinib can effectively target the BCR-ABL oncoprotein in a majority of patients with chronic myeloid leukemia (CML).	imatinib	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
25006453-3	2014	Imatinib, a PDGFR antagonist, may be beneficial in the treatment of both conditions because of its potent antiproliferative effect.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	12-17
24753251-8	2014	Treatment of primary cells from newly diagnosed CML patients in chronic phase as well as BCR-ABL(+) cell lines with imatinib increased IRF-8 transcription.	imatinib	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
24753251-8	2014	Treatment of primary cells from newly diagnosed CML patients in chronic phase as well as BCR-ABL(+) cell lines with imatinib increased IRF-8 transcription.	imatinib	116-124	interferon regulatory factor 8	Homo sapiens	135-140
24753251-9	2014	Furthermore, IRF-8 expression in cell line models was necessary for imatinib-induced antitumor responses.	imatinib	68-76	interferon regulatory factor 8	Homo sapiens	13-18
24732112-4	2014	The effect of both OSAE, OSWE, pure compound EUG and positive control imatinib (IMT) was investigated in THP-1 cells by studying the following markers: lipopolysaccharide (LPS) induced tumor necrosis factor alpha (TNF-alpha) secretion by ELISA, gene expression of inflammatory markers (TNF-alpha, IL-6, MIP-1alpha and MCP-1) by real time PCR and translocation of nuclear factor kappa B (NF-kappaB) by confocol microscopy.	imatinib	70-78	GLI family zinc finger 2	Homo sapiens	105-110
24759231-0	2014	Gleevec/imatinib, an ABL2 kinase inhibitor, protects tumor and endothelial cells from semaphorin-induced cytoskeleton collapse and loss of cell motility.	imatinib	0-7	ABL proto-oncogene 2, non-receptor tyrosine kinase	Homo sapiens	21-25
24759231-0	2014	Gleevec/imatinib, an ABL2 kinase inhibitor, protects tumor and endothelial cells from semaphorin-induced cytoskeleton collapse and loss of cell motility.	imatinib	8-16	ABL proto-oncogene 2, non-receptor tyrosine kinase	Homo sapiens	21-25
24759231-4	2014	We now demonstrate that Gleevec (imatinib, STI571), an ABL2 tyrosine kinase inhibitor, abrogates SEMA3A&F-induced stress fiber loss in glioblastoma cells and endothelial cells and diminishes their ability to inhibit migration.	imatinib	33-41	ABL proto-oncogene 2, non-receptor tyrosine kinase	Homo sapiens	55-59
24759231-4	2014	We now demonstrate that Gleevec (imatinib, STI571), an ABL2 tyrosine kinase inhibitor, abrogates SEMA3A&F-induced stress fiber loss in glioblastoma cells and endothelial cells and diminishes their ability to inhibit migration.	imatinib	33-41	semaphorin 3A	Homo sapiens	97-103
24759231-4	2014	We now demonstrate that Gleevec (imatinib, STI571), an ABL2 tyrosine kinase inhibitor, abrogates SEMA3A&F-induced stress fiber loss in glioblastoma cells and endothelial cells and diminishes their ability to inhibit migration.	imatinib	43-49	ABL proto-oncogene 2, non-receptor tyrosine kinase	Homo sapiens	55-59
24759231-4	2014	We now demonstrate that Gleevec (imatinib, STI571), an ABL2 tyrosine kinase inhibitor, abrogates SEMA3A&F-induced stress fiber loss in glioblastoma cells and endothelial cells and diminishes their ability to inhibit migration.	imatinib	43-49	semaphorin 3A	Homo sapiens	97-103
24885658-9	2014	These trends predict sensitivity to agents such as paclitaxel (ABCB1 substrate) and imatinib (c-KIT inhibitor) would be altered with extended passage.	imatinib	84-92	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	94-99
24705490-1	2014	C-abl oncogene 1, nonreceptor tyrosine kinase (ABL1) kinase inhibitors such as imatinib mesylate (imatinib) are effective in managing chronic myeloid leukemia (CML) but incapable of eliminating leukemia stem cells (LSCs), suggesting that kinase-independent pathways support LSC survival.	imatinib	79-96	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	47-51
24705490-1	2014	C-abl oncogene 1, nonreceptor tyrosine kinase (ABL1) kinase inhibitors such as imatinib mesylate (imatinib) are effective in managing chronic myeloid leukemia (CML) but incapable of eliminating leukemia stem cells (LSCs), suggesting that kinase-independent pathways support LSC survival.	imatinib	79-87	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	47-51
24705490-3	2014	Importantly, we found that although breakpoint cluster region (BCR)-ABL1 kinase remained effectively inhibited by imatinib under hypoxia, apoptosis became partially suppressed.	imatinib	114-122	BCR activator of RhoGEF and GTPase	Mus musculus	63-66
24705490-3	2014	Importantly, we found that although breakpoint cluster region (BCR)-ABL1 kinase remained effectively inhibited by imatinib under hypoxia, apoptosis became partially suppressed.	imatinib	114-122	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	68-72
24705490-6	2014	In vitro, HIF1-alpha is stabilized during hypoxia, and its expression and transcriptional activity can be partially attenuated by concurrent imatinib treatment.	imatinib	141-149	hypoxia inducible factor 1, alpha subunit	Mus musculus	10-20
24835010-0	2014	C-Abl inhibitor imatinib enhances insulin production by beta cells: c-Abl negatively regulates insulin production via interfering with the expression of NKx2.2 and GLUT-2.	imatinib	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
24638003-9	2014	When comparing the two arms, imatinib therapy was associated with higher RFS in patients with a KIT exon 11 deletion of any type, but not a KIT exon 11 insertion or point mutation, KIT exon 9 mutation, PDGFRA mutation, or wild-type tumor, although some of these patient groups were small.	imatinib	29-37	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	96-99
24638003-12	2014	Patients with KIT exon 11 deletions assigned to 1 year of adjuvant imatinib had a longer RFS.	imatinib	67-75	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-17
24836440-8	2014	Finally, RNAi targeting STAT5B but not STAT5A sensitizes human BCR-ABL-positive cell lines to imatinib-treatment.	imatinib	94-102	signal transducer and activator of transcription 5B	Homo sapiens	24-30
24835010-0	2014	C-Abl inhibitor imatinib enhances insulin production by beta cells: c-Abl negatively regulates insulin production via interfering with the expression of NKx2.2 and GLUT-2.	imatinib	16-24	insulin	Homo sapiens	34-41
24836440-8	2014	Finally, RNAi targeting STAT5B but not STAT5A sensitizes human BCR-ABL-positive cell lines to imatinib-treatment.	imatinib	94-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
24835010-0	2014	C-Abl inhibitor imatinib enhances insulin production by beta cells: c-Abl negatively regulates insulin production via interfering with the expression of NKx2.2 and GLUT-2.	imatinib	16-24	insulin	Homo sapiens	95-102
24835010-0	2014	C-Abl inhibitor imatinib enhances insulin production by beta cells: c-Abl negatively regulates insulin production via interfering with the expression of NKx2.2 and GLUT-2.	imatinib	16-24	NK2 homeobox 2	Homo sapiens	153-159
24835010-0	2014	C-Abl inhibitor imatinib enhances insulin production by beta cells: c-Abl negatively regulates insulin production via interfering with the expression of NKx2.2 and GLUT-2.	imatinib	16-24	solute carrier family 2 member 2	Homo sapiens	164-170
24835010-2	2014	Imatinib specifically inhibits the tyrosine kinase, c-Abl.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-57
24835010-3	2014	However, the mechanism of how Imatinib treatment can lead to increased insulin level is unclear.	imatinib	30-38	insulin	Homo sapiens	71-78
24835010-4	2014	Specifically, there is little investigation into whether Imatinib directly affects beta cells to promote insulin production.	imatinib	57-65	insulin	Homo sapiens	105-112
24835010-5	2014	In this study, we showed that Imatinib significantly induced insulin expression in both glucose-stimulated and resting beta cells.	imatinib	30-38	insulin	Homo sapiens	61-68
24820332-8	2014	The clinically used PDGFR antagonist imatinib did not relieve mechanical pain in a nerve injury model as determined by Von Frey assay.	imatinib	37-45	platelet derived growth factor receptor beta	Homo sapiens	20-25
24675360-4	2014	Moreover, ST2 overexpression is normalized following imatinib mesylate therapy, whereas IL-33 counteracts in vitro imatinib mesylate-induced growth arrest in CML CD34(+) progenitors via reactivation of the STAT5 pathway, thus supporting the notion that IL-33 may impede the antiproliferative effects of imatinib mesylate on CD34(+) progenitors in CML.	imatinib	53-70	ST2	Homo sapiens	10-13
24675360-4	2014	Moreover, ST2 overexpression is normalized following imatinib mesylate therapy, whereas IL-33 counteracts in vitro imatinib mesylate-induced growth arrest in CML CD34(+) progenitors via reactivation of the STAT5 pathway, thus supporting the notion that IL-33 may impede the antiproliferative effects of imatinib mesylate on CD34(+) progenitors in CML.	imatinib	115-132	interleukin 33	Homo sapiens	88-93
24675360-4	2014	Moreover, ST2 overexpression is normalized following imatinib mesylate therapy, whereas IL-33 counteracts in vitro imatinib mesylate-induced growth arrest in CML CD34(+) progenitors via reactivation of the STAT5 pathway, thus supporting the notion that IL-33 may impede the antiproliferative effects of imatinib mesylate on CD34(+) progenitors in CML.	imatinib	115-132	CD34 molecule	Homo sapiens	162-166
24675360-4	2014	Moreover, ST2 overexpression is normalized following imatinib mesylate therapy, whereas IL-33 counteracts in vitro imatinib mesylate-induced growth arrest in CML CD34(+) progenitors via reactivation of the STAT5 pathway, thus supporting the notion that IL-33 may impede the antiproliferative effects of imatinib mesylate on CD34(+) progenitors in CML.	imatinib	115-132	signal transducer and activator of transcription 5A	Homo sapiens	206-211
24675360-4	2014	Moreover, ST2 overexpression is normalized following imatinib mesylate therapy, whereas IL-33 counteracts in vitro imatinib mesylate-induced growth arrest in CML CD34(+) progenitors via reactivation of the STAT5 pathway, thus supporting the notion that IL-33 may impede the antiproliferative effects of imatinib mesylate on CD34(+) progenitors in CML.	imatinib	115-132	interleukin 33	Homo sapiens	88-93
24675360-4	2014	Moreover, ST2 overexpression is normalized following imatinib mesylate therapy, whereas IL-33 counteracts in vitro imatinib mesylate-induced growth arrest in CML CD34(+) progenitors via reactivation of the STAT5 pathway, thus supporting the notion that IL-33 may impede the antiproliferative effects of imatinib mesylate on CD34(+) progenitors in CML.	imatinib	115-132	CD34 molecule	Homo sapiens	162-166
24675360-4	2014	Moreover, ST2 overexpression is normalized following imatinib mesylate therapy, whereas IL-33 counteracts in vitro imatinib mesylate-induced growth arrest in CML CD34(+) progenitors via reactivation of the STAT5 pathway, thus supporting the notion that IL-33 may impede the antiproliferative effects of imatinib mesylate on CD34(+) progenitors in CML.	imatinib	115-132	signal transducer and activator of transcription 5A	Homo sapiens	206-211
24675360-8	2014	Taken together, our results provide evidence that IL-33/ST2 signaling may represent a novel cytokine-mediated mechanism contributing to CML progenitor growth and support a role for this pathway in CML maintenance and imatinib mesylate resistance.	imatinib	217-234	interleukin 33	Homo sapiens	50-55
24675360-8	2014	Taken together, our results provide evidence that IL-33/ST2 signaling may represent a novel cytokine-mediated mechanism contributing to CML progenitor growth and support a role for this pathway in CML maintenance and imatinib mesylate resistance.	imatinib	217-234	ST2	Homo sapiens	56-59
24819355-1	2014	We have investigated in vitro the metabolic capability of 3 extrahepatic cytochromes P-450, CYP1A1, 1B1 and 2J2, known to be over-expressed in various tumors, to biotransform 5 tyrosine kinase inhibitors (TKI): dasatinib, imatinib, nilotinib, sorafenib and sunitinib.	imatinib	222-230	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	92-103
24860788-7	2014	Integrin alpha5 inhibitory antibody inhibited adhesion of Ph+ leukemia to human fibronectin and acted synergistically with imatinib to induce Ph+ leukemia cell apoptosis.	imatinib	123-131	integrin subunit alpha 5	Homo sapiens	0-15
24828813-5	2014	CSF-1R is also sensitive to Imatinib and this sensitivity is altered by mutation D802V.	imatinib	28-36	colony stimulating factor 1 receptor	Homo sapiens	0-6
24855354-1	2014	PURPOSE: Imatinib inhibits platelet-derived growth factor receptor (PDGFR), and evidence shows that PDGFR participates in the development and progression of cervical cancer.	imatinib	9-17	platelet derived growth factor receptor beta	Homo sapiens	27-66
24855380-0	2014	Antitumor activity of sorafenib and imatinib in a patient with thymic carcinoma harboring c-KIT exon 13 missense mutation K642E.	imatinib	36-44	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	90-95
24855354-1	2014	PURPOSE: Imatinib inhibits platelet-derived growth factor receptor (PDGFR), and evidence shows that PDGFR participates in the development and progression of cervical cancer.	imatinib	9-17	platelet derived growth factor receptor beta	Homo sapiens	68-73
24855354-14	2014	CONCLUSION: These findings indicate that the nano-sized FR-targeted PDGFR antagonist imatinib liposomes may constitute a promising strategy in cervical cancer therapy through the combination of active targeting and molecular targeting.	imatinib	85-93	platelet derived growth factor receptor beta	Homo sapiens	68-73
24685695-5	2014	Silencing H19 expression sensitized leukemic cells to undergo imatinib-induced apoptosis and inhibited Bcr-Abl-induced tumor growth.	imatinib	62-70	H19 imprinted maternally expressed transcript	Homo sapiens	10-13
24492162-1	2014	BACKGROUND: We conducted a phase I trial of cisplatin/pemetrexed/imatinib mesylate, an oral platelet-derived growth factor receptor (PDGFR) inhibitor, in chemonaive patients with malignant pleural mesothelioma (MPM).	imatinib	65-82	platelet derived growth factor receptor beta	Homo sapiens	92-131
24788138-4	2014	An imatinib-resistant activating mutation of the receptor tyrosine kinase KIT (KIT D816V) is most frequently present in transformed mast cells and is associated with all clinical forms of the disease.	imatinib	3-11	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	74-77
24788138-4	2014	An imatinib-resistant activating mutation of the receptor tyrosine kinase KIT (KIT D816V) is most frequently present in transformed mast cells and is associated with all clinical forms of the disease.	imatinib	3-11	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	79-82
24445143-5	2014	Tyrosine-phosphorylated IRF5 displayed reduced transcriptional activity that was partially restored by imatinib mesylate (IM).	imatinib	103-120	interferon regulatory factor 5	Homo sapiens	24-28
24103790-5	2014	In recent years, ABCC10 inhibitors, including cepharanthine, lapatinib, erlotinib, nilotinib, imatinib, sildenafil, and vardenafil, have been reported to overcome ABCC10-mediated MDR.	imatinib	94-102	ATP binding cassette subfamily C member 10	Homo sapiens	17-23
24103790-5	2014	In recent years, ABCC10 inhibitors, including cepharanthine, lapatinib, erlotinib, nilotinib, imatinib, sildenafil, and vardenafil, have been reported to overcome ABCC10-mediated MDR.	imatinib	94-102	ATP binding cassette subfamily C member 10	Homo sapiens	163-169
24492162-1	2014	BACKGROUND: We conducted a phase I trial of cisplatin/pemetrexed/imatinib mesylate, an oral platelet-derived growth factor receptor (PDGFR) inhibitor, in chemonaive patients with malignant pleural mesothelioma (MPM).	imatinib	65-82	platelet derived growth factor receptor beta	Homo sapiens	133-138
24317392-0	2014	A new KIT mutation (N505I) in acral melanoma confers constitutive signaling, favors tumorigenic properties, and is sensitive to imatinib.	imatinib	128-136	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	6-9
24486648-7	2014	Imatinib inhibited the growth of common myeloid progenitors expressing Hes1 with FIP1L1-PDGFRalpha, but not with imatinib-resistant FIP1L1-PDGFRalpha mutants harboring T674I or D842V.	imatinib	0-8	hes family bHLH transcription factor 1	Mus musculus	71-75
24486648-7	2014	Imatinib inhibited the growth of common myeloid progenitors expressing Hes1 with FIP1L1-PDGFRalpha, but not with imatinib-resistant FIP1L1-PDGFRalpha mutants harboring T674I or D842V.	imatinib	0-8	FIP1 like 1 (S. cerevisiae)	Mus musculus	81-87
24486648-7	2014	Imatinib inhibited the growth of common myeloid progenitors expressing Hes1 with FIP1L1-PDGFRalpha, but not with imatinib-resistant FIP1L1-PDGFRalpha mutants harboring T674I or D842V.	imatinib	0-8	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	88-98
24486648-8	2014	In contrast, ponatinib efficiently eradicated leukemic cells expressing Hes1 and the imatinib-resistant FLP1L1-PDGFRAlpha mutant in vitro and in vivo.	imatinib	85-93	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	111-121
24772479-0	2014	Identification and functional characterization of imatinib-sensitive DTD1-PDGFRB and CCDC88C-PDGFRB fusion genes in eosinophilia-associated myeloid/lymphoid neoplasms.	imatinib	50-58	D-aminoacyl-tRNA deacylase 1	Homo sapiens	69-73
24772479-0	2014	Identification and functional characterization of imatinib-sensitive DTD1-PDGFRB and CCDC88C-PDGFRB fusion genes in eosinophilia-associated myeloid/lymphoid neoplasms.	imatinib	50-58	platelet derived growth factor receptor beta	Homo sapiens	74-80
24772479-0	2014	Identification and functional characterization of imatinib-sensitive DTD1-PDGFRB and CCDC88C-PDGFRB fusion genes in eosinophilia-associated myeloid/lymphoid neoplasms.	imatinib	50-58	coiled-coil domain containing 88C	Homo sapiens	85-92
24772479-0	2014	Identification and functional characterization of imatinib-sensitive DTD1-PDGFRB and CCDC88C-PDGFRB fusion genes in eosinophilia-associated myeloid/lymphoid neoplasms.	imatinib	50-58	platelet derived growth factor receptor beta	Homo sapiens	93-99
24772479-1	2014	Eosinophilia-associated myeloid neoplasms with rearrangement of chromosome bands 5q31-33 are frequently associated with PDGFRB fusion genes, which are exquisitely sensitive to treatment with imatinib.	imatinib	191-199	platelet derived growth factor receptor beta	Homo sapiens	120-126
24502926-8	2014	Furthermore, BMSCs elevated proto-oncogene BCL6 expression in the CML cells in response to imatinib treatment, suggesting the possible role of BCL6 in stroma-mediated TKI resistance.	imatinib	91-99	BCL6 transcription repressor	Homo sapiens	43-47
24502926-8	2014	Furthermore, BMSCs elevated proto-oncogene BCL6 expression in the CML cells in response to imatinib treatment, suggesting the possible role of BCL6 in stroma-mediated TKI resistance.	imatinib	91-99	BCL6 transcription repressor	Homo sapiens	143-147
24502926-13	2014	CXCR4 inhibition with BKT140 antagonist efficiently cooperated with imatinib in vitro and in vivo.	imatinib	68-76	C-X-C motif chemokine receptor 4	Homo sapiens	0-5
24552773-0	2014	Ponatinib induces apoptosis in imatinib-resistant human mast cells by dephosphorylating mutant D816V KIT and silencing beta-catenin signaling.	imatinib	31-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	101-104
24552773-4	2014	We discovered that ponatinib abrogated the phosphorylation of KIT harboring either V560G (sensitive to imatinib) or D816V mutation (resistant to imatinib) and the downstream signaling transduction.	imatinib	103-111	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	62-65
24552773-4	2014	We discovered that ponatinib abrogated the phosphorylation of KIT harboring either V560G (sensitive to imatinib) or D816V mutation (resistant to imatinib) and the downstream signaling transduction.	imatinib	145-153	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	62-65
24310825-3	2014	METHODS: We report four pediatric patients with various malignancies (chronic myelogenous leukemia, acute lymphoblastic leukemia, and glioma/renal cell carcinoma) who developed nephrotic syndrome during treatment with TK inhibitors (imatinib, sunitinib, dasatinib, and quizartinib).	imatinib	233-241	TXK tyrosine kinase	Homo sapiens	218-220
24552773-0	2014	Ponatinib induces apoptosis in imatinib-resistant human mast cells by dephosphorylating mutant D816V KIT and silencing beta-catenin signaling.	imatinib	31-39	catenin beta 1	Homo sapiens	119-131
24855825-0	2014	The MEK1/2 inhibitor U0126 reverses imatinib resistance through down-regulating activation of Lyn/ERK signaling pathway in imatinib-resistant K562R leukemia cells.	imatinib	36-44	mitogen-activated protein kinase kinase 1	Homo sapiens	4-10
24855825-5	2014	Our results showed that abnormal activation of the BCR-ABL-independent Lyn/ERK signaling pathway was involved in imatinib-resistance of K562R cells.	imatinib	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
24855825-0	2014	The MEK1/2 inhibitor U0126 reverses imatinib resistance through down-regulating activation of Lyn/ERK signaling pathway in imatinib-resistant K562R leukemia cells.	imatinib	36-44	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	94-97
24855825-0	2014	The MEK1/2 inhibitor U0126 reverses imatinib resistance through down-regulating activation of Lyn/ERK signaling pathway in imatinib-resistant K562R leukemia cells.	imatinib	36-44	EPH receptor B2	Homo sapiens	98-101
24855825-0	2014	The MEK1/2 inhibitor U0126 reverses imatinib resistance through down-regulating activation of Lyn/ERK signaling pathway in imatinib-resistant K562R leukemia cells.	imatinib	123-131	mitogen-activated protein kinase kinase 1	Homo sapiens	4-10
24855825-0	2014	The MEK1/2 inhibitor U0126 reverses imatinib resistance through down-regulating activation of Lyn/ERK signaling pathway in imatinib-resistant K562R leukemia cells.	imatinib	123-131	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	94-97
24855825-0	2014	The MEK1/2 inhibitor U0126 reverses imatinib resistance through down-regulating activation of Lyn/ERK signaling pathway in imatinib-resistant K562R leukemia cells.	imatinib	123-131	EPH receptor B2	Homo sapiens	98-101
24855825-2	2014	The BCR-ABL tyrosine kinase inhibitor imatinib is the standard treatment for CML.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
24855825-5	2014	Our results showed that abnormal activation of the BCR-ABL-independent Lyn/ERK signaling pathway was involved in imatinib-resistance of K562R cells.	imatinib	113-121	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	71-74
24855825-5	2014	Our results showed that abnormal activation of the BCR-ABL-independent Lyn/ERK signaling pathway was involved in imatinib-resistance of K562R cells.	imatinib	113-121	EPH receptor B2	Homo sapiens	75-78
24855825-6	2014	Furthermore, p-Lyn and p-ERK were up-regulated after treatment with imatinib alone.	imatinib	68-76	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	15-18
24855825-6	2014	Furthermore, p-Lyn and p-ERK were up-regulated after treatment with imatinib alone.	imatinib	68-76	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	23-28
24855825-8	2014	In conclusion, our studies suggest that the combination of imatinib and an inhibitor of the ERK signaling pathway may be effective in imatinib-resistant CML patients.	imatinib	134-142	EPH receptor B2	Homo sapiens	92-95
24790651-3	2014	However, most advanced GISTs responding to imatinib progress within 2-3 years due to heterogeneous subclones harboring a range of imatinib-resistant secondary KIT mutations.	imatinib	130-138	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	159-162
24021153-2	2014	RESULTS: As tested by colony-forming cell assays using clinical specimens, both number and size of total colonies derived from CD34(+) CML cells were significantly reduced by fenretinide, and by combining fenretinide with imatinib.	imatinib	222-230	CD34 molecule	Homo sapiens	127-131
24789045-0	2014	Geminin overexpression promotes imatinib sensitive breast cancer: a novel treatment approach for aggressive breast cancers, including a subset of triple negative.	imatinib	32-40	geminin DNA replication inhibitor	Homo sapiens	0-7
24789045-9	2014	Inhibiting c-Abl expression or activity (using imatinib or nilotinib) prevented geminin Y150 phosphorylation, inactivated the protein, and most importantly converted overexpressed geminin from an oncogene to an apoptosis inducer.	imatinib	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-16
24789045-9	2014	Inhibiting c-Abl expression or activity (using imatinib or nilotinib) prevented geminin Y150 phosphorylation, inactivated the protein, and most importantly converted overexpressed geminin from an oncogene to an apoptosis inducer.	imatinib	47-55	geminin DNA replication inhibitor	Homo sapiens	80-87
24789045-9	2014	Inhibiting c-Abl expression or activity (using imatinib or nilotinib) prevented geminin Y150 phosphorylation, inactivated the protein, and most importantly converted overexpressed geminin from an oncogene to an apoptosis inducer.	imatinib	47-55	geminin DNA replication inhibitor	Homo sapiens	180-187
24789045-11	2014	Moreover, established geminin overexpressing orthotopic tumors regressed when treated with imatinib or nilotinib.	imatinib	91-99	geminin DNA replication inhibitor	Homo sapiens	22-29
24789045-12	2014	Our studies support imatinib/nilotonib as a novel treatment option for patients with aggressive breast cancer (including a subset of TNBCs)-overexpressing geminin and nuclear c-Abl.	imatinib	20-28	geminin DNA replication inhibitor	Homo sapiens	155-162
24789045-12	2014	Our studies support imatinib/nilotonib as a novel treatment option for patients with aggressive breast cancer (including a subset of TNBCs)-overexpressing geminin and nuclear c-Abl.	imatinib	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-180
24414484-6	2014	Patients with >10% Bcr-Abl levels were found to have 25.0% of suboptimal response and 3.57% of failure to imatinib at standard dose.	imatinib	109-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
24775308-0	2014	Combination of the ABL kinase inhibitor imatinib with the Janus kinase 2 inhibitor TG101348 for targeting residual BCR-ABL-positive cells.	imatinib	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
24680683-3	2014	In this study, we explored the function of RPS27a in leukemia cells by using CML cell line K562 cells and its imatinib resistant cell line K562/G01 cells.	imatinib	110-118	ribosomal protein S27a	Homo sapiens	43-49
24581936-0	2014	Association of genotypes and haplotypes of multi-drug transporter genes ABCB1 and ABCG2 with clinical response to imatinib mesylate in chronic myeloid leukemia patients.	imatinib	114-122	ATP binding cassette subfamily B member 1	Homo sapiens	72-77
24680683-5	2014	Further analysis revealed that RPS27a knockdown by shRNA in both K562 and K562G01 cells inhibited the cell viability, induced cell cycle arrest at S and G2/M phases and increased cell apoptosis induced by imatinib.	imatinib	205-213	ribosomal protein S27a	Homo sapiens	31-37
24680683-6	2014	Combination of shRNA with imatinib treatment could lead to more cleaved PARP and cleaved caspase-3 expression in RPS27a knockdown cells.	imatinib	26-34	collagen type XI alpha 2 chain	Homo sapiens	72-76
24680683-6	2014	Combination of shRNA with imatinib treatment could lead to more cleaved PARP and cleaved caspase-3 expression in RPS27a knockdown cells.	imatinib	26-34	ribosomal protein S27a	Homo sapiens	113-119
24569990-8	2014	Imatinib, a c-Abl-selective inhibitor, also specifically blocked PKCdelta Tyr-155 phosphorylation.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-17
24569990-8	2014	Imatinib, a c-Abl-selective inhibitor, also specifically blocked PKCdelta Tyr-155 phosphorylation.	imatinib	0-8	protein kinase C delta	Homo sapiens	65-73
24569990-9	2014	Dasatinib and imatinib both blocked binding of PKCdelta to importin-alpha and nuclear import, demonstrating that tyrosine kinase inhibitors can inhibit nuclear accumulation of PKCdelta.	imatinib	14-22	protein kinase C delta	Homo sapiens	47-55
24569990-9	2014	Dasatinib and imatinib both blocked binding of PKCdelta to importin-alpha and nuclear import, demonstrating that tyrosine kinase inhibitors can inhibit nuclear accumulation of PKCdelta.	imatinib	14-22	protein kinase C delta	Homo sapiens	176-184
24783183-3	2014	Sunitinib, an oral multitargeted receptor tyrosine kinase inhibitor that inhibits kinases such as KIT, PDGFR (platelet-derived growth factor recepter), and VEGFR (vascular endothelial growth factor receptor), was recently approved for the treatment of imatinib-refractory GIST.	imatinib	252-260	kinase insert domain receptor	Homo sapiens	163-206
24424174-9	2014	Imatinib and mepolizumab, a humanized anti-interleukin 5 monoclonal antibody, may be useful in patients with eosinophilic myositis as part of a hypereosinophilic syndrome.	imatinib	0-8	interleukin 5	Homo sapiens	43-56
24569263-10	2014	Imatinib-resistant/-intolerant patients with CML-CP can experience long-term benefit with dasatinib therapy, particularly if achieving BCR-ABL <=10% at 3 months.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
24591204-0	2014	Pretransplant administration of imatinib for allo-HSCT in patients with BCR-ABL-positive acute lymphoblastic leukemia.	imatinib	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
23584476-1	2014	Most gastrointestinal stromal tumors (GISTs) contain KIT or PDGFRA kinase gain-of-function mutations, and therefore respond clinically to imatinib and other tyrosine kinase inhibitor (TKI) therapies.	imatinib	138-146	platelet derived growth factor receptor alpha	Homo sapiens	60-66
23584476-6	2014	Validations in treatment-naive (GIST-T1, GIST882) vs imatinib-resistant GISTs (GIST48, GIST430) demonstrated that: (1) CDC37 interacts with oncogenic KIT; (2) CDC37 regulates expression and activation of KIT and downstream signaling intermediates in GIST; and (3) unlike direct HSP90 inhibition, CDC37 knockdown accomplishes prolonged KIT inhibition (>20 days) in GIST.	imatinib	53-61	cell division cycle 37, HSP90 cochaperone	Homo sapiens	119-124
23584476-7	2014	These studies highlight CDC37 as a key biologic vulnerability in both imatinib-sensitive and imatinib-resistant GIST.	imatinib	70-78	cell division cycle 37, HSP90 cochaperone	Homo sapiens	24-29
23584476-7	2014	These studies highlight CDC37 as a key biologic vulnerability in both imatinib-sensitive and imatinib-resistant GIST.	imatinib	93-101	cell division cycle 37, HSP90 cochaperone	Homo sapiens	24-29
24783183-2	2014	Several recent findings that there are activating mutations in the KIT and PDGFRA (platelet-derived growth factor receptor-alpha) genes of GISTs provide the rationale for using targeted therapies such as imatinib or sunitinib.	imatinib	204-212	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	67-70
24783183-2	2014	Several recent findings that there are activating mutations in the KIT and PDGFRA (platelet-derived growth factor receptor-alpha) genes of GISTs provide the rationale for using targeted therapies such as imatinib or sunitinib.	imatinib	204-212	platelet derived growth factor receptor alpha	Homo sapiens	75-81
24783183-2	2014	Several recent findings that there are activating mutations in the KIT and PDGFRA (platelet-derived growth factor receptor-alpha) genes of GISTs provide the rationale for using targeted therapies such as imatinib or sunitinib.	imatinib	204-212	platelet derived growth factor receptor alpha	Homo sapiens	83-128
24581936-0	2014	Association of genotypes and haplotypes of multi-drug transporter genes ABCB1 and ABCG2 with clinical response to imatinib mesylate in chronic myeloid leukemia patients.	imatinib	114-122	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	82-87
24504921-8	2014	Mechanistically, depletion of the transcription factor GATA4 resulting in decreased levels of its prosurvival targets Bcl-2 and Bcl-XL was an underlying cause of imatinib toxicity.	imatinib	162-170	GATA binding protein 4	Homo sapiens	55-60
24333732-0	2014	Imatinib sensitizes endometrial cancer cells to cisplatin by targeting CD117-positive growth-competent cells.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	71-76
24333732-7	2014	Imatinib was confirmed to selectively target CD117(+) cells in vitro, and synergistically enhanced the anti-tumor effect of low dose cisplatin in vivo, which showed only modest effects when used as a single use.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	45-50
24333732-9	2014	Targeting of the SCF/CD117 axis by imatinib sensitized endometrial cancer cells to cisplatin, proposing a novel therapeutic strategy for this tumor type.	imatinib	35-43	KIT ligand	Homo sapiens	17-20
24333732-9	2014	Targeting of the SCF/CD117 axis by imatinib sensitized endometrial cancer cells to cisplatin, proposing a novel therapeutic strategy for this tumor type.	imatinib	35-43	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	21-26
24215657-0	2014	OCT1 genetic variants are associated with long term outcomes in imatinib treated chronic myeloid leukemia patients.	imatinib	64-72	solute carrier family 22 member 1	Homo sapiens	0-4
24215657-2	2014	Imatinib is actively transported into cells by the SLC22A1 transporter (hOCT1) and its genetic variants may affect intracellular drug import.	imatinib	0-8	solute carrier family 22 member 1	Homo sapiens	51-58
24215657-2	2014	Imatinib is actively transported into cells by the SLC22A1 transporter (hOCT1) and its genetic variants may affect intracellular drug import.	imatinib	0-8	solute carrier family 22 member 1	Homo sapiens	72-77
24215657-3	2014	We studied the effect of SLC22A1 genetic variants on long-term outcomes of imatinib treated patients.	imatinib	75-83	solute carrier family 22 member 1	Homo sapiens	25-32
24382642-0	2014	Drug resistance and BCR-ABL kinase domain mutations in Philadelphia chromosome-positive acute lymphoblastic leukemia from the imatinib to the second-generation tyrosine kinase inhibitor era: The main changes are in the type of mutations, but not in the frequency of mutation involvement.	imatinib	126-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
24382642-5	2014	RESULTS: BCR-ABL KD mutations were detected in 70% of imatinib-resistant patients, with T315I, E255K, and Y253H mutations accounting for 75% of cases.	imatinib	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
24382642-10	2014	BCR-ABL KD mutation screening of patients with Ph+ ALL who are receiving imatinib or second-generation TKIs would be a precious ally for timely treatment optimization.	imatinib	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
24758502-5	2014	Pharmacogenomics have been successful in designing drugs to overcome not only the primary resistance of GISTs to the action of imatinib (e.g. GISTs with a substitution of Asp842Val in exon 18 PDGFRA or SDHB-deficient GISTs), but also the secondary resistance caused by secondary mutation of a gene encoding either the receptor tyrosine kinase or other molecules involved in the respective signalling cascade.	imatinib	127-135	platelet derived growth factor receptor alpha	Homo sapiens	192-198
24504921-8	2014	Mechanistically, depletion of the transcription factor GATA4 resulting in decreased levels of its prosurvival targets Bcl-2 and Bcl-XL was an underlying cause of imatinib toxicity.	imatinib	162-170	BCL2 apoptosis regulator	Homo sapiens	118-123
24504921-8	2014	Mechanistically, depletion of the transcription factor GATA4 resulting in decreased levels of its prosurvival targets Bcl-2 and Bcl-XL was an underlying cause of imatinib toxicity.	imatinib	162-170	BCL2 like 1	Homo sapiens	128-134
23683876-0	2014	Association of MDR1 gene polymorphism (G2677T) with imatinib response in Egyptian chronic myeloid leukemia patients.	imatinib	52-60	ATP binding cassette subfamily B member 1	Homo sapiens	15-19
24504921-9	2014	Consistent with this, GATA4 haploinsufficient mice were more susceptible to imatinib, and myocyte-specific up-regulation of GATA4 or Bcl-2 protected against drug-induced cardiotoxicity.	imatinib	76-84	GATA binding protein 4	Mus musculus	22-27
24468189-3	2014	Nobiletin-exerted BR on jejunal contractility was abolished in the presence of c-kit receptor tyrosine kinase inhibitor imatinib or Ca(2+) channel blocker verapamil.	imatinib	120-128	KIT proto-oncogene receptor tyrosine kinase	Rattus norvegicus	79-109
24464935-6	2014	STI571, an inhibitor of cAbl, blocked induction/activation of Mst1 and H2O2-induced cell death.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-28
24464935-6	2014	STI571, an inhibitor of cAbl, blocked induction/activation of Mst1 and H2O2-induced cell death.	imatinib	0-6	macrophage stimulating 1	Homo sapiens	62-66
24407160-11	2014	We also examined drug effects on Ba/F3 cells expressing two clinically relevant, imatinib-resistant, mutant forms of FIP1L1-PDGFRA, namely T674I and D842V.	imatinib	81-89	FIP1 like 1 (S. cerevisiae)	Mus musculus	117-123
24407160-11	2014	We also examined drug effects on Ba/F3 cells expressing two clinically relevant, imatinib-resistant, mutant forms of FIP1L1-PDGFRA, namely T674I and D842V.	imatinib	81-89	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	124-130
24407160-13	2014	In summary, novel PDGFR-targeting TKIs may be alternative agents for the treatment of patients with imatinib-resistant chronic eosinophilic leukemia.	imatinib	100-108	platelet derived growth factor receptor beta	Homo sapiens	18-23
23683876-14	2014	CONCLUSION: Determination of MDR1 polymorphisms (G2677T) might be useful in response prediction to therapy with imatinib in patients with CML.	imatinib	112-120	ATP binding cassette subfamily B member 1	Homo sapiens	29-33
24136016-8	2014	Suppression of the initiation of autophagy by 3-methyladenine or small interfering RNA (siRNA) against beclin-1 attenuated the imatinib-mediated cytotoxicity.	imatinib	127-135	beclin 1	Homo sapiens	103-111
24717604-0	2014	[Treatment with imatinib for refractory PAH].	imatinib	16-24	phenylalanine hydroxylase	Homo sapiens	40-43
24292246-0	2014	Imatinib responsiveness in canine mast cell tumors carrying novel mutations of c-KIT exon 11.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	79-84
24186003-0	2014	RNA-seq identifies clinically relevant fusion genes in leukemia including a novel MEF2D/CSF1R fusion responsive to imatinib.	imatinib	115-123	colony stimulating factor 1 receptor	Homo sapiens	88-93
24456693-0	2014	BCR-ABL kinase domain mutations, including 2 novel mutations in imatinib resistant Malaysian chronic myeloid leukemia patients-Frequency and clinical outcome.	imatinib	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
24456693-1	2014	Discovery of imatinib mesylate (IM) as the targeted BCR-ABL protein tyrosine kinase inhibitor (TKI) has resulted in its use as the frontline therapy for chronic myeloid leukemia (CML) across the world.	imatinib	13-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
23616342-2	2014	METHODS: Newborn rat pups were treated daily with the KIT inhibitor imatinib mesylate (IM).	imatinib	68-85	KIT proto-oncogene receptor tyrosine kinase	Rattus norvegicus	54-57
24691473-1	2014	Glutathione peroxidase activity was previously determined to be elevated in lymphocytes obtained from patients treated with the Bcr-Abl kinase inhibitor imatinib mesylate.	imatinib	153-170	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
24691473-3	2014	The levels of GPx-1 were significantly increased following treatment with imatinib.	imatinib	74-82	glutathione peroxidase 1	Homo sapiens	14-19
24691473-4	2014	This increase was not due to altered steady-state mRNA levels, and appeared to be dependent on the expression of Bcr-Abl, as no increases were observed following imatinib treatment of cells that did not express the fusion protein.	imatinib	162-170	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
24691473-6	2014	Treatment of those same cells used in the imatinib studies with rapamycin, an inhibitor of mTOR, resulted in elevated GPx-1 and GPx-4 protein levels independent of Bcr-Abl expression.	imatinib	42-50	mechanistic target of rapamycin kinase	Homo sapiens	91-95
24691473-6	2014	Treatment of those same cells used in the imatinib studies with rapamycin, an inhibitor of mTOR, resulted in elevated GPx-1 and GPx-4 protein levels independent of Bcr-Abl expression.	imatinib	42-50	glutathione peroxidase 1	Homo sapiens	118-123
24691473-6	2014	Treatment of those same cells used in the imatinib studies with rapamycin, an inhibitor of mTOR, resulted in elevated GPx-1 and GPx-4 protein levels independent of Bcr-Abl expression.	imatinib	42-50	glutathione peroxidase 4	Homo sapiens	128-133
25117044-9	2014	However, the dramatic response to imatinib emphasizes the need to study the presence of the fusion product FIP1L1/PDGFRA in all patients with eosinophilia of unknown etiology.	imatinib	34-42	factor interacting with PAPOLA and CPSF1	Homo sapiens	107-113
25117044-9	2014	However, the dramatic response to imatinib emphasizes the need to study the presence of the fusion product FIP1L1/PDGFRA in all patients with eosinophilia of unknown etiology.	imatinib	34-42	platelet derived growth factor receptor alpha	Homo sapiens	114-120
24481545-2	2014	The aim of this study was to examine if TNC causes neuronal apoptosis after subarachnoid hemorrhage (SAH), a deadly cerebrovascular disorder, using imatinib mesylate (a selective inhibitor of platelet-derived growth factor receptor [PDGFR] that is reported to suppress TNC induction) and recombinant TNC.	imatinib	148-165	tenascin C	Rattus norvegicus	40-43
24481545-4	2014	PDGFR inactivation by an intraperitoneal injection of imatinib mesylate prevented neuronal apoptosis, as well as MAPKs activation and TNC induction in the cerebral cortex at 24 h. A cisternal injection of recombinant TNC reactivated MAPKs and abolished anti-apoptotic effects of imatinib mesylate.	imatinib	54-71	tenascin C	Rattus norvegicus	217-220
24186003-0	2014	RNA-seq identifies clinically relevant fusion genes in leukemia including a novel MEF2D/CSF1R fusion responsive to imatinib.	imatinib	115-123	myocyte enhancer factor 2D	Homo sapiens	82-87
24660038-0	2014	ABCB1 haplotypes are associated with P-gp activity and affect a major molecular response in chronic myeloid leukemia patients treated with a standard dose of imatinib.	imatinib	158-166	ATP binding cassette subfamily B member 1	Homo sapiens	0-5
24660038-0	2014	ABCB1 haplotypes are associated with P-gp activity and affect a major molecular response in chronic myeloid leukemia patients treated with a standard dose of imatinib.	imatinib	158-166	ATP binding cassette subfamily B member 1	Homo sapiens	37-41
24484970-2	2014	Anaplastic GIST, with pleomorphic cells and loss of CD117, until recently have only been reported in patients with chronic imatinib mesylate treatment.	imatinib	123-140	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	52-57
24798723-1	2014	BACKGROUND: MDR1 gene polymorphisms were demonstrated to be associated with interindividual variability of imatinib response for chronic myeloid leukemia (CML) patients in several studies; however, the results have been inconclusive.	imatinib	107-115	ATP binding cassette subfamily B member 1	Homo sapiens	12-16
24798723-2	2014	MATERIALS & METHODS: To clarify the effect of common MDR1 variants on clinical response to imatinib, we performed a meta-analysis to quantify the accumulated information from genetic association studies.	imatinib	95-103	ATP binding cassette subfamily B member 1	Homo sapiens	57-61
24798723-3	2014	After a thorough search of the published literature, we undertook a meta-analysis to evaluate the effect of MDR1 C1236T, G2677T and C3435T polymorphisms on imatinib response.	imatinib	156-164	ATP binding cassette subfamily B member 1	Homo sapiens	108-112
24798723-4	2014	RESULTS: Our pooled data showed a significant association between MDR1 C1236T polymorphism and the increasing risk of imatinib resistance in Asian CML patients.	imatinib	118-126	ATP binding cassette subfamily B member 1	Homo sapiens	66-70
24798723-6	2014	CONCLUSION: The synonymous MDR1 C1236T polymorphism might be a risk factor for nonoptimal clinical response to imatinib in Asian CML patients.	imatinib	111-119	ATP binding cassette subfamily B member 1	Homo sapiens	27-31
24724051-5	2014	Addition of the first generation ABL1 class TKI imatinib to intensive chemotherapy dramatically increased the survival for children with Ph(+) ALL and established that many patients can be cured without HSCT.	imatinib	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-37
24669761-0	2014	Discovery of imatinib-responsive FIP1L1-PDGFRA mutation during refractory acute myeloid leukemia transformation of chronic myelomonocytic leukemia.	imatinib	13-21	factor interacting with PAPOLA and CPSF1	Homo sapiens	33-39
24669761-0	2014	Discovery of imatinib-responsive FIP1L1-PDGFRA mutation during refractory acute myeloid leukemia transformation of chronic myelomonocytic leukemia.	imatinib	13-21	platelet derived growth factor receptor alpha	Homo sapiens	40-46
24366361-7	2014	In contrast, good-risk patients with IKZF1 wild-type responded remarkably well to imatinib-containing regimens, providing a rationale to potentially avoid hematopoietic stem-cell transplantation in this subset of patients.	imatinib	82-90	IKAROS family zinc finger 1	Homo sapiens	37-42
24401847-6	2014	Moreover, treatment of MLMVEC with the c-Abl inhibitor imatinib increased catalase and GPx-1 protein in a posttranscriptional fashion.	imatinib	55-63	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	39-44
24401847-6	2014	Moreover, treatment of MLMVEC with the c-Abl inhibitor imatinib increased catalase and GPx-1 protein in a posttranscriptional fashion.	imatinib	55-63	catalase	Mus musculus	74-82
24401847-6	2014	Moreover, treatment of MLMVEC with the c-Abl inhibitor imatinib increased catalase and GPx-1 protein in a posttranscriptional fashion.	imatinib	55-63	glutathione peroxidase 1	Mus musculus	87-92
23542172-10	2014	Treatment with a specific peptide that inhibits Y211 phosphorylation of PCNA or with the c-Abl pharmacological inhibitor imatinib suppressed HGFL-induced cell proliferation.	imatinib	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-94
24681707-7	2014	In Ph+ ALL, major growth-inhibitory effects of the Hsp32-targeting drugs were observed in imatinib-sensitive and imatinib-resistant cells.	imatinib	90-98	heme oxygenase 1	Homo sapiens	51-56
24681707-7	2014	In Ph+ ALL, major growth-inhibitory effects of the Hsp32-targeting drugs were observed in imatinib-sensitive and imatinib-resistant cells.	imatinib	113-121	heme oxygenase 1	Homo sapiens	51-56
24681707-8	2014	Hsp32-targeting drugs were found to synergize with imatinib, nilotinib, and bendamustine in producing growth inhibition and apoptosis in Ph+ ALL cells.	imatinib	51-59	heme oxygenase 1	Homo sapiens	0-5
24681707-9	2014	A siRNA against Hsp32 was found to inhibit growth and survival of ALL cells and to synergize with imatinib in suppressing the growth of ALL cells.	imatinib	98-106	heme oxygenase 1	Homo sapiens	16-21
23542172-10	2014	Treatment with a specific peptide that inhibits Y211 phosphorylation of PCNA or with the c-Abl pharmacological inhibitor imatinib suppressed HGFL-induced cell proliferation.	imatinib	121-129	LOC105369252	Homo sapiens	141-145
24408322-3	2014	We tested proteins from the bone marrow microenvironment and found that FGF2 promotes resistance to imatinib in vitro.	imatinib	100-108	fibroblast growth factor 2	Homo sapiens	72-76
24626299-0	2014	BEX1 promotes imatinib-induced apoptosis by binding to and antagonizing BCL-2.	imatinib	14-22	brain expressed X-linked 1	Homo sapiens	0-4
24626299-0	2014	BEX1 promotes imatinib-induced apoptosis by binding to and antagonizing BCL-2.	imatinib	14-22	BCL2 apoptosis regulator	Homo sapiens	72-77
24626299-1	2014	An enhanced anti-apoptotic capacity of tumor cells plays an important role in the process of breakpoint cluster region/Abelson tyrosine kinase gene (BCR/ABL)-independent imatinib resistance.	imatinib	170-178	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
24626299-2	2014	We have previously demonstrated that brain expressed X-linked 1 (BEX1) was silenced in secondary imatinib-resistant K562 cells and that re-expression of BEX1 can restore imatinib sensitivity resulting in the induction of apoptosis.	imatinib	97-105	brain expressed X-linked 1	Homo sapiens	37-63
24626299-2	2014	We have previously demonstrated that brain expressed X-linked 1 (BEX1) was silenced in secondary imatinib-resistant K562 cells and that re-expression of BEX1 can restore imatinib sensitivity resulting in the induction of apoptosis.	imatinib	97-105	brain expressed X-linked 1	Homo sapiens	65-69
24626299-2	2014	We have previously demonstrated that brain expressed X-linked 1 (BEX1) was silenced in secondary imatinib-resistant K562 cells and that re-expression of BEX1 can restore imatinib sensitivity resulting in the induction of apoptosis.	imatinib	170-178	brain expressed X-linked 1	Homo sapiens	37-63
24626299-2	2014	We have previously demonstrated that brain expressed X-linked 1 (BEX1) was silenced in secondary imatinib-resistant K562 cells and that re-expression of BEX1 can restore imatinib sensitivity resulting in the induction of apoptosis.	imatinib	170-178	brain expressed X-linked 1	Homo sapiens	65-69
24626299-2	2014	We have previously demonstrated that brain expressed X-linked 1 (BEX1) was silenced in secondary imatinib-resistant K562 cells and that re-expression of BEX1 can restore imatinib sensitivity resulting in the induction of apoptosis.	imatinib	170-178	brain expressed X-linked 1	Homo sapiens	153-157
24626299-8	2014	Additionally, we found that this region is essential for BEX1-regulated imatinib-induced apoptosis.	imatinib	72-80	brain expressed X-linked 1	Homo sapiens	57-61
24626299-9	2014	Furthermore, we demonstrated that the interaction between BCL-2 and BEX1 promotes imatinib-induced apoptosis by suppressing the formation of anti-apoptotic BCL-2/BCL-2-associated X protein (BAX) heterodimers.	imatinib	82-90	BCL2 apoptosis regulator	Homo sapiens	58-63
24626299-9	2014	Furthermore, we demonstrated that the interaction between BCL-2 and BEX1 promotes imatinib-induced apoptosis by suppressing the formation of anti-apoptotic BCL-2/BCL-2-associated X protein (BAX) heterodimers.	imatinib	82-90	brain expressed X-linked 1	Homo sapiens	68-72
24626299-9	2014	Furthermore, we demonstrated that the interaction between BCL-2 and BEX1 promotes imatinib-induced apoptosis by suppressing the formation of anti-apoptotic BCL-2/BCL-2-associated X protein (BAX) heterodimers.	imatinib	82-90	BCL2 apoptosis regulator	Homo sapiens	156-161
24626299-9	2014	Furthermore, we demonstrated that the interaction between BCL-2 and BEX1 promotes imatinib-induced apoptosis by suppressing the formation of anti-apoptotic BCL-2/BCL-2-associated X protein (BAX) heterodimers.	imatinib	82-90	BCL2 associated X, apoptosis regulator	Homo sapiens	162-188
24626299-9	2014	Furthermore, we demonstrated that the interaction between BCL-2 and BEX1 promotes imatinib-induced apoptosis by suppressing the formation of anti-apoptotic BCL-2/BCL-2-associated X protein (BAX) heterodimers.	imatinib	82-90	BCL2 associated X, apoptosis regulator	Homo sapiens	190-193
24626299-10	2014	Our results revealed an interaction between BEX1 and BCL-2 and a novel mechanism of imatinib resistance mediated by the BEX1/BCL-2 pathway.	imatinib	84-92	brain expressed X-linked 1	Homo sapiens	44-48
24626299-10	2014	Our results revealed an interaction between BEX1 and BCL-2 and a novel mechanism of imatinib resistance mediated by the BEX1/BCL-2 pathway.	imatinib	84-92	brain expressed X-linked 1	Homo sapiens	120-124
24626299-10	2014	Our results revealed an interaction between BEX1 and BCL-2 and a novel mechanism of imatinib resistance mediated by the BEX1/BCL-2 pathway.	imatinib	84-92	BCL2 apoptosis regulator	Homo sapiens	125-130
24603487-5	2014	Our data demonstrated that compared with wild-type K562 cells, the higher percentage of ABCG2+ cells corresponded to the higher SP fraction in K562/ABCG2 (ABCG2 overexpressing) and K562/IMR (resistance to imatinib) cells, which exhibited enhanced drug resistance along with downregulated phosphatase and tensin homologue deleted on chromosome -10 (PTEN) and activated phosphorylated-Akt (p-Akt).	imatinib	205-213	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	88-93
24487968-0	2014	Curcumin derivative C817 inhibits proliferation of imatinib-resistant chronic myeloid leukemia cells with wild-type or mutant Bcr-Abl in vitro.	imatinib	51-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
24599309-4	2014	Several studies revealed that imatinib mesylate inhibits osteoclast differentiation through the M-CSFR pathway and activates osteoblast differentiation through PDGFR pathway, two key cells involved in the vicious cycle controlling the tumour development.	imatinib	30-47	platelet derived growth factor receptor, beta polypeptide	Mus musculus	160-165
24599309-11	2014	A phospho-receptor tyrosine kinase array kit revealed that PDGFRalpha, among 7 other receptors (PDFGFRbeta, Axl, RYK, EGFR, EphA2 and 10, IGF1R), appears as one of the main molecular targets for imatinib mesylate.	imatinib	195-203	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	59-69
24487968-9	2014	C817 (0.5 or 1 mumol/L) dose-dependently inhibited the phosphorylation of Bcr-Abl and downstream proteins STAT-5 and CrkL in imatinib-resistant K562/G01 cells.	imatinib	125-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
24577808-8	2014	Identification of rearranged PDGFRA or PDGFRB is critical because of the exquisite responsiveness of these diseases to imatinib.	imatinib	119-127	platelet derived growth factor receptor alpha	Homo sapiens	29-35
24577808-8	2014	Identification of rearranged PDGFRA or PDGFRB is critical because of the exquisite responsiveness of these diseases to imatinib.	imatinib	119-127	platelet derived growth factor receptor beta	Homo sapiens	39-45
24487968-9	2014	C817 (0.5 or 1 mumol/L) dose-dependently inhibited the phosphorylation of Bcr-Abl and downstream proteins STAT-5 and CrkL in imatinib-resistant K562/G01 cells.	imatinib	125-133	signal transducer and activator of transcription 5A	Homo sapiens	106-112
24487968-9	2014	C817 (0.5 or 1 mumol/L) dose-dependently inhibited the phosphorylation of Bcr-Abl and downstream proteins STAT-5 and CrkL in imatinib-resistant K562/G01 cells.	imatinib	125-133	CRK like proto-oncogene, adaptor protein	Homo sapiens	117-121
24487968-11	2014	CONCLUSION: C817 is a promising compound for treatment of CML patients with Bcr-Abl kinase domain mutations that confer imatinib resistance.	imatinib	120-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
24596204-1	2014	FGF2 induces imatinib resistance in CML cells via reactivation of FGFR3-RAS-MAPK signaling.	imatinib	13-21	fibroblast growth factor 2	Homo sapiens	0-4
24596204-1	2014	FGF2 induces imatinib resistance in CML cells via reactivation of FGFR3-RAS-MAPK signaling.	imatinib	13-21	fibroblast growth factor receptor 3	Homo sapiens	66-71
24847647-1	2014	Mutations in the kinase domain of Bcr-Abl are the most common cause of resistance to therapy with Imatinib in patients with chronic myelogenous leukaemia (CML).	imatinib	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
24479586-7	2014	Furthermore, stem cell factor (SCF)-stimulated c-Kit activation and melanocyte proliferation were completely abrogated by imatinib.	imatinib	122-130	KIT ligand	Homo sapiens	13-29
24479586-7	2014	Furthermore, stem cell factor (SCF)-stimulated c-Kit activation and melanocyte proliferation were completely abrogated by imatinib.	imatinib	122-130	KIT ligand	Homo sapiens	31-34
24479586-7	2014	Furthermore, stem cell factor (SCF)-stimulated c-Kit activation and melanocyte proliferation were completely abrogated by imatinib.	imatinib	122-130	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	47-52
24479586-8	2014	CONCLUSIONS: Inactivation of c-Kit signalling by imatinib has inhibitory effects on melanocyte survival, proliferation and melanogenesis, which explains the clinical hypopigmentation seen in patients with CML.	imatinib	49-57	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	29-34
24107928-0	2014	Interaction of the efflux transporters ABCB1 and ABCG2 with imatinib, nilotinib, and dasatinib.	imatinib	60-68	ATP binding cassette subfamily B member 1	Homo sapiens	39-44
24107928-0	2014	Interaction of the efflux transporters ABCB1 and ABCG2 with imatinib, nilotinib, and dasatinib.	imatinib	60-68	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	49-54
24107928-1	2014	The efflux transporters adenosine triphosphate (ATP)-binding cassette (ABC)B1 and ABCG2 have been demonstrated to interact with the tyrosine kinase inhibitors (TKIs) imatinib, nilotinib, and dasatinib.	imatinib	166-174	ATP binding cassette subfamily B member 1	Homo sapiens	71-77
24107928-1	2014	The efflux transporters adenosine triphosphate (ATP)-binding cassette (ABC)B1 and ABCG2 have been demonstrated to interact with the tyrosine kinase inhibitors (TKIs) imatinib, nilotinib, and dasatinib.	imatinib	166-174	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	82-87
24500518-2	2014	Inhibition of BCR-ABL using Abl-specific kinase inhibitors (TKI) such as imatinib induces remarkable clinical responses.	imatinib	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
24847647-2	2014	Second generation Bcr-Abl inhibitors, such as Nilotinib and Dasatinib, are able to overcome most Imatinib- resistant mutants, with the exception of the T315I substitution.	imatinib	97-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
24847658-2	2014	On the basis of their activity against the spectrum of BCR-ABL mutations that have shown to be the most prominent mechanism of resistance to imatinib, new TKIs have been classified as second generation (such as nilotinib, dasatinib and bosutinib) or third generation (also cover- ing T315I such as ponatinib) TKIs.	imatinib	141-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
24527087-0	2014	In vitro effects of imatinib on CD34+ cells of patients with chronic myeloid leukemia in the megakaryocytic crisis phase.	imatinib	20-28	CD34 molecule	Homo sapiens	32-36
24598853-4	2014	However, most drugs, including new KIT D816V-blocking agents, have failed to achieve long-lasting remissions in advanced systemic mastocytosis, and there is a similar problem in chronic myeloid leukemia, where imatinib-resistant patients sometimes fail to achieve remission, even with second- or third-line BCR-ABL1 specific tyrosine kinase inhibitors.	imatinib	210-218	BCR activator of RhoGEF and GTPase	Homo sapiens	307-315
24444465-0	2014	High-resolution melting analysis is a sensitive diagnostic tool to detect imatinib-resistant and imatinib-sensitive PDGFRA exon 18 mutations in gastrointestinal stromal tumors.	imatinib	97-105	platelet derived growth factor receptor alpha	Homo sapiens	116-122
23934627-7	2014	Inhibition of AURKA could be useful to overcome imatinib-resistance mediated by Bcr-Abl mutants.	imatinib	48-56	aurora kinase A	Mus musculus	14-19
24367893-3	2014	Upon treatment with both imatinib and dasatinib, BCR-ABL1-expressing Ba/F3 cells underwent rapid apoptosis, whereas SNX2-ABL1-expressing Ba/F3 cells showed poorer sensitivity toward these TKIs and could proliferate in the presence of a low dose of dasatinib.	imatinib	25-33	BCR activator of RhoGEF and GTPase	Mus musculus	49-57
24367893-3	2014	Upon treatment with both imatinib and dasatinib, BCR-ABL1-expressing Ba/F3 cells underwent rapid apoptosis, whereas SNX2-ABL1-expressing Ba/F3 cells showed poorer sensitivity toward these TKIs and could proliferate in the presence of a low dose of dasatinib.	imatinib	25-33	sorting nexin 2	Mus musculus	116-120
24367893-3	2014	Upon treatment with both imatinib and dasatinib, BCR-ABL1-expressing Ba/F3 cells underwent rapid apoptosis, whereas SNX2-ABL1-expressing Ba/F3 cells showed poorer sensitivity toward these TKIs and could proliferate in the presence of a low dose of dasatinib.	imatinib	25-33	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	53-57
24269846-0	2014	Single-cell analysis of K562 cells: an imatinib-resistant subpopulation is adherent and has upregulated expression of BCR-ABL mRNA and protein.	imatinib	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
24269846-6	2014	Furthermore, treatment with the BCR-ABL tyrosine kinase inhibitor, imatinib, reduced cell viability more rapidly in K562/NonAdh compared with K562/Adh cells (p < 0.005) both at single and bulk cell levels.	imatinib	67-75	BCR activator of RhoGEF and GTPase	Homo sapiens	32-35
24469953-0	2014	Reduced ABCG2 and increased SLC22A1 mRNA expression are associated with imatinib response in chronic myeloid leukemia.	imatinib	72-80	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	8-13
24469953-0	2014	Reduced ABCG2 and increased SLC22A1 mRNA expression are associated with imatinib response in chronic myeloid leukemia.	imatinib	72-80	solute carrier family 22 member 1	Homo sapiens	28-35
24527087-6	2014	Imatinib significantly induced G1 arrest, reduced the phosphorylation of cyclin-dependent kinase 1 and retinoblastoma proteins and inhibited the proliferation of CD34+ cells from patients with CML in the megakaryocytic crisis phase.	imatinib	0-8	cyclin dependent kinase 1	Homo sapiens	73-98
24527087-6	2014	Imatinib significantly induced G1 arrest, reduced the phosphorylation of cyclin-dependent kinase 1 and retinoblastoma proteins and inhibited the proliferation of CD34+ cells from patients with CML in the megakaryocytic crisis phase.	imatinib	0-8	CD34 molecule	Homo sapiens	162-166
24527087-7	2014	Annexin V/propidium iodide and caspase-3 activity showed that imatinib induced apoptosis.	imatinib	62-70	annexin A5	Homo sapiens	0-9
24527087-7	2014	Annexin V/propidium iodide and caspase-3 activity showed that imatinib induced apoptosis.	imatinib	62-70	caspase 3	Homo sapiens	31-40
24527087-8	2014	Western blot analysis and protein tyrosine kinase activity assays showed that imatinib inhibited BCR-ABL protein tyrosine kinase activity.	imatinib	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
24764730-0	2014	FIP1L1-PDGFRA-Positive Chronic Eosinophilic Leukemia: A Low-Burden Disease with Dramatic Response to Imatinib - A Report of 5 Cases from South India.	imatinib	101-109	factor interacting with PAPOLA and CPSF1	Homo sapiens	0-6
24764730-0	2014	FIP1L1-PDGFRA-Positive Chronic Eosinophilic Leukemia: A Low-Burden Disease with Dramatic Response to Imatinib - A Report of 5 Cases from South India.	imatinib	101-109	platelet derived growth factor receptor alpha	Homo sapiens	7-13
24764730-1	2014	OBJECTIVE: Eosinophilia associated with FIP1L1-PDGFRA rearrangement represents a subset of chronic eosinophilic leukemia and affected patients are sensitive to imatinib treatment.	imatinib	160-168	factor interacting with PAPOLA and CPSF1	Homo sapiens	40-46
24764730-1	2014	OBJECTIVE: Eosinophilia associated with FIP1L1-PDGFRA rearrangement represents a subset of chronic eosinophilic leukemia and affected patients are sensitive to imatinib treatment.	imatinib	160-168	platelet derived growth factor receptor alpha	Homo sapiens	47-53
24335106-3	2014	At 3 months, more patients had EMR failure (ie, BCR-ABL(IS) >10%) on imatinib (33%) than on nilotinib (9%-11%); similarly at 6 months, 16% of patients in the imatinib arm vs 3% and 7% in the nilotinib arms had EMR failure.	imatinib	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
24586514-1	2014	Resistance to imatinib (Gleevec ) in cancer cells is frequently because of acquired point mutations in the kinase domain of BCR-ABL.	imatinib	14-22	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	128-131
24352644-1	2014	PURPOSE: In addition to mutated BCR-ABL1 kinase, the organic cation transporter 1 (OCT1, encoded by SLC22A1) has been considered to contribute to imatinib resistance in patients with chronic myeloid leukemia (CML).	imatinib	146-154	solute carrier family 22 member 1	Homo sapiens	53-81
23934954-3	2014	Interferon alpha (IFN) induces hematologic and cytogenetic remissions and interestingly, improved outcome was reported with the combination of interferon and imatinib.	imatinib	158-166	interferon alpha 1	Homo sapiens	18-21
25674429-2	2014	Imatinib mesylate, a tyrosine kinase inhibitor of platelet derived growth factor receptor-alpha and -beta, c-fms, c-kit, abl and arg kinase (imatinib targets), has been shown to prevent tumor progression in early studies of recurrent gliomas, but has shown weak activity in randomized controlled trials.	imatinib	0-17	colony stimulating factor 1 receptor	Homo sapiens	107-112
25674429-2	2014	Imatinib mesylate, a tyrosine kinase inhibitor of platelet derived growth factor receptor-alpha and -beta, c-fms, c-kit, abl and arg kinase (imatinib targets), has been shown to prevent tumor progression in early studies of recurrent gliomas, but has shown weak activity in randomized controlled trials.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	114-119
25674429-2	2014	Imatinib mesylate, a tyrosine kinase inhibitor of platelet derived growth factor receptor-alpha and -beta, c-fms, c-kit, abl and arg kinase (imatinib targets), has been shown to prevent tumor progression in early studies of recurrent gliomas, but has shown weak activity in randomized controlled trials.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-124
24352644-1	2014	PURPOSE: In addition to mutated BCR-ABL1 kinase, the organic cation transporter 1 (OCT1, encoded by SLC22A1) has been considered to contribute to imatinib resistance in patients with chronic myeloid leukemia (CML).	imatinib	146-154	solute carrier family 22 member 1	Homo sapiens	83-87
24385214-1	2014	Most gastrointestinal stromal tumors (GIST) are caused by oncogenic KIT or platelet-derived growth factor receptor activation, and the small molecule kinase inhibitor imatinib mesylate is an effective first-line therapy for metastatic or unresectable GIST.	imatinib	167-184	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	68-71
24352644-1	2014	PURPOSE: In addition to mutated BCR-ABL1 kinase, the organic cation transporter 1 (OCT1, encoded by SLC22A1) has been considered to contribute to imatinib resistance in patients with chronic myeloid leukemia (CML).	imatinib	146-154	solute carrier family 22 member 1	Homo sapiens	100-107
24352644-2	2014	As data are conflicting as to whether OCT1 transports imatinib and may serve as a clinical biomarker, we used a combination of different approaches including animal experiments to elucidate comprehensively the impact of OCT1 on cellular imatinib uptake.	imatinib	237-245	solute carrier family 22 member 1	Homo sapiens	220-224
24417566-1	2014	The success of imatinib, a BCR-ABL inhibitor for the treatment of chronic myelogenous leukemia, has created a great impetus for the development of additional kinase inhibitors as therapeutic agents.	imatinib	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
26580056-0	2014	In Silico Design of Monomolecular Drug Carriers for the Tyrosine Kinase Inhibitor Drug Imatinib Based on Calix- and Thiacalix[n]arene Host Molecules: A DFT and Molecular Dynamics Study.	imatinib	87-95	TXK tyrosine kinase	Homo sapiens	56-71
26580056-1	2014	The use of functionalized calix- and thia-calix[n]arenes is proposed as the basis for our in silico design of a suitable drug carrier for the tyrosine kinase inhibitor, Imatinib.	imatinib	169-177	TXK tyrosine kinase	Homo sapiens	142-157
24523596-2	2014	ABCG2/BCRP is referred to as a "half-type" ABC transporter, functioning as a homodimer, and transports anticancer agents such as irinotecan, 7-ethyl-10-hydroxycamptothecin (SN-38), gefitinib, imatinib, methotrexate, and mitoxantrone from cells.	imatinib	192-200	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
24323036-7	2014	Fluctuation of BCR-ABL transcript levels below the MMR threshold (>= two consecutive positive values) was observed in 31% of patients after imatinib discontinuation.	imatinib	143-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
24378417-3	2014	In a pilot study, imatinib, a c-kit/PDGF-receptor inhibitor, induced partial regression of AIDS-associated KS (AIDS-KS) in five of 10 patients.	imatinib	18-26	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	30-35
24523596-2	2014	ABCG2/BCRP is referred to as a "half-type" ABC transporter, functioning as a homodimer, and transports anticancer agents such as irinotecan, 7-ethyl-10-hydroxycamptothecin (SN-38), gefitinib, imatinib, methotrexate, and mitoxantrone from cells.	imatinib	192-200	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	6-10
24523596-6	2014	Importantly, many recently developed molecular-targeted cancer drugs, such as the tyrosine kinase inhisbitors, imatinib mesylate, gefitinib, and others, can also interact with ABCG2/BCRP.	imatinib	111-128	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	176-181
24523596-6	2014	Importantly, many recently developed molecular-targeted cancer drugs, such as the tyrosine kinase inhisbitors, imatinib mesylate, gefitinib, and others, can also interact with ABCG2/BCRP.	imatinib	111-128	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	182-186
24091144-6	2014	When we analyzed the gene expression values of LYN, an increase was observed only in advanced stages of the disease, however, when we analyzed the ratio between LYN and PTEN genes, the group of resistant patients in chronic phase in imatinib or nilotinib treatment (CP-IN) also showed a significant increase.	imatinib	233-241	phosphatase and tensin homolog	Homo sapiens	169-173
24140598-6	2014	Moreover, the synergism resulting from the combined use of boswellic acid and imatinib, which directly inhibits PDGFR-beta activity, on activated HSCs offers new perspectives for the development of therapeutic strategies that could implement molecules affecting diverse players of this molecular circuit, thus paving the way to multi-drug low-dose regimens for liver fibrosis.	imatinib	78-86	platelet derived growth factor receptor beta	Homo sapiens	112-122
24091144-10	2014	Our data suggest that the LYN/PTEN expression ratio may be a sensitive monitor of disease progression in unmutated CML patients under imatinib or nilotinib treatment.	imatinib	134-142	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	26-29
24091144-10	2014	Our data suggest that the LYN/PTEN expression ratio may be a sensitive monitor of disease progression in unmutated CML patients under imatinib or nilotinib treatment.	imatinib	134-142	phosphatase and tensin homolog	Homo sapiens	30-34
24100660-2	2014	However, a substantial number of patients develop resistance to imatinib treatment due to the emergence of clones carrying mutations in the protein BCR-ABL.	imatinib	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	148-155
24100660-7	2014	The combination of NVP-BEZ235 with a BCR-ABL kinase inhibitor, imatinib, or nilotinib, induced a more pronounced colony growth inhibition, whereas the combination of NVP-BEZ235 and nilotinib was more effective in inducing apoptosis and reducing the phosphorylation of AKT, 4E-BP1, and S6 kinase.	imatinib	63-71	AKT serine/threonine kinase 1	Homo sapiens	268-271
24100660-7	2014	The combination of NVP-BEZ235 with a BCR-ABL kinase inhibitor, imatinib, or nilotinib, induced a more pronounced colony growth inhibition, whereas the combination of NVP-BEZ235 and nilotinib was more effective in inducing apoptosis and reducing the phosphorylation of AKT, 4E-BP1, and S6 kinase.	imatinib	63-71	eukaryotic translation initiation factor 4E binding protein 1	Homo sapiens	273-279
24177958-7	2014	When these cells were simultaneously treated with a c-ABL kinase inhibitor, STI571, or a c-ABL-specific siRNA along with adriamycin, the p53-dependent p21 induction was dramatically diminished, even though p53 is substantially induced.	imatinib	76-82	tumor protein p53	Homo sapiens	137-140
24177958-7	2014	When these cells were simultaneously treated with a c-ABL kinase inhibitor, STI571, or a c-ABL-specific siRNA along with adriamycin, the p53-dependent p21 induction was dramatically diminished, even though p53 is substantially induced.	imatinib	76-82	cyclin dependent kinase inhibitor 1A	Homo sapiens	151-154
24300419-7	2014	Treatment of dendritic cells with inhibitors of c-kit activation such as imatinib mesylate (Gleevec) induces breach of T-cell tolerance, skewing of responses toward Th1, and activation of natural killer cells.	imatinib	92-99	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	48-53
24177958-9	2014	On the contrary, when cells were treated with a relatively high dose of adriamycin (0.4 mug/ml) cells became apoptotic, and the simultaneous presence of a c-ABL kinase inhibitor STI571 augmented the extent of apoptosis.	imatinib	178-184	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-160
24300419-7	2014	Treatment of dendritic cells with inhibitors of c-kit activation such as imatinib mesylate (Gleevec) induces breach of T-cell tolerance, skewing of responses toward Th1, and activation of natural killer cells.	imatinib	73-90	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	48-53
24300419-7	2014	Treatment of dendritic cells with inhibitors of c-kit activation such as imatinib mesylate (Gleevec) induces breach of T-cell tolerance, skewing of responses toward Th1, and activation of natural killer cells.	imatinib	92-99	negative elongation factor complex member C/D	Homo sapiens	165-168
24300419-7	2014	Treatment of dendritic cells with inhibitors of c-kit activation such as imatinib mesylate (Gleevec) induces breach of T-cell tolerance, skewing of responses toward Th1, and activation of natural killer cells.	imatinib	73-90	negative elongation factor complex member C/D	Homo sapiens	165-168
24112092-0	2014	Mammalian target of rapamycin inhibitor rapamycin enhances anti-leukemia effect of imatinib on Ph+ acute lymphoblastic leukemia cells.	imatinib	83-91	mechanistic target of rapamycin kinase	Homo sapiens	0-29
24374144-0	2014	p-Stat3 and bcr/abl gene expression in chronic myeloid leukemia and their relation to imatinib therapy.	imatinib	86-94	signal transducer and activator of transcription 3	Homo sapiens	2-7
24258348-1	2014	Treatment of chronic myeloid leukemia (CML) has been drastically changed by the emergence of the ABL tyrosine kinase inhibitor (TKI), imatinib mesylate.	imatinib	134-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-100
24258348-3	2014	Point mutations within the ABL kinase domain that interfere with imatinib binding are the most critical cause of imatinib resistance.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-30
24258348-3	2014	Point mutations within the ABL kinase domain that interfere with imatinib binding are the most critical cause of imatinib resistance.	imatinib	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-30
24490049-0	2014	Durable response with a combination of imatinib and sorafenib in KIT exon 17 mutant gastrointestinal stromal tumor.	imatinib	39-47	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	65-68
24490049-1	2014	Imatinib, a selective KIT tyrosine-kinase inhibitor is considered standard first line therapy in metastatic gastrointestinal stromal tumors (GISTs).	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	22-25
24130113-1	2014	GNF-2, a tyrosine kinase inhibitor, was developed to overcome imatinib-resistant mutations found in CML patients.	imatinib	62-70	growth and fatness 2	Mus musculus	0-5
24374144-0	2014	p-Stat3 and bcr/abl gene expression in chronic myeloid leukemia and their relation to imatinib therapy.	imatinib	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
24374144-3	2014	Imatinib treatment was found to suppress the expression of p-Stat3 in bone marrow cells.	imatinib	0-8	signal transducer and activator of transcription 3	Homo sapiens	61-66
24415355-0	2014	Homoharringtonine contributes to imatinib sensitivity by blocking the EphB4/RhoA pathway in chronic myeloid leukemia cell lines.	imatinib	33-41	EPH receptor B4	Homo sapiens	70-75
24284036-5	2014	Blockade of PDGF-beta receptors (imatinib) had no effect on the pattern of the HVR in Hyperoxia rats, although it attenuated ventilatory depression during the late phase of the HVR in Control rats.	imatinib	33-41	platelet derived growth factor subunit B	Rattus norvegicus	12-21
24415355-0	2014	Homoharringtonine contributes to imatinib sensitivity by blocking the EphB4/RhoA pathway in chronic myeloid leukemia cell lines.	imatinib	33-41	ras homolog family member A	Homo sapiens	76-80
24415355-1	2014	The purpose was to investigate the role of EphB4 in imatinib (IM) resistance and the mechanism responsible for homoharringtonine (HHT) contributing to imatinib sensitivity for a chronic myeloid leukemia (CML) cell lines.	imatinib	52-60	EPH receptor B4	Homo sapiens	43-48
24634785-3	2014	Introduction of imatinib (IM) and other tyrosine kinase inhibitors (TKIs) has radically improved the outcome of patients with CML and some other diseases with BCR/ABL expression.	imatinib	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-166
25593988-2	2014	However, acquired resistance to imatinib, dasatinib or nilotinib (1(st) and 2(nd) generation TKIs), due in part to BCR-ABL1 kinase mutations, has been largely described.	imatinib	32-40	BCR activator of RhoGEF and GTPase	Mus musculus	115-123
24472312-0	2014	Ponatinib efficiently kills imatinib-resistant chronic eosinophilic leukemia cells harboring gatekeeper mutant T674I FIP1L1-PDGFRalpha: roles of Mcl-1 and beta-catenin.	imatinib	28-36	FIP1 like 1 (S. cerevisiae)	Mus musculus	117-123
24472312-1	2014	BACKGROUND: T674I FIP1L1-PDGFRalpha in a subset of chronic eosinophilic leukemia (CEL) is a gatekeeper mutation that is resistant to many tyrosine kinase inhibitors (TKIs) (e.g., imatinib, nilotinib and dasatinib), similar to T315I Bcr-Abl.	imatinib	179-187	FIP1 like 1 (S. cerevisiae)	Mus musculus	18-24
24095864-8	2014	The administration of the anticancer drug imatinib, which is a substrate of CYP3A, to mice at 12weeks after gastrectomy resulted in an increase in the metabolic rate, suggesting a possible decrease in drug effectiveness.	imatinib	42-50	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	76-81
27774462-8	2014	Accordingly, leukemia stem cells of CML selected in low oxygen are refractory to the Bcr/Abl inhibitor imatinib mesylate.	imatinib	103-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
27774462-9	2014	Bcr/Abl protein suppression turned out to be actually determined when glucose shortage complicated the effects of low oxygen, indicating that ischemia-like conditions are the driving force of leukemia stem cell refractoriness to imatinib mesylate.	imatinib	229-246	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
24456946-0	2014	Imatinib-induced postoperative periorbital purpura: GASP (Gleevec-Associated Surgical Purpura) in a woman with imatinib-treated chronic myelogenous leukemia.	imatinib	0-8	G protein-coupled receptor associated sorting protein 1	Homo sapiens	52-56
24456946-0	2014	Imatinib-induced postoperative periorbital purpura: GASP (Gleevec-Associated Surgical Purpura) in a woman with imatinib-treated chronic myelogenous leukemia.	imatinib	0-8	G protein-coupled receptor associated sorting protein 1	Homo sapiens	58-93
24456946-0	2014	Imatinib-induced postoperative periorbital purpura: GASP (Gleevec-Associated Surgical Purpura) in a woman with imatinib-treated chronic myelogenous leukemia.	imatinib	111-119	G protein-coupled receptor associated sorting protein 1	Homo sapiens	52-56
24456946-0	2014	Imatinib-induced postoperative periorbital purpura: GASP (Gleevec-Associated Surgical Purpura) in a woman with imatinib-treated chronic myelogenous leukemia.	imatinib	111-119	G protein-coupled receptor associated sorting protein 1	Homo sapiens	58-93
24454763-2	2014	Imatinib inhibits c-Abl, c-Kit, and PDGFRs.	imatinib	0-8	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	18-23
24454763-2	2014	Imatinib inhibits c-Abl, c-Kit, and PDGFRs.	imatinib	0-8	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	25-30
24454763-4	2014	In this study, we investigated the contribution of c-Kit inhibition by imatinib in reversal of hyperglycemia in NOD mice.	imatinib	71-79	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	51-56
24454763-5	2014	METHODS: The T670I mutation in c-Kit, which confers imatinib resistance, was engineered into the mouse genome and bred onto the NOD background.	imatinib	52-60	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	31-36
24606652-0	2014	[Molecular response and prognostic factors of patients with Philadelphia chromosome/BCR-ABL-positive acute lymphoblastic leukemia treated by imatinib with chemotherapy].	imatinib	141-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
24606652-1	2014	OBJECTIVE: To evaluate the molecular response and prognostic factors of patients with Philadelphia chromosome/BCR-ABL-positive acute lymphoblastic leukaemia (Ph+ ALL) treated by imatinib with chemotherapy.	imatinib	178-186	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
24606652-11	2014	allo-HSCT, imatinib combined in the first cycle of induction therapy and female were independent favorable factors for DFS (P<0.01, 0.05 and 0.01, respectively), BCR-ABL mRNA reduction at least 1 log from baseline after the first induction therapy and allo-HSCT were independent favorable factors for OS (P=0.011 and 0.027, respectively).	imatinib	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	165-172
24465953-5	2014	Targeting GAS2 also sensitized K562 cells to Imatinib mesylate (IM).	imatinib	45-62	growth arrest specific 2	Homo sapiens	10-14
23208504-9	2014	Finally, upregulation of miR-138 upon imatinib treatment is associated with the enhancement of GATA1 activity, which binds to the miR-138 promoter.	imatinib	38-46	GATA binding protein 1	Homo sapiens	95-100
24454763-8	2014	RESULTS: In vitro expansion of HSCs from NOD.c-Kit(wt) mice was sensitive to imatinib, while expansion of HSCs from NOD.c-Kit(T670I) mice was insensitive to imatinib.	imatinib	77-85	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	45-50
23208504-13	2014	Therefore, miR-138, by virtue of a BCR-ABL/GATA1/miR-138 circuitry, is a tumor suppressor miRNA implicated in the pathogenesis of CML and its clinical response to imatinib.	imatinib	163-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
24219857-4	2014	The results show that the good bioavailability of imatinib is highly likely achieved by its active absorption from the intestine and that its active elimination through the intestinal mucosa is mediated by a synergistic activity of organic cation transporter 1 in the basolateral membrane and the added activity of two efflux proteins (P-glycoprotein and breast cancer resistant protein) in the apical membrane of enterocytes of the rat ileum.	imatinib	50-58	solute carrier family 22 member 1	Rattus norvegicus	232-260
23208504-13	2014	Therefore, miR-138, by virtue of a BCR-ABL/GATA1/miR-138 circuitry, is a tumor suppressor miRNA implicated in the pathogenesis of CML and its clinical response to imatinib.	imatinib	163-171	GATA binding protein 1	Homo sapiens	43-48
24577437-0	2014	CD117 (c-kit) expression on CD34+ cells participates in the cytogenetic response to imatinib in patients with chronic myeloid leukemia in the first chronic phase.	imatinib	84-92	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-5
24455115-2	2014	With the appearance of the first Tyrosine Kinase Inhibitor (TKI) (imatinib) and based on the results of the pivotal IRIS trial, imatinib monotherapy was the new treatment of choice for CML, according to the ELN recommendations.	imatinib	128-136	elastin	Homo sapiens	207-210
24455116-4	2014	Imatinib binds to BCR-ABL kinase domain by preventing the transfer of a phosphate group to tyrosine on the protein substrate and the subsequent activation of phosphorylated protein.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
24217767-0	2014	MiR-320a downregulation is associated with imatinib resistance in gastrointestinal stromal tumors.	imatinib	43-51	microRNA 320a	Homo sapiens	0-8
24217767-7	2014	We found that low expression of miR-320a was correlated with short time to imatinib resistance, and proposed the potential mechanism of miR-320a for imatinib resistance.	imatinib	75-83	microRNA 320a	Homo sapiens	32-40
24217767-7	2014	We found that low expression of miR-320a was correlated with short time to imatinib resistance, and proposed the potential mechanism of miR-320a for imatinib resistance.	imatinib	75-83	microRNA 320a	Homo sapiens	136-144
24217767-7	2014	We found that low expression of miR-320a was correlated with short time to imatinib resistance, and proposed the potential mechanism of miR-320a for imatinib resistance.	imatinib	149-157	microRNA 320a	Homo sapiens	32-40
24217767-7	2014	We found that low expression of miR-320a was correlated with short time to imatinib resistance, and proposed the potential mechanism of miR-320a for imatinib resistance.	imatinib	149-157	microRNA 320a	Homo sapiens	136-144
24577437-0	2014	CD117 (c-kit) expression on CD34+ cells participates in the cytogenetic response to imatinib in patients with chronic myeloid leukemia in the first chronic phase.	imatinib	84-92	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	7-12
24577437-0	2014	CD117 (c-kit) expression on CD34+ cells participates in the cytogenetic response to imatinib in patients with chronic myeloid leukemia in the first chronic phase.	imatinib	84-92	CD34 molecule	Homo sapiens	28-32
24577437-2	2014	Later years with imatinib and second-generation tyrosine kinase inhibitors showed a variety of resistance mechanisms and it became obvious that the bcr-abl chimeric gene is not the only enemy to fight.	imatinib	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	148-155
24577437-6	2014	RESULTS: The percentage of CD34+ cells expressing c-kit (CD117) isolated from bone marrow samples of 54 CML patients treated with standard-dose imatinib was significantly lower among imatinib responders.	imatinib	144-152	CD34 molecule	Homo sapiens	27-31
24577437-6	2014	RESULTS: The percentage of CD34+ cells expressing c-kit (CD117) isolated from bone marrow samples of 54 CML patients treated with standard-dose imatinib was significantly lower among imatinib responders.	imatinib	144-152	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	50-55
24577437-6	2014	RESULTS: The percentage of CD34+ cells expressing c-kit (CD117) isolated from bone marrow samples of 54 CML patients treated with standard-dose imatinib was significantly lower among imatinib responders.	imatinib	144-152	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	57-62
24577437-6	2014	RESULTS: The percentage of CD34+ cells expressing c-kit (CD117) isolated from bone marrow samples of 54 CML patients treated with standard-dose imatinib was significantly lower among imatinib responders.	imatinib	183-191	CD34 molecule	Homo sapiens	27-31
24577437-6	2014	RESULTS: The percentage of CD34+ cells expressing c-kit (CD117) isolated from bone marrow samples of 54 CML patients treated with standard-dose imatinib was significantly lower among imatinib responders.	imatinib	183-191	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	50-55
24577437-6	2014	RESULTS: The percentage of CD34+ cells expressing c-kit (CD117) isolated from bone marrow samples of 54 CML patients treated with standard-dose imatinib was significantly lower among imatinib responders.	imatinib	183-191	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	57-62
24009127-0	2014	Cessation of imatinib mesylate may lead to sustained hematologic and molecular remission in FIP1L1-PDGFRA-mutated hypereosinophilic syndrome.	imatinib	13-30	factor interacting with PAPOLA and CPSF1	Homo sapiens	92-98
24009127-0	2014	Cessation of imatinib mesylate may lead to sustained hematologic and molecular remission in FIP1L1-PDGFRA-mutated hypereosinophilic syndrome.	imatinib	13-30	platelet derived growth factor receptor alpha	Homo sapiens	99-105
25520136-7	2014	After imatinib (IM) treatment, patients with m-bcr showed higher BCR-ABL relative concentrations in both CML-CP and ALL groups.	imatinib	6-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
24088895-4	2014	In this study, treatment of the K562 CML stem/progenitor cell line with activin A followed by a subtoxic concentration of the Bcr-Abl inhibitor imatinib strongly induced growth inhibition and apoptosis compared with simultaneous treatment with activin A and imatinib.	imatinib	144-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
24088895-4	2014	In this study, treatment of the K562 CML stem/progenitor cell line with activin A followed by a subtoxic concentration of the Bcr-Abl inhibitor imatinib strongly induced growth inhibition and apoptosis compared with simultaneous treatment with activin A and imatinib.	imatinib	258-266	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
24088895-7	2014	More than 90% of the activin A-induced increases in glycophorin A-positive cells were sensitive to imatinib.	imatinib	99-107	glycophorin A (MNS blood group)	Homo sapiens	52-65
24088895-8	2014	However, only some of original glycophorin A-positive cells in the activin A treatment group were sensitive to imatinib.	imatinib	111-119	glycophorin A (MNS blood group)	Homo sapiens	31-44
24088895-9	2014	Sequential treatment with activin A and imatinib decreased Bcr-Abl, procaspase-3, Mcl-1, and Bcl-xL and also induced cleavage of procaspase-3/poly(ADP-ribose)polymerase.	imatinib	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
24088895-9	2014	Sequential treatment with activin A and imatinib decreased Bcr-Abl, procaspase-3, Mcl-1, and Bcl-xL and also induced cleavage of procaspase-3/poly(ADP-ribose)polymerase.	imatinib	40-48	caspase 3	Homo sapiens	68-80
24088895-9	2014	Sequential treatment with activin A and imatinib decreased Bcr-Abl, procaspase-3, Mcl-1, and Bcl-xL and also induced cleavage of procaspase-3/poly(ADP-ribose)polymerase.	imatinib	40-48	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	82-87
24088895-9	2014	Sequential treatment with activin A and imatinib decreased Bcr-Abl, procaspase-3, Mcl-1, and Bcl-xL and also induced cleavage of procaspase-3/poly(ADP-ribose)polymerase.	imatinib	40-48	BCL2 like 1	Homo sapiens	93-99
24088895-9	2014	Sequential treatment with activin A and imatinib decreased Bcr-Abl, procaspase-3, Mcl-1, and Bcl-xL and also induced cleavage of procaspase-3/poly(ADP-ribose)polymerase.	imatinib	40-48	caspase 3	Homo sapiens	129-141
24088895-10	2014	The reduction of erythroid differentiation in p38 MAPK dominant-negative mutants or by short hairpin RNA knockdown of p38 MAPK decreased the growth inhibition and apoptosis mediated by sequential treatment with activin A and imatinib.	imatinib	225-233	mitogen-activated protein kinase 14	Homo sapiens	46-49
24088895-10	2014	The reduction of erythroid differentiation in p38 MAPK dominant-negative mutants or by short hairpin RNA knockdown of p38 MAPK decreased the growth inhibition and apoptosis mediated by sequential treatment with activin A and imatinib.	imatinib	225-233	mitogen-activated protein kinase 14	Homo sapiens	118-121
24088895-11	2014	Furthermore, the same inhibition level of multidrug resistance 1 expression was observed in cells treated with activin A alone, treated sequentially with activin A and imatinib, or treated simultaneously with activin A and imatinib.	imatinib	168-176	ATP binding cassette subfamily B member 1	Homo sapiens	42-64
24088895-11	2014	Furthermore, the same inhibition level of multidrug resistance 1 expression was observed in cells treated with activin A alone, treated sequentially with activin A and imatinib, or treated simultaneously with activin A and imatinib.	imatinib	223-231	ATP binding cassette subfamily B member 1	Homo sapiens	42-64
24641422-0	2014	Low level of TERC gene amplification between chronic myeloid leukaemia patients resistant and respond to imatinib mesylate treatment.	imatinib	105-122	telomerase RNA component	Homo sapiens	13-17
24969884-0	2014	Silencing of suppressor of cytokine signaling-3 due to methylation results in phosphorylation of STAT3 in imatinib resistant BCR-ABL positive chronic myeloid leukemia cells.	imatinib	106-114	suppressor of cytokine signaling 3	Homo sapiens	13-47
24969884-0	2014	Silencing of suppressor of cytokine signaling-3 due to methylation results in phosphorylation of STAT3 in imatinib resistant BCR-ABL positive chronic myeloid leukemia cells.	imatinib	106-114	signal transducer and activator of transcription 3	Homo sapiens	97-102
24969884-0	2014	Silencing of suppressor of cytokine signaling-3 due to methylation results in phosphorylation of STAT3 in imatinib resistant BCR-ABL positive chronic myeloid leukemia cells.	imatinib	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
24969884-2	2014	Imatinib mesylate is a tyrosine kinase inhibitor that specifically targets the BCR-ABL protein and induces hematological remission in patients with chronic myeloid leukemia (CML).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
24969884-4	2014	We here investigated the methylation profile of SOCS-3 gene and its downstream effects in a BCR-ABL positive CML cells resistant to imatinib.	imatinib	132-140	suppressor of cytokine signaling 3	Homo sapiens	48-54
24969884-4	2014	We here investigated the methylation profile of SOCS-3 gene and its downstream effects in a BCR-ABL positive CML cells resistant to imatinib.	imatinib	132-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
24969884-5	2014	MATERIALS AND METHODS: BCR-ABL positive CML cells resistant to imatinib (K562-R) were developed by overexposure of K562 cell lines to the drug.	imatinib	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
24969884-16	2014	Activation of STAT3 protein leads to uncontrolled cell proliferation in imatinib resistant BCR-ABL due to DNA methylation of the SOCS-3 gene.	imatinib	72-80	signal transducer and activator of transcription 3	Homo sapiens	14-19
24969884-16	2014	Activation of STAT3 protein leads to uncontrolled cell proliferation in imatinib resistant BCR-ABL due to DNA methylation of the SOCS-3 gene.	imatinib	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
24969884-16	2014	Activation of STAT3 protein leads to uncontrolled cell proliferation in imatinib resistant BCR-ABL due to DNA methylation of the SOCS-3 gene.	imatinib	72-80	suppressor of cytokine signaling 3	Homo sapiens	129-135
24969884-17	2014	Thus SOCS-3 provides a suitable candidate for mechanisms underlying the development of imatinib resistant in CML patients.	imatinib	87-95	suppressor of cytokine signaling 3	Homo sapiens	5-11
24641422-2	2014	This present study was aimed to investigate copy number amplification status of TERC gene in chronic myeloid leukaemia (CML) patients who were being treated with imatinib mesylate (IM).	imatinib	162-179	telomerase RNA component	Homo sapiens	80-84
25087954-0	2014	Distinct interaction of nilotinib and imatinib with P-Glycoprotein in intracellular accumulation and cytotoxicity in CML Cell Line K562 cells.	imatinib	38-46	ATP binding cassette subfamily B member 1	Homo sapiens	52-66
25087954-6	2014	Inhibition experiments in K562 cells, and examination of the cellular uptake using influx transporter-transfected human embryonic kidney (HEK) 293 cells, suggested that the influx transporters OCT1 and OATP1A2, which have been reported to mediate accumulation of imatinib in CML cells, contributed little to the uptake of nilotinib.	imatinib	263-271	solute carrier family 22 member 1	Homo sapiens	193-197
25087954-6	2014	Inhibition experiments in K562 cells, and examination of the cellular uptake using influx transporter-transfected human embryonic kidney (HEK) 293 cells, suggested that the influx transporters OCT1 and OATP1A2, which have been reported to mediate accumulation of imatinib in CML cells, contributed little to the uptake of nilotinib.	imatinib	263-271	solute carrier organic anion transporter family member 1A2	Homo sapiens	202-209
25087954-7	2014	Nilotinib was found to accumulate in imatinib-resistant K562 (K562/IM) cells overexpressing the efflux transporter P-glycoprotein (P-gp), although cytotoxic assays showed that K562/IM cells displayed 20000-fold greater resistance to nilotinib over the parent K562 cells.	imatinib	37-45	ATP binding cassette subfamily B member 1	Homo sapiens	115-129
25087954-7	2014	Nilotinib was found to accumulate in imatinib-resistant K562 (K562/IM) cells overexpressing the efflux transporter P-glycoprotein (P-gp), although cytotoxic assays showed that K562/IM cells displayed 20000-fold greater resistance to nilotinib over the parent K562 cells.	imatinib	37-45	ATP binding cassette subfamily B member 1	Homo sapiens	131-135
24524084-3	2014	Imatinib can reduce TCR-triggered T cell activation by inhibiting the phosphorylation of tyrosine kinases such as Lck, ZAP70, LAT, and PLC gamma 1 early in the TCR signaling pathway.	imatinib	0-8	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	114-117
24280068-0	2014	Imatinib analogs as potential agents for PET imaging of Bcr-Abl and c-KIT expression at a kinase level.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
24280068-0	2014	Imatinib analogs as potential agents for PET imaging of Bcr-Abl and c-KIT expression at a kinase level.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	68-73
24524084-3	2014	Imatinib can reduce TCR-triggered T cell activation by inhibiting the phosphorylation of tyrosine kinases such as Lck, ZAP70, LAT, and PLC gamma 1 early in the TCR signaling pathway.	imatinib	0-8	zeta chain of T cell receptor associated protein kinase 70	Homo sapiens	119-124
24280068-1	2014	We synthesized two series of imatinib mesylate (STI-571) analogs to develop a Bcr-Abl and c-KIT receptor-specific labeling agent for positron emission tomography (PET) imaging to measure Bcr-Abl and c-KIT expression levels in a mouse model.	imatinib	29-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
24280068-1	2014	We synthesized two series of imatinib mesylate (STI-571) analogs to develop a Bcr-Abl and c-KIT receptor-specific labeling agent for positron emission tomography (PET) imaging to measure Bcr-Abl and c-KIT expression levels in a mouse model.	imatinib	29-46	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	90-95
24280068-1	2014	We synthesized two series of imatinib mesylate (STI-571) analogs to develop a Bcr-Abl and c-KIT receptor-specific labeling agent for positron emission tomography (PET) imaging to measure Bcr-Abl and c-KIT expression levels in a mouse model.	imatinib	29-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	187-194
24524084-3	2014	Imatinib can reduce TCR-triggered T cell activation by inhibiting the phosphorylation of tyrosine kinases such as Lck, ZAP70, LAT, and PLC gamma 1 early in the TCR signaling pathway.	imatinib	0-8	linker for activation of T cells	Homo sapiens	126-129
24280068-1	2014	We synthesized two series of imatinib mesylate (STI-571) analogs to develop a Bcr-Abl and c-KIT receptor-specific labeling agent for positron emission tomography (PET) imaging to measure Bcr-Abl and c-KIT expression levels in a mouse model.	imatinib	29-46	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	199-204
24524084-3	2014	Imatinib can reduce TCR-triggered T cell activation by inhibiting the phosphorylation of tyrosine kinases such as Lck, ZAP70, LAT, and PLC gamma 1 early in the TCR signaling pathway.	imatinib	0-8	phospholipase C gamma 1	Homo sapiens	135-146
24524084-7	2014	Pretreatment with SEA prevents the inhibitory effects of imatinib on TCR signaling, which leads to T cell proliferation and IL-2 production.	imatinib	57-65	interleukin 2	Homo sapiens	124-128
24963404-4	2014	Imatinib, an oral targeted therapy, inhibits tyrosine kinases specifically BCR-ABL, c-KIT, and PDGFRA.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
24205792-4	2014	Although sunitinib malate, a multi-kinase inhibitor, has shown effectiveness against imatinib-resistant GISTs, recent studies have indicated that some imatinib-resistant GISTs harboring secondary mutations in the KIT activation loop were also resistant to sunitinib.	imatinib	85-93	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	213-216
24205792-4	2014	Although sunitinib malate, a multi-kinase inhibitor, has shown effectiveness against imatinib-resistant GISTs, recent studies have indicated that some imatinib-resistant GISTs harboring secondary mutations in the KIT activation loop were also resistant to sunitinib.	imatinib	151-159	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	213-216
24963404-4	2014	Imatinib, an oral targeted therapy, inhibits tyrosine kinases specifically BCR-ABL, c-KIT, and PDGFRA.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	84-89
24963404-4	2014	Imatinib, an oral targeted therapy, inhibits tyrosine kinases specifically BCR-ABL, c-KIT, and PDGFRA.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	95-101
25408862-5	2014	Using the technique, we have detected 0.2 nM anti-BSA and 15 muM anti-cancer drug (imatinib) with an enzyme modified surface.	imatinib	83-91	latexin	Homo sapiens	61-64
24963404-5	2014	Apart from its remarkable success in CML and GIST, Imatinib benefits various other tumors caused by Imatinib-specific abnormalities of PDGFR and c-KIT.	imatinib	51-59	platelet derived growth factor receptor beta	Homo sapiens	135-140
25408862-6	2014	The achieved effective charge detection limit is ~0.25 electron charge/mum2, corresponding to ~0.3 fg/mm2 for imatinib, which is orders of magnitude better than traditional label-free optical detection methods.	imatinib	110-118	trafficking protein particle complex subunit 1	Homo sapiens	71-75
24963404-5	2014	Apart from its remarkable success in CML and GIST, Imatinib benefits various other tumors caused by Imatinib-specific abnormalities of PDGFR and c-KIT.	imatinib	51-59	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	145-150
24963404-5	2014	Apart from its remarkable success in CML and GIST, Imatinib benefits various other tumors caused by Imatinib-specific abnormalities of PDGFR and c-KIT.	imatinib	100-108	platelet derived growth factor receptor beta	Homo sapiens	135-140
24963404-5	2014	Apart from its remarkable success in CML and GIST, Imatinib benefits various other tumors caused by Imatinib-specific abnormalities of PDGFR and c-KIT.	imatinib	100-108	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	145-150
24963404-6	2014	Imatinib has also been proven to be effective in steroid-refractory chronic graft-versus-host disease because of its anti-PDGFR action.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	122-127
24322486-7	2014	The treatment of platelet-derived growth factor alpha (PDGFRA)-positive HES with imatinib demonstrated long-lasting efficacy and low likelihood of drug resistance.	imatinib	81-89	platelet derived growth factor receptor alpha	Homo sapiens	55-61
24334603-0	2014	Gambogic acid induces apoptosis in imatinib-resistant chronic myeloid leukemia cells via inducing proteasome inhibition and caspase-dependent Bcr-Abl downregulation.	imatinib	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
24334603-2	2014	Bcr-Abl-T315I is the predominant mutation that causes resistance to imatinib, cytotoxic drugs, and the second-generation tyrosine kinase inhibitors.	imatinib	68-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
24334603-8	2014	RESULTS: Gambogic acid induced apoptosis and cell proliferation inhibition in CML cells and inhibited the growth of imatinib-resistant Bcr-Abl-T315I xenografts in nude mice.	imatinib	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
24334603-10	2014	CONCLUSIONS: These findings suggest an alternative strategy to overcome imatinib resistance by enhancing Bcr-Abl downregulation with the medicinal compound gambogic acid, which may have great clinical significance in imatinib-resistant cancer therapy.	imatinib	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-112
24334603-10	2014	CONCLUSIONS: These findings suggest an alternative strategy to overcome imatinib resistance by enhancing Bcr-Abl downregulation with the medicinal compound gambogic acid, which may have great clinical significance in imatinib-resistant cancer therapy.	imatinib	217-225	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-112
25648025-0	2014	Status of leptin in MBCR-ABL p210 positive chronic myeloid leukemia patients before and after imatinib therapy: a conflicting scenario.	imatinib	94-102	leptin	Homo sapiens	10-16
25648025-3	2014	There are few and conflicting reports about the status of serum leptin levels and recently alteration in leptin has been reported due to imatinib mesylate.	imatinib	137-154	leptin	Homo sapiens	105-111
25648025-15	2014	Imatinib itself may increase leptin levels, and, as leptin plays an active role in the pathophysiology of CML, this conflicting scenario needs further investigation.	imatinib	0-8	leptin	Homo sapiens	29-35
24662099-5	2014	In this study we have characterized the effect of Imatinib, an inhibitor of GSAP, in the 3xTg mice, a mouse model of AD with plaques and tangles.	imatinib	50-58	gamma-secretase activating protein	Mus musculus	76-80
24077846-2	2014	We hypothesized that imatinib plus sequential chemotherapy will result in significant leukemia cell cytoreduction in patients with Philadelphia chromosome positive acute lymphoblastic leukemia, allowing collection of normal hematopoietic stem cells uncontaminated by residual BCR/ABL1(+) lymphoblasts and thus reduce the likelihood of relapse after autologous stem cell transplantation for patients under 60 years of age without sibling donors.	imatinib	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	280-284
25006277-1	2014	The prognosis of patients with chronic myeloid leukemia (CML) has changed radically since the advent of imatinib mesylate, a selective inhibitor of BCR-ABL tyrosine kinase.	imatinib	104-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	148-155
25006280-0	2014	Incidence of BCR-ABL transcript variants in patients with chronic myeloid leukemia: Their correlation with presenting features, risk scores and response to treatment with imatinib mesylate.	imatinib	171-188	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
24293258-4	2014	The patient"s BCR-ABL transcript disappeared after 6 months of treatment with imatinib, while the JAK2V617F mutation remained positive.	imatinib	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
24662099-7	2014	By contrast, Imatinib-treated animals had a significant increase in CTF-beta and a significant reduction in GSAP expression levels.	imatinib	13-21	gamma-secretase activating protein	Mus musculus	108-112
24662099-9	2014	In vitro studies confirmed that Imatinib prevents Abeta formation by modulating gamma-secretase activity and GSAP levels.	imatinib	32-40	amyloid beta (A4) precursor protein	Mus musculus	50-55
24662099-9	2014	In vitro studies confirmed that Imatinib prevents Abeta formation by modulating gamma-secretase activity and GSAP levels.	imatinib	32-40	gamma-secretase activating protein	Mus musculus	109-113
26030751-0	2014	Multiple Copies of BCR/ABL Fusion Signals and t(3;21) in a Chronic Myeloid Leukemia: Patient with Blast Crisis - A Rare Event with Imatinib Mesylate (Gleevec)-Resistance in an Indian Patient.	imatinib	131-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
24635438-0	2014	Significant antitumor effectiveness of imatinib in c- kit negative gastrointestinal stromal tumor -  case report.	imatinib	39-47	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	51-57
26030751-2	2014	The duplication of Ph chromosome is a recurring abnormality acquired during disease progression, whereas intrachromosomal amplification of BCR/ABL is a rare phenomenon and has been associated with imatinib mesylate (IM) therapy resistance.	imatinib	197-214	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-146
23989453-2	2014	Despite their clinical activity in many patients with CML, the BCR-ABL kinase inhibitors (BCR-ABL-KIs) imatinib, dasatinib, and nilotinib provide only transient leukemia reduction in patients with Ph+ ALL.	imatinib	103-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
23989453-2	2014	Despite their clinical activity in many patients with CML, the BCR-ABL kinase inhibitors (BCR-ABL-KIs) imatinib, dasatinib, and nilotinib provide only transient leukemia reduction in patients with Ph+ ALL.	imatinib	103-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
24635438-6	2014	We therefore consider imatinib mesylate an appropriate therapy for c- kit negative GIST bearing PDGFRA mutations.	imatinib	22-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	67-73
24635438-6	2014	We therefore consider imatinib mesylate an appropriate therapy for c- kit negative GIST bearing PDGFRA mutations.	imatinib	22-39	platelet derived growth factor receptor alpha	Homo sapiens	96-102
24190424-5	2014	The cells were exposed to tumor necrosis factor alpha (TNF-alpha), a known inductor of Egr-1, to c-Abl inhibitor STI-571 and to small interfering RNA (siRNA)-Egr-1, respectively.	imatinib	113-120	tumor necrosis factor	Homo sapiens	55-64
24262285-3	2014	Univariate analysis revealed that significant factors associated with not attaining a major molecular response (MMR) were the presence of the minor BCR-ABL1 fusion gene, a low daily dose of TKI, and the emergence of BCR-ABL1 kinase domain mutations conferring resistance to imatinib.	imatinib	274-282	BCR activator of RhoGEF and GTPase	Homo sapiens	216-224
24293093-0	2014	Functional polymorphism of CYP2B6 G15631T is associated with hematologic and cytogenetic response in chronic myeloid leukemia patients treated with imatinib.	imatinib	148-156	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	27-33
24293093-3	2014	The present study aimed to understand the functional impact of CYP2B6 15631G>T polymorphism on the response of imatinib in CML patients and its relation to CML susceptibility.	imatinib	114-122	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	63-69
24384849-5	2014	Treatment with tyrosine kinase inhibitors (TKIs) such as imatinib, sunitinib, and regorafenib is effective in controlling unresectable disease; however, drug resistance caused by secondary KIT or PDGFRA mutations eventually develops in 90% of cases.	imatinib	57-65	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	189-192
24384849-5	2014	Treatment with tyrosine kinase inhibitors (TKIs) such as imatinib, sunitinib, and regorafenib is effective in controlling unresectable disease; however, drug resistance caused by secondary KIT or PDGFRA mutations eventually develops in 90% of cases.	imatinib	57-65	platelet derived growth factor receptor alpha	Homo sapiens	196-202
25150313-0	2014	MiR-200c sensitizes clear-cell renal cell carcinoma cells to sorafenib and imatinib by targeting heme oxygenase-1.	imatinib	75-83	microRNA 200c	Homo sapiens	0-8
25150313-0	2014	MiR-200c sensitizes clear-cell renal cell carcinoma cells to sorafenib and imatinib by targeting heme oxygenase-1.	imatinib	75-83	heme oxygenase 1	Homo sapiens	97-113
25150313-5	2014	We provided evidences to elucidate that miR-200c could sensitize ccRCC cells to sorafenib or imatinib to inhibit cell proliferation, at least partly by targeting HO-1.	imatinib	93-101	microRNA 200c	Homo sapiens	40-48
25150313-5	2014	We provided evidences to elucidate that miR-200c could sensitize ccRCC cells to sorafenib or imatinib to inhibit cell proliferation, at least partly by targeting HO-1.	imatinib	93-101	heme oxygenase 1	Homo sapiens	162-166
25748132-7	2014	Given that potential disease modifying drugs, bosentan and imatinib, reverse the expression and transcriptional activity of Fli1, the studies on the pathological process of double heterozygous mice and the impact of these transcription factors on various cell types may provide a new clue to further understand the pathogenesis of SSc leading to the development of new therapies.	imatinib	59-67	Friend leukemia integration 1	Mus musculus	124-128
25171229-1	2014	BACKGROUND: Imatinib is a tyrosine kinase inhibitor of BCR-ABL, ABL, PDGFR-alpha and -beta, KIT, and DDR.	imatinib	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
24727986-1	2014	In gastrointestinal stromal tumors (GIST), molecularly targeted therapies, starting with imatinib, are directed against an activating mutation of KIT or PDGFRA, which drives the disease.	imatinib	89-97	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	146-149
25171229-1	2014	BACKGROUND: Imatinib is a tyrosine kinase inhibitor of BCR-ABL, ABL, PDGFR-alpha and -beta, KIT, and DDR.	imatinib	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-62
25171229-1	2014	BACKGROUND: Imatinib is a tyrosine kinase inhibitor of BCR-ABL, ABL, PDGFR-alpha and -beta, KIT, and DDR.	imatinib	12-20	platelet derived growth factor receptor alpha	Homo sapiens	69-104
25227759-4	2014	Using an in vitro system, our results indicate that the TKIs gefitinib and imatinib abrogate the ability of ABCG2 to protect cells against ciprofloxacin-induced phototoxicity.	imatinib	75-83	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	108-113
24322003-4	2014	The aim of this study was to investigate the consequences of ABCG2 SNPs for transport and efficacy of TKIs [imatinib, N-desmethyl imatinib (CGP74588), dasatinib, nilotinib, and bosutinib].	imatinib	108-116	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	61-66
24322003-8	2014	It was found that ABCG2 expression provided better protection against CGP74588 than its parent compound, imatinib.	imatinib	105-113	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	18-23
24322003-9	2014	ABCG2 421C>A, 623T>C, 886G>C, and 1574T>G reduced cell membrane expression of ABCG2 and the protective effect of ABCG2 against imatinib, CGP74588, dasatinib, and nilotinib cytotoxicity.	imatinib	139-147	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
24322003-9	2014	ABCG2 421C>A, 623T>C, 886G>C, and 1574T>G reduced cell membrane expression of ABCG2 and the protective effect of ABCG2 against imatinib, CGP74588, dasatinib, and nilotinib cytotoxicity.	imatinib	139-147	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	90-95
24322003-9	2014	ABCG2 421C>A, 623T>C, 886G>C, and 1574T>G reduced cell membrane expression of ABCG2 and the protective effect of ABCG2 against imatinib, CGP74588, dasatinib, and nilotinib cytotoxicity.	imatinib	139-147	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	90-95
24322003-11	2014	Furthermore, the active imatinib metabolite CGP74588 is influenced by ABCG2 expression to a greater extent than the parent compound.	imatinib	24-32	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	70-75
24727986-1	2014	In gastrointestinal stromal tumors (GIST), molecularly targeted therapies, starting with imatinib, are directed against an activating mutation of KIT or PDGFRA, which drives the disease.	imatinib	89-97	platelet derived growth factor receptor alpha	Homo sapiens	153-159
24105694-8	2013	By 12 months, the cumulative molecular response rates (ie, BCR-ABL/abl <= 0.01 [IS: molecular responses graded as molecular response 4 (MR4)]) were 14% and 25%, respectively, for the subgroup treated with imatinib at a dose of 400 mg and the PegIFN90 subgroup.	imatinib	208-216	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
24756783-3	2014	Imatinib is a rationally designed oral signal transduction inhibitor that specifically targets several protein tyrosine kinases, Abl, Arg (Abl-related gene), the stem cell factor receptor (c-KIT), platelet-derived growth factor receptor (PDGF-R), and their oncogenic forms, most notably BCR-ABL.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-132
24756783-3	2014	Imatinib is a rationally designed oral signal transduction inhibitor that specifically targets several protein tyrosine kinases, Abl, Arg (Abl-related gene), the stem cell factor receptor (c-KIT), platelet-derived growth factor receptor (PDGF-R), and their oncogenic forms, most notably BCR-ABL.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-142
24756783-3	2014	Imatinib is a rationally designed oral signal transduction inhibitor that specifically targets several protein tyrosine kinases, Abl, Arg (Abl-related gene), the stem cell factor receptor (c-KIT), platelet-derived growth factor receptor (PDGF-R), and their oncogenic forms, most notably BCR-ABL.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	189-194
24756783-3	2014	Imatinib is a rationally designed oral signal transduction inhibitor that specifically targets several protein tyrosine kinases, Abl, Arg (Abl-related gene), the stem cell factor receptor (c-KIT), platelet-derived growth factor receptor (PDGF-R), and their oncogenic forms, most notably BCR-ABL.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	197-236
24106839-3	2013	Imatinib is notable in that it is highly selective for its kinase target, Abl, over other closely related tyrosine kinases, such as Src.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-77
24106839-3	2013	Imatinib is notable in that it is highly selective for its kinase target, Abl, over other closely related tyrosine kinases, such as Src.	imatinib	0-8	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	132-135
24106839-4	2013	In addition, imatinib is highly sensitive to the phosphorylation state of Abl"s activation loop, which is believed to be a general characteristic of all inhibitors that stabilize a similar inactive ATP-binding site conformation.	imatinib	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-77
24106839-5	2013	In this report, we perform a systematic analysis of a diverse series of ATP-competitive inhibitors that stabilize a similar inactive ATP-binding site conformation as imatinib with the tyrosine kinases Src and Abl.	imatinib	166-174	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	201-204
24106839-5	2013	In this report, we perform a systematic analysis of a diverse series of ATP-competitive inhibitors that stabilize a similar inactive ATP-binding site conformation as imatinib with the tyrosine kinases Src and Abl.	imatinib	166-174	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-212
24132921-0	2013	Large-scale analysis of PDGFRA mutations in melanomas and evaluation of their sensitivity to tyrosine kinase inhibitors imatinib and crenolanib.	imatinib	120-128	platelet derived growth factor receptor alpha	Homo sapiens	24-30
24132921-4	2013	We analyzed the genetic mutations of PDGFRA in Chinese patients with melanoma and determined the inhibitory potency of TKIs, such as imatinib and crenolanib, on mutant PDGFRA.	imatinib	133-141	platelet derived growth factor receptor alpha	Homo sapiens	168-174
24132921-6	2013	Activities of mutations in response to imatinib and crenolanib were analyzed by Western blotting of tyrosine-phosphorylated PDGFRA and cell proliferation assays.	imatinib	39-47	platelet derived growth factor receptor alpha	Homo sapiens	124-130
24132921-11	2013	Crenolanib showed higher potency than imatinib in inhibiting the kinase activity of PDGFRA.	imatinib	38-46	platelet derived growth factor receptor alpha	Homo sapiens	84-90
24756783-3	2014	Imatinib is a rationally designed oral signal transduction inhibitor that specifically targets several protein tyrosine kinases, Abl, Arg (Abl-related gene), the stem cell factor receptor (c-KIT), platelet-derived growth factor receptor (PDGF-R), and their oncogenic forms, most notably BCR-ABL.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	238-244
24756783-3	2014	Imatinib is a rationally designed oral signal transduction inhibitor that specifically targets several protein tyrosine kinases, Abl, Arg (Abl-related gene), the stem cell factor receptor (c-KIT), platelet-derived growth factor receptor (PDGF-R), and their oncogenic forms, most notably BCR-ABL.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	287-294
24756783-8	2014	Clonal evolution, amplification, or overexpression of BCR-ABL as well as mutations in the catalytic domain, P-loop, and other mutations have been demonstrated to play a role in primary and secondary resistance to imatinib, respectively.	imatinib	213-221	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
24756785-4	2014	One such inhibitor, nilotinib, was rationally designed to increase its affinity and specificity for the oncogenic tyrosine kinase Bcr-Abl compared with imatinib and has been shown to be effective after imatinib failure.	imatinib	202-210	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
24367707-2	2013	Use of the pharmacological inhibitor imatinib, which targets the Abl family of non-receptor tyrosine kinases (Abl and Arg), as well as other tyrosine kinases including the platelet-derived growth factor receptor (PDGFR), Kit, colony stimulating factor 1 receptor (CSF1R), and discoidin domain receptors, has shown protective effects in animal models of inflammation, sepsis, and other pathologies characterized by enhanced vascular permeability.	imatinib	37-45	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	65-68
24367707-2	2013	Use of the pharmacological inhibitor imatinib, which targets the Abl family of non-receptor tyrosine kinases (Abl and Arg), as well as other tyrosine kinases including the platelet-derived growth factor receptor (PDGFR), Kit, colony stimulating factor 1 receptor (CSF1R), and discoidin domain receptors, has shown protective effects in animal models of inflammation, sepsis, and other pathologies characterized by enhanced vascular permeability.	imatinib	37-45	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	110-113
24323358-5	2013	In both mice and humans, the KIT oncoprotein inhibitor imatinib polarized TAMs to become M2-like, a process which involved TAM interaction with apoptotic tumor cells leading to the induction of CCAAT/enhancer binding protein (C/EBP) transcription factors.	imatinib	55-63	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	29-32
24132921-14	2013	Our study suggests that patients with melanoma harboring certain PDGFRA mutations may benefit from imatinib and crenolanib treatment.	imatinib	99-107	platelet derived growth factor receptor alpha	Homo sapiens	65-71
24839736-1	2013	BACKGROUND: To assess the response and the impact on the overall survival (OS) on c-KIT-positive (CD117+) gastrointestinal stromal tumours (GISTs) patients treated with imatinib mesylate.	imatinib	169-186	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	82-87
24117365-0	2013	A common novel splice variant of SLC22A1 (OCT1) is associated with impaired responses to imatinib in patients with chronic myeloid leukaemia.	imatinib	89-97	solute carrier family 22 member 1	Homo sapiens	33-40
24117365-0	2013	A common novel splice variant of SLC22A1 (OCT1) is associated with impaired responses to imatinib in patients with chronic myeloid leukaemia.	imatinib	89-97	solute carrier family 22 member 1	Homo sapiens	42-46
24117365-2	2013	Changes in solute carrier family 22 (organic cation transporter), member 1 (SLC22A1, also termed OCT1), the main transporter for imatinib, have been proposed as a possible predictive factor.	imatinib	129-137	solute carrier family 22 member 1	Homo sapiens	76-83
24117365-2	2013	Changes in solute carrier family 22 (organic cation transporter), member 1 (SLC22A1, also termed OCT1), the main transporter for imatinib, have been proposed as a possible predictive factor.	imatinib	129-137	solute carrier family 22 member 1	Homo sapiens	97-101
23575252-1	2013	INTRODUCTION: ABL1 kinase mutations represent a major mechanism of imatinib resistance in Philadelphia-positive (Ph+) patients.	imatinib	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-18
24056763-4	2013	DNA damage promoted the recruitment of MyoD to phosphorylated Nbs1 (pNbs1)-containing repair foci, and this effect was abrogated by either ABL knockdown or the ABL kinase inhibitor imatinib.	imatinib	181-189	myogenic differentiation 1	Homo sapiens	39-43
24056763-4	2013	DNA damage promoted the recruitment of MyoD to phosphorylated Nbs1 (pNbs1)-containing repair foci, and this effect was abrogated by either ABL knockdown or the ABL kinase inhibitor imatinib.	imatinib	181-189	nibrin	Homo sapiens	62-66
24056763-4	2013	DNA damage promoted the recruitment of MyoD to phosphorylated Nbs1 (pNbs1)-containing repair foci, and this effect was abrogated by either ABL knockdown or the ABL kinase inhibitor imatinib.	imatinib	181-189	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-163
24095296-2	2013	Three BCR-ABL inhibitors, imatinib, nilotinib, and dasatinib, have been approved by the US Food and Drug Administration for first-line treatment of patients with newly diagnosed CML in chronic phase (CML-CP).	imatinib	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-13
23716303-7	2013	Inhibition of FYN and FAK phosphorylation each increased tumor cell sensitivity to imatinib.	imatinib	83-91	FYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	14-17
23716303-7	2013	Inhibition of FYN and FAK phosphorylation each increased tumor cell sensitivity to imatinib.	imatinib	83-91	protein tyrosine kinase 2	Homo sapiens	22-25
23942795-5	2013	RESULTS: Dasatinib demonstrates efficacy against most BCR-ABL mutations arising during imatinib therapy and is effective in treating patients with imatinib resistance due to other mechanisms.	imatinib	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
23716303-8	2013	Furthermore, a FAK-selective inhibitor (TAG372) induced apoptosis of imatinib-resistant GIST-T1 cells and decreased the imatinib IC50 .	imatinib	69-77	protein tyrosine kinase 2	Homo sapiens	15-18
23716303-8	2013	Furthermore, a FAK-selective inhibitor (TAG372) induced apoptosis of imatinib-resistant GIST-T1 cells and decreased the imatinib IC50 .	imatinib	120-128	protein tyrosine kinase 2	Homo sapiens	15-18
23716303-9	2013	These results indicate that FYN or FAK might be potential therapeutic targets to overcome resistance to imatinib in GISTs.	imatinib	104-112	FYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	28-31
23716303-9	2013	These results indicate that FYN or FAK might be potential therapeutic targets to overcome resistance to imatinib in GISTs.	imatinib	104-112	protein tyrosine kinase 2	Homo sapiens	35-38
23659595-8	2013	CONCLUSION: Imatinib has a therapeutic role in the presence of an imatinib-sensitive KIT mutation or in KIT816-unmutated patients with aggressive SM.	imatinib	12-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	85-88
23659595-3	2013	Here, the authors report significant symptomatic, cutaneous and systemic response to imatinib in a case of childhood onset indolent D816V KIT unmutated systemic mastocytosis (SM).	imatinib	85-93	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	138-141
23659595-8	2013	CONCLUSION: Imatinib has a therapeutic role in the presence of an imatinib-sensitive KIT mutation or in KIT816-unmutated patients with aggressive SM.	imatinib	66-74	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	85-88
23659595-10	2013	However, the authors have demonstrated the usefulness of imatinib in the treatment of c-KIT-negative indolent SM with extensive cutaneous involvement.	imatinib	57-65	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	86-91
24210993-1	2013	ABCB1/P-glycoprotein (Pgp) and ABCG2/BCRP overexpression have been described as related to imatinib resistance in chronic myeloid leukemia (CML).	imatinib	91-99	phosphoglycolate phosphatase	Homo sapiens	0-20
24369323-0	2013	Correlation of imatinib resistance with the mutational status of KIT and PDGFRA genes in gastrointestinal stromal tumors: a meta-analysis.	imatinib	15-23	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	65-68
24369323-0	2013	Correlation of imatinib resistance with the mutational status of KIT and PDGFRA genes in gastrointestinal stromal tumors: a meta-analysis.	imatinib	15-23	platelet derived growth factor receptor alpha	Homo sapiens	73-79
24369323-3	2013	Our meta-analysis aimed to investigate the association between imatinib resistance and KIT and PDGFRA mutations in GIST.	imatinib	63-71	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	87-90
24369323-3	2013	Our meta-analysis aimed to investigate the association between imatinib resistance and KIT and PDGFRA mutations in GIST.	imatinib	63-71	platelet derived growth factor receptor alpha	Homo sapiens	95-101
24369323-9	2013	Total imatinib resistance was found in 35.5 % of PDGFRA-mutant tumors (OR = 2.9, P = 0.038), 33.7% of wild-type tumors (KIT and PDGFRA non-mutant tumors; OR = 2.8, P = 0.002), and 27.4% of KIT-mutant tumors (OR = 0.3, P = 0.001).	imatinib	6-14	platelet derived growth factor receptor alpha	Homo sapiens	49-55
24369323-9	2013	Total imatinib resistance was found in 35.5 % of PDGFRA-mutant tumors (OR = 2.9, P = 0.038), 33.7% of wild-type tumors (KIT and PDGFRA non-mutant tumors; OR = 2.8, P = 0.002), and 27.4% of KIT-mutant tumors (OR = 0.3, P = 0.001).	imatinib	6-14	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	120-123
24369323-9	2013	Total imatinib resistance was found in 35.5 % of PDGFRA-mutant tumors (OR = 2.9, P = 0.038), 33.7% of wild-type tumors (KIT and PDGFRA non-mutant tumors; OR = 2.8, P = 0.002), and 27.4% of KIT-mutant tumors (OR = 0.3, P = 0.001).	imatinib	6-14	platelet derived growth factor receptor alpha	Homo sapiens	128-134
24369323-9	2013	Total imatinib resistance was found in 35.5 % of PDGFRA-mutant tumors (OR = 2.9, P = 0.038), 33.7% of wild-type tumors (KIT and PDGFRA non-mutant tumors; OR = 2.8, P = 0.002), and 27.4% of KIT-mutant tumors (OR = 0.3, P = 0.001).	imatinib	6-14	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	189-192
24369323-10	2013	Primary imatinib resistance was found in 50.0% of PDGFRA-mutant tumors (OR = 10.9, P = 0.031), 33.4% of wild-type tumors (OR = 5.9, P = 0.060), and 8.9% of KIT-mutant tumors (OR = 0.2, P = 0.025).	imatinib	8-16	platelet derived growth factor receptor alpha	Homo sapiens	50-56
24369323-10	2013	Primary imatinib resistance was found in 50.0% of PDGFRA-mutant tumors (OR = 10.9, P = 0.031), 33.4% of wild-type tumors (OR = 5.9, P = 0.060), and 8.9% of KIT-mutant tumors (OR = 0.2, P = 0.025).	imatinib	8-16	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	156-159
24369323-14	2013	Our meta-analysis indicates that imatinib resistance is closely associated with KIT and PDGFRA genotypes in GIST.	imatinib	33-41	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	80-83
24369323-14	2013	Our meta-analysis indicates that imatinib resistance is closely associated with KIT and PDGFRA genotypes in GIST.	imatinib	33-41	platelet derived growth factor receptor alpha	Homo sapiens	88-94
24369323-15	2013	Thus, the mutational status of KIT and PDGFRA might predict response to imatinib in GIST patients.	imatinib	72-80	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	31-34
24369323-15	2013	Thus, the mutational status of KIT and PDGFRA might predict response to imatinib in GIST patients.	imatinib	72-80	platelet derived growth factor receptor alpha	Homo sapiens	39-45
24176282-0	2013	Enhanced adhesion/migration and induction of Pyk2 expression in K562 cells following imatinib exposure.	imatinib	85-93	protein tyrosine kinase 2 beta	Homo sapiens	45-49
24176282-3	2013	Imatinib induced upregulation of Pyk2 mRNA and protein levels.	imatinib	0-8	protein tyrosine kinase 2 beta	Homo sapiens	33-37
24176282-4	2013	Pyk2 inhibition resulted in a reduction of K562 cells" adhesion and migration subsequent to imatinib treatment.	imatinib	92-100	protein tyrosine kinase 2 beta	Homo sapiens	0-4
24210993-1	2013	ABCB1/P-glycoprotein (Pgp) and ABCG2/BCRP overexpression have been described as related to imatinib resistance in chronic myeloid leukemia (CML).	imatinib	91-99	phosphoglycolate phosphatase	Homo sapiens	22-25
24210993-1	2013	ABCB1/P-glycoprotein (Pgp) and ABCG2/BCRP overexpression have been described as related to imatinib resistance in chronic myeloid leukemia (CML).	imatinib	91-99	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	31-36
24210993-1	2013	ABCB1/P-glycoprotein (Pgp) and ABCG2/BCRP overexpression have been described as related to imatinib resistance in chronic myeloid leukemia (CML).	imatinib	91-99	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	37-41
24210993-3	2013	Imatinib-induced Crkl phosphorylated protein (pCrkl) reduction was more pronounced in K562 (Pgp-negative) than in K562-Lucena (Pgp-positive) CML cell line.	imatinib	0-8	CRK like proto-oncogene, adaptor protein	Homo sapiens	17-21
24210993-3	2013	Imatinib-induced Crkl phosphorylated protein (pCrkl) reduction was more pronounced in K562 (Pgp-negative) than in K562-Lucena (Pgp-positive) CML cell line.	imatinib	0-8	phosphoglycolate phosphatase	Homo sapiens	92-95
24210993-3	2013	Imatinib-induced Crkl phosphorylated protein (pCrkl) reduction was more pronounced in K562 (Pgp-negative) than in K562-Lucena (Pgp-positive) CML cell line.	imatinib	0-8	phosphoglycolate phosphatase	Homo sapiens	127-130
24210993-4	2013	Expressive pCrkl reduction levels after in vitro imatinib treatment was observed in samples from patients exhibiting lower Pgp activity levels compared with patients exhibiting higher Pgp activity levels (p=0.0045).	imatinib	49-57	phosphoglycolate phosphatase	Homo sapiens	123-126
24210993-5	2013	Pgp activity in association with pCrkl reduction levels might help to distinguish between imatinib-resistant and imatinib-sensitive CML cells.	imatinib	90-98	phosphoglycolate phosphatase	Homo sapiens	0-3
24210993-5	2013	Pgp activity in association with pCrkl reduction levels might help to distinguish between imatinib-resistant and imatinib-sensitive CML cells.	imatinib	113-121	phosphoglycolate phosphatase	Homo sapiens	0-3
23883175-8	2013	After 6 years of imatinib, the cumulative probability [95% CI] of reaching a >=4 log reduction of BCR-ABL was 48% [16%; 92%] for patients of the EEC group and 84% [63%; 97%] for patients of the No EEC group.	imatinib	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
24167056-5	2013	Among the differentially expressed proteins, heme oxygenase-1 (HO-1) was found in the sunitinib and imatinib mesylate treatment groups, which possibly acts as a specific target for synthetic lethality in combinational treatment.	imatinib	100-108	heme oxygenase 1	Homo sapiens	45-61
24167056-5	2013	Among the differentially expressed proteins, heme oxygenase-1 (HO-1) was found in the sunitinib and imatinib mesylate treatment groups, which possibly acts as a specific target for synthetic lethality in combinational treatment.	imatinib	100-108	heme oxygenase 1	Homo sapiens	63-67
24012109-2	2013	Despite the great efficacy of the Bcr-Abl-specific inhibitor imatinib, resistance to this drug is recognized as a major problem in CML treatment.	imatinib	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
24012109-3	2013	We found that in LAMA84 cells, characterized by imatinib-resistance caused by BCR-ABL1 gene amplification, the pro-survival protein kinase CK2 is up-regulated as compared to the sensitive cells.	imatinib	48-56	BCR activator of RhoGEF and GTPase	Homo sapiens	78-86
24012109-7	2013	CK2 and Bcr-Abl are members of the same multi-protein complex(es) in imatinib-resistant cells as demonstrated by co-immunoprecipitation and co-sedimentation in glycerol gradients.	imatinib	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-15
24012109-10	2013	Consistently, knockdown of CK2alpha expression by siRNA restores the sensitivity of resistant LAMA84 cells to low imatinib concentrations.	imatinib	114-122	casein kinase 2 alpha 2	Homo sapiens	27-35
24012109-11	2013	Remarkably, the CK2/Bcr-Abl interaction and the sensitization towards imatinib obtained by CK2-inhibition in LAMA84 is observable also in other imatinib-resistant CML cell lines.	imatinib	144-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
24260131-4	2013	Catalytic mTOR inhibition also results in upregulation of SESN3 expression in cells harboring the TKI-insensitive T315I-BCR-ABL mutant, which is resistant to imatinib mesylate.	imatinib	158-175	mechanistic target of rapamycin kinase	Homo sapiens	10-14
24191057-4	2013	Binding of the ATP-site inhibitor imatinib leads to an unexpected open conformation of the multidomain SH3-SH2-kinase c-Abl core, whose relevance is confirmed by cellular assays on Bcr-Abl.	imatinib	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-123
24191057-4	2013	Binding of the ATP-site inhibitor imatinib leads to an unexpected open conformation of the multidomain SH3-SH2-kinase c-Abl core, whose relevance is confirmed by cellular assays on Bcr-Abl.	imatinib	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	181-188
24260231-5	2013	Inhibition of these kinases by their inhibitors, imatinib, sorafenib, or JakI-1, significantly abbreviated Chk1 activation, and drastically enhanced apoptosis induced by etoposide.	imatinib	49-57	checkpoint kinase 1	Homo sapiens	107-111
24260131-4	2013	Catalytic mTOR inhibition also results in upregulation of SESN3 expression in cells harboring the TKI-insensitive T315I-BCR-ABL mutant, which is resistant to imatinib mesylate.	imatinib	158-175	sestrin 3	Homo sapiens	58-63
24236021-2	2013	The inhibitors such as imatinib, dasatinib and nilotinib are effective drugs but are resistant to some BCR-ABL mutations.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
24892939-2	2013	The management of CML was revolutionized more than a decade ago with the introduction of imatinib, a targeted inhibitor of the BCR-ABL protein.	imatinib	89-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
24203930-0	2013	Imatinib therapy in a patient with suspected chronic neutrophilic leukemia and FIP1L1-PDGFRA rearrangement.	imatinib	0-8	factor interacting with PAPOLA and CPSF1	Homo sapiens	79-85
24203930-0	2013	Imatinib therapy in a patient with suspected chronic neutrophilic leukemia and FIP1L1-PDGFRA rearrangement.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	86-92
24223922-12	2013	CONCLUSION: Patients with advanced GIST harboring a KIT exon 11 mutation have the best response rate and long-term survival with imatinib treatment.	imatinib	129-137	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	52-55
24033272-3	2013	BCR-ABL1 negative patients received weekly asparaginase during intensification, while BCR-ABL1+ patients received daily imatinib.	imatinib	120-128	BCR activator of RhoGEF and GTPase	Homo sapiens	86-94
24223824-3	2013	The present study aimed at identifying mutations in the BIM sequence that could lead to imatinib resistance independently of BCR-ABL mutations.	imatinib	88-96	BCL2 like 11	Homo sapiens	56-59
24223824-4	2013	EXPERIMENTAL DESIGN: BIM coding sequence analysis was performed in 72 imatinib-treated CML patients from a French population of our centre and in 29 healthy controls (reference population) as a case-control study.	imatinib	70-78	BCL2 like 11	Homo sapiens	21-24
24223824-12	2013	CONCLUSION: These results suggest that the analysis of the c465C>T SNP of BIM could be useful for predicting the outcome of imatinib-treated CML patients.	imatinib	127-135	BCL2 like 11	Homo sapiens	77-80
23394826-14	2013	In clinical studies using midazolam or anticancer drugs (irinotecan and imatinib) as known CYP3A4 substrates in combination with SJW, decreased plasma levels of these drugs were observed, which was expected as a consequence of CYP3A4 induction.	imatinib	72-80	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	91-97
23394826-14	2013	In clinical studies using midazolam or anticancer drugs (irinotecan and imatinib) as known CYP3A4 substrates in combination with SJW, decreased plasma levels of these drugs were observed, which was expected as a consequence of CYP3A4 induction.	imatinib	72-80	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	227-233
23891770-6	2013	Beyond its direct effect on tumor cells by inhibiting the tyrosine kinase domain of the abl gene, imatinib has been reported to reduce the Bcr-Abl-mediated secretion of the angiogenesis factor VEGF and hence to interfere with angiogenesis.	imatinib	98-106	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	88-91
23891770-6	2013	Beyond its direct effect on tumor cells by inhibiting the tyrosine kinase domain of the abl gene, imatinib has been reported to reduce the Bcr-Abl-mediated secretion of the angiogenesis factor VEGF and hence to interfere with angiogenesis.	imatinib	98-106	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	143-146
23891770-6	2013	Beyond its direct effect on tumor cells by inhibiting the tyrosine kinase domain of the abl gene, imatinib has been reported to reduce the Bcr-Abl-mediated secretion of the angiogenesis factor VEGF and hence to interfere with angiogenesis.	imatinib	98-106	vascular endothelial growth factor A	Mus musculus	193-197
23913859-7	2013	Moreover, using a murine treatment model of bleomycin-induced pulmonary fibrosis we found that inhibition of TGFbeta/PDGF and ErbB pathways with imatinib plus lapatinib, respectively, not only prevented myofibroblast gene expression to a greater extent than either drug alone, but also essentially stabilized gas exchange (oxygen saturation) as an overall measure of lung function.	imatinib	145-153	transforming growth factor, beta 1	Mus musculus	109-116
23913859-7	2013	Moreover, using a murine treatment model of bleomycin-induced pulmonary fibrosis we found that inhibition of TGFbeta/PDGF and ErbB pathways with imatinib plus lapatinib, respectively, not only prevented myofibroblast gene expression to a greater extent than either drug alone, but also essentially stabilized gas exchange (oxygen saturation) as an overall measure of lung function.	imatinib	145-153	epidermal growth factor receptor	Mus musculus	126-130
24129092-1	2013	The development of resistance to imatinib mesylate may partly depend on high bcr-abl expression levels or point mutation(s).	imatinib	33-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
24308033-6	2013	GSI combined with either rCCN3 or imatinib reduced K562 colony formation with enhanced reduction of NOTCH1 signalling observed with combination treatments.	imatinib	34-42	notch receptor 1	Homo sapiens	100-106
23676790-0	2013	Detection of BCR-ABL kinase domain mutations in patients with chronic myeloid leukemia on imatinib.	imatinib	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
23676790-1	2013	BCR-ABL tyrosine kinase domain mutations are the most important factor contributing to imatinib-resistance in patients with chronic myeloid leukemia.	imatinib	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
23676790-5	2013	This report expands the spectrum of BCR-ABL mutations and stresses the use of mutation testing in imatinib-resistant patients for continuation of treatment procedure.	imatinib	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
23775094-1	2013	INTRODUCTION: The discovery of activating KIT and PDGFRalpha mutations in gastrointestinal stromal tumors (GISTs) represented a milestone as it allowed clinicians to use tyrosine kinase inhibitors, like imatinib, to treat this sarcoma.	imatinib	203-211	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	42-45
23775094-1	2013	INTRODUCTION: The discovery of activating KIT and PDGFRalpha mutations in gastrointestinal stromal tumors (GISTs) represented a milestone as it allowed clinicians to use tyrosine kinase inhibitors, like imatinib, to treat this sarcoma.	imatinib	203-211	platelet derived growth factor receptor alpha	Homo sapiens	50-60
23615556-0	2013	Long-term follow-up of treatment with imatinib in eosinophilia-associated myeloid/lymphoid neoplasms with PDGFR rearrangements in blast phase.	imatinib	38-46	platelet derived growth factor receptor beta	Homo sapiens	106-111
24125838-0	2013	CUEDC2 sensitizes chronic myeloid leukemic cells to imatinib treatment.	imatinib	52-60	CUE domain containing 2	Homo sapiens	0-6
23972517-3	2013	The results showed that Wnt5a augmented the effects of Imatinib Mesylate on inhibiting CML cells proliferation and inducing apoptosis in vitro; Wnt5a enhanced the inhibition effect of Imatinib Mesylate on the growth of K562 cells xenograft tumour in an animal model.	imatinib	55-72	Wnt family member 5A	Homo sapiens	24-29
23972517-0	2013	Wnt5a enhances the response of CML cells to Imatinib Mesylate through JNK activation and gamma-catenin inhibition.	imatinib	44-61	Wnt family member 5A	Homo sapiens	0-5
23972517-3	2013	The results showed that Wnt5a augmented the effects of Imatinib Mesylate on inhibiting CML cells proliferation and inducing apoptosis in vitro; Wnt5a enhanced the inhibition effect of Imatinib Mesylate on the growth of K562 cells xenograft tumour in an animal model.	imatinib	184-201	Wnt family member 5A	Homo sapiens	144-149
23972517-5	2013	When inhibiting the activity of JNK, the influence of Wnt5a on the effects of Imatinib Mesylate was attenuated.	imatinib	78-95	mitogen-activated protein kinase 8	Homo sapiens	32-35
24125838-4	2013	Knockdown of CUEDC2 in K562 cells resulted in decreased cell apoptosis after imatinib treatment; when CUEDC2 was overexpressed in K562/G01 cells, imatinib induced more cell apoptosis.	imatinib	77-85	CUE domain containing 2	Homo sapiens	13-19
24125838-4	2013	Knockdown of CUEDC2 in K562 cells resulted in decreased cell apoptosis after imatinib treatment; when CUEDC2 was overexpressed in K562/G01 cells, imatinib induced more cell apoptosis.	imatinib	146-154	CUE domain containing 2	Homo sapiens	13-19
24125838-4	2013	Knockdown of CUEDC2 in K562 cells resulted in decreased cell apoptosis after imatinib treatment; when CUEDC2 was overexpressed in K562/G01 cells, imatinib induced more cell apoptosis.	imatinib	146-154	CUE domain containing 2	Homo sapiens	102-108
24125838-6	2013	Our data suggested that the expression level of CUEDC2 has an inverse correlation with imatinib resistance and activity of NF-kappaB signaling pathway in CML cells, CUEDC2 could regulate imatinib sensitivity in CML cells at least partially through NF-kappaB signaling pathway.	imatinib	87-95	CUE domain containing 2	Homo sapiens	48-54
23972517-5	2013	When inhibiting the activity of JNK, the influence of Wnt5a on the effects of Imatinib Mesylate was attenuated.	imatinib	78-95	Wnt family member 5A	Homo sapiens	54-59
23972517-0	2013	Wnt5a enhances the response of CML cells to Imatinib Mesylate through JNK activation and gamma-catenin inhibition.	imatinib	44-61	mitogen-activated protein kinase 8	Homo sapiens	70-73
23972517-6	2013	Moreover, JNK suppressed beta-catenin and its target gene Survivin, and enhanced the effects of Imatinib Mesylate.	imatinib	96-113	mitogen-activated protein kinase 8	Homo sapiens	10-13
23972517-7	2013	These results suggest that Wnt5a can enhance the efficacy of Imatinib Mesylate through JNK/beta-catenin/Survivin and gamma-catenin/beta-catenin/Survivin pathways.	imatinib	61-78	Wnt family member 5A	Homo sapiens	27-32
24125838-6	2013	Our data suggested that the expression level of CUEDC2 has an inverse correlation with imatinib resistance and activity of NF-kappaB signaling pathway in CML cells, CUEDC2 could regulate imatinib sensitivity in CML cells at least partially through NF-kappaB signaling pathway.	imatinib	87-95	nuclear factor kappa B subunit 1	Homo sapiens	248-257
24125838-6	2013	Our data suggested that the expression level of CUEDC2 has an inverse correlation with imatinib resistance and activity of NF-kappaB signaling pathway in CML cells, CUEDC2 could regulate imatinib sensitivity in CML cells at least partially through NF-kappaB signaling pathway.	imatinib	187-195	CUE domain containing 2	Homo sapiens	48-54
24125838-6	2013	Our data suggested that the expression level of CUEDC2 has an inverse correlation with imatinib resistance and activity of NF-kappaB signaling pathway in CML cells, CUEDC2 could regulate imatinib sensitivity in CML cells at least partially through NF-kappaB signaling pathway.	imatinib	187-195	nuclear factor kappa B subunit 1	Homo sapiens	123-132
24125838-6	2013	Our data suggested that the expression level of CUEDC2 has an inverse correlation with imatinib resistance and activity of NF-kappaB signaling pathway in CML cells, CUEDC2 could regulate imatinib sensitivity in CML cells at least partially through NF-kappaB signaling pathway.	imatinib	187-195	CUE domain containing 2	Homo sapiens	165-171
24125838-6	2013	Our data suggested that the expression level of CUEDC2 has an inverse correlation with imatinib resistance and activity of NF-kappaB signaling pathway in CML cells, CUEDC2 could regulate imatinib sensitivity in CML cells at least partially through NF-kappaB signaling pathway.	imatinib	187-195	nuclear factor kappa B subunit 1	Homo sapiens	248-257
23972517-7	2013	These results suggest that Wnt5a can enhance the efficacy of Imatinib Mesylate through JNK/beta-catenin/Survivin and gamma-catenin/beta-catenin/Survivin pathways.	imatinib	61-78	mitogen-activated protein kinase 8	Homo sapiens	87-90
23972517-7	2013	These results suggest that Wnt5a can enhance the efficacy of Imatinib Mesylate through JNK/beta-catenin/Survivin and gamma-catenin/beta-catenin/Survivin pathways.	imatinib	61-78	catenin beta 1	Homo sapiens	91-103
23972517-7	2013	These results suggest that Wnt5a can enhance the efficacy of Imatinib Mesylate through JNK/beta-catenin/Survivin and gamma-catenin/beta-catenin/Survivin pathways.	imatinib	61-78	catenin beta 1	Homo sapiens	131-143
23972517-2	2013	The research is aimed at determining whether Wnt5a affects the effects of Imatinib Mesylate against BCR-ABL positive CML cells (K562 cells and KU812 cells) and which signalling proteins are involved in.	imatinib	74-91	Wnt family member 5A	Homo sapiens	45-50
23972517-2	2013	The research is aimed at determining whether Wnt5a affects the effects of Imatinib Mesylate against BCR-ABL positive CML cells (K562 cells and KU812 cells) and which signalling proteins are involved in.	imatinib	74-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
24196611-7	2013	A phosphorylated isoform of Abi1 that stains positively in these microcompartments disappears after treatment with the tyrosine kinase inhibitor STI571 (Glivec ).	imatinib	145-151	abl interactor 1	Homo sapiens	28-32
23877223-7	2013	The activation antigen CD69 was reduced in the MDR cell line and treatment with imatinib further decreased the expressed levels.	imatinib	80-88	CD69 molecule	Homo sapiens	23-27
23702733-6	2013	Moreover, in in vitro experiments, KIT mutants with concurrent KRAS mutation showed resistance to imatinib, a receptor tyrosine kinase inhibitor used in GIST treatment.	imatinib	98-106	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	35-38
23702733-6	2013	Moreover, in in vitro experiments, KIT mutants with concurrent KRAS mutation showed resistance to imatinib, a receptor tyrosine kinase inhibitor used in GIST treatment.	imatinib	98-106	KRAS proto-oncogene, GTPase	Homo sapiens	63-67
24196611-10	2013	As phosphorylation of Abi1 could be pharmaceutically targeted with STI571, this indicates a possible therapeutic option to prevent the gain of a metastatic phenotype in colorectal cancer.	imatinib	67-73	abl interactor 1	Homo sapiens	22-26
24146755-6	2013	We can inhibit these events and promote the survival of DSS-treated Rassf1a knockout mice with intraperitoneal injection of the c-Abl and c-Abl related protein tyrosine kinase inhibitor, imatinib/gleevec.	imatinib	187-195	Ras association (RalGDS/AF-6) domain family member 1	Mus musculus	68-75
23994742-11	2013	In addition, platelet-derived growth factor-beta receptor (PDGF-betaR) blocker imatinib reduced p38 phosphorylation and also mimicked the pro-apoptotic effect of SSD in LO2 cells.	imatinib	79-87	mitogen-activated protein kinase 14	Homo sapiens	96-99
24101380-5	2013	Combined Irf8 deletion and constitutive beta-catenin activation result in progression of CML into fatal blast crisis, elevated leukemic potential of BCR-ABL-induced LICs, and Imatinib resistance.	imatinib	175-183	interferon regulatory factor 8	Mus musculus	9-13
24101380-5	2013	Combined Irf8 deletion and constitutive beta-catenin activation result in progression of CML into fatal blast crisis, elevated leukemic potential of BCR-ABL-induced LICs, and Imatinib resistance.	imatinib	175-183	catenin (cadherin associated protein), beta 1	Mus musculus	40-52
24146755-6	2013	We can inhibit these events and promote the survival of DSS-treated Rassf1a knockout mice with intraperitoneal injection of the c-Abl and c-Abl related protein tyrosine kinase inhibitor, imatinib/gleevec.	imatinib	187-195	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	128-133
24146755-6	2013	We can inhibit these events and promote the survival of DSS-treated Rassf1a knockout mice with intraperitoneal injection of the c-Abl and c-Abl related protein tyrosine kinase inhibitor, imatinib/gleevec.	imatinib	187-195	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	138-143
24155950-8	2013	These results open novel possibilities for the treatment of Bcr-Abl-positive leukemias, especially in the imatinib, dasatinib and nilotinib-resistant CML cases.	imatinib	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
24119229-0	2013	Tyrosine kinases inhibition by Imatinib slows progression in chronic anti-thy1 glomerulosclerosis of the rat.	imatinib	31-39	Thy-1 cell surface antigen	Rattus norvegicus	74-78
24119229-9	2013	Imatinib administration was paralled by significant reductions in tubulointerstitial accumulation of matrix proteins (-44%), collagen I deposition (-86%), expression of TGF-beta1 (-30%), production of fibronectin (-23%), myofibroblast differentiation (-87%), macrophage infiltration (-36%) and cell proliferation (-45%), respectively.	imatinib	0-8	transforming growth factor, beta 1	Rattus norvegicus	169-178
24124608-0	2013	GSTT1 copy number gain and ZNF overexpression are predictors of poor response to imatinib in gastrointestinal stromal tumors.	imatinib	81-89	glutathione S-transferase theta 1	Homo sapiens	0-5
24119229-9	2013	Imatinib administration was paralled by significant reductions in tubulointerstitial accumulation of matrix proteins (-44%), collagen I deposition (-86%), expression of TGF-beta1 (-30%), production of fibronectin (-23%), myofibroblast differentiation (-87%), macrophage infiltration (-36%) and cell proliferation (-45%), respectively.	imatinib	0-8	fibronectin 1	Rattus norvegicus	201-212
24119229-12	2013	CONCLUSIONS: Therapy with Imatinib limits the progressive course of chronic anti-thy1 glomerulosclerosis towards tubulointerstitial fibrosis and renal insufficiency.	imatinib	26-34	Thy-1 cell surface antigen	Rattus norvegicus	81-85
24112389-11	2013	However, treatment with imatinib and GNF-5 inhibited the ovalbumin-induced increase in IL-13 and CCL2 as well as airway resistance and smooth muscle growth in animals.	imatinib	24-32	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	57-66
24112389-11	2013	However, treatment with imatinib and GNF-5 inhibited the ovalbumin-induced increase in IL-13 and CCL2 as well as airway resistance and smooth muscle growth in animals.	imatinib	24-32	interleukin 13	Mus musculus	87-92
24112389-11	2013	However, treatment with imatinib and GNF-5 inhibited the ovalbumin-induced increase in IL-13 and CCL2 as well as airway resistance and smooth muscle growth in animals.	imatinib	24-32	chemokine (C-C motif) ligand 2	Mus musculus	97-101
24147007-10	2013	Instead, persistent treatment for several days with imatinib, an ABL kinase inhibitor, was required to cause the enhanced and the CQ-insensitive apoptotic response to TRAIL.	imatinib	52-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-68
24147007-10	2013	Instead, persistent treatment for several days with imatinib, an ABL kinase inhibitor, was required to cause the enhanced and the CQ-insensitive apoptotic response to TRAIL.	imatinib	52-60	TNF superfamily member 10	Homo sapiens	167-172
24729782-6	2013	The Src kinase inhibitor PP2 was active only in cells grown on ripples, while the Abl inhibitors dasatinib and imatinib suppressed beta-catenin translocation on both structures.	imatinib	111-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-85
24729782-6	2013	The Src kinase inhibitor PP2 was active only in cells grown on ripples, while the Abl inhibitors dasatinib and imatinib suppressed beta-catenin translocation on both structures.	imatinib	111-119	catenin beta 1	Homo sapiens	131-143
24124608-0	2013	GSTT1 copy number gain and ZNF overexpression are predictors of poor response to imatinib in gastrointestinal stromal tumors.	imatinib	81-89	zinc finger protein 763	Homo sapiens	27-30
24124608-3	2013	We performed an association study between copy number alterations (CNAs) identified from array CGH and gene expression analyses results for four wild-type GISTs and an imatinib-resistant PDGFRA D842V mutant GIST, and compared the results to those obtained from 27 GISTs with KIT mutations.	imatinib	168-176	platelet derived growth factor receptor alpha	Homo sapiens	187-193
24124608-7	2013	Surprisingly, all four malignant GISTs with KIT exon 11 deletion mutations with primary resistance to imatinib had an increased GSTT1 CN and mRNA expression level of GSTT1.	imatinib	102-110	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	44-47
24124608-7	2013	Surprisingly, all four malignant GISTs with KIT exon 11 deletion mutations with primary resistance to imatinib had an increased GSTT1 CN and mRNA expression level of GSTT1.	imatinib	102-110	glutathione S-transferase theta 1	Homo sapiens	128-133
24124608-7	2013	Surprisingly, all four malignant GISTs with KIT exon 11 deletion mutations with primary resistance to imatinib had an increased GSTT1 CN and mRNA expression level of GSTT1.	imatinib	102-110	glutathione S-transferase theta 1	Homo sapiens	166-171
24124608-8	2013	Increased mRNA expression of GSTT1 and ZNF could be predictors of a poor response to imatinib.	imatinib	85-93	glutathione S-transferase theta 1	Homo sapiens	29-34
24124608-8	2013	Increased mRNA expression of GSTT1 and ZNF could be predictors of a poor response to imatinib.	imatinib	85-93	zinc finger protein 763	Homo sapiens	39-42
24124608-9	2013	Our integrative approach reveals that for patients with wild-type (or imatinib-resistant) GISTs, attempts to target VEGFRs and IGF1R may be reasonable options.	imatinib	70-78	insulin like growth factor 1 receptor	Homo sapiens	127-132
23892407-6	2013	c-Abl was inhibited with Imatinib or by overexpressing a dominant negative form of c-Abl (K290R).	imatinib	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
23489324-5	2013	Imatinib mesylate (imatinib) is the first-line therapy for patients with abnormalities of PDGFRA/B, whereas patients with FGFR1 fusions are resistant to this therapy and carry a poor prognosis.	imatinib	0-17	platelet derived growth factor receptor alpha	Homo sapiens	90-96
23489324-5	2013	Imatinib mesylate (imatinib) is the first-line therapy for patients with abnormalities of PDGFRA/B, whereas patients with FGFR1 fusions are resistant to this therapy and carry a poor prognosis.	imatinib	19-27	platelet derived growth factor receptor alpha	Homo sapiens	90-96
23918469-4	2013	We found that the novel variants, E184K, D185N, T259P, and D288N, were associated with impaired estrone-3-sulfate, imatinib, and methotrexate transport (~20-50% of wild-type control); function was retained by OATP1A2-V255I.	imatinib	115-123	solute carrier organic anion transporter family member 1A2	Homo sapiens	209-216
23755839-9	2013	Of the 19 R0-resected young adult patients, one patient with small intestinal GIST harboring KIT exon 11 deletion mutation developed recurrence and showed partial responses for imatinib.	imatinib	177-185	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	93-96
23892407-12	2013	In DOX-resistant cells, Imatinib treatment reduced IkappaBalpha tyrosine phosphorylation and NF-kappaB activity.	imatinib	24-32	NFKB inhibitor alpha	Homo sapiens	51-63
23892407-12	2013	In DOX-resistant cells, Imatinib treatment reduced IkappaBalpha tyrosine phosphorylation and NF-kappaB activity.	imatinib	24-32	nuclear factor kappa B subunit 1	Homo sapiens	93-102
24457249-0	2013	A new KIT gene mutation in thymic cancer and a promising response to imatinib.	imatinib	69-77	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	6-9
24245631-3	2013	Both models describe the competition of leukemic and normal cells, however Model 1 also describes the dynamics of BCR-ABL, the oncogene targeted by imatinib, at the sub-cellular level.	imatinib	148-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
23891189-0	2013	XIAP and P-glycoprotein co-expression is related to imatinib resistance in chronic myeloid leukemia cells.	imatinib	52-60	X-linked inhibitor of apoptosis	Homo sapiens	0-4
23891189-0	2013	XIAP and P-glycoprotein co-expression is related to imatinib resistance in chronic myeloid leukemia cells.	imatinib	52-60	ATP binding cassette subfamily B member 1	Homo sapiens	9-23
23891189-4	2013	Imatinib increased XIAP and Pgp expression in K562-Lucena cells, while in K562 cells a downregulation of these proteins was observed, suggesting that imatinib induces an increment of MDR phenotype of CML cells that previously exhibit high levels of Pgp/XIAP co-expression.	imatinib	0-8	X-linked inhibitor of apoptosis	Homo sapiens	19-23
23891189-4	2013	Imatinib increased XIAP and Pgp expression in K562-Lucena cells, while in K562 cells a downregulation of these proteins was observed, suggesting that imatinib induces an increment of MDR phenotype of CML cells that previously exhibit high levels of Pgp/XIAP co-expression.	imatinib	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	28-31
23891189-4	2013	Imatinib increased XIAP and Pgp expression in K562-Lucena cells, while in K562 cells a downregulation of these proteins was observed, suggesting that imatinib induces an increment of MDR phenotype of CML cells that previously exhibit high levels of Pgp/XIAP co-expression.	imatinib	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	249-252
23891189-4	2013	Imatinib increased XIAP and Pgp expression in K562-Lucena cells, while in K562 cells a downregulation of these proteins was observed, suggesting that imatinib induces an increment of MDR phenotype of CML cells that previously exhibit high levels of Pgp/XIAP co-expression.	imatinib	0-8	X-linked inhibitor of apoptosis	Homo sapiens	253-257
23891189-4	2013	Imatinib increased XIAP and Pgp expression in K562-Lucena cells, while in K562 cells a downregulation of these proteins was observed, suggesting that imatinib induces an increment of MDR phenotype of CML cells that previously exhibit high levels of Pgp/XIAP co-expression.	imatinib	150-158	ATP binding cassette subfamily B member 1	Homo sapiens	249-252
23891189-4	2013	Imatinib increased XIAP and Pgp expression in K562-Lucena cells, while in K562 cells a downregulation of these proteins was observed, suggesting that imatinib induces an increment of MDR phenotype of CML cells that previously exhibit high levels of Pgp/XIAP co-expression.	imatinib	150-158	X-linked inhibitor of apoptosis	Homo sapiens	253-257
23953880-0	2013	Imatinib induces demethylation of miR-203 gene: an epigenetic mechanism of anti-tumor effect of imatinib.	imatinib	0-8	microRNA 203a	Homo sapiens	34-41
23953880-0	2013	Imatinib induces demethylation of miR-203 gene: an epigenetic mechanism of anti-tumor effect of imatinib.	imatinib	96-104	microRNA 203a	Homo sapiens	34-41
23953880-5	2013	Imatinib induced the demethylation of the miR-203 promoter region, resulting in low expression of targeted BCR-ABL1 gene, and loss of proliferation of leukemic cells.	imatinib	0-8	microRNA 203a	Homo sapiens	42-49
23953880-5	2013	Imatinib induced the demethylation of the miR-203 promoter region, resulting in low expression of targeted BCR-ABL1 gene, and loss of proliferation of leukemic cells.	imatinib	0-8	BCR activator of RhoGEF and GTPase	Homo sapiens	107-115
23953880-6	2013	In conclusion, demethylation of miR-203 is one of the molecular mechanisms of imatinib-induced inhibition of BCR-ABL1-positive leukemic cells.	imatinib	78-86	microRNA 203a	Homo sapiens	32-39
23953880-6	2013	In conclusion, demethylation of miR-203 is one of the molecular mechanisms of imatinib-induced inhibition of BCR-ABL1-positive leukemic cells.	imatinib	78-86	BCR activator of RhoGEF and GTPase	Homo sapiens	109-117
23816609-1	2013	Dasatinib is a second-generation BCR-ABL inhibitor approved for the treatment of patients with chronic myeloid leukemia, both in the frontline and in the imatinib-resistant/intolerant settings.	imatinib	154-162	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
23146907-6	2013	Impairment of Abl expression or Abl kinase activity with imatinib mesylate enhanced HNSCC matrix degradation and 3D collagen invasion, functions that were impaired in MDA-MB-231.	imatinib	57-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-35
24123600-0	2013	High imatinib dose overcomes insufficient response associated with ABCG2 haplotype in chronic myelogenous leukemia patients.	imatinib	5-13	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	67-72
23146907-9	2013	Imatinib-treated HNSCC cells had increased EGFR, Erk1/2 and Src activation, enhancing cortactin pY421 and pS405/418 required for invadopodia function.	imatinib	0-8	epidermal growth factor receptor	Homo sapiens	43-47
24123600-9	2013	Lower response rates associated with "non- favorable" ABCG2 haplotypes may be overcome by increasing the imatinib daily dose up to 600 mg/d.	imatinib	105-113	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	54-59
23146907-10	2013	Imatinib stimulated shedding of the EGFR ligand heparin-binding EGF-like growth factor (HB-EGF) from HNSCC cells, where soluble HB-EGF enhanced invadopodia ECM degradation in HNSCC but not in MDA-MB-231.	imatinib	0-8	heparin binding EGF like growth factor	Homo sapiens	88-94
23146907-10	2013	Imatinib stimulated shedding of the EGFR ligand heparin-binding EGF-like growth factor (HB-EGF) from HNSCC cells, where soluble HB-EGF enhanced invadopodia ECM degradation in HNSCC but not in MDA-MB-231.	imatinib	0-8	heparin binding EGF like growth factor	Homo sapiens	128-134
23146907-9	2013	Imatinib-treated HNSCC cells had increased EGFR, Erk1/2 and Src activation, enhancing cortactin pY421 and pS405/418 required for invadopodia function.	imatinib	0-8	mitogen-activated protein kinase 3	Homo sapiens	49-55
23146907-9	2013	Imatinib-treated HNSCC cells had increased EGFR, Erk1/2 and Src activation, enhancing cortactin pY421 and pS405/418 required for invadopodia function.	imatinib	0-8	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	60-63
23146907-9	2013	Imatinib-treated HNSCC cells had increased EGFR, Erk1/2 and Src activation, enhancing cortactin pY421 and pS405/418 required for invadopodia function.	imatinib	0-8	cortactin	Homo sapiens	86-95
23146907-10	2013	Imatinib stimulated shedding of the EGFR ligand heparin-binding EGF-like growth factor (HB-EGF) from HNSCC cells, where soluble HB-EGF enhanced invadopodia ECM degradation in HNSCC but not in MDA-MB-231.	imatinib	0-8	epidermal growth factor receptor	Homo sapiens	36-40
23146907-10	2013	Imatinib stimulated shedding of the EGFR ligand heparin-binding EGF-like growth factor (HB-EGF) from HNSCC cells, where soluble HB-EGF enhanced invadopodia ECM degradation in HNSCC but not in MDA-MB-231.	imatinib	0-8	heparin binding EGF like growth factor	Homo sapiens	48-86
23887971-2	2013	On the basis of its involvement in CML pathogenesis, we hypothesized that KIT may govern responses of CML cells to imatinib.	imatinib	115-123	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	74-77
23820134-0	2013	Imatinib-associated tumour response in a dog with a non-resectable gastrointestinal stromal tumour harbouring a c-kit exon 11 deletion mutation.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	112-117
23820134-5	2013	The c-kit mutation found in the tumour cells appears to be a mutation driving oncogenesis, as evidenced by the partial remission elicited by imatinib in this dog.	imatinib	141-149	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	4-9
24098519-7	2013	Interestingly, RhoA activity was observed to affect cell survival in the presence of imatinib through the SAPK/JNK pathway.	imatinib	85-93	ras homolog family member A	Homo sapiens	15-19
24052062-4	2013	Imatinib, a TKI with targets that include the breakpoint cluster region-Abelson (bcr-abl) fusion protein kinase and mast/stem cell growth factor receptor kinase (c-Kit), was the first clinically successful drug of this type and revolutionized the treatment and prognosis of chronic myeloid leukemia and gastrointestinal stromal tumors.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	162-167
23975171-2	2013	They have represented a paradigm of molecular-targeted therapies for solid tumors since the discovery of KIT mutations and KIT expression in GIST in 1998, which opened the way to the use of imatinib, a tyrosine kinase inhibitor able to inhibit the growth of cells expressing KIT-mutant isoforms.	imatinib	190-198	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	105-108
23975171-2	2013	They have represented a paradigm of molecular-targeted therapies for solid tumors since the discovery of KIT mutations and KIT expression in GIST in 1998, which opened the way to the use of imatinib, a tyrosine kinase inhibitor able to inhibit the growth of cells expressing KIT-mutant isoforms.	imatinib	190-198	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	123-126
23975171-2	2013	They have represented a paradigm of molecular-targeted therapies for solid tumors since the discovery of KIT mutations and KIT expression in GIST in 1998, which opened the way to the use of imatinib, a tyrosine kinase inhibitor able to inhibit the growth of cells expressing KIT-mutant isoforms.	imatinib	190-198	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	123-126
24053143-6	2013	In addition, we confirm the association of the ETV6-ABL1 fusion with imatinib resistance reported so far in three other patients, while recording excellent response to the 2nd generation tyrosine kinase inhibitor (TKI) nilotinib.	imatinib	69-77	ETS variant transcription factor 6	Homo sapiens	47-51
24053143-6	2013	In addition, we confirm the association of the ETV6-ABL1 fusion with imatinib resistance reported so far in three other patients, while recording excellent response to the 2nd generation tyrosine kinase inhibitor (TKI) nilotinib.	imatinib	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-56
24053143-7	2013	In summary, we highlight the value of ETV6 FISH as a diagnostic test and the therapy resistance of ETV6-ABL1 positive disorders to imatinib.	imatinib	131-139	ETS variant transcription factor 6	Homo sapiens	99-103
24053143-7	2013	In summary, we highlight the value of ETV6 FISH as a diagnostic test and the therapy resistance of ETV6-ABL1 positive disorders to imatinib.	imatinib	131-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-108
23860199-4	2013	The KIT protooncogene or, less frequently, platelet-derived growth factor receptor alpha is mutated in GIST; the gene products of both are inhibited by imatinib mesylate.	imatinib	152-169	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	4-7
24004697-0	2013	Proliferation inhibition and apoptosis induction of imatinib-resistant chronic myeloid leukemia cells via PPP2R5C down-regulation.	imatinib	52-60	protein phosphatase 2 regulatory subunit B'gamma	Homo sapiens	106-113
24004697-1	2013	Despite the success of imatinib and other tyrosine kinase inhibitors (TKIs), chronic myeloid leukemia (CML) remains largely incurable, and a number of CML patients die due to Abl mutation-related drug resistance and blast crisis.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-178
24004697-11	2013	In conclusion, the suppression of PPP2R5C by RNA interference could inhibit proliferation and effectively induce apoptosis in CML cells that were either imatinib sensitive or resistant.	imatinib	153-161	protein phosphatase 2 regulatory subunit B'gamma	Homo sapiens	34-41
24004697-12	2013	Down-regulating PPP2R5C gene expression might be considered as a new therapeutic target strategy for CML, particularly for imatinib-resistant CML.	imatinib	123-131	protein phosphatase 2 regulatory subunit B'gamma	Homo sapiens	16-23
23760739-2	2013	The greatest difference between the CCI curves at 5 years after initiating imatinib therapy was observed for the BCR-ABL1 transcripts at 3 months.	imatinib	75-83	BCR activator of RhoGEF and GTPase	Homo sapiens	113-121
23760739-4	2013	Therefore, the examination of BCR-ABL1 transcripts at 3 months may help in early identification of patients who are likely to perform poorly with imatinib.	imatinib	146-154	BCR activator of RhoGEF and GTPase	Homo sapiens	30-38
23613107-5	2013	Of interest, the oncogenic Bcr/Abl fusion protein but not its mRNA levels were quickly reduced upon alantolactone exposure in imatinib-sensitive and -resistant K562 cells.	imatinib	126-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
23775718-4	2013	Mast cell inhibition with imatinib ameliorated cytokine release from skin biopsies and led to a correlative decrease in granulocyte-macrophage colony-stimulating factor and white blood cells in transgenic sickle mice.	imatinib	26-34	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	120-168
23775962-0	2013	Imatinib for melanomas harboring mutationally activated or amplified KIT arising on mucosal, acral, and chronically sun-damaged skin.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	69-72
23775962-2	2013	PATIENTS AND METHODS: We conducted a multicenter phase II trial of imatinib in metastatic mucosal, acral, or chronically sun-damaged (CSD) melanoma with KIT amplifications and/or mutations.	imatinib	67-75	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	153-156
23775962-15	2013	Imatinib can be effective when tumors harbor KIT mutations, but not if KIT is amplified only.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	45-48
23775962-16	2013	NRAS mutations and KIT copy number gain may be mechanisms of therapeutic resistance to imatinib.	imatinib	87-95	NRAS proto-oncogene, GTPase	Homo sapiens	0-4
23775962-16	2013	NRAS mutations and KIT copy number gain may be mechanisms of therapeutic resistance to imatinib.	imatinib	87-95	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	19-22
24007855-1	2013	We present a case of a 42-year old female with the rare diagnosis of a myeloproliferative syndrome harboring both a BCR-ABL transclocation and a JAK2V617F mutation.Initially diagnosed with a CML, the patient underwent treatment with imatinib followed by dasatinib.	imatinib	233-241	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
23860199-4	2013	The KIT protooncogene or, less frequently, platelet-derived growth factor receptor alpha is mutated in GIST; the gene products of both are inhibited by imatinib mesylate.	imatinib	152-169	platelet derived growth factor receptor alpha	Homo sapiens	43-88
23707389-8	2013	CBY-driven cytoplasmic accumulation of beta catenin is also a component of BCR-ABL1+ cell response to the TK inhibitor Imatinib (IM).	imatinib	119-127	catenin beta 1	Homo sapiens	39-51
23707389-8	2013	CBY-driven cytoplasmic accumulation of beta catenin is also a component of BCR-ABL1+ cell response to the TK inhibitor Imatinib (IM).	imatinib	119-127	BCR activator of RhoGEF and GTPase	Homo sapiens	75-83
23906052-2	2013	These studies have led to the rapid development of many BCR-ABL specific tyrosine kinase inhibitors (TKIs), such as Imatinib, Nilotinib and Dasatinib, which have improved 10-years survival to more than 80%.	imatinib	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
23657159-1	2013	Cytochrome P450 (CYP) 3A4 is considered the most important enzyme in imatinib biotransformation.	imatinib	69-77	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-25
23657159-2	2013	In a randomized, crossover study, 10 healthy subjects were administered gemfibrozil 600 mg or placebo twice daily for 6 days, and imatinib 200 mg on day 3, to study the significance of CYP2C8 in imatinib pharmacokinetics.	imatinib	195-203	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	185-191
23657159-6	2013	Our findings indicate significant participation of CYP2C8 in the metabolism of imatinib in humans, and support involvement of an intestinal influx transporter in imatinib absorption.	imatinib	79-87	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	51-57
23759247-0	2013	The role of TC-PTP (PTPN2) in modulating sensitivity to imatinib and interferon-alpha in CML cell line, KT-1 cells.	imatinib	56-64	protein tyrosine phosphatase, non-receptor type 2	Mus musculus	12-18
23505219-8	2013	Fibroblast migration was potently induced by PDGF-D and CCA conditioned medium and was significantly inhibited by PDGFRbeta blockade with Imatinib and by silencing PDGF-D expression in CCA cells.	imatinib	138-146	platelet derived growth factor receptor beta	Homo sapiens	114-123
23876601-2	2013	Because patients treated with imatinib and other tyrosine kinase inhibitors achieve lower levels of detectable disease, quantitation of BCR-ABL1 transcripts with quantitative RT-PCR has become an essential tool in chronic myeloid leukemia monitoring.	imatinib	30-38	BCR activator of RhoGEF and GTPase	Homo sapiens	136-144
23759247-0	2013	The role of TC-PTP (PTPN2) in modulating sensitivity to imatinib and interferon-alpha in CML cell line, KT-1 cells.	imatinib	56-64	protein tyrosine phosphatase, non-receptor type 2	Mus musculus	20-25
23759247-4	2013	Suppression of TC-PTP induced activation of STAT5, leading to imatinib resistance, while prolonged phosphorylation of STAT1 was induced by IFN-alpha, triggering cell death in KT-1 cells.	imatinib	62-70	protein tyrosine phosphatase, non-receptor type 2	Mus musculus	15-21
23759247-4	2013	Suppression of TC-PTP induced activation of STAT5, leading to imatinib resistance, while prolonged phosphorylation of STAT1 was induced by IFN-alpha, triggering cell death in KT-1 cells.	imatinib	62-70	signal transducer and activator of transcription 5A	Mus musculus	44-49
23759247-5	2013	These findings suggest that TC-PTP modulates sensitivity to imatinib and IFN-alpha in CML.	imatinib	60-68	protein tyrosine phosphatase, non-receptor type 2	Mus musculus	28-34
23198834-4	2013	Moreover, there is reported a small proportion of wild-type GISTs for both KIT and PDGFRA genes, and tumors more often acquire secondary mutations on KIT, that results into imatinib resistance.	imatinib	173-181	platelet derived growth factor receptor alpha	Homo sapiens	83-89
23982058-1	2013	Imatinib is the treatment of choice for FIP1L1/PDGFRA (F/P)-associated chronic eosinophilic leukemia (F/P CEL), but its optimal dosing, duration, and possibility of discontinuation are still a matter of debate.	imatinib	0-8	factor interacting with PAPOLA and CPSF1	Homo sapiens	40-46
23982058-1	2013	Imatinib is the treatment of choice for FIP1L1/PDGFRA (F/P)-associated chronic eosinophilic leukemia (F/P CEL), but its optimal dosing, duration, and possibility of discontinuation are still a matter of debate.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	47-53
23947692-1	2013	Imatinib mesylate is a selective protein tyrosine kinase inhibitor, which can inhibit BCR/Abl, PDGF-R, c-KIT, c-fms, TCR/Abl, Lck, FLT-3 and MAPKs activities on various cell types.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
23198834-3	2013	The presence and type of KIT/PDGFRA mutations help to predict the imatinib mesylate therapy, a selective tyrosine kinase inhibitor.	imatinib	66-74	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	25-28
23198834-3	2013	The presence and type of KIT/PDGFRA mutations help to predict the imatinib mesylate therapy, a selective tyrosine kinase inhibitor.	imatinib	66-74	platelet derived growth factor receptor alpha	Homo sapiens	29-35
23198834-4	2013	Moreover, there is reported a small proportion of wild-type GISTs for both KIT and PDGFRA genes, and tumors more often acquire secondary mutations on KIT, that results into imatinib resistance.	imatinib	173-181	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	150-153
23947692-1	2013	Imatinib mesylate is a selective protein tyrosine kinase inhibitor, which can inhibit BCR/Abl, PDGF-R, c-KIT, c-fms, TCR/Abl, Lck, FLT-3 and MAPKs activities on various cell types.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	95-101
23947692-1	2013	Imatinib mesylate is a selective protein tyrosine kinase inhibitor, which can inhibit BCR/Abl, PDGF-R, c-KIT, c-fms, TCR/Abl, Lck, FLT-3 and MAPKs activities on various cell types.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	103-108
23786773-0	2013	The DREAM complex mediates GIST cell quiescence and is a novel therapeutic target to enhance imatinib-induced apoptosis.	imatinib	93-101	potassium voltage-gated channel interacting protein 3	Homo sapiens	4-9
23947692-1	2013	Imatinib mesylate is a selective protein tyrosine kinase inhibitor, which can inhibit BCR/Abl, PDGF-R, c-KIT, c-fms, TCR/Abl, Lck, FLT-3 and MAPKs activities on various cell types.	imatinib	0-17	colony stimulating factor 1 receptor	Homo sapiens	110-115
23947692-1	2013	Imatinib mesylate is a selective protein tyrosine kinase inhibitor, which can inhibit BCR/Abl, PDGF-R, c-KIT, c-fms, TCR/Abl, Lck, FLT-3 and MAPKs activities on various cell types.	imatinib	0-17	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	117-120
23947692-1	2013	Imatinib mesylate is a selective protein tyrosine kinase inhibitor, which can inhibit BCR/Abl, PDGF-R, c-KIT, c-fms, TCR/Abl, Lck, FLT-3 and MAPKs activities on various cell types.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-93
23947692-1	2013	Imatinib mesylate is a selective protein tyrosine kinase inhibitor, which can inhibit BCR/Abl, PDGF-R, c-KIT, c-fms, TCR/Abl, Lck, FLT-3 and MAPKs activities on various cell types.	imatinib	0-17	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	126-129
23947692-1	2013	Imatinib mesylate is a selective protein tyrosine kinase inhibitor, which can inhibit BCR/Abl, PDGF-R, c-KIT, c-fms, TCR/Abl, Lck, FLT-3 and MAPKs activities on various cell types.	imatinib	0-17	fms related receptor tyrosine kinase 3	Homo sapiens	131-136
23947692-2	2013	On immune system, imatinib has antiproliferative activity and immunomodulatory effects in lymphocytes, macrophages, mast cells and dendritic cells with abrogating multiple signal transduction pathways involved in pathogenesis of autoimmune diseases e.g. inhibiting IFN-gamma, TNF-alpha, IL-1beta and IL-17 pro-inflammatory cytokines and MMPs secretion.	imatinib	18-26	interferon gamma	Homo sapiens	265-274
23947692-2	2013	On immune system, imatinib has antiproliferative activity and immunomodulatory effects in lymphocytes, macrophages, mast cells and dendritic cells with abrogating multiple signal transduction pathways involved in pathogenesis of autoimmune diseases e.g. inhibiting IFN-gamma, TNF-alpha, IL-1beta and IL-17 pro-inflammatory cytokines and MMPs secretion.	imatinib	18-26	tumor necrosis factor	Homo sapiens	276-285
23947692-2	2013	On immune system, imatinib has antiproliferative activity and immunomodulatory effects in lymphocytes, macrophages, mast cells and dendritic cells with abrogating multiple signal transduction pathways involved in pathogenesis of autoimmune diseases e.g. inhibiting IFN-gamma, TNF-alpha, IL-1beta and IL-17 pro-inflammatory cytokines and MMPs secretion.	imatinib	18-26	interleukin 1 beta	Homo sapiens	287-295
23947692-2	2013	On immune system, imatinib has antiproliferative activity and immunomodulatory effects in lymphocytes, macrophages, mast cells and dendritic cells with abrogating multiple signal transduction pathways involved in pathogenesis of autoimmune diseases e.g. inhibiting IFN-gamma, TNF-alpha, IL-1beta and IL-17 pro-inflammatory cytokines and MMPs secretion.	imatinib	18-26	interleukin 17A	Homo sapiens	300-305
23198834-4	2013	Moreover, there is reported a small proportion of wild-type GISTs for both KIT and PDGFRA genes, and tumors more often acquire secondary mutations on KIT, that results into imatinib resistance.	imatinib	173-181	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	75-78
24009732-0	2013	The conformational control inhibitor of tyrosine kinases DCC-2036 is effective for imatinib-resistant cells expressing T674I FIP1L1-PDGFRalpha.	imatinib	83-91	deleted in colorectal carcinoma	Mus musculus	57-60
24009732-0	2013	The conformational control inhibitor of tyrosine kinases DCC-2036 is effective for imatinib-resistant cells expressing T674I FIP1L1-PDGFRalpha.	imatinib	83-91	FIP1 like 1 (S. cerevisiae)	Mus musculus	125-131
24009732-0	2013	The conformational control inhibitor of tyrosine kinases DCC-2036 is effective for imatinib-resistant cells expressing T674I FIP1L1-PDGFRalpha.	imatinib	83-91	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	132-142
24009732-1	2013	The cells expressing the T674I point mutant of FIP1-like-1-platelet-derived growth factor receptor alpha (FIP1L1-PDGFRalpha) in hypereosinophilics syndrome (HES) are resistant to imatinib and some second-generation tyrosine kinase inhibitors (TKIs).	imatinib	179-187	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	113-123
24009732-10	2013	DCC-2036 may be a potential compound to treat imatinib-resistant HES.	imatinib	46-54	deleted in colorectal carcinoma	Mus musculus	0-3
24019750-2	2013	ABCB1 SNPs and haplotypes have been suggested to influence the pharmacokinetics and therapeutic outcome of the tyrosine kinase inhibitor (TKI) imatinib, used for treatment of chronic myeloid leukemia (CML).	imatinib	143-151	ATP binding cassette subfamily B member 1	Homo sapiens	0-5
24019750-4	2013	Functional studies of variant ABCB1 transport of imatinib as well as other TKIs might aid the interpretation of results from in vivo association studies, but are currently lacking.	imatinib	49-57	ATP binding cassette subfamily B member 1	Homo sapiens	30-35
24019750-5	2013	The aim of this study was to investigate the consequences of ABCB1 variant haplotypes for transport and efficacy of TKIs (imatinib, its major metabolite N-desmethyl imatinib [CGP74588], dasatinib, nilotinib, and bosutinib) in CML cells.	imatinib	122-130	ATP binding cassette subfamily B member 1	Homo sapiens	61-66
24019750-8	2013	It was found that dasatinib and the imatinib metabolite CGP74588 are effectively transported by ABCB1, while imatinib, nilotinib, and bosutinib are comparatively weaker ABCB1 substrates.	imatinib	36-44	ATP binding cassette subfamily B member 1	Homo sapiens	96-101
24019750-8	2013	It was found that dasatinib and the imatinib metabolite CGP74588 are effectively transported by ABCB1, while imatinib, nilotinib, and bosutinib are comparatively weaker ABCB1 substrates.	imatinib	109-117	ATP binding cassette subfamily B member 1	Homo sapiens	169-174
23786773-3	2013	In line with this notion, we have previously shown that imatinib induces GIST cell quiescence in vitro through the APC(CDH1)-SKP2-p27(Kip1) signaling axis.	imatinib	56-64	cadherin 1	Homo sapiens	115-123
23786773-3	2013	In line with this notion, we have previously shown that imatinib induces GIST cell quiescence in vitro through the APC(CDH1)-SKP2-p27(Kip1) signaling axis.	imatinib	56-64	interferon alpha inducible protein 27	Homo sapiens	130-133
23786773-3	2013	In line with this notion, we have previously shown that imatinib induces GIST cell quiescence in vitro through the APC(CDH1)-SKP2-p27(Kip1) signaling axis.	imatinib	56-64	cyclin dependent kinase inhibitor 1B	Homo sapiens	134-138
23786773-5	2013	Importantly, inhibition of DREAM complex formation by depletion of the DREAM regulatory kinase DYRK1A or its target LIN52 was found to enhance imatinib-induced cell death.	imatinib	143-151	potassium voltage-gated channel interacting protein 3	Homo sapiens	27-32
23786773-5	2013	Importantly, inhibition of DREAM complex formation by depletion of the DREAM regulatory kinase DYRK1A or its target LIN52 was found to enhance imatinib-induced cell death.	imatinib	143-151	potassium voltage-gated channel interacting protein 3	Homo sapiens	71-76
23786773-5	2013	Importantly, inhibition of DREAM complex formation by depletion of the DREAM regulatory kinase DYRK1A or its target LIN52 was found to enhance imatinib-induced cell death.	imatinib	143-151	dual specificity tyrosine phosphorylation regulated kinase 1A	Homo sapiens	95-101
23786773-5	2013	Importantly, inhibition of DREAM complex formation by depletion of the DREAM regulatory kinase DYRK1A or its target LIN52 was found to enhance imatinib-induced cell death.	imatinib	143-151	lin-52 DREAM MuvB core complex component	Homo sapiens	116-121
23786773-7	2013	Inhibition of this process enhances imatinib-induced apoptosis, which opens the opportunity for future therapeutic interventions to target the DREAM complex for more efficient imatinib responses.	imatinib	36-44	potassium voltage-gated channel interacting protein 3	Homo sapiens	143-148
23786773-7	2013	Inhibition of this process enhances imatinib-induced apoptosis, which opens the opportunity for future therapeutic interventions to target the DREAM complex for more efficient imatinib responses.	imatinib	176-184	potassium voltage-gated channel interacting protein 3	Homo sapiens	143-148
24371782-0	2013	Leptin modification in chronic myeloid leukemia patients treated with imatinib: An emerging effect of targeted therapy.	imatinib	70-78	leptin	Homo sapiens	0-6
24371782-1	2013	We evaluated serum leptin levels in 9 young chronic myeloid leukemia (CML) patients under imatinib therapy during a long-term follow-up.	imatinib	90-98	leptin	Homo sapiens	19-25
24371782-6	2013	One patient recovered the leptin normal value after imatinib suspension.	imatinib	52-60	leptin	Homo sapiens	26-32
24371782-8	2013	This study suggests that imatinib therapy may result in leptin alteration.	imatinib	25-33	leptin	Homo sapiens	56-62
23598363-12	2013	Our findings indicate that imatinib protects oocytes from cisplatin-induced cell death by inhibiting c-Abl kinase, which would otherwise activate TAp73-BAX-mediated apoptosis.	imatinib	27-35	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	101-106
23749639-5	2013	Expression and phosphorylation of eIF4B relied upon Abl kinase activity in both v-Abl- and Bcr-Abl-expressing leukemic cells based on their blockade by the Abl kinase inhibitor imatinib.	imatinib	177-185	eukaryotic translation initiation factor 4B	Mus musculus	34-39
23749639-5	2013	Expression and phosphorylation of eIF4B relied upon Abl kinase activity in both v-Abl- and Bcr-Abl-expressing leukemic cells based on their blockade by the Abl kinase inhibitor imatinib.	imatinib	177-185	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	52-55
23749639-7	2013	In contrast, silencing eIF4B sensitized Abl-transformed cells to imatinib-induced apoptosis and also inhibited their growth as engrafted tumors in nude mice.	imatinib	65-73	eukaryotic translation initiation factor 4B	Mus musculus	23-28
23749639-7	2013	In contrast, silencing eIF4B sensitized Abl-transformed cells to imatinib-induced apoptosis and also inhibited their growth as engrafted tumors in nude mice.	imatinib	65-73	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	40-43
23433665-0	2013	Frequency of ABL gene mutations in chronic myeloid leukemia patients resistant to imatinib and results of treatment switch to second-generation tyrosine kinase inhibitors.	imatinib	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
23433665-5	2013	The aim of this study was to determine the type and frequency of ABL mutations in patients who were resistant to imatinib or had lost the response, and to analyze the effect of second-generation TKI on their outcome.	imatinib	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-68
23433665-6	2013	PATIENTS AND METHODS: The presence of ABL mutations in 45 CML patients resistant to imatinib was evaluated by direct sequencing and was correlated with the results of the cytogenetic study (performed in 39 cases).	imatinib	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-41
23433665-11	2013	CONCLUSION: The frequency of ABL mutations in CML patients resistant to imatinib is high and is more frequent among those with clonal cytogenetic evolution.	imatinib	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-32
23598363-3	2013	Recently, the c-Abl kinase inhibitor imatinib mesylate (imatinib) has become the focus of research as a fertoprotective drug against cisplatin.	imatinib	37-54	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	14-19
23598363-3	2013	Recently, the c-Abl kinase inhibitor imatinib mesylate (imatinib) has become the focus of research as a fertoprotective drug against cisplatin.	imatinib	37-45	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	14-19
23598363-12	2013	Our findings indicate that imatinib protects oocytes from cisplatin-induced cell death by inhibiting c-Abl kinase, which would otherwise activate TAp73-BAX-mediated apoptosis.	imatinib	27-35	transformation related protein 73	Mus musculus	146-151
23598363-8	2013	While imatinib was unable to block cisplatin-induced DNA damage and damage response, such as the upregulation of p53, imatinib inhibited the cisplatin-induced nuclear accumulation of c-Abl/TAp73 and the subsequent downregulation of TAp63 and upregulation of Bax, thereby abrogating oocyte cell death.	imatinib	118-126	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	183-188
23598363-8	2013	While imatinib was unable to block cisplatin-induced DNA damage and damage response, such as the upregulation of p53, imatinib inhibited the cisplatin-induced nuclear accumulation of c-Abl/TAp73 and the subsequent downregulation of TAp63 and upregulation of Bax, thereby abrogating oocyte cell death.	imatinib	118-126	transformation related protein 73	Mus musculus	189-194
23598363-12	2013	Our findings indicate that imatinib protects oocytes from cisplatin-induced cell death by inhibiting c-Abl kinase, which would otherwise activate TAp73-BAX-mediated apoptosis.	imatinib	27-35	BCL2-associated X protein	Mus musculus	152-155
23598363-8	2013	While imatinib was unable to block cisplatin-induced DNA damage and damage response, such as the upregulation of p53, imatinib inhibited the cisplatin-induced nuclear accumulation of c-Abl/TAp73 and the subsequent downregulation of TAp63 and upregulation of Bax, thereby abrogating oocyte cell death.	imatinib	118-126	BCL2-associated X protein	Mus musculus	258-261
23883479-1	2013	The first tyrosine kinase inhibitor (TKI) imatinib mesylate (imatinib) targets the kinase domain of BCR-ABL and induces apoptosis in newly diagnosed chronic myeloid leukaemia (CML).	imatinib	42-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
23904774-5	2013	The Kit inhibitor imatinib mesylate is approved for aggressive sm.	imatinib	18-35	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	4-7
23883479-1	2013	The first tyrosine kinase inhibitor (TKI) imatinib mesylate (imatinib) targets the kinase domain of BCR-ABL and induces apoptosis in newly diagnosed chronic myeloid leukaemia (CML).	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
23591991-8	2013	Imatinib mesylate inhibited Pdgfr-beta activation and Acta2(-/-) SMC proliferation in vitro and neointimal formation with vascular injury in vivo.	imatinib	0-17	platelet derived growth factor receptor, beta polypeptide	Mus musculus	28-38
23591991-8	2013	Imatinib mesylate inhibited Pdgfr-beta activation and Acta2(-/-) SMC proliferation in vitro and neointimal formation with vascular injury in vivo.	imatinib	0-17	actin alpha 2, smooth muscle, aorta	Mus musculus	54-59
23930677-4	2013	When combined with TPL, both doxorubicin and imatinib downregulate Nrf2 and HIF-1alpha expression at protein and mRNA levels.	imatinib	45-53	NFE2 like bZIP transcription factor 2	Homo sapiens	67-71
23157309-0	2013	Sorafenib is effective for imatinib-resistant FIP1L1/PDGFRA T674I mutation-positive acute myeloid leukemia with eosinophilia.	imatinib	27-35	factor interacting with PAPOLA and CPSF1	Homo sapiens	46-52
23434731-0	2013	Cleavage of BCR-ABL transcripts at the T315I point mutation by DNAzyme promotes apoptotic cell death in imatinib-resistant BCR-ABL leukemic cells.	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
23434731-0	2013	Cleavage of BCR-ABL transcripts at the T315I point mutation by DNAzyme promotes apoptotic cell death in imatinib-resistant BCR-ABL leukemic cells.	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-130
23434731-2	2013	Although the TK inhibitor imatinib mesylate, which targets the BCR-ABL protein, has been proven to be effective in controlling leukemic growth, imatinib resistance has been observed with disease relapse because of point mutations in the ABL gene that inhibit imatinib efficacy.	imatinib	26-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
23434731-2	2013	Although the TK inhibitor imatinib mesylate, which targets the BCR-ABL protein, has been proven to be effective in controlling leukemic growth, imatinib resistance has been observed with disease relapse because of point mutations in the ABL gene that inhibit imatinib efficacy.	imatinib	26-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-70
23434731-2	2013	Although the TK inhibitor imatinib mesylate, which targets the BCR-ABL protein, has been proven to be effective in controlling leukemic growth, imatinib resistance has been observed with disease relapse because of point mutations in the ABL gene that inhibit imatinib efficacy.	imatinib	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
23434731-2	2013	Although the TK inhibitor imatinib mesylate, which targets the BCR-ABL protein, has been proven to be effective in controlling leukemic growth, imatinib resistance has been observed with disease relapse because of point mutations in the ABL gene that inhibit imatinib efficacy.	imatinib	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-70
23434731-3	2013	In this study, we designed oligodeoxyribozymes (DNAzymes) that specifically target and cleave both the junction sequence and the site of the point mutation (T315I), conferring imatinib resistance in BCR-ABL mRNA.	imatinib	176-184	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	199-206
23434731-5	2013	Selective cleavage of T315I-mutant ABL mRNA by DNAzyme (T315I Dz) led to cell cycle arrest in G0/G1 phase, with induction of caspase-3/-7 in imatinib-resistant BCR-ABL-positive cells harboring the T315I mutation.	imatinib	141-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
23434731-5	2013	Selective cleavage of T315I-mutant ABL mRNA by DNAzyme (T315I Dz) led to cell cycle arrest in G0/G1 phase, with induction of caspase-3/-7 in imatinib-resistant BCR-ABL-positive cells harboring the T315I mutation.	imatinib	141-149	caspase 3	Homo sapiens	125-137
23434731-5	2013	Selective cleavage of T315I-mutant ABL mRNA by DNAzyme (T315I Dz) led to cell cycle arrest in G0/G1 phase, with induction of caspase-3/-7 in imatinib-resistant BCR-ABL-positive cells harboring the T315I mutation.	imatinib	141-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-167
23434731-6	2013	Moreover, cotreatment with the DNAzyme targeting the T315I mutation and imatinib resulted in enhanced inhibition of proliferation and induction of apoptosis in T315I leukemic cells as compared with imatinib alone, thereby antagonizing imatinib resistance in CML cells bearing T315I-mutant BCR-ABL.	imatinib	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	289-296
23434731-6	2013	Moreover, cotreatment with the DNAzyme targeting the T315I mutation and imatinib resulted in enhanced inhibition of proliferation and induction of apoptosis in T315I leukemic cells as compared with imatinib alone, thereby antagonizing imatinib resistance in CML cells bearing T315I-mutant BCR-ABL.	imatinib	198-206	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	289-296
23434731-6	2013	Moreover, cotreatment with the DNAzyme targeting the T315I mutation and imatinib resulted in enhanced inhibition of proliferation and induction of apoptosis in T315I leukemic cells as compared with imatinib alone, thereby antagonizing imatinib resistance in CML cells bearing T315I-mutant BCR-ABL.	imatinib	198-206	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	289-296
23434731-7	2013	Therefore, cleavage of T315I-mutant ABL mRNA by DNAzyme combined with imatinib treatment may be an alternative approach to overcoming imatinib resistance in leukemic cells.	imatinib	134-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-39
23567324-1	2013	A novel double-mutant KIT in GIST that responds to Imatinib.	imatinib	51-59	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	22-25
23567324-3	2013	Generally only one KIT mutation is found in primary tumors and the majority of mutations affecting KIT exon 11 is sensitive to Imatinib.	imatinib	127-135	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	99-102
23567324-5	2013	The relative affinities for ATP and Imatinib of each single (W557G, Y578C) and double (W557G/Y578C) mutant KITs were predicted by in silico studies (computer-based molecular simulations), and compared with those obtained for known Imatinib sensitive and resistant KIT mutants.	imatinib	36-44	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	107-110
23553655-1	2013	Four breakpoint cluster region (BCR)-ABL1 tyrosine kinase inhibitors (TKIs) are currently available for the treatment of chronic myeloid leukemia (CML): imatinib, nilotinib, dasatinib, and bosutinib.	imatinib	153-161	BCR activator of RhoGEF and GTPase	Homo sapiens	32-35
23930677-4	2013	When combined with TPL, both doxorubicin and imatinib downregulate Nrf2 and HIF-1alpha expression at protein and mRNA levels.	imatinib	45-53	hypoxia inducible factor 1 subunit alpha	Homo sapiens	76-86
23936456-2	2013	Tyrosine kinase inhibitors (TKI) that target BCR/ABL, such as imatinib, have improved treatment of Ph(+)ALL and are generally incorporated into induction regimens.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
23754495-2	2013	We focused on Anxa1 because it is one of the major proteins upregulated in imatinib-sensitive KCL22S cells versus imatinib-resistant KCL22R.	imatinib	75-83	annexin A1	Homo sapiens	14-19
23754495-2	2013	We focused on Anxa1 because it is one of the major proteins upregulated in imatinib-sensitive KCL22S cells versus imatinib-resistant KCL22R.	imatinib	114-122	annexin A1	Homo sapiens	14-19
23754495-5	2013	Among the proteins identified, we studied the interaction of Anxa1 with two phosphatases, Shp1 and Shp2, which were recently identified as biomarkers of imatinib sensitivity in patients affected by chronic myeloid leukemia.	imatinib	153-161	annexin A1	Homo sapiens	61-66
23754495-5	2013	Among the proteins identified, we studied the interaction of Anxa1 with two phosphatases, Shp1 and Shp2, which were recently identified as biomarkers of imatinib sensitivity in patients affected by chronic myeloid leukemia.	imatinib	153-161	nuclear receptor subfamily 0 group B member 2	Homo sapiens	90-94
23754495-5	2013	Among the proteins identified, we studied the interaction of Anxa1 with two phosphatases, Shp1 and Shp2, which were recently identified as biomarkers of imatinib sensitivity in patients affected by chronic myeloid leukemia.	imatinib	153-161	protein tyrosine phosphatase non-receptor type 11	Homo sapiens	99-103
23723070-8	2013	Pretreatment with specific c-Abl inhibitor, imatinib mesylate, and knock down of c-Abl significantly decreased the caveolin-1 phosphorylation after H2O2 exposure and abolished the inhibitory effect of AICAR on the caveolin-1 phosphorylation.	imatinib	44-61	caveolin 1	Homo sapiens	115-125
23998582-0	2013	[Effect of bortezomib on reverse multidrug resistance and XIAP expression in imatinib-resistant primary cells of chronic myeloid leukemia in blastic crisis].	imatinib	77-85	X-linked inhibitor of apoptosis	Homo sapiens	58-62
23998582-1	2013	This study was aimed to explore the effects of proteasome inhibitor bortezomib on the drug sensitivity of imatinib-resistant primary cells in blastic phase of chronic myeloid leukemia (CML) and the expression of XIAP.	imatinib	106-114	X-linked inhibitor of apoptosis	Homo sapiens	212-216
23704092-7	2013	Highly sensitive patient-specific BCR-ABL DNA PCR showed persistence of the original CML clone in all patients with stable UMRD, even several years after imatinib withdrawal.	imatinib	154-162	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
23719297-7	2013	In vitro coincubation of B cells with plasma from CML patients on TKI or with imatinib, dasatinib, or nilotinib induced significant and dose-dependent inhibition of Bruton"s tyrosine kinase and indirectly its downstream substrate, phospholipase-C-gamma2, both important in B-cell signaling and survival.	imatinib	78-86	Bruton tyrosine kinase	Homo sapiens	165-189
23719297-7	2013	In vitro coincubation of B cells with plasma from CML patients on TKI or with imatinib, dasatinib, or nilotinib induced significant and dose-dependent inhibition of Bruton"s tyrosine kinase and indirectly its downstream substrate, phospholipase-C-gamma2, both important in B-cell signaling and survival.	imatinib	78-86	phospholipase C gamma 2	Homo sapiens	231-253
23681919-2	2013	We have recently produced a mouse model for imatinib resistant gastrointestinal stromal tumor (GIST) carrying the Kit(V558Delta) and Kit(T669I) (human KIT(T670I) ) mutations found in imatinib-resistant GIST.	imatinib	44-52	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	114-117
23681919-2	2013	We have recently produced a mouse model for imatinib resistant gastrointestinal stromal tumor (GIST) carrying the Kit(V558Delta) and Kit(T669I) (human KIT(T670I) ) mutations found in imatinib-resistant GIST.	imatinib	44-52	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	133-136
23681919-2	2013	We have recently produced a mouse model for imatinib resistant gastrointestinal stromal tumor (GIST) carrying the Kit(V558Delta) and Kit(T669I) (human KIT(T670I) ) mutations found in imatinib-resistant GIST.	imatinib	44-52	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	99-100
23935374-2	2013	Successful targeting of c-KIT and PDGFRA with imatinib, a tyrosine kinase inhibitor (TKI), has had a major impact in advanced GIST and as an adjuvant and neoadjuvant treatment.	imatinib	46-54	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	24-29
23935374-2	2013	Successful targeting of c-KIT and PDGFRA with imatinib, a tyrosine kinase inhibitor (TKI), has had a major impact in advanced GIST and as an adjuvant and neoadjuvant treatment.	imatinib	46-54	platelet derived growth factor receptor alpha	Homo sapiens	34-40
23922791-4	2013	Thus, blocking PDGFR receptor activation with imatinib has shown promising activity in the treatment of advanced and metastatic DFSP.	imatinib	46-54	platelet derived growth factor receptor beta	Homo sapiens	15-20
23922791-9	2013	Of note, we identified newly emerged 8 non-synonymous somatic mutations of the genes (ACAP2, CARD10, KIAA0556, PAAQR7, PPP1R39, SAFB2, STARD9, and ZFYVE9) in the imatinib-resistant tumor tissue.	imatinib	162-170	katanin interacting protein	Homo sapiens	101-109
23922791-9	2013	Of note, we identified newly emerged 8 non-synonymous somatic mutations of the genes (ACAP2, CARD10, KIAA0556, PAAQR7, PPP1R39, SAFB2, STARD9, and ZFYVE9) in the imatinib-resistant tumor tissue.	imatinib	162-170	zinc finger FYVE-type containing 9	Homo sapiens	147-153
23922791-10	2013	This study revealed diverse possible candidate mechanisms by which imatinib resistance to PDGFRB inhibition may arise in DFSP, and highlights the usefulness of whole-genome sequencing in identifying drug resistance mechanisms and in pursuing genome-directed, personalized anti-cancer therapy.	imatinib	67-75	platelet derived growth factor receptor beta	Homo sapiens	90-96
23866735-0	2013	Down-regulation of miR-181c in imatinib-resistant chronic myeloid leukemia.	imatinib	31-39	microRNA 181c	Homo sapiens	19-27
23866735-3	2013	Only one differentially expressed miRNA, miR-181c, was found when the imatinib-resistant group was compared with imatinib-responders.	imatinib	70-78	microRNA 181c	Homo sapiens	41-49
23866735-3	2013	Only one differentially expressed miRNA, miR-181c, was found when the imatinib-resistant group was compared with imatinib-responders.	imatinib	113-121	microRNA 181c	Homo sapiens	41-49
23866735-4	2013	Significant down-regulation of miR-181c in imatinib-resistant versus imatinib-responders was confirmed by qRT-PCR.	imatinib	43-51	microRNA 181c	Homo sapiens	31-39
23866735-4	2013	Significant down-regulation of miR-181c in imatinib-resistant versus imatinib-responders was confirmed by qRT-PCR.	imatinib	69-77	microRNA 181c	Homo sapiens	31-39
23650173-5	2013	F342S is located in the ATP-binding P-loop and is homologous to a c-Abl kinase mutation conferring resistance to imatinib.	imatinib	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-71
23833101-0	2013	CD34-negative solitary fibrous tumour resistant to imatinib.	imatinib	51-59	CD34 molecule	Homo sapiens	0-4
23833101-7	2013	Imatinib, a multityrosine kinase inhibitor with targets, including platelet-derived growth factor receptor (PDGFR)-alpha and PDGFR-beta, has antitumour activity in some patients with SFT.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	108-120
23833101-7	2013	Imatinib, a multityrosine kinase inhibitor with targets, including platelet-derived growth factor receptor (PDGFR)-alpha and PDGFR-beta, has antitumour activity in some patients with SFT.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	125-135
23833101-8	2013	Unfortunately, imatinib treatment failed to control disease progression in the present case that expressed PDGFR-beta, but not PDGFR-alpha.	imatinib	15-23	platelet derived growth factor receptor beta	Homo sapiens	107-117
23833101-9	2013	This report described a case of CD34-negative SFT resistant to imatinib.	imatinib	63-71	CD34 molecule	Homo sapiens	32-36
23720340-10	2013	Imatinib has a therapeutic role in the presence of an imatinib-sensitive KIT mutation or in KITD816-unmutated patients.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
23720340-10	2013	Imatinib has a therapeutic role in the presence of an imatinib-sensitive KIT mutation or in KITD816-unmutated patients.	imatinib	54-62	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
23839611-0	2013	Imatinib in neurofibromatosis type 2.	imatinib	0-8	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	12-36
23394475-4	2013	This study aimed to investigate the allele and genotype frequencies of single nucleotide polymorphisms (SNPs) of SLCO1B3 (T334G) and CYP3A5*3 in CML patients undergoing imatinib treatment and to determine whether SNPs of these two genes could predict the response of imatinib therapy in CML patients.	imatinib	169-177	solute carrier organic anion transporter family member 1B3	Homo sapiens	113-120
23277196-2	2013	As the oncogenic BCR-ABL kinase is the target of the first approved small-molecule kinase inhibitor imatinib, we will first focus on the structural and mechanistic basis for imatinib resistance.	imatinib	100-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
23277196-2	2013	As the oncogenic BCR-ABL kinase is the target of the first approved small-molecule kinase inhibitor imatinib, we will first focus on the structural and mechanistic basis for imatinib resistance.	imatinib	174-182	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
23277196-3	2013	We will then show ways how next generations of BCR-ABL inhibitors and alternative targeting strategies have helped to offer effective treatment options for imatinib-resistant patients.	imatinib	156-164	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
23660976-6	2013	Co-treatment of cisplatin with the Abl kinase inhibitor, imatinib, reduced the accumulation of p53 and PUMAalpha in the Abl(+/+) but not in the Abl(mu/mu) kidneys.	imatinib	57-65	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	35-38
23660976-6	2013	Co-treatment of cisplatin with the Abl kinase inhibitor, imatinib, reduced the accumulation of p53 and PUMAalpha in the Abl(+/+) but not in the Abl(mu/mu) kidneys.	imatinib	57-65	transformation related protein 53, pseudogene	Mus musculus	95-98
23660976-6	2013	Co-treatment of cisplatin with the Abl kinase inhibitor, imatinib, reduced the accumulation of p53 and PUMAalpha in the Abl(+/+) but not in the Abl(mu/mu) kidneys.	imatinib	57-65	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	120-123
23660976-6	2013	Co-treatment of cisplatin with the Abl kinase inhibitor, imatinib, reduced the accumulation of p53 and PUMAalpha in the Abl(+/+) but not in the Abl(mu/mu) kidneys.	imatinib	57-65	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	144-153
23648119-5	2013	Efficacy of imatinib in GISTs with KIT exon 13 was evaluated and compared with published data.	imatinib	12-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	35-38
23394475-4	2013	This study aimed to investigate the allele and genotype frequencies of single nucleotide polymorphisms (SNPs) of SLCO1B3 (T334G) and CYP3A5*3 in CML patients undergoing imatinib treatment and to determine whether SNPs of these two genes could predict the response of imatinib therapy in CML patients.	imatinib	169-177	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	133-139
23394475-4	2013	This study aimed to investigate the allele and genotype frequencies of single nucleotide polymorphisms (SNPs) of SLCO1B3 (T334G) and CYP3A5*3 in CML patients undergoing imatinib treatment and to determine whether SNPs of these two genes could predict the response of imatinib therapy in CML patients.	imatinib	267-275	solute carrier organic anion transporter family member 1B3	Homo sapiens	113-120
23394475-4	2013	This study aimed to investigate the allele and genotype frequencies of single nucleotide polymorphisms (SNPs) of SLCO1B3 (T334G) and CYP3A5*3 in CML patients undergoing imatinib treatment and to determine whether SNPs of these two genes could predict the response of imatinib therapy in CML patients.	imatinib	267-275	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	133-139
23394475-12	2013	CONCLUSION: CYP3A5*3 polymorphism was associated with imatinib efficacy while the SNP SLCO1B3 (T334G) was not associated with the response to imatinib treatment in Egyptian patients with CML in chronic phase.	imatinib	54-62	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	12-18
23394475-13	2013	These results prompt us to explore the effect of CYP3A5*3 in CML patients taking imatinib in a larger scale study.	imatinib	81-89	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	49-55
23394612-0	2013	The roles of epigenetic modifications of proapoptotic BID and BIM genes in imatinib-resistant chronic myeloid leukemia cells.	imatinib	75-83	BH3 interacting domain death agonist	Homo sapiens	54-57
23394612-0	2013	The roles of epigenetic modifications of proapoptotic BID and BIM genes in imatinib-resistant chronic myeloid leukemia cells.	imatinib	75-83	BCL2 like 11	Homo sapiens	62-65
23394612-3	2013	We detected higher expression levels of BIM and BID genes and lower expression levels of EZH2, EED2, SIRT1, and SUZ12 genes in imatinib-resistant K562/IMA-3 cells compared to imatinib-non-resistant K562 cells.	imatinib	127-135	BCL2 like 11	Homo sapiens	40-43
23394612-3	2013	We detected higher expression levels of BIM and BID genes and lower expression levels of EZH2, EED2, SIRT1, and SUZ12 genes in imatinib-resistant K562/IMA-3 cells compared to imatinib-non-resistant K562 cells.	imatinib	127-135	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	89-93
23394612-3	2013	We detected higher expression levels of BIM and BID genes and lower expression levels of EZH2, EED2, SIRT1, and SUZ12 genes in imatinib-resistant K562/IMA-3 cells compared to imatinib-non-resistant K562 cells.	imatinib	127-135	sirtuin 1	Homo sapiens	101-106
23394612-3	2013	We detected higher expression levels of BIM and BID genes and lower expression levels of EZH2, EED2, SIRT1, and SUZ12 genes in imatinib-resistant K562/IMA-3 cells compared to imatinib-non-resistant K562 cells.	imatinib	127-135	SUZ12 polycomb repressive complex 2 subunit	Homo sapiens	112-117
24250632-7	2013	Compound 2c (IC50 = 100 muM) with p-nitro substituent was the most active compound compared to imatinib(IC50 = 98 muM) in MCF-7 cell line.	imatinib	95-103	latexin	Homo sapiens	114-117
23322583-0	2013	Growth failure in children with chronic myeloid leukemia receiving imatinib is due to disruption of GH/IGF-1 axis.	imatinib	67-75	insulin like growth factor 1	Homo sapiens	103-108
23715577-1	2013	PURPOSE: Dasatinib is a potent BCR-ABL inhibitor with proven efficacy in adults with newly diagnosed chronic myeloid leukemia (CML) in chronic phase (CP) and in imatinib-resistant/intolerant disease.	imatinib	161-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
23186533-0	2013	Recurrent CEP85L-PDGFRB fusion in patient with t(5;6) and imatinib-responsive myeloproliferative neoplasm with eosinophilia.	imatinib	58-66	centrosomal protein 85 like	Homo sapiens	10-16
23186533-0	2013	Recurrent CEP85L-PDGFRB fusion in patient with t(5;6) and imatinib-responsive myeloproliferative neoplasm with eosinophilia.	imatinib	58-66	platelet derived growth factor receptor beta	Homo sapiens	17-23
23722018-8	2013	Reactivity for DOG1 may aid in the diagnosis of GISTs, which fail to express c-kit antigen, and lead to appropriate treatment with imatinib mesylate, an inhibitor of the KIT tyrosine kinase.	imatinib	131-148	anoctamin 1	Homo sapiens	15-19
23322583-14	2013	CONCLUSIONS: This study demonstrates that imatinib results in growth failure in children with CML by disturbing the GH:IGF-1 axis.	imatinib	42-50	insulin like growth factor 1	Homo sapiens	119-124
23722018-8	2013	Reactivity for DOG1 may aid in the diagnosis of GISTs, which fail to express c-kit antigen, and lead to appropriate treatment with imatinib mesylate, an inhibitor of the KIT tyrosine kinase.	imatinib	131-148	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	170-173
23322583-15	2013	GH stimulation test and serum IGF-1 levels should be performed in children on treatment with imatinib who have growth retardation.	imatinib	93-101	insulin like growth factor 1	Homo sapiens	30-35
23582185-2	2013	Many activating c-Kit mutations have been shown to be highly sensitive to imatinib mesylate, although the majority of patients with c-Kit mutant melanoma eventually progress on this inhibitor.	imatinib	74-91	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	16-21
23582185-4	2013	Four imatinib-resistant and six nilotinib-resistant sublines had acquired additional, secondary c-Kit mutations.	imatinib	5-13	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	96-101
23582185-5	2013	The secondary A829P c-Kit mutation rendered cells resistant to imatinib, but did not suppress the activity of the tyrosine kinase inhibitors nilotinib and dasatinib.	imatinib	63-71	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	20-25
23582185-6	2013	Sublines with an additional T670I c-Kit mutation showed resistance to imatinib, nilotinib and dasatinib, but responded to sunitinib.	imatinib	70-78	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	34-39
23787070-3	2013	Imatinib (STI571) is the first drug in the family of Bcr-Abl tyrosine kinase inhibitors while Nilotinib (AMN107) and Dasatinib (BMS-345825) are second generation drugs that are intended to have less resistance and intolerance than imatinib.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
23813934-0	2013	Imatinib tackles lymphoma via the PDGFRbeta+ pericyte.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	34-43
23632889-2	2013	Here, we report that imatinib, a tyrosine kinase inhibitor of platelet-derived growth factor receptor beta (PDGFRbeta), impaired growth of lymphoma in both human xenograft and murine allograft models.	imatinib	21-29	platelet derived growth factor receptor beta	Homo sapiens	62-106
23632889-2	2013	Here, we report that imatinib, a tyrosine kinase inhibitor of platelet-derived growth factor receptor beta (PDGFRbeta), impaired growth of lymphoma in both human xenograft and murine allograft models.	imatinib	21-29	platelet derived growth factor receptor beta	Homo sapiens	108-117
23632889-5	2013	In vivo, imatinib induced apoptosis of tumor-associated PDGFRbeta(+) pericytes and loss of perivascular integrity.	imatinib	9-17	platelet derived growth factor receptor beta	Homo sapiens	56-65
23632889-6	2013	In vitro, imatinib inhibited PDGFRbeta(+) VSMC proliferation and PDGF-BB signaling, whereas small interfering RNA knockdown of PDGFRbeta in pericytes protected them against imatinib-mediated growth inhibition.	imatinib	10-18	platelet derived growth factor receptor beta	Homo sapiens	29-38
23632889-6	2013	In vitro, imatinib inhibited PDGFRbeta(+) VSMC proliferation and PDGF-BB signaling, whereas small interfering RNA knockdown of PDGFRbeta in pericytes protected them against imatinib-mediated growth inhibition.	imatinib	173-181	platelet derived growth factor receptor beta	Homo sapiens	127-136
23632889-9	2013	Last, microarray analysis (Gene Expression Omnibus database accession number GSE30752) of PDGFRbeta(+) VSMCs following imatinib treatment showed down-regulation of genes implicated in vascular cell proliferation, survival, and assembly, including those representing multiple pathways downstream of PDGFRbeta.	imatinib	119-127	platelet derived growth factor receptor beta	Homo sapiens	90-99
23632889-9	2013	Last, microarray analysis (Gene Expression Omnibus database accession number GSE30752) of PDGFRbeta(+) VSMCs following imatinib treatment showed down-regulation of genes implicated in vascular cell proliferation, survival, and assembly, including those representing multiple pathways downstream of PDGFRbeta.	imatinib	119-127	platelet derived growth factor receptor beta	Homo sapiens	298-307
23826126-2	2013	Imatinib, a BCR-Abl tyrosine kinase inhibitor, is a successful front-line treatment for chronic myelogenous leukemia (CML).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
23826126-3	2013	However, resistance to imatinib may be acquired by BCR-Abl mutations or hyperactivation of Src family kinases such as Lyn.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
23826126-3	2013	However, resistance to imatinib may be acquired by BCR-Abl mutations or hyperactivation of Src family kinases such as Lyn.	imatinib	23-31	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	118-121
23826126-12	2013	Thus, MIB/MS analysis identified MEK and IKKalpha as important downstream targets of Lyn, suggesting that co-targeting these kinases may provide a unique strategy to inhibit Lyn-dependent imatinib-resistant CML.	imatinib	188-196	MIB E3 ubiquitin protein ligase 1	Homo sapiens	6-9
23826126-12	2013	Thus, MIB/MS analysis identified MEK and IKKalpha as important downstream targets of Lyn, suggesting that co-targeting these kinases may provide a unique strategy to inhibit Lyn-dependent imatinib-resistant CML.	imatinib	188-196	mitogen-activated protein kinase kinase 7	Homo sapiens	33-36
23826126-12	2013	Thus, MIB/MS analysis identified MEK and IKKalpha as important downstream targets of Lyn, suggesting that co-targeting these kinases may provide a unique strategy to inhibit Lyn-dependent imatinib-resistant CML.	imatinib	188-196	component of inhibitor of nuclear factor kappa B kinase complex	Homo sapiens	41-49
23826126-12	2013	Thus, MIB/MS analysis identified MEK and IKKalpha as important downstream targets of Lyn, suggesting that co-targeting these kinases may provide a unique strategy to inhibit Lyn-dependent imatinib-resistant CML.	imatinib	188-196	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	85-88
23826126-12	2013	Thus, MIB/MS analysis identified MEK and IKKalpha as important downstream targets of Lyn, suggesting that co-targeting these kinases may provide a unique strategy to inhibit Lyn-dependent imatinib-resistant CML.	imatinib	188-196	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	174-177
23787070-3	2013	Imatinib (STI571) is the first drug in the family of Bcr-Abl tyrosine kinase inhibitors while Nilotinib (AMN107) and Dasatinib (BMS-345825) are second generation drugs that are intended to have less resistance and intolerance than imatinib.	imatinib	10-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
23787115-8	2013	The concentrations of tumor necrosis factor-alpha, interleukin (IL)-1beta, IL-6 and myeloperoxidase in BAL fluid were significantly inhibited by imatinib or nilotinib in mice of ALI during neutropenia recovery.	imatinib	145-153	tumor necrosis factor	Mus musculus	22-49
23576565-8	2013	Similar results were obtained after selection of imatinib-resistant DOG1- and KIT-negative cells derived from parental DOG1 and KIT-positive GIST cells, where a 5,000-fold increase in IGFBP5 mRNA transcripts were documented.	imatinib	49-57	anoctamin 1	Homo sapiens	68-72
23787115-8	2013	The concentrations of tumor necrosis factor-alpha, interleukin (IL)-1beta, IL-6 and myeloperoxidase in BAL fluid were significantly inhibited by imatinib or nilotinib in mice of ALI during neutropenia recovery.	imatinib	145-153	interleukin 1 beta	Mus musculus	51-73
23787115-8	2013	The concentrations of tumor necrosis factor-alpha, interleukin (IL)-1beta, IL-6 and myeloperoxidase in BAL fluid were significantly inhibited by imatinib or nilotinib in mice of ALI during neutropenia recovery.	imatinib	145-153	interleukin 6	Mus musculus	75-79
23787115-8	2013	The concentrations of tumor necrosis factor-alpha, interleukin (IL)-1beta, IL-6 and myeloperoxidase in BAL fluid were significantly inhibited by imatinib or nilotinib in mice of ALI during neutropenia recovery.	imatinib	145-153	myeloperoxidase	Mus musculus	84-99
23787115-9	2013	The mRNA expressions of platelet-derived growth factor receptor-beta and c-KIT in imatinib or nilotinib group were significantly lower than LPS group.	imatinib	82-90	platelet derived growth factor receptor, beta polypeptide	Mus musculus	24-68
23787115-9	2013	The mRNA expressions of platelet-derived growth factor receptor-beta and c-KIT in imatinib or nilotinib group were significantly lower than LPS group.	imatinib	82-90	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	73-78
23576565-1	2013	Gastrointestinal stromal tumors (GIST) are characterized by activating mutations of KIT or platelet-derived growth factor receptor alpha(PDGFRA), which can be therapeutically targeted by tyrosine kinase inhibitors (TKI) such as imatinib.	imatinib	228-236	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	84-87
23576565-1	2013	Gastrointestinal stromal tumors (GIST) are characterized by activating mutations of KIT or platelet-derived growth factor receptor alpha(PDGFRA), which can be therapeutically targeted by tyrosine kinase inhibitors (TKI) such as imatinib.	imatinib	228-236	platelet derived growth factor receptor alpha	Homo sapiens	91-136
23576565-1	2013	Gastrointestinal stromal tumors (GIST) are characterized by activating mutations of KIT or platelet-derived growth factor receptor alpha(PDGFRA), which can be therapeutically targeted by tyrosine kinase inhibitors (TKI) such as imatinib.	imatinib	228-236	platelet derived growth factor receptor alpha	Homo sapiens	137-143
23840364-1	2013	Advanced gastrointestinal stromal tumors (GIST), a KIT oncogene-driven tumor, on imatinib mesylate (IM) treatment may develop secondary KIT mutations to confer IM-resistant phenotype.	imatinib	81-98	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	51-54
23840364-1	2013	Advanced gastrointestinal stromal tumors (GIST), a KIT oncogene-driven tumor, on imatinib mesylate (IM) treatment may develop secondary KIT mutations to confer IM-resistant phenotype.	imatinib	81-98	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	136-139
23576565-8	2013	Similar results were obtained after selection of imatinib-resistant DOG1- and KIT-negative cells derived from parental DOG1 and KIT-positive GIST cells, where a 5,000-fold increase in IGFBP5 mRNA transcripts were documented.	imatinib	49-57	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	78-81
23576565-8	2013	Similar results were obtained after selection of imatinib-resistant DOG1- and KIT-negative cells derived from parental DOG1 and KIT-positive GIST cells, where a 5,000-fold increase in IGFBP5 mRNA transcripts were documented.	imatinib	49-57	anoctamin 1	Homo sapiens	119-123
23576565-8	2013	Similar results were obtained after selection of imatinib-resistant DOG1- and KIT-negative cells derived from parental DOG1 and KIT-positive GIST cells, where a 5,000-fold increase in IGFBP5 mRNA transcripts were documented.	imatinib	49-57	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	128-131
23576565-8	2013	Similar results were obtained after selection of imatinib-resistant DOG1- and KIT-negative cells derived from parental DOG1 and KIT-positive GIST cells, where a 5,000-fold increase in IGFBP5 mRNA transcripts were documented.	imatinib	49-57	insulin like growth factor binding protein 5	Homo sapiens	184-190
23592754-3	2013	The KIT tyrosine kinase inhibitor imatinib mesylate markedly prolongs the survival of patients with gastrointestinal stromal tumors (GIST) by direct effects on tumor cells as well as by indirect immunostimulatory effects on T and NK cells.	imatinib	34-42	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	4-7
23592754-7	2013	Moreover, GIST were infiltrated by a homogeneous subset of cytokine-secreting CD56(bright) (NCAM1) NK cells that accumulated in tumor foci after imatinib mesylate treatment.	imatinib	145-162	neural cell adhesion molecule 1	Homo sapiens	78-82
23592754-7	2013	Moreover, GIST were infiltrated by a homogeneous subset of cytokine-secreting CD56(bright) (NCAM1) NK cells that accumulated in tumor foci after imatinib mesylate treatment.	imatinib	145-162	neural cell adhesion molecule 1	Homo sapiens	92-97
23749045-4	2013	Imatinib or a blocking anti-stem cell factor (SCF) mAb also inhibited colony formation of two cell lines expressing C-KIT and SCF, and decreased P-AKT.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	116-121
23766461-0	2013	Can "specific" OCT1 inhibitors be used to determine OCT1 transporter activity toward imatinib?	imatinib	85-93	solute carrier family 22 member 1	Homo sapiens	15-19
23766461-0	2013	Can "specific" OCT1 inhibitors be used to determine OCT1 transporter activity toward imatinib?	imatinib	85-93	solute carrier family 22 member 1	Homo sapiens	52-56
23629659-6	2013	Inhibition of BCR-ABL using either imatinib or shRNA-mediated silencing led to the activation of SPTLC1 and to increased apoptosis in both K562 and LAMA-84 cells.	imatinib	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
23629659-6	2013	Inhibition of BCR-ABL using either imatinib or shRNA-mediated silencing led to the activation of SPTLC1 and to increased apoptosis in both K562 and LAMA-84 cells.	imatinib	35-43	serine palmitoyltransferase long chain base subunit 1	Homo sapiens	97-103
23749045-4	2013	Imatinib or a blocking anti-stem cell factor (SCF) mAb also inhibited colony formation of two cell lines expressing C-KIT and SCF, and decreased P-AKT.	imatinib	0-8	KIT ligand	Homo sapiens	126-129
23749045-4	2013	Imatinib or a blocking anti-stem cell factor (SCF) mAb also inhibited colony formation of two cell lines expressing C-KIT and SCF, and decreased P-AKT.	imatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	147-150
23462796-0	2013	Imatinib mesilate-induced phosphatidylinositol 3-kinase signalling and improved survival in insulin-producing cells: role of Src homology 2-containing inositol 5"-phosphatase interaction with c-Abl.	imatinib	0-17	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	125-128
23576564-1	2013	The imatinib paradigm in chronic myelogenous leukemia (CML) established continuous BCR-ABL inhibition as a design principle for ABL tyrosine kinase inhibitors (TKI).	imatinib	4-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
23576564-1	2013	The imatinib paradigm in chronic myelogenous leukemia (CML) established continuous BCR-ABL inhibition as a design principle for ABL tyrosine kinase inhibitors (TKI).	imatinib	4-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-90
23420410-7	2013	Additionally, imatinib is a promising targeted therapy for patients whose tumors harbor a KIT mutation in exons 11 and 13.	imatinib	14-22	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	90-93
23462796-8	2013	RESULTS: Imatinib stimulated ERK(thr202/tyr204) phosphorylation in a c-Abl-dependent manner.	imatinib	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-74
23440701-0	2013	Induction of autophagy by Imatinib sequesters Bcr-Abl in autophagosomes and down-regulates Bcr-Abl protein.	imatinib	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
23440701-0	2013	Induction of autophagy by Imatinib sequesters Bcr-Abl in autophagosomes and down-regulates Bcr-Abl protein.	imatinib	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
23440701-3	2013	We have previously demonstrated that imatinib can induce autophagy in Bcr-Abl expressing cells.	imatinib	37-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
23440701-4	2013	Autophagy has been associated with the clearance of large macromolecular signaling complexes and abnormal proteins, however, the contribution of autophagy to the turnover of Bcr-Abl protein in imatinib treated cells is unknown.	imatinib	193-201	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-181
23440701-5	2013	In this study, we show that following imatinib treatment, Bcr-Abl is sequestered into vesicular structures that co-localize with the autophagy marker LC3 or GABARAP.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
23440701-5	2013	In this study, we show that following imatinib treatment, Bcr-Abl is sequestered into vesicular structures that co-localize with the autophagy marker LC3 or GABARAP.	imatinib	38-46	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	150-153
23440701-5	2013	In this study, we show that following imatinib treatment, Bcr-Abl is sequestered into vesicular structures that co-localize with the autophagy marker LC3 or GABARAP.	imatinib	38-46	GABA type A receptor-associated protein	Homo sapiens	157-164
23440701-8	2013	Bcr-Abl protein expression was reduced with imatinib treatment.	imatinib	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
23440701-9	2013	Inhibition of both autophagy and proteasome activity in imatinib treated cells was required to restore Bcr-Abl protein levels to those of untreated cells.	imatinib	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
23440701-10	2013	This ability to down-regulate Bcr-Abl protein levels through the induction of autophagy may be an additional and important feature of the activity of imatinib.	imatinib	150-158	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
23462796-9	2013	Imatinib, but not sunitinib, also stimulated IRS-1(tyr612), Akt(ser473) and Akt(thr308) phosphorylation.	imatinib	0-8	insulin receptor substrate 1	Homo sapiens	45-50
23462796-9	2013	Imatinib, but not sunitinib, also stimulated IRS-1(tyr612), Akt(ser473) and Akt(thr308) phosphorylation.	imatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	60-63
23462796-0	2013	Imatinib mesilate-induced phosphatidylinositol 3-kinase signalling and improved survival in insulin-producing cells: role of Src homology 2-containing inositol 5"-phosphatase interaction with c-Abl.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	192-197
23462796-8	2013	RESULTS: Imatinib stimulated ERK(thr202/tyr204) phosphorylation in a c-Abl-dependent manner.	imatinib	9-17	mitogen-activated protein kinase 1	Homo sapiens	29-32
23456621-0	2013	Secondary mutations of c-KIT contribute to acquired resistance to imatinib and decrease efficacy of sunitinib in Chinese patients with gastrointestinal stromal tumors.	imatinib	66-74	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	23-28
23462796-9	2013	Imatinib, but not sunitinib, also stimulated IRS-1(tyr612), Akt(ser473) and Akt(thr308) phosphorylation.	imatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	76-79
23462796-12	2013	In line with this, imatinib decreased the phosphorylation of SHIP2 but not of PTEN.	imatinib	19-27	inositol polyphosphate phosphatase like 1	Homo sapiens	61-66
23462796-13	2013	c-Abl co-immunoprecipitated with SHIP2 and its binding to SHIP2 was largely reduced by imatinib but not by sunitinib.	imatinib	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
23462796-13	2013	c-Abl co-immunoprecipitated with SHIP2 and its binding to SHIP2 was largely reduced by imatinib but not by sunitinib.	imatinib	87-95	inositol polyphosphate phosphatase like 1	Homo sapiens	33-38
23462796-13	2013	c-Abl co-immunoprecipitated with SHIP2 and its binding to SHIP2 was largely reduced by imatinib but not by sunitinib.	imatinib	87-95	inositol polyphosphate phosphatase like 1	Homo sapiens	58-63
23462796-14	2013	Imatinib increased total beta-catenin levels and cell viability, whereas sunitinib exerted negative effects on cell viability.	imatinib	0-8	catenin beta 1	Homo sapiens	25-37
23462796-15	2013	CONCLUSIONS/INTERPRETATION: Imatinib inhibition of c-Abl in beta cells decreases SHIP2 activity, which results in enhanced signalling downstream of PI3 kinase.	imatinib	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-56
23462796-15	2013	CONCLUSIONS/INTERPRETATION: Imatinib inhibition of c-Abl in beta cells decreases SHIP2 activity, which results in enhanced signalling downstream of PI3 kinase.	imatinib	28-36	inositol polyphosphate phosphatase like 1	Homo sapiens	81-86
23540855-0	2013	Imatinib and prostate cancer: lessons learned from targeting the platelet-derived growth factor receptor.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	65-104
23540855-2	2013	Imatinib mesylate is a potent inhibitor of the platelet-derived growth factor receptor (PDGFR) and its activity has been tested in preclinical models and in Phase I and II clinical trials.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	47-86
23540855-2	2013	Imatinib mesylate is a potent inhibitor of the platelet-derived growth factor receptor (PDGFR) and its activity has been tested in preclinical models and in Phase I and II clinical trials.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	88-93
23540855-3	2013	AREAS COVERED: This review summarizes the preclinical data on PDGF/PDGFR in prostate cancer, and reviews the clinical and correlative data using imatinib as a PDGFR inhibitor.	imatinib	145-153	platelet derived growth factor receptor beta	Homo sapiens	159-164
23540855-6	2013	Correlations of pharmacodynamic monitoring of imatinib-induced PDGFR inhibition with progression-free and overall survival outcomes have led to the hypothesis that PDGF may function as a homeostatic factor in bone metastases.	imatinib	46-54	platelet derived growth factor receptor beta	Homo sapiens	63-68
23613267-0	2013	Two CML patients who subsequently developed features of essential thrombocythemia with JAK2-V617F mutation while in complete cytogenetic remission after treatment with imatinib mesylate.	imatinib	168-185	Janus kinase 2	Homo sapiens	87-91
23705634-1	2013	INTRODUCTION: Some inhibitors of tyrosine kinase, as imatinib, erlotinib and sunitinib have antihyperglycemic effects but the mechanisms are not totally clear.	imatinib	53-61	TXK tyrosine kinase	Homo sapiens	33-48
23610110-0	2013	Rare, germline mutation of KIT with imatinib-resistant multiple GI stromal tumors and mastocytosis.	imatinib	36-44	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	27-30
23212150-0	2013	Randomized comparison of prophylactic and minimal residual disease-triggered imatinib after allogeneic stem cell transplantation for BCR-ABL1-positive acute lymphoblastic leukemia.	imatinib	77-85	BCR activator of RhoGEF and GTPase	Homo sapiens	133-141
23212150-8	2013	In conclusion, post-transplant imatinib results in a low relapse rate, durable remissions and excellent long-term outcome in patients with BCR-ABL1-positive ALL irrespective of whether it is given prophylactically or MRD-triggered.	imatinib	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-147
23212150-9	2013	Reappearance of BCR-ABL1 transcripts early after SCT or at higher levels identifies a small subset of patients who do not benefit sufficiently from imatinib, and in whom alternative approaches should be explored.	imatinib	148-156	BCR activator of RhoGEF and GTPase	Homo sapiens	16-24
23859518-8	2013	Indeed patients with metastatic GIST and duplication within exon 9 of KIT deserve to receive twice the dose of imatinib, while GIST with PDGFRA p.D842 V mutation are resistant to this drug.	imatinib	111-119	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	70-73
23456621-1	2013	The aim of this study was to investigate the associations between secondary mutations of c-KIT/PDGFRalpha and acquired imatinib resistance or efficacy of sunitinib in Chinese patients with gastrointestinal stromal tumors (GISTs).	imatinib	119-127	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	89-94
23456621-1	2013	The aim of this study was to investigate the associations between secondary mutations of c-KIT/PDGFRalpha and acquired imatinib resistance or efficacy of sunitinib in Chinese patients with gastrointestinal stromal tumors (GISTs).	imatinib	119-127	platelet derived growth factor receptor alpha	Homo sapiens	95-105
23456621-6	2013	After imatinib treatment, 25 of 38 (65.8 %) resistant tumors had secondary mutations in c-KIT exon 13 (n = 10), exon 14 (n = 1), exon 17 (n = 12) and exon 18 (n = 2), while no secondary mutations of c-KIT were found in 14 sensitive tumors (P < 0.001), indicating the close association of c-KIT secondary mutations with imatinib-acquired resistance.	imatinib	6-14	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	88-93
23456621-6	2013	After imatinib treatment, 25 of 38 (65.8 %) resistant tumors had secondary mutations in c-KIT exon 13 (n = 10), exon 14 (n = 1), exon 17 (n = 12) and exon 18 (n = 2), while no secondary mutations of c-KIT were found in 14 sensitive tumors (P < 0.001), indicating the close association of c-KIT secondary mutations with imatinib-acquired resistance.	imatinib	322-330	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	88-93
23456621-8	2013	Secondary mutations of c-KIT were significantly associated with acquired resistance to imatinib in Chinese GIST patients, and whether secondary mutations of c-KIT could influence the efficacy of sunitinib needed to be further investigated.	imatinib	87-95	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	23-28
23894705-0	2013	Use of a KIT-specific monoclonal antibody to bypass imatinib resistance in gastrointestinal stromal tumors.	imatinib	52-60	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	9-12
23536723-0	2013	Suppression of survivin induced by a BCR-ABL/JAK2/STAT3 pathway sensitizes imatinib-resistant CML cells to different cytotoxic drugs.	imatinib	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
23536723-0	2013	Suppression of survivin induced by a BCR-ABL/JAK2/STAT3 pathway sensitizes imatinib-resistant CML cells to different cytotoxic drugs.	imatinib	75-83	Janus kinase 2	Homo sapiens	45-49
23536723-0	2013	Suppression of survivin induced by a BCR-ABL/JAK2/STAT3 pathway sensitizes imatinib-resistant CML cells to different cytotoxic drugs.	imatinib	75-83	signal transducer and activator of transcription 3	Homo sapiens	50-55
23564048-3	2013	In K562 CML cells, all drugs tested, in combination with imatinib impaired the expression or cellular distribution of LC3 and Beclin 1 (autophagy markers) and reduced the recovery of cells following drug withdrawal.	imatinib	57-65	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	118-121
23564048-3	2013	In K562 CML cells, all drugs tested, in combination with imatinib impaired the expression or cellular distribution of LC3 and Beclin 1 (autophagy markers) and reduced the recovery of cells following drug withdrawal.	imatinib	57-65	beclin 1	Homo sapiens	126-134
23894705-2	2013	We have recently demonstrated that a monoclonal antibody targeting KIT could potentially bypass imatinib resistance in preclinical models of GIST.	imatinib	96-104	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	67-70
23815902-0	2013	[Efficacy of dasatinib in treatment of imatinib-resistant BCR/ABL positive leukemia].	imatinib	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
23315207-0	2013	Ex vivo evaluation of imatinib mesylate for induction of cell death on canine neoplastic mast cells with mutations in c-Kit exon 11 via apoptosis.	imatinib	22-39	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	118-123
23315207-3	2013	We hypothesize that the selective tyrosine kinase inhibitor imatinib mesylate inhibits signal transduction and induces apoptosis when tested in cutaneous canine mast cell tumour samples positive for mutation in c-kit exon 11.	imatinib	60-77	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	211-216
23315207-8	2013	Our results demonstrate that STI-571 induces Caspase-dependent apoptosis in a canine neoplastic mast cells possessing mutations in c-kit exon 11.	imatinib	29-36	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	131-136
23815902-1	2013	This study was aimed to evaluate the efficacy and safety of dasatinib in BCR/ABL positive leukemia patients with primary or secondary resistance to imatinib.	imatinib	148-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
23815902-4	2013	The results showed that the median duration of dasatinib therapy was 8 (1-66) months in the 27 imatinib-resistant BCR/ABL positive leukemia cases, with a median follow-up of 54 (3-75) months.	imatinib	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
23815902-10	2013	It is concluded that dasatinib is an effective drug in imatinib-resistant BCR/ABL positive leukemia patients, the better curative effect and better tolerance has been observed in patients who received dasatinib in stable disease.	imatinib	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
22797058-7	2013	Imatinib (Gleevec), a clinical drug that blocks c-Kit kinase activity, also demonstrated its inhibition potency on OTICs.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	48-53
23984520-0	2013	[Annexin A1 increases the sensitivity of K562 cell to imatinib].	imatinib	54-62	annexin A1	Homo sapiens	1-11
23984520-2	2013	Previous research showed that ANXA1 could increase markedly with multiple increase of drug resistance in K562/imatinib cell lines in vitro.	imatinib	110-118	annexin A1	Homo sapiens	30-35
23984520-4	2013	Cell growth inhibition experiment via MTT and cell proliferation experiment via MTS showed that K562-pEGFP-N1-ANXA1 cell strain was more sensitive to imatinib than the K562-pEGFP-N1 cell strain, and however the ability of proliferation of K562-pEGFP-N1-ANXA1 cell strain did not change compared with the negative control.	imatinib	150-158	annexin A1	Homo sapiens	110-115
23984520-4	2013	Cell growth inhibition experiment via MTT and cell proliferation experiment via MTS showed that K562-pEGFP-N1-ANXA1 cell strain was more sensitive to imatinib than the K562-pEGFP-N1 cell strain, and however the ability of proliferation of K562-pEGFP-N1-ANXA1 cell strain did not change compared with the negative control.	imatinib	150-158	annexin A1	Homo sapiens	253-258
23984520-7	2013	The deduction was that ANXA1 may make the K562-pEGFP-N1-ANXA1 cell strain more sensitive to imatinib due to the increased uptake of imatinib via the increase of ANXA1 and the interaction between ANXA1 and beta-actin in the K562-pEGFP-N1-ANXA1 cell strain in vitro.	imatinib	92-100	annexin A1	Homo sapiens	23-28
23984520-7	2013	The deduction was that ANXA1 may make the K562-pEGFP-N1-ANXA1 cell strain more sensitive to imatinib due to the increased uptake of imatinib via the increase of ANXA1 and the interaction between ANXA1 and beta-actin in the K562-pEGFP-N1-ANXA1 cell strain in vitro.	imatinib	92-100	annexin A1	Homo sapiens	56-61
23984520-7	2013	The deduction was that ANXA1 may make the K562-pEGFP-N1-ANXA1 cell strain more sensitive to imatinib due to the increased uptake of imatinib via the increase of ANXA1 and the interaction between ANXA1 and beta-actin in the K562-pEGFP-N1-ANXA1 cell strain in vitro.	imatinib	92-100	annexin A1	Homo sapiens	56-61
23984520-7	2013	The deduction was that ANXA1 may make the K562-pEGFP-N1-ANXA1 cell strain more sensitive to imatinib due to the increased uptake of imatinib via the increase of ANXA1 and the interaction between ANXA1 and beta-actin in the K562-pEGFP-N1-ANXA1 cell strain in vitro.	imatinib	92-100	annexin A1	Homo sapiens	56-61
23984520-7	2013	The deduction was that ANXA1 may make the K562-pEGFP-N1-ANXA1 cell strain more sensitive to imatinib due to the increased uptake of imatinib via the increase of ANXA1 and the interaction between ANXA1 and beta-actin in the K562-pEGFP-N1-ANXA1 cell strain in vitro.	imatinib	92-100	POTE ankyrin domain family member F	Homo sapiens	205-215
23984520-7	2013	The deduction was that ANXA1 may make the K562-pEGFP-N1-ANXA1 cell strain more sensitive to imatinib due to the increased uptake of imatinib via the increase of ANXA1 and the interaction between ANXA1 and beta-actin in the K562-pEGFP-N1-ANXA1 cell strain in vitro.	imatinib	92-100	annexin A1	Homo sapiens	56-61
23984520-7	2013	The deduction was that ANXA1 may make the K562-pEGFP-N1-ANXA1 cell strain more sensitive to imatinib due to the increased uptake of imatinib via the increase of ANXA1 and the interaction between ANXA1 and beta-actin in the K562-pEGFP-N1-ANXA1 cell strain in vitro.	imatinib	132-140	annexin A1	Homo sapiens	23-28
23984520-7	2013	The deduction was that ANXA1 may make the K562-pEGFP-N1-ANXA1 cell strain more sensitive to imatinib due to the increased uptake of imatinib via the increase of ANXA1 and the interaction between ANXA1 and beta-actin in the K562-pEGFP-N1-ANXA1 cell strain in vitro.	imatinib	132-140	annexin A1	Homo sapiens	56-61
23984520-7	2013	The deduction was that ANXA1 may make the K562-pEGFP-N1-ANXA1 cell strain more sensitive to imatinib due to the increased uptake of imatinib via the increase of ANXA1 and the interaction between ANXA1 and beta-actin in the K562-pEGFP-N1-ANXA1 cell strain in vitro.	imatinib	132-140	annexin A1	Homo sapiens	56-61
23984520-7	2013	The deduction was that ANXA1 may make the K562-pEGFP-N1-ANXA1 cell strain more sensitive to imatinib due to the increased uptake of imatinib via the increase of ANXA1 and the interaction between ANXA1 and beta-actin in the K562-pEGFP-N1-ANXA1 cell strain in vitro.	imatinib	132-140	annexin A1	Homo sapiens	56-61
23984520-7	2013	The deduction was that ANXA1 may make the K562-pEGFP-N1-ANXA1 cell strain more sensitive to imatinib due to the increased uptake of imatinib via the increase of ANXA1 and the interaction between ANXA1 and beta-actin in the K562-pEGFP-N1-ANXA1 cell strain in vitro.	imatinib	132-140	POTE ankyrin domain family member F	Homo sapiens	205-215
23984520-7	2013	The deduction was that ANXA1 may make the K562-pEGFP-N1-ANXA1 cell strain more sensitive to imatinib due to the increased uptake of imatinib via the increase of ANXA1 and the interaction between ANXA1 and beta-actin in the K562-pEGFP-N1-ANXA1 cell strain in vitro.	imatinib	132-140	annexin A1	Homo sapiens	56-61
23827110-1	2013	OBJECTIVE: To investigate the effect of up-regulated expression of tumor suppressor gene p14(ARF) on apoptosis of chronic myeloid leukemia (CML) cells and its interaction with imatinib.	imatinib	176-184	ribonuclease P/MRP subunit p14	Homo sapiens	89-92
23827110-8	2013	Imatinib significantly inhibited the proliferation of K562-p14(ARF) cells in a dose-dependent manner.	imatinib	0-8	ribonuclease P/MRP subunit p14	Homo sapiens	59-62
23668619-3	2013	Imatinib is a tirosin-kinase inhibitors (TKI) active against CSF1-receptor whose activity in naive PVNS was already described.	imatinib	0-8	colony stimulating factor 1	Homo sapiens	61-65
23827110-10	2013	CONCLUSION: Increased p14(ARF) gene expression could induce apoptosis of CML cells; Moreover, it could enhance inhibitory effect on cell proliferation when combined with imatinib.	imatinib	170-178	ribonuclease P/MRP subunit p14	Homo sapiens	22-25
23827112-0	2013	[Effect of VE-cadherin on sensitivity to Imatinib in Sup-B15 Philadelphia chromosome positive acute lymphoblastic leukemia cells].	imatinib	41-49	cadherin 5	Homo sapiens	11-22
23827112-1	2013	OBJECTIVE: To investigate the sensitivity of imatinib mesylate (IM) on Sup-B15 Ph+ acute lymphoblastic leukemia (ALL) cells knockdown of VE-cadherin (CD144), and to further explore its mechanism.	imatinib	45-62	cadherin 5	Homo sapiens	137-148
23827112-1	2013	OBJECTIVE: To investigate the sensitivity of imatinib mesylate (IM) on Sup-B15 Ph+ acute lymphoblastic leukemia (ALL) cells knockdown of VE-cadherin (CD144), and to further explore its mechanism.	imatinib	45-62	cadherin 5	Homo sapiens	150-155
23691243-9	2013	Inhibition of Abl with STI571 rescued the multi-lobular WAVE2-KD 3D phenotype whereas overexpression of Abl kinase phenocopied the WAVE2-KD phenotype.	imatinib	23-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-17
23668619-4	2013	We report on two PVNS patients who responded to imatinib after failure to nilotinib, another CSF1-receptor inhibitor.	imatinib	48-56	colony stimulating factor 1	Homo sapiens	93-97
23515925-0	2013	Early molecular response and female sex strongly predict stable undetectable BCR-ABL1, the criteria for imatinib discontinuation in patients with CML.	imatinib	104-112	BCR activator of RhoGEF and GTPase	Homo sapiens	77-85
23642185-0	2013	Imatinib mesylate inhibits cell growth of malignant peripheral nerve sheath tumors in vitro and in vivo through suppression of PDGFR-beta.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	127-137
23515925-11	2013	The findings justify the focus on rapid reduction of BCR-ABL1 as a strategy to maximize potential suitability for imatinib discontinuation studies.	imatinib	114-122	BCR activator of RhoGEF and GTPase	Homo sapiens	53-61
23642185-5	2013	Imatinib mesylate effectively suppressed MPNST cell growth in vitro at concentrations similar to those used clinically (1.46 - 4.6 muM) in three of six cell lines.	imatinib	0-17	latexin	Homo sapiens	131-134
23065514-1	2013	The BCR-ABL T315I mutation causes resistance to imatinib, nilotinib and dasatinib in chronic myeloid leukemia.	imatinib	48-56	BCR activator of RhoGEF and GTPase	Homo sapiens	4-9
23480638-1	2013	BACKGROUND: Acquired resistance to imatinib is frequently caused by secondary KIT mutations.	imatinib	35-43	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	78-81
23518411-1	2013	The capacity of imatinib mesylate to reverse established pulmonary arterial hypertension (PAH) has been attributed to a reduction in pulmonary arterial muscularization via inhibition of platelet-derived growth factor receptor-beta on vascular smooth muscle cells.	imatinib	16-33	platelet derived growth factor receptor beta	Rattus norvegicus	186-230
23518411-4	2013	The prevention of pulmonary hypertension by imatinib blocked these changes in pulmonary leukocyte content and induced elevations in pulmonary interferon-gamma, tumor necrosis factor alpha, and IL-10, corresponding to the enhanced activity of splenic NK cells ex vivo.	imatinib	44-52	interferon gamma	Rattus norvegicus	142-187
23518411-4	2013	The prevention of pulmonary hypertension by imatinib blocked these changes in pulmonary leukocyte content and induced elevations in pulmonary interferon-gamma, tumor necrosis factor alpha, and IL-10, corresponding to the enhanced activity of splenic NK cells ex vivo.	imatinib	44-52	interleukin 10	Rattus norvegicus	193-198
23374223-4	2013	Imatinib (Glivec( )) is a tyrosine kinase inhibitor specific for PDGF-Rs, c-KappaIotaTau and BCR-ABL.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
23420553-0	2013	Apoptosis in chronic myeloid leukemia cells transiently treated with imatinib or dasatinib is caused by residual BCR-ABL kinase inhibition.	imatinib	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
23395818-3	2013	Inhibition of the mammalian target of rapamycin (mTOR) in imatinib-resistant BCR-ABL1-positive cells was effective in vitro, but in a pilot clinical trial, only a few patients responded to the treatment.	imatinib	58-66	mechanistic target of rapamycin kinase	Homo sapiens	18-47
23395818-3	2013	Inhibition of the mammalian target of rapamycin (mTOR) in imatinib-resistant BCR-ABL1-positive cells was effective in vitro, but in a pilot clinical trial, only a few patients responded to the treatment.	imatinib	58-66	mechanistic target of rapamycin kinase	Homo sapiens	49-53
23459373-0	2013	Extracellular domain c-kit mutation with duplication of Ser501Ala502 found in gastrointestinal stromal tumors is more imatinib- and nilotinib-sensitive than that with duplication of Ala502Tyr503.	imatinib	118-126	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	21-26
23459373-13	2013	Although mutation sites of KIT-Dup-Ser501Ala502 and KIT-Dup-Ala502Tyr503 are closely located, imatinib- and nilotinib-sensitive KIT-Dup-Ser501Ala502 are distinguishable from KIT-Dup-Ala502Tyr503.	imatinib	94-102	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	27-30
23459373-8	2013	The inhibitory effect of selective tyrosine kinase inhibitors, imatinib and nilotinib, on KIT-Dup-Ser501Ala502 was examined and compared with that of KIT-Dup-Ala502Tyr503.	imatinib	63-71	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	90-93
23459373-13	2013	Although mutation sites of KIT-Dup-Ser501Ala502 and KIT-Dup-Ala502Tyr503 are closely located, imatinib- and nilotinib-sensitive KIT-Dup-Ser501Ala502 are distinguishable from KIT-Dup-Ala502Tyr503.	imatinib	94-102	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	52-55
23459373-12	2013	In fact, a patient with KIT-Dup-Ser501Ala502 showed long-term stable disease with administration of the usual dose of 400 mg imatinib.	imatinib	125-133	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	24-27
23459373-13	2013	Although mutation sites of KIT-Dup-Ser501Ala502 and KIT-Dup-Ala502Tyr503 are closely located, imatinib- and nilotinib-sensitive KIT-Dup-Ser501Ala502 are distinguishable from KIT-Dup-Ala502Tyr503.	imatinib	94-102	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	52-55
23394269-8	2013	The ratio of CD4+CD25+Foxp3+ cells in blood was significantly higher at 30 and 60 days after imatinib therapy than that at the time of pre-imatinib in 20 patients (P = 0.019 and 0.001, respectively).	imatinib	93-101	CD4 molecule	Homo sapiens	13-16
23761821-0	2013	Multiple copies of BCR-ABL fusion gene on two isodicentric Philadelphia chromosomes in an imatinib mesylate-resistant chronic myeloid leukemia patient.	imatinib	90-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
23394269-8	2013	The ratio of CD4+CD25+Foxp3+ cells in blood was significantly higher at 30 and 60 days after imatinib therapy than that at the time of pre-imatinib in 20 patients (P = 0.019 and 0.001, respectively).	imatinib	93-101	forkhead box P3	Homo sapiens	22-27
23459373-13	2013	Although mutation sites of KIT-Dup-Ser501Ala502 and KIT-Dup-Ala502Tyr503 are closely located, imatinib- and nilotinib-sensitive KIT-Dup-Ser501Ala502 are distinguishable from KIT-Dup-Ala502Tyr503.	imatinib	94-102	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	52-55
23761821-2	2013	Amplification or duplication of the BCR-ABL gene has been found to be one of the key factors leading to drug resistance to imatinib mesylate (IM).	imatinib	123-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
22710719-9	2013	As p27 overexpression is reported to induce erythroid differentiation in K562, we explored the effect of MYC on imatinib-dependent induction of p27.	imatinib	112-120	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	105-108
22710719-9	2013	As p27 overexpression is reported to induce erythroid differentiation in K562, we explored the effect of MYC on imatinib-dependent induction of p27.	imatinib	112-120	interferon alpha inducible protein 27	Homo sapiens	144-147
22710719-0	2013	MYC antagonizes the differentiation induced by imatinib in chronic myeloid leukemia cells through downregulation of p27(KIP1.).	imatinib	47-55	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	0-3
22710719-10	2013	We show that MYC abrogated the imatinib-induced upregulation of p27 concomitantly with the differentiation inhibition, suggesting that MYC inhibits differentiation by antagonizing the imatinib-mediated upregulation of p27.	imatinib	31-39	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	13-16
22710719-0	2013	MYC antagonizes the differentiation induced by imatinib in chronic myeloid leukemia cells through downregulation of p27(KIP1.).	imatinib	47-55	interferon alpha inducible protein 27	Homo sapiens	116-119
22710719-10	2013	We show that MYC abrogated the imatinib-induced upregulation of p27 concomitantly with the differentiation inhibition, suggesting that MYC inhibits differentiation by antagonizing the imatinib-mediated upregulation of p27.	imatinib	31-39	interferon alpha inducible protein 27	Homo sapiens	64-67
22710719-0	2013	MYC antagonizes the differentiation induced by imatinib in chronic myeloid leukemia cells through downregulation of p27(KIP1.).	imatinib	47-55	cyclin dependent kinase inhibitor 1B	Homo sapiens	120-124
22710719-10	2013	We show that MYC abrogated the imatinib-induced upregulation of p27 concomitantly with the differentiation inhibition, suggesting that MYC inhibits differentiation by antagonizing the imatinib-mediated upregulation of p27.	imatinib	31-39	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	135-138
22710719-4	2013	We found that imatinib upregulated the cell cycle inhibitor p27(KIP1) (p27) in a time- and -concentration dependent manner, and that the extent of imatinib-mediated differentiation was severely decreased in cells with depleted p27.	imatinib	14-22	cyclin dependent kinase inhibitor 1B	Homo sapiens	60-68
22710719-10	2013	We show that MYC abrogated the imatinib-induced upregulation of p27 concomitantly with the differentiation inhibition, suggesting that MYC inhibits differentiation by antagonizing the imatinib-mediated upregulation of p27.	imatinib	31-39	interferon alpha inducible protein 27	Homo sapiens	218-221
22710719-4	2013	We found that imatinib upregulated the cell cycle inhibitor p27(KIP1) (p27) in a time- and -concentration dependent manner, and that the extent of imatinib-mediated differentiation was severely decreased in cells with depleted p27.	imatinib	14-22	interferon alpha inducible protein 27	Homo sapiens	60-63
22710719-10	2013	We show that MYC abrogated the imatinib-induced upregulation of p27 concomitantly with the differentiation inhibition, suggesting that MYC inhibits differentiation by antagonizing the imatinib-mediated upregulation of p27.	imatinib	184-192	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	13-16
22710719-4	2013	We found that imatinib upregulated the cell cycle inhibitor p27(KIP1) (p27) in a time- and -concentration dependent manner, and that the extent of imatinib-mediated differentiation was severely decreased in cells with depleted p27.	imatinib	14-22	interferon alpha inducible protein 27	Homo sapiens	71-74
22710719-6	2013	MYC is overexpressed in untreated CML and is associated to poor response to imatinib.	imatinib	76-84	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	0-3
22710719-10	2013	We show that MYC abrogated the imatinib-induced upregulation of p27 concomitantly with the differentiation inhibition, suggesting that MYC inhibits differentiation by antagonizing the imatinib-mediated upregulation of p27.	imatinib	184-192	interferon alpha inducible protein 27	Homo sapiens	64-67
22710719-7	2013	Using K562 sublines with conditional MYC expression (induced by Zn(2+) or activated by 4-hydroxy-tamoxifen) we show that MYC prevented the erythroid differentiation induced by imatinib and dasatinib.	imatinib	176-184	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	121-124
22710719-10	2013	We show that MYC abrogated the imatinib-induced upregulation of p27 concomitantly with the differentiation inhibition, suggesting that MYC inhibits differentiation by antagonizing the imatinib-mediated upregulation of p27.	imatinib	184-192	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	135-138
22710719-10	2013	We show that MYC abrogated the imatinib-induced upregulation of p27 concomitantly with the differentiation inhibition, suggesting that MYC inhibits differentiation by antagonizing the imatinib-mediated upregulation of p27.	imatinib	184-192	interferon alpha inducible protein 27	Homo sapiens	218-221
23770790-0	2013	Profile of BCR-ABL transcript levels based on Sokal prognostic score in chronic myeloid leukemia patients treated with imatinib.	imatinib	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-18
23607741-0	2013	Alterations of Gab2 signalling complexes in imatinib and dasatinib treated chronic myeloid leukaemia cells.	imatinib	44-52	GRB2 associated binding protein 2	Homo sapiens	15-19
23607741-4	2013	In the course of that project, we noticed that two clinically relevant drugs, imatinib and dasatinib, provoke distinct alterations in the electrophoretic mobility of Gab2, its signalling output and protein interactions.	imatinib	78-86	GRB2 associated binding protein 2	Homo sapiens	166-170
23607741-6	2013	FINDINGS: Using stable isotope labelling by amino acids in cell culture (SILAC)-based quantitative mass spectrometry (MS), we show now that imatinib and dasatinib provoke distinct effects on the phosphorylation status and interactome of Gab2.	imatinib	140-148	GRB2 associated binding protein 2	Homo sapiens	237-241
23607741-10	2013	In addition, we also identify novel components of the Gab2 signalling complex, such as casein kinases, stathmins and PIP1 as well as known interaction partners whose association with Gab2 is disrupted by imatinib and/or dasatinib.	imatinib	204-212	GRB2 associated binding protein 2	Homo sapiens	54-58
23607741-10	2013	In addition, we also identify novel components of the Gab2 signalling complex, such as casein kinases, stathmins and PIP1 as well as known interaction partners whose association with Gab2 is disrupted by imatinib and/or dasatinib.	imatinib	204-212	GRB2 associated binding protein 2	Homo sapiens	183-187
23613979-5	2013	In this study, we investigate the effect of ACM on the sensitivity of human CML cell line K562 to Bcr-Abl specific inhibitor imatinib (STI571, Gleevec).	imatinib	125-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
23613979-5	2013	In this study, we investigate the effect of ACM on the sensitivity of human CML cell line K562 to Bcr-Abl specific inhibitor imatinib (STI571, Gleevec).	imatinib	135-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
23613979-8	2013	Sequential treatment with ACM and imatinib induced Bcr-Abl down-regulation, cytochrome c release into the cytosol, and caspase-3 activation, as well as decreased Mcl-1 and Bcl-xL expressions, but did not affect Fas ligand/Fas death receptor and procaspase-8 expressions.	imatinib	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
23613979-8	2013	Sequential treatment with ACM and imatinib induced Bcr-Abl down-regulation, cytochrome c release into the cytosol, and caspase-3 activation, as well as decreased Mcl-1 and Bcl-xL expressions, but did not affect Fas ligand/Fas death receptor and procaspase-8 expressions.	imatinib	34-42	cytochrome c, somatic	Homo sapiens	76-88
23613979-8	2013	Sequential treatment with ACM and imatinib induced Bcr-Abl down-regulation, cytochrome c release into the cytosol, and caspase-3 activation, as well as decreased Mcl-1 and Bcl-xL expressions, but did not affect Fas ligand/Fas death receptor and procaspase-8 expressions.	imatinib	34-42	caspase 3	Homo sapiens	119-128
23613979-8	2013	Sequential treatment with ACM and imatinib induced Bcr-Abl down-regulation, cytochrome c release into the cytosol, and caspase-3 activation, as well as decreased Mcl-1 and Bcl-xL expressions, but did not affect Fas ligand/Fas death receptor and procaspase-8 expressions.	imatinib	34-42	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	162-167
23613979-8	2013	Sequential treatment with ACM and imatinib induced Bcr-Abl down-regulation, cytochrome c release into the cytosol, and caspase-3 activation, as well as decreased Mcl-1 and Bcl-xL expressions, but did not affect Fas ligand/Fas death receptor and procaspase-8 expressions.	imatinib	34-42	BCL2 like 1	Homo sapiens	172-178
23613979-9	2013	ACM/imatinib sequential treatment-induced apoptosis was suppressed by a caspase-9 inhibitor and a caspase-3 inhibitor, indicating that the caspase cascade is involved in this apoptosis.	imatinib	4-12	caspase 9	Homo sapiens	72-81
23613979-9	2013	ACM/imatinib sequential treatment-induced apoptosis was suppressed by a caspase-9 inhibitor and a caspase-3 inhibitor, indicating that the caspase cascade is involved in this apoptosis.	imatinib	4-12	caspase 3	Homo sapiens	98-107
23613955-0	2013	Inhibition of BCR/ABL protein expression by miR-203 sensitizes for imatinib mesylate.	imatinib	67-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
23613955-0	2013	Inhibition of BCR/ABL protein expression by miR-203 sensitizes for imatinib mesylate.	imatinib	67-84	microRNA 203a	Homo sapiens	44-51
23613955-1	2013	Selective inhibition of BCR/ABL expression by RNA interference has been demonstrated as an effective strategy in CML treatment and a reversal to imatinib resistance.	imatinib	145-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
23613955-5	2013	Furthermore, miR-203 increased sensitivity to imatinib in BaF3-BCR/ABL(T315I) cells, thereby antagonizing the main mechanism of resistance to imatinib.	imatinib	46-54	microRNA 203a	Homo sapiens	13-20
23613955-5	2013	Furthermore, miR-203 increased sensitivity to imatinib in BaF3-BCR/ABL(T315I) cells, thereby antagonizing the main mechanism of resistance to imatinib.	imatinib	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
23613955-5	2013	Furthermore, miR-203 increased sensitivity to imatinib in BaF3-BCR/ABL(T315I) cells, thereby antagonizing the main mechanism of resistance to imatinib.	imatinib	142-150	microRNA 203a	Homo sapiens	13-20
23613955-5	2013	Furthermore, miR-203 increased sensitivity to imatinib in BaF3-BCR/ABL(T315I) cells, thereby antagonizing the main mechanism of resistance to imatinib.	imatinib	142-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
23556431-1	2013	BACKGROUND: The use of imatinib, an ABL tyrosine kinase inhibitor, has led to a dramatic change in the management of BCR-ABL-positive leukemia patients.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
23556431-2	2013	However, resistance to imatinib mediated by mutations in the BCR-ABL domain has become a major problem in the treatment of these patients.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
23637779-3	2013	We initially observed that imatinib (IM), an inhibitor targeting the tyrosine kinase activity of c-Kit concomitantly down-regulated the expression of c-Kit and accelerated the Epo-driven differentiation of erythroblasts in the absence of SCF.	imatinib	27-35	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	97-102
23637779-3	2013	We initially observed that imatinib (IM), an inhibitor targeting the tyrosine kinase activity of c-Kit concomitantly down-regulated the expression of c-Kit and accelerated the Epo-driven differentiation of erythroblasts in the absence of SCF.	imatinib	27-35	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	150-155
23637779-3	2013	We initially observed that imatinib (IM), an inhibitor targeting the tyrosine kinase activity of c-Kit concomitantly down-regulated the expression of c-Kit and accelerated the Epo-driven differentiation of erythroblasts in the absence of SCF.	imatinib	27-35	erythropoietin	Homo sapiens	176-179
23637779-3	2013	We initially observed that imatinib (IM), an inhibitor targeting the tyrosine kinase activity of c-Kit concomitantly down-regulated the expression of c-Kit and accelerated the Epo-driven differentiation of erythroblasts in the absence of SCF.	imatinib	27-35	KIT ligand	Homo sapiens	238-241
23637779-3	2013	We initially observed that imatinib (IM), an inhibitor targeting the tyrosine kinase activity of c-Kit concomitantly down-regulated the expression of c-Kit and accelerated the Epo-driven differentiation of erythroblasts in the absence of SCF.	imatinib	37-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	97-102
23637779-3	2013	We initially observed that imatinib (IM), an inhibitor targeting the tyrosine kinase activity of c-Kit concomitantly down-regulated the expression of c-Kit and accelerated the Epo-driven differentiation of erythroblasts in the absence of SCF.	imatinib	37-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	150-155
23637779-3	2013	We initially observed that imatinib (IM), an inhibitor targeting the tyrosine kinase activity of c-Kit concomitantly down-regulated the expression of c-Kit and accelerated the Epo-driven differentiation of erythroblasts in the absence of SCF.	imatinib	37-39	erythropoietin	Homo sapiens	176-179
23637779-3	2013	We initially observed that imatinib (IM), an inhibitor targeting the tyrosine kinase activity of c-Kit concomitantly down-regulated the expression of c-Kit and accelerated the Epo-driven differentiation of erythroblasts in the absence of SCF.	imatinib	37-39	KIT ligand	Homo sapiens	238-241
23613627-13	2013	Expression of bcl-2 mRNA in the transplanted GISTs was markedly downregulated (P < 0.01) in the PS-ASODN group (7.245 +- 0.739) compared with the imatinib group (14.153 +- 1.618) and liposome negative control group (16.396 +- 1.351).	imatinib	149-157	B cell leukemia/lymphoma 2	Mus musculus	14-19
22641215-1	2013	Resistance to imatinib (IM) and other tyrosine kinase inhibitors (TKI)s is an increasing problem in leukemias caused by expression of BCR-ABL1.	imatinib	14-22	BCR activator of RhoGEF and GTPase	Homo sapiens	134-142
22641215-3	2013	Notably, the steady state levels of two ALT NHEJ proteins, poly-(ADP-ribose) polymerase 1 (PARP1) and DNA ligase IIIalpha, were increased in the BCR-ABL1-positive CML cell line K562 and, to a greater extent, in its imatinib-resistant (IMR) derivative.	imatinib	215-223	poly(ADP-ribose) polymerase 1	Homo sapiens	59-89
22641215-3	2013	Notably, the steady state levels of two ALT NHEJ proteins, poly-(ADP-ribose) polymerase 1 (PARP1) and DNA ligase IIIalpha, were increased in the BCR-ABL1-positive CML cell line K562 and, to a greater extent, in its imatinib-resistant (IMR) derivative.	imatinib	215-223	poly(ADP-ribose) polymerase 1	Homo sapiens	91-96
22641215-3	2013	Notably, the steady state levels of two ALT NHEJ proteins, poly-(ADP-ribose) polymerase 1 (PARP1) and DNA ligase IIIalpha, were increased in the BCR-ABL1-positive CML cell line K562 and, to a greater extent, in its imatinib-resistant (IMR) derivative.	imatinib	215-223	BCR activator of RhoGEF and GTPase	Homo sapiens	145-153
23770790-1	2013	AIM: to elucidate the pattern of molecular response assessed by logarithmic reduction in BCR-ABL transcription levels based on Sokal prognostic score in chronic phase chronic myeloid leukemia (CML) patients receiving Imatinib treatment.	imatinib	217-225	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
23770790-8	2013	After 18 months of Imatinib treatment, the undetected BCR-ABL transcript level (complete MR) were 7(70%), 8(66.7%), and 9(50%) in low-, intermediate-, and high risk group patients, respectively (p=0.417).	imatinib	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
23370613-0	2013	The new iodoacetamidobenzofuran derivative TR120 decreases STAT5 expression and induces antitumor effects in imatinib-sensitive and imatinib-resistant BCR-ABL-expressing leukemia cells.	imatinib	132-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-158
23370613-1	2013	The identification of novel compounds modulating the expression/activity of molecular targets downstream to BCR-ABL could be a new approach in the treatment of chronic myeloid leukemias (CMLs) resistant to imatinib or other BCR-ABL-targeted molecules.	imatinib	206-214	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
23370613-8	2013	Considering that STAT5 is a BCR-ABL molecular target that plays a key role in the pathogenesis of CML as well as in BCR-ABL-mediated resistance to apoptosis, TR120 could potentially be a useful novel agent in the treatment of imatinib-resistant CML.	imatinib	226-234	signal transducer and activator of transcription 5A	Homo sapiens	17-22
23432194-3	2013	ABCA3 protected leukaemic cells from the cytotoxic effects of the tyrosine kinase inhibitors imatinib, dasatinib, and nilotinib.	imatinib	93-101	ATP binding cassette subfamily A member 3	Homo sapiens	0-5
23400594-9	2013	STAT5A attenuation was also active at inhibiting growth of CML CD34(+) cells from patients with acquired resistance to imatinib.	imatinib	119-127	signal transducer and activator of transcription 5A	Homo sapiens	0-6
23400594-9	2013	STAT5A attenuation was also active at inhibiting growth of CML CD34(+) cells from patients with acquired resistance to imatinib.	imatinib	119-127	CD34 molecule	Homo sapiens	63-67
23174907-9	2013	Furthermore, CD90+ cells enhanced the motility of EpCAM+ cells when cocultured in vitro through the activation of transforming growth factor beta (TGF-beta) signaling, whereas imatinib mesylate suppressed TGFB1 expression in CD90+ cells as well as CD90+ cell-induced motility of EpCAM+ cells.	imatinib	176-193	transforming growth factor beta 1	Homo sapiens	205-210
23751892-0	2013	A ZMYM2-FGFR1 8p11 myeloproliferative neoplasm with a novel nonsense RUNX1 mutation and tumor lysis upon imatinib treatment.	imatinib	105-113	zinc finger MYM-type containing 2	Homo sapiens	2-7
23751892-0	2013	A ZMYM2-FGFR1 8p11 myeloproliferative neoplasm with a novel nonsense RUNX1 mutation and tumor lysis upon imatinib treatment.	imatinib	105-113	fibroblast growth factor receptor 1	Homo sapiens	8-13
23751892-0	2013	A ZMYM2-FGFR1 8p11 myeloproliferative neoplasm with a novel nonsense RUNX1 mutation and tumor lysis upon imatinib treatment.	imatinib	105-113	RUNX family transcription factor 1	Homo sapiens	69-74
23751892-3	2013	Here we report on a case with a t(8;13)(p11.2;q12.1) ZMYM2-FGFR1 fusion, with massive tumor lysis upon tyrosine kinase inhibition with imatinib.	imatinib	135-143	zinc finger MYM-type containing 2	Homo sapiens	53-58
23751892-3	2013	Here we report on a case with a t(8;13)(p11.2;q12.1) ZMYM2-FGFR1 fusion, with massive tumor lysis upon tyrosine kinase inhibition with imatinib.	imatinib	135-143	fibroblast growth factor receptor 1	Homo sapiens	59-64
23596478-2	2013	Imatinib mesylate (IM), an inhibitor of the tyrosine kinase activity of BCR-ABL, has been used as a first-line therapy for CML.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
23596478-2	2013	Imatinib mesylate (IM), an inhibitor of the tyrosine kinase activity of BCR-ABL, has been used as a first-line therapy for CML.	imatinib	19-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
23174907-8	2013	In cell lines, CD90+ cells showed abundant expression of c-Kit and in vitro chemosensitivity to imatinib mesylate.	imatinib	96-113	Thy-1 cell surface antigen	Homo sapiens	15-19
23174907-9	2013	Furthermore, CD90+ cells enhanced the motility of EpCAM+ cells when cocultured in vitro through the activation of transforming growth factor beta (TGF-beta) signaling, whereas imatinib mesylate suppressed TGFB1 expression in CD90+ cells as well as CD90+ cell-induced motility of EpCAM+ cells.	imatinib	176-193	Thy-1 cell surface antigen	Homo sapiens	225-229
23174907-9	2013	Furthermore, CD90+ cells enhanced the motility of EpCAM+ cells when cocultured in vitro through the activation of transforming growth factor beta (TGF-beta) signaling, whereas imatinib mesylate suppressed TGFB1 expression in CD90+ cells as well as CD90+ cell-induced motility of EpCAM+ cells.	imatinib	176-193	Thy-1 cell surface antigen	Homo sapiens	225-229
23375402-3	2013	Here, we present a case report of TC with c-Kit mutation, who has relapsed after exposure to multiple lines of combination chemotherapy, but he has shown an impressive and long lasting response to sunitinib after imatinib failure.	imatinib	213-221	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	42-47
23544168-0	2013	Imatinib and Dasatinib Inhibit Hemangiosarcoma and Implicate PDGFR-beta and Src in Tumor Growth.	imatinib	0-8	platelet derived growth factor receptor beta	Canis lupus familiaris	61-71
23818358-0	2013	miR-17 in imatinib resistance and response to tyrosine kinase inhibitors in chronic myeloid leukemia cells.	imatinib	10-18	microRNA 17	Homo sapiens	0-6
23818358-1	2013	PURPOSE: In this study we examined the expression levels of miR-17 which possesses oncogenic activities through downregulation of CDKN1A, p21 and E2F1 tumor suppressor genes, in imatinib sensitive and resistant chronic myeloid leukemia (CML) cells.	imatinib	178-186	microRNA 17	Homo sapiens	60-66
23818358-2	2013	On the other hand, we also determined the expression levels of miR-17 in response to tyrosine kinase inhibitors imatinib, nilotinib and dasatinib used for the treatment of CML.	imatinib	112-120	microRNA 17	Homo sapiens	63-69
23818358-4	2013	RESULTS: The results revealed significant increase in the expression levels of miR-17 in imatinib sensitive and resistant cells compared to peripheral blood mononuclear cells (PBMCs).	imatinib	89-97	microRNA 17	Homo sapiens	79-85
23818358-5	2013	On the other hand, significant decrease was observed in miR-17 levels in response to imatinib, nilotinib and dasatinib.	imatinib	85-93	microRNA 17	Homo sapiens	56-62
23337400-1	2013	Imatinib is a highly effective drug for the treatment of chronic myeloid leukemia (CML) that targets the BCR-ABL kinase.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-112
23313020-1	2013	Imatinib mesylate inhibits signaling of tyrosine kinase receptors, including PDGFRalpha, and has been used for human cancer therapy.	imatinib	0-17	platelet derived growth factor receptor alpha	Homo sapiens	77-87
23544168-0	2013	Imatinib and Dasatinib Inhibit Hemangiosarcoma and Implicate PDGFR-beta and Src in Tumor Growth.	imatinib	0-8	SRC proto-oncogene, non-receptor tyrosine kinase	Canis lupus familiaris	76-79
23544168-4	2013	We report here on the use of the TKIs imatinib and dasatinib in canine hemangiosarcoma and their effects on platelet-derived growth factor receptor beta (PDGFR-beta) and Src inhibition.	imatinib	38-46	platelet derived growth factor receptor beta	Canis lupus familiaris	108-152
23544168-4	2013	We report here on the use of the TKIs imatinib and dasatinib in canine hemangiosarcoma and their effects on platelet-derived growth factor receptor beta (PDGFR-beta) and Src inhibition.	imatinib	38-46	platelet derived growth factor receptor beta	Canis lupus familiaris	154-164
23544168-4	2013	We report here on the use of the TKIs imatinib and dasatinib in canine hemangiosarcoma and their effects on platelet-derived growth factor receptor beta (PDGFR-beta) and Src inhibition.	imatinib	38-46	SRC proto-oncogene, non-receptor tyrosine kinase	Canis lupus familiaris	170-173
23544168-6	2013	Dasatinib also inhibited the phosphorylation of the shared PDGFR-beta target at a concentration approximately 1000 times less than that needed by imatinib and effectively blocked Src phosphorylation.	imatinib	146-154	platelet derived growth factor receptor beta	Canis lupus familiaris	59-69
23544168-8	2013	Despite the higher concentrations needed in cell-based assays, imatinib significantly inhibited tumor growth (P < .05) in a tumor xenograft model, highlighting that disruption of PDGFR-beta/PDGF signaling may be important in targeting the angiogenic nature of these tumors.	imatinib	63-71	platelet derived growth factor receptor beta	Canis lupus familiaris	182-192
23247615-1	2013	A flow-based route to imatinib, the API of Gleevec, was developed and the general procedure then used to generate a number of analogues which were screened for biological activity against Abl1.	imatinib	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	188-192
22665066-4	2013	Second-generation tyrosine kinase inhibitors (dasatinib and nilotinib) and short hairpin RNA against bcr-abl also downregulated DR4 and DR5 expression in Ph(+) leukemia cells, and transfection of bcr-abl into a Ph(-) leukemia cell line induced DR4 and DR5 expression, which was abrogated by imatinib treatment.	imatinib	291-299	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
22665066-5	2013	Accordingly, Ph(+) leukemia cells that had been pretreated with imatinib showed resistance to the pro-apoptotic activity of recombinant human soluble TRAIL.	imatinib	64-72	TNF superfamily member 10	Homo sapiens	150-155
22665066-3	2013	Here we demonstrate that imatinib specifically downregulated DR4 and DR5 expression in cell lines and clinical samples of Ph(+) leukemia.	imatinib	25-33	TNF receptor superfamily member 10a	Homo sapiens	61-64
22665066-3	2013	Here we demonstrate that imatinib specifically downregulated DR4 and DR5 expression in cell lines and clinical samples of Ph(+) leukemia.	imatinib	25-33	TNF receptor superfamily member 10b	Homo sapiens	69-72
23247657-0	2013	The synthesis of Bcr-Abl inhibiting anticancer pharmaceutical agents imatinib, nilotinib and dasatinib.	imatinib	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
23247657-1	2013	Imatinib (1), nilotinib (2) and dasatinib (3) are Bcr-Abl tyrosine kinase inhibitors approved for the treatment of chronic myelogenous leukemia (CML).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
23117072-1	2013	BACKGROUND: This study explored the impact of genetic polymorphisms in cytochrome P450 (CYP) enzymes and transporters on the plasma trough concentration of imatinib mesylate (IM) and clinical response in chronic myeloid leukemia (CML).	imatinib	156-173	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	71-86
23446756-0	2013	Overcoming chronic myeloid leukemia stem cell resistance to imatinib by also targeting JAK2.	imatinib	60-68	Janus kinase 2	Homo sapiens	87-91
23348204-2	2013	Altered morphology and loss of CD117 reactivity has been described previously after chronic imatinib treatment; however, this phenomenon has not been reported in imatinib-naive tumors.	imatinib	92-100	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	31-36
23348204-12	2013	However, 2 imatinib-resistant tumors showed coexistence of KIT exon 11 and exon 13 mutations.	imatinib	11-19	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	59-62
23117072-1	2013	BACKGROUND: This study explored the impact of genetic polymorphisms in cytochrome P450 (CYP) enzymes and transporters on the plasma trough concentration of imatinib mesylate (IM) and clinical response in chronic myeloid leukemia (CML).	imatinib	156-173	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	88-91
23433851-0	2013	Arginine homozygosity in codon 72 of p53 correlates with failure to imatinib response in chronic myeloid leukemia.	imatinib	68-76	tumor protein p53	Homo sapiens	37-40
23201011-0	2013	Dihydroartemisinin inhibits the Bcr/Abl oncogene at the mRNA level in chronic myeloid leukemia sensitive or resistant to imatinib.	imatinib	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
23201011-1	2013	Due to the mutations of the Bcr/Abl oncogene that obstacle the binding of the protein with imatinib, the resistance to imatinib has developed in a significant portion of chronic myeloid leukemia (CML) patients.	imatinib	91-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
23201011-1	2013	Due to the mutations of the Bcr/Abl oncogene that obstacle the binding of the protein with imatinib, the resistance to imatinib has developed in a significant portion of chronic myeloid leukemia (CML) patients.	imatinib	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
23201011-3	2013	Inhibiting the amplification of Bcr/Abl oncogene is believed to be a new effective strategy to override the imatinib resistance on CML cells.	imatinib	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
23201011-5	2013	Moreover, dihydroartemisinin could also lead to the inhibition of the Bcr/Abl protein expression and tyrosine kinase activity, and strongly suppress on the downstream signals of Bcr/Abl, which included inhibition of tyrosine kinase activity of AKT and ERK, promotion of cytochrome c release from the mitochondria and the consequential activation of caspase-9/3 in imatinib-resistant CML cells.	imatinib	364-372	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185
23433851-1	2013	PURPOSE: In this study, the role of the polymorphism at codon 72 of tumor protein p53 gene (TP53) was investigated regarding the response to treatment with imatinib in chronic myeloid leukemia (CML).	imatinib	156-164	tumor protein p53	Homo sapiens	82-85
23433851-1	2013	PURPOSE: In this study, the role of the polymorphism at codon 72 of tumor protein p53 gene (TP53) was investigated regarding the response to treatment with imatinib in chronic myeloid leukemia (CML).	imatinib	156-164	tumor protein p53	Homo sapiens	92-96
23433851-10	2013	CONCLUSION: The findings suggest that in CML patients, TP53 codon 72 polymorphism may contribute to a high Sokal score and failure to imatinib treatment.	imatinib	134-142	tumor protein p53	Homo sapiens	55-59
23278256-0	2013	BCR-ABL1 transcript at 3 months predicts long-term outcomes following second generation tyrosine kinase inhibitor therapy in the patients with chronic myeloid leukaemia in chronic phase who failed Imatinib.	imatinib	197-205	BCR activator of RhoGEF and GTPase	Homo sapiens	0-8
23278256-1	2013	The BCR-ABL1 transcript level at 3 months can predict long-term outcomes following frontline therapy with Imatinib or Dasatinib in chronic myeloid leukaemia (CML) patients.	imatinib	106-114	BCR activator of RhoGEF and GTPase	Homo sapiens	4-12
23302228-4	2013	The response of the homologous recombination protein RAD51 to radiation is inhibited by the small-molecule tyrosine kinase inhibitor imatinib.	imatinib	133-141	RAD51 recombinase	Homo sapiens	53-58
23278256-9	2013	In conclusion, the BCR-ABL1 transcript level at 3 months is the most relevant surrogate for outcomes following 2GTKI therapy after Imatinib failure.	imatinib	131-139	BCR activator of RhoGEF and GTPase	Homo sapiens	19-27
30349606-6	2013	Motesanib, sorafenib, vandetanib, sunitinib, lenvatinib, imatinib and cabozantinib are multi-kinase inhibitors that have the ability of inhibiting the rearranged during transection (RET) and vascular endothelial growth factor receptor (VEGFR), and other kinases, and have been used in advanced differentiated thyroid carcinoma.	imatinib	57-65	ret proto-oncogene	Homo sapiens	182-185
23299198-6	2013	Imatinib, a selective inhibitor targeting Abl as well as c-kit and the platelet-derived growth factor receptor, has been tested for the efficacy and toxicities in metastatic melanoma patients, suggesting that imatinib may increase the progression-free survival and overall survival in selected melanoma patients harboring mutations in c-kit gene.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-45
23299198-6	2013	Imatinib, a selective inhibitor targeting Abl as well as c-kit and the platelet-derived growth factor receptor, has been tested for the efficacy and toxicities in metastatic melanoma patients, suggesting that imatinib may increase the progression-free survival and overall survival in selected melanoma patients harboring mutations in c-kit gene.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	57-62
23299198-6	2013	Imatinib, a selective inhibitor targeting Abl as well as c-kit and the platelet-derived growth factor receptor, has been tested for the efficacy and toxicities in metastatic melanoma patients, suggesting that imatinib may increase the progression-free survival and overall survival in selected melanoma patients harboring mutations in c-kit gene.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	335-340
23299198-6	2013	Imatinib, a selective inhibitor targeting Abl as well as c-kit and the platelet-derived growth factor receptor, has been tested for the efficacy and toxicities in metastatic melanoma patients, suggesting that imatinib may increase the progression-free survival and overall survival in selected melanoma patients harboring mutations in c-kit gene.	imatinib	209-217	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	57-62
23299198-6	2013	Imatinib, a selective inhibitor targeting Abl as well as c-kit and the platelet-derived growth factor receptor, has been tested for the efficacy and toxicities in metastatic melanoma patients, suggesting that imatinib may increase the progression-free survival and overall survival in selected melanoma patients harboring mutations in c-kit gene.	imatinib	209-217	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	335-340
23299198-7	2013	The current status of c-kit mutation and the standard for selection of imatinib-sensitive patients have been tentatively established.	imatinib	71-79	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	22-27
23299198-10	2013	In selected subsets of melanoma patients harboring genetic alterations of c-kit, imatinib may be a promising agent.	imatinib	81-89	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	74-79
23206668-7	2013	Patients on imatinib whose tumours harbour mutations in exon 11 of the KIT gene tend to have superior RFS compared with patients with exon 9 mutations.	imatinib	12-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	71-74
23691445-0	2013	A novel t(3;12)(q21;p13) translocation in a patient with accelerated chronic myeloid leukemia after imatinib and nilotinib therapy.	imatinib	100-108	H3 histone pseudogene 6	Homo sapiens	20-23
23385615-7	2013	Patients with hypereosinophilic MPNs associated with PDGFRA and PDGFRB fusion genes are responsive to imatinib.	imatinib	102-110	platelet derived growth factor receptor alpha	Homo sapiens	53-59
23385615-7	2013	Patients with hypereosinophilic MPNs associated with PDGFRA and PDGFRB fusion genes are responsive to imatinib.	imatinib	102-110	platelet derived growth factor receptor beta	Homo sapiens	64-70
23341130-0	2013	A novel small molecule RAD51 inactivator overcomes imatinib-resistance in chronic myeloid leukaemia.	imatinib	51-59	RAD51 recombinase	Homo sapiens	23-28
30349606-6	2013	Motesanib, sorafenib, vandetanib, sunitinib, lenvatinib, imatinib and cabozantinib are multi-kinase inhibitors that have the ability of inhibiting the rearranged during transection (RET) and vascular endothelial growth factor receptor (VEGFR), and other kinases, and have been used in advanced differentiated thyroid carcinoma.	imatinib	57-65	kinase insert domain receptor	Homo sapiens	191-234
30349606-6	2013	Motesanib, sorafenib, vandetanib, sunitinib, lenvatinib, imatinib and cabozantinib are multi-kinase inhibitors that have the ability of inhibiting the rearranged during transection (RET) and vascular endothelial growth factor receptor (VEGFR), and other kinases, and have been used in advanced differentiated thyroid carcinoma.	imatinib	57-65	kinase insert domain receptor	Homo sapiens	236-241
22845311-0	2013	Degree of kinase inhibition achieved in vitro by imatinib and nilotinib is decreased by high levels of ABCB1 but not ABCG2.	imatinib	49-57	ATP binding cassette subfamily B member 1	Homo sapiens	103-108
24426336-2	2013	We want to present a case of IHES with chromosomal mosaicism for inversion of chromosome 3(p25, p26), who achieved complete remission after treatment with Imatinib and short course of prednisolone.	imatinib	155-163	tubulin polymerization promoting protein	Homo sapiens	91-94
24426336-2	2013	We want to present a case of IHES with chromosomal mosaicism for inversion of chromosome 3(p25, p26), who achieved complete remission after treatment with Imatinib and short course of prednisolone.	imatinib	155-163	transmembrane p24 trafficking protein 3	Homo sapiens	96-99
23675289-0	2013	Predictive Value of Pretreatment BCR-ABL(IS) Transcript level on Response to Imatinib Therapy in Egyptian Patients with Chronic Phase Chronic Myeloid Leukemia (CPCML).	imatinib	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
23083077-3	2013	We tested the hypothesis that imatinib, a clinically available inhibitor of PDGFR-beta, Mast/stem cell growth factor receptor (c-kit) and cAbl, would reduce the severity of dermal fibrosis in a murine model.	imatinib	30-38	platelet derived growth factor receptor, beta polypeptide	Mus musculus	76-86
23083077-3	2013	We tested the hypothesis that imatinib, a clinically available inhibitor of PDGFR-beta, Mast/stem cell growth factor receptor (c-kit) and cAbl, would reduce the severity of dermal fibrosis in a murine model.	imatinib	30-38	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	127-132
23083077-3	2013	We tested the hypothesis that imatinib, a clinically available inhibitor of PDGFR-beta, Mast/stem cell growth factor receptor (c-kit) and cAbl, would reduce the severity of dermal fibrosis in a murine model.	imatinib	30-38	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	138-142
23345330-5	2013	Sox4-deficient pro-B cells, particularly those expressing the stem cell factor receptor c-Kit, readily underwent apoptosis, and even more so when c-Kit activity was inhibited by imatinib.	imatinib	178-186	SRY (sex determining region Y)-box 4	Mus musculus	0-4
23345330-5	2013	Sox4-deficient pro-B cells, particularly those expressing the stem cell factor receptor c-Kit, readily underwent apoptosis, and even more so when c-Kit activity was inhibited by imatinib.	imatinib	178-186	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	146-151
23160178-4	2013	The increased SMS in K562 cells was caused by the presence of Bcr-abl, a hallmark of CML; stable expression of Bcr-abl elevated SMS activity in HL-60 cells while inhibition of the tyrosine kinase activity of Bcr-abl with Imatinib mesylate decreased SMS activity in K562 cells.	imatinib	221-238	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
23160178-4	2013	The increased SMS in K562 cells was caused by the presence of Bcr-abl, a hallmark of CML; stable expression of Bcr-abl elevated SMS activity in HL-60 cells while inhibition of the tyrosine kinase activity of Bcr-abl with Imatinib mesylate decreased SMS activity in K562 cells.	imatinib	221-238	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
23160178-4	2013	The increased SMS in K562 cells was caused by the presence of Bcr-abl, a hallmark of CML; stable expression of Bcr-abl elevated SMS activity in HL-60 cells while inhibition of the tyrosine kinase activity of Bcr-abl with Imatinib mesylate decreased SMS activity in K562 cells.	imatinib	221-238	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
22976128-0	2013	Imatinib-dependent tyrosine phosphorylation profiling of Bcr-Abl-positive chronic myeloid leukemia cells.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
22845311-1	2013	Imatinib and nilotinib interact with ABCB1 and ABCG2.	imatinib	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	37-42
22845311-1	2013	Imatinib and nilotinib interact with ABCB1 and ABCG2.	imatinib	0-8	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	47-52
22845311-3	2013	Here, in vitro, Bcr-Abl kinase inhibition was used to elucidate the impact of ABCB1/ABCG2 overexpression on imatinib and nilotinib transport.	imatinib	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
22845311-3	2013	Here, in vitro, Bcr-Abl kinase inhibition was used to elucidate the impact of ABCB1/ABCG2 overexpression on imatinib and nilotinib transport.	imatinib	108-116	ATP binding cassette subfamily B member 1	Homo sapiens	78-83
22845311-3	2013	Here, in vitro, Bcr-Abl kinase inhibition was used to elucidate the impact of ABCB1/ABCG2 overexpression on imatinib and nilotinib transport.	imatinib	108-116	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	84-89
22845311-4	2013	High levels of ABCB1 protein in K562-Dox cells resulted in a significantly increased 50% inhibitory concentration (IC(50)) compared with parental K562 cells for imatinib (IC(50)(IM); 9 microM to 19 microM, p = 0.002) and nilotinib (IC(50)(NIL); 345 nM to 620 nM, p = 0.013).	imatinib	161-169	ATP binding cassette subfamily B member 1	Homo sapiens	15-20
22845311-8	2013	Imatinib and nilotinib appear to be transported by ABCB1 but do not interact strongly with ABCG2.	imatinib	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	51-56
23536354-4	2013	In recent years, targeted therapy with imatinib mesylate, which inhibits KIT kinase activity, represents the other cornerstone for the treatment of GIST.	imatinib	39-56	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
23382202-0	2013	Anti-KIT monoclonal antibody inhibits imatinib-resistant gastrointestinal stromal tumor growth.	imatinib	38-46	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	5-8
23382202-4	2013	Treatment of GIST with imatinib, a small-molecule tyrosine kinase inhibitor, inhibits KIT-mediated signaling and initially results in disease control in 70-85% of patients with KIT-positive GIST.	imatinib	23-31	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	86-89
23382202-4	2013	Treatment of GIST with imatinib, a small-molecule tyrosine kinase inhibitor, inhibits KIT-mediated signaling and initially results in disease control in 70-85% of patients with KIT-positive GIST.	imatinib	23-31	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	177-180
22821812-3	2013	We also found that CAFs express platelet-derived growth factor receptor (PDGFR) at a high level and that imatinib therapy targeting PDGFR in CAFs inhibits growth and metastasis of human colon cancer.	imatinib	105-113	platelet derived growth factor receptor beta	Homo sapiens	132-137
23663336-6	2013	The proportion of patients in the first remission (CR1) in the imatinib group was higher than that in control group (20/23 vs 6/12, P = 0.038).	imatinib	63-71	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	51-54
23316053-4	2013	Selective inhibitors of Bcr-Abl, of which imatinib is the prototype, have had a tremendous impact on clinical outcomes in chronic myelogenous leukemia and revolutionized the field of targeted cancer therapy.	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
22821812-3	2013	We also found that CAFs express platelet-derived growth factor receptor (PDGFR) at a high level and that imatinib therapy targeting PDGFR in CAFs inhibits growth and metastasis of human colon cancer.	imatinib	105-113	T-box transcription factor 1	Homo sapiens	141-145
23420105-5	2013	Moreover, in the 1-methyl-4-phenyl-1,2,4,6-tetrahydropyridine (MPTP) mouse model, dopamine deficiency caused increased phosphorylation of both Tyr15-Cdk5 and Thr75-DARPP-32 in the striatum, which could be attenuated by administration of L-3,4-dihydroxyphenylalanine and imatinib (STI-571), a selective c-Abl inhibitor.	imatinib	270-278	cyclin-dependent kinase 5	Mus musculus	143-153
23301703-7	2013	GZD824 represents a promising lead candidate for development of Bcr-Abl inhibitors to overcome acquired imatinib resistance.	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
23301703-1	2013	Bcr-Abl(T315I) mutation-induced imatinib resistance remains a major challenge for clinical management of chronic myelogenous leukemia (CML).	imatinib	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
23420105-5	2013	Moreover, in the 1-methyl-4-phenyl-1,2,4,6-tetrahydropyridine (MPTP) mouse model, dopamine deficiency caused increased phosphorylation of both Tyr15-Cdk5 and Thr75-DARPP-32 in the striatum, which could be attenuated by administration of L-3,4-dihydroxyphenylalanine and imatinib (STI-571), a selective c-Abl inhibitor.	imatinib	280-287	cyclin-dependent kinase 5	Mus musculus	143-153
23196876-5	2013	In this study, we demonstrated that NVP-AUY922 (AUY922), a new class of HSP90AA1 inhibitor, is effective in inhibiting the growth of GIST cells expressing mutant KIT protein, the imatinib-sensitive GIST882 and imatinib-resistant GIST48 cells.	imatinib	179-187	heat shock protein 90 alpha family class A member 1	Homo sapiens	72-80
23383963-0	2013	SPARC expression in CML is associated to imatinib treatment and to inhibition of leukemia cell proliferation.	imatinib	41-49	secreted protein acidic and cysteine rich	Homo sapiens	0-5
23383963-6	2013	Finally we analyzed the interaction between exogenous SPARC and imatinib (IM), in vitro, using ATP-lite and cell cycle analysis.	imatinib	64-72	secreted protein acidic and cysteine rich	Homo sapiens	54-59
23324740-3	2013	Although tyrosine kinase inhibitors, such as the BCR-ABL inhibitor imatinib, have demonstrated remarkable efficacy in the clinic, drug-resistant leukemias emerge in some patients because of either the acquisition of point mutations or amplification of the tyrosine kinase, resulting in a poor long-term prognosis.	imatinib	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
23196876-5	2013	In this study, we demonstrated that NVP-AUY922 (AUY922), a new class of HSP90AA1 inhibitor, is effective in inhibiting the growth of GIST cells expressing mutant KIT protein, the imatinib-sensitive GIST882 and imatinib-resistant GIST48 cells.	imatinib	210-218	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	162-165
23233089-0	2013	Downregulation of gamma-catenin inhibits CML cell growth and potentiates             the response of CML cells to imatinib through beta-catenin inhibition.	imatinib	114-122	catenin beta 1	Homo sapiens	131-143
23108698-2	2013	Imatinib inhibits PDGFR kinase activity at therapeutically relevant doses.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	18-23
23108698-18	2013	Further study is warranted as imatinib can be delivered at levels that inhibit PDGFR.	imatinib	30-38	platelet derived growth factor receptor beta	Homo sapiens	79-84
23372106-2	2013	Five currently available BCR-ABL inhibitors form the mainstay of CML treatment, including first-generation imatinib and more potent second-generation BCR-ABL inhibitors dasatinib and nilotinib, with bosutinib and ponatinib having been recently approved for market inclusion.	imatinib	107-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
22875622-5	2013	In the overall population, the OCTN1 C allele (rs1050152), a simple combination of polymorphisms in the hOCT1 gene and another combination in the genes involved in imatinib uptake were significantly associated with major molecular response.	imatinib	164-172	solute carrier family 22 member 4	Homo sapiens	31-36
23233201-7	2013	Overexpression of PECAM-1 in BCR/ABL-expressing cells, including K562 human             leukemia cells, enhanced cell adhesion and partially inhibited imatinib-induced             apoptosis involving mitochondria depolarization and caspase-3 cleavage, at least             partly, in an ITIM-independent manner.	imatinib	151-159	BCR activator of RhoGEF and GTPase	Homo sapiens	29-32
23233089-4	2013	Furthermore, downregulation             of gamma-catenin by siRNA inhibited the proliferation and colony formation of CML             cells and the expression of the c-Myc and cyclin D1 genes; downregulation of gamma-catenin             also potentiated the effects of imatinib (inhibiting CML cell proliferation and             inducing apoptosis) and suppressed the anti-apoptotic genes Bcl-xL and survivin.	imatinib	269-277	cyclin D1	Homo sapiens	176-185
23233201-0	2013	PECAM-1 is involved in BCR/ABL signaling and may downregulate imatinib-induced             apoptosis of Philadelphia chromosome-positive leukemia cells.	imatinib	62-70	platelet and endothelial cell adhesion molecule 1	Homo sapiens	0-7
23233201-8	2013	These data suggest that PECAM-1 may play             a role in regulation of apoptosis as well as adhesion of BCR/ABL-expressing cells             to modulate their imatinib sensitivity and would be a possible candidate for therapeutic             target in Ph+ leukemias.	imatinib	165-173	platelet and endothelial cell adhesion molecule 1	Homo sapiens	24-31
23233201-8	2013	These data suggest that PECAM-1 may play             a role in regulation of apoptosis as well as adhesion of BCR/ABL-expressing cells             to modulate their imatinib sensitivity and would be a possible candidate for therapeutic             target in Ph+ leukemias.	imatinib	165-173	BCR activator of RhoGEF and GTPase	Homo sapiens	110-113
23233201-3	2013	The BCR/ABL fusion tyrosine kinase is expressed in chronic myeloid             leukemia and Philadelphia-positive (Ph+) acute lymphoblastic leukemia cells, and             its inhibition by the clinically used tyrosine kinase inhibitors imatinib or dasatinib             induces apoptosis of these cells.	imatinib	237-245	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
23233201-8	2013	These data suggest that PECAM-1 may play             a role in regulation of apoptosis as well as adhesion of BCR/ABL-expressing cells             to modulate their imatinib sensitivity and would be a possible candidate for therapeutic             target in Ph+ leukemias.	imatinib	165-173	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-117
23233201-5	2013	Studies using imatinib and dasatinib as well             as transient expression experiments in 293T cells revealed that PECAM-1 was phosphorylated             directly by BCR/ABL, which was enhanced by the imatinib-resistant E255K and T315I             mutations, or partly by the Src family tyrosine kinases, including Lyn, which             were activated dependently or independently on BCR/ABL.	imatinib	14-22	platelet and endothelial cell adhesion molecule 1	Homo sapiens	121-128
23233201-5	2013	Studies using imatinib and dasatinib as well             as transient expression experiments in 293T cells revealed that PECAM-1 was phosphorylated             directly by BCR/ABL, which was enhanced by the imatinib-resistant E255K and T315I             mutations, or partly by the Src family tyrosine kinases, including Lyn, which             were activated dependently or independently on BCR/ABL.	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-179
23233201-5	2013	Studies using imatinib and dasatinib as well             as transient expression experiments in 293T cells revealed that PECAM-1 was phosphorylated             directly by BCR/ABL, which was enhanced by the imatinib-resistant E255K and T315I             mutations, or partly by the Src family tyrosine kinases, including Lyn, which             were activated dependently or independently on BCR/ABL.	imatinib	207-215	platelet and endothelial cell adhesion molecule 1	Homo sapiens	121-128
23233201-5	2013	Studies using imatinib and dasatinib as well             as transient expression experiments in 293T cells revealed that PECAM-1 was phosphorylated             directly by BCR/ABL, which was enhanced by the imatinib-resistant E255K and T315I             mutations, or partly by the Src family tyrosine kinases, including Lyn, which             were activated dependently or independently on BCR/ABL.	imatinib	207-215	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-179
23233201-5	2013	Studies using imatinib and dasatinib as well             as transient expression experiments in 293T cells revealed that PECAM-1 was phosphorylated             directly by BCR/ABL, which was enhanced by the imatinib-resistant E255K and T315I             mutations, or partly by the Src family tyrosine kinases, including Lyn, which             were activated dependently or independently on BCR/ABL.	imatinib	207-215	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	321-324
23233201-5	2013	Studies using imatinib and dasatinib as well             as transient expression experiments in 293T cells revealed that PECAM-1 was phosphorylated             directly by BCR/ABL, which was enhanced by the imatinib-resistant E255K and T315I             mutations, or partly by the Src family tyrosine kinases, including Lyn, which             were activated dependently or independently on BCR/ABL.	imatinib	207-215	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	391-398
23233201-7	2013	Overexpression of PECAM-1 in BCR/ABL-expressing cells, including K562 human             leukemia cells, enhanced cell adhesion and partially inhibited imatinib-induced             apoptosis involving mitochondria depolarization and caspase-3 cleavage, at least             partly, in an ITIM-independent manner.	imatinib	151-159	platelet and endothelial cell adhesion molecule 1	Homo sapiens	18-25
23420128-0	2013	Expression of stem cell factor in gastrointestinal stromal tumors: Implications for proliferation and imatinib resistance.	imatinib	102-110	KIT ligand	Homo sapiens	14-30
23218026-0	2013	Imatinib and Nilotinib inhibit Bcr-Abl-induced ROS through targeted degradation of the NADPH oxidase subunit p22phox.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
23218026-0	2013	Imatinib and Nilotinib inhibit Bcr-Abl-induced ROS through targeted degradation of the NADPH oxidase subunit p22phox.	imatinib	0-8	cytochrome b-245 alpha chain	Homo sapiens	109-116
23218026-4	2013	In this study, using the K562 CML cell line we showed that inhibition of Bcr-Abl signalling, by either Imatinib or Nilotinib, led to a significant reduction in ROS levels which was concurrent with the GSK-3beta dependent, post-translational down-regulation of the small membrane-bound protein p22phox, an essential component of the Nox complex.	imatinib	103-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
23218026-4	2013	In this study, using the K562 CML cell line we showed that inhibition of Bcr-Abl signalling, by either Imatinib or Nilotinib, led to a significant reduction in ROS levels which was concurrent with the GSK-3beta dependent, post-translational down-regulation of the small membrane-bound protein p22phox, an essential component of the Nox complex.	imatinib	103-111	glycogen synthase kinase 3 beta	Homo sapiens	201-210
23218026-4	2013	In this study, using the K562 CML cell line we showed that inhibition of Bcr-Abl signalling, by either Imatinib or Nilotinib, led to a significant reduction in ROS levels which was concurrent with the GSK-3beta dependent, post-translational down-regulation of the small membrane-bound protein p22phox, an essential component of the Nox complex.	imatinib	103-111	cytochrome b-245 alpha chain	Homo sapiens	293-300
23420128-4	2013	However, primary resistance to imatinib in GISTs with wild-type KIT and acquired resistance in GISTs with mutant KIT are becoming increasingly significant problems.	imatinib	31-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	64-67
23420128-5	2013	The aims of this study were to detect the expression and function of SCF in 68 GIST samples, and to explore the relationship between SCF activity and imatinib resistance using immunohistochemical staining and western blot analysis.	imatinib	150-158	KIT ligand	Homo sapiens	133-136
23525192-0	2013	Phase I clinical trial combining imatinib mesylate and IL-2 in refractory cancer patients: IL-2 interferes with the pharmacokinetics of imatinib mesylate.	imatinib	33-50	interleukin 2	Homo sapiens	91-95
23420128-8	2013	We also found increased SCF expression in GIST cells treated with imatinib.	imatinib	66-74	KIT ligand	Homo sapiens	24-27
23525192-0	2013	Phase I clinical trial combining imatinib mesylate and IL-2 in refractory cancer patients: IL-2 interferes with the pharmacokinetics of imatinib mesylate.	imatinib	136-153	interleukin 2	Homo sapiens	91-95
23420128-10	2013	Imatinib was not able to inhibit the activity of SCF, while it promoted the expression of SCF, which may have contributed to acquired imatinib resistance.	imatinib	0-8	KIT ligand	Homo sapiens	90-93
23420128-10	2013	Imatinib was not able to inhibit the activity of SCF, while it promoted the expression of SCF, which may have contributed to acquired imatinib resistance.	imatinib	134-142	KIT ligand	Homo sapiens	90-93
23611226-0	2013	[FIP1L1-PDGFRA positive chronic eosinophilic leukemia with imatinib-resistant T674I mutant of PDGFRA gene: a case report and literature review].	imatinib	59-67	factor interacting with PAPOLA and CPSF1	Homo sapiens	1-7
23127916-0	2013	Polymorphisms in OCTN1 and OCTN2 transporters genes are associated with prolonged time to progression in unresectable gastrointestinal stromal tumours treated with imatinib therapy.	imatinib	164-172	solute carrier family 22 member 4	Homo sapiens	17-22
23127916-0	2013	Polymorphisms in OCTN1 and OCTN2 transporters genes are associated with prolonged time to progression in unresectable gastrointestinal stromal tumours treated with imatinib therapy.	imatinib	164-172	solute carrier family 22 member 5	Homo sapiens	27-32
23127916-2	2013	Response to imatinib mainly depends from KIT and PDGFRalpha mutational status.	imatinib	12-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	41-44
23127916-2	2013	Response to imatinib mainly depends from KIT and PDGFRalpha mutational status.	imatinib	12-20	platelet derived growth factor receptor alpha	Homo sapiens	49-59
23127916-9	2013	In conclusion, in this study we showed that SLC22A4 and SLC22A5 genotypes may be an important predictor of time to progression in GIST patients receiving imatinib therapy.	imatinib	154-162	solute carrier family 22 member 4	Homo sapiens	44-51
23127916-9	2013	In conclusion, in this study we showed that SLC22A4 and SLC22A5 genotypes may be an important predictor of time to progression in GIST patients receiving imatinib therapy.	imatinib	154-162	solute carrier family 22 member 5	Homo sapiens	56-63
22410779-2	2013	The tyrosine kinase inhibitor imatinib effectively treats CML, but acquired resistance can develop because of BCR-ABL mutations.	imatinib	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
23319661-2	2013	Gleevec, a well-known therapeutic agent against chronic myelogenous leukemia, is an effective inhibitor of Abl tyrosine kinase.	imatinib	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-110
23209290-7	2013	In subsequent cellular studies with imatinib, a kinase inhibitor that reportedly prevents the interaction of GSAP with the C-terminal fragment of amyloid precursor protein, a concentration-dependent decrease in amyloid-beta levels was observed.	imatinib	36-44	gamma-secretase activating protein	Mus musculus	109-113
23209290-7	2013	In subsequent cellular studies with imatinib, a kinase inhibitor that reportedly prevents the interaction of GSAP with the C-terminal fragment of amyloid precursor protein, a concentration-dependent decrease in amyloid-beta levels was observed.	imatinib	36-44	amyloid beta (A4) precursor protein	Mus musculus	146-171
23277171-2	2013	Coupled with the development of tyrosine kinase inhibitors such as imatinib, c-kit has emerged as a viable drug target in what seems to be a validated therapeutic concept.	imatinib	67-75	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	77-82
23223357-0	2013	The hOCT1 SNPs M420del and M408V alter imatinib uptake and M420del modifies clinical outcome in imatinib-treated chronic myeloid leukemia.	imatinib	39-47	solute carrier family 22 member 1	Homo sapiens	4-9
23223357-0	2013	The hOCT1 SNPs M420del and M408V alter imatinib uptake and M420del modifies clinical outcome in imatinib-treated chronic myeloid leukemia.	imatinib	96-104	solute carrier family 22 member 1	Homo sapiens	4-9
23223357-3	2013	In the present study, we analyzed the effect of 23 hOCT1 SNPs on imatinib treatment outcome in newly diagnosed CML patients using MassARRAY sequencing and pyrosequencing.	imatinib	65-73	solute carrier family 22 member 1	Homo sapiens	51-56
23223358-1	2013	BCR-ABL1 compound mutations can confer high-level resistance to imatinib and other ABL1 tyrosine kinase inhibitors (TKIs).	imatinib	64-72	BCR activator of RhoGEF and GTPase	Homo sapiens	0-8
23223358-1	2013	BCR-ABL1 compound mutations can confer high-level resistance to imatinib and other ABL1 tyrosine kinase inhibitors (TKIs).	imatinib	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-8
23611226-0	2013	[FIP1L1-PDGFRA positive chronic eosinophilic leukemia with imatinib-resistant T674I mutant of PDGFRA gene: a case report and literature review].	imatinib	59-67	platelet derived growth factor receptor alpha	Homo sapiens	8-14
23611226-0	2013	[FIP1L1-PDGFRA positive chronic eosinophilic leukemia with imatinib-resistant T674I mutant of PDGFRA gene: a case report and literature review].	imatinib	59-67	platelet derived growth factor receptor alpha	Homo sapiens	94-100
23204129-0	2013	PLK1 inhibitors synergistically potentiate HDAC inhibitor lethality in imatinib mesylate-sensitive or -resistant BCR/ABL+ leukemia cells in vitro and in vivo.	imatinib	71-88	polo like kinase 1	Homo sapiens	0-4
23204129-0	2013	PLK1 inhibitors synergistically potentiate HDAC inhibitor lethality in imatinib mesylate-sensitive or -resistant BCR/ABL+ leukemia cells in vitro and in vivo.	imatinib	71-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
23204129-10	2013	CONCLUSIONS: These findings suggest that concomitant PLK1 and HDAC inhibition is active against imatinib mesylate-sensitive or refractory CML and ALL cells both in vitro and in vivo and that this strategy warrants further evaluation in the setting of BCR/ABL(+) leukemias.	imatinib	96-113	polo like kinase 1	Homo sapiens	53-57
23204129-10	2013	CONCLUSIONS: These findings suggest that concomitant PLK1 and HDAC inhibition is active against imatinib mesylate-sensitive or refractory CML and ALL cells both in vitro and in vivo and that this strategy warrants further evaluation in the setting of BCR/ABL(+) leukemias.	imatinib	96-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	251-258
23204129-5	2013	RESULTS: Cotreatment with BI2536 and vorinostat synergistically induced cell death in parental or imatinib mesylate-resistant BCR/ABL(+) cells and primary CD34(+) bone marrow cells but was minimally toxic to normal cells.	imatinib	98-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
23175686-1	2013	Molecular response to imatinib (IM) in chronic myeloid leukemia (CML) is associated with a biphasic but heterogeneous decline of BCR-ABL transcript levels.	imatinib	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
23087024-12	2013	CONCLUSIONS: We report a novel mode of action for imatinib, demonstrating TPH1 down-regulation via inhibition of PDGFR-beta signaling.	imatinib	50-58	tryptophan hydroxylase 1	Mus musculus	74-78
23288640-4	2013	Second generation tyrosine kinase inhibitors (TKIs) have allowed for effective treatment of some patients with imatinib resistance, but bcr-abl mutants such as T315I remain problematic.	imatinib	111-119	TXK tyrosine kinase	Homo sapiens	18-33
23326179-6	2013	Imatinib mesylate is an oral agent that is a selective protein tyrosine kinase inhibitor of the KIT protein tyrosine kinase, and it has demonstrated clinical benefit and objective tumor responses in most GIST patients in phase II and III trials.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	96-99
23326179-7	2013	The presence and the type of KIT or PDGFRA mutation are predictive of response to imatinib therapy in patients with advanced and metastatic disease.	imatinib	82-90	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	29-32
23326179-7	2013	The presence and the type of KIT or PDGFRA mutation are predictive of response to imatinib therapy in patients with advanced and metastatic disease.	imatinib	82-90	platelet derived growth factor receptor alpha	Homo sapiens	36-42
23087024-0	2013	Imatinib attenuates hypoxia-induced pulmonary arterial hypertension pathology via reduction in 5-hydroxytryptamine through inhibition of tryptophan hydroxylase 1 expression.	imatinib	0-8	tryptophan hydroxylase 1	Mus musculus	137-161
23087024-7	2013	Imatinib attenuated hypoxia-induced increases in Tph1 expression in pulmonary endothelial cells in vitro via inhibition of the PDGFR-beta pathway.	imatinib	0-8	tryptophan hydroxylase 1	Mus musculus	49-53
23087024-12	2013	CONCLUSIONS: We report a novel mode of action for imatinib, demonstrating TPH1 down-regulation via inhibition of PDGFR-beta signaling.	imatinib	50-58	platelet derived growth factor receptor, beta polypeptide	Mus musculus	113-123
23087024-7	2013	Imatinib attenuated hypoxia-induced increases in Tph1 expression in pulmonary endothelial cells in vitro via inhibition of the PDGFR-beta pathway.	imatinib	0-8	platelet derived growth factor receptor, beta polypeptide	Mus musculus	127-137
23087024-13	2013	Our data reveal interplay between PDGF and 5-HT pathways within PAH, demonstrating TPH1-dependent imatinib efficacy in collagen-mediated mechanisms of fibrosis.	imatinib	98-106	tryptophan hydroxylase 1	Mus musculus	83-87
23232855-1	2013	Rearrangement of the PDGFRA gene defines a distinct group of hematopoietic neoplasms that commonly present with persistent eosinophilia and are highly sensitive to low-dose imatinib mesylate treatment.	imatinib	173-190	platelet derived growth factor receptor alpha	Homo sapiens	21-27
23232855-8	2013	Despite its aggressive clinical behavior attributed to myeloid sarcoma in general, the presence of PDGFRA rearrangement in this case conferred a high sensitivity to imatinib treatment and a favorable clinical outcome.	imatinib	165-173	platelet derived growth factor receptor alpha	Homo sapiens	99-105
23674887-2	2013	Bosutinib effectively overcomes the majority of imatinib-resistance-conferring BCR-ABL mutations except V299L and T315I.	imatinib	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
23043437-1	2013	With the manufacture of imatinib, researchers introduced tyrosine kinase inhibitors (TKIs) into the clinical setting in 2000 to treat cancers; approximately fifteen other TKIs soon followed.	imatinib	24-32	TXK tyrosine kinase	Homo sapiens	57-72
23484077-0	2013	HOXA4 gene promoter hypermethylation as an epigenetic mechanism mediating resistance to imatinib mesylate in chronic myeloid leukemia patients.	imatinib	88-105	homeobox A4	Homo sapiens	0-5
23053257-0	2013	Two-year adjuvant imatinib mesylate after complete resection of localized, high-risk GIST with KIT exon 11 mutation.	imatinib	18-35	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	95-98
23116058-0	2013	The BCL2L11 (BIM) deletion polymorphism is a possible criterion for discontinuation of imatinib in chronic myeloid leukaemia patients.	imatinib	87-95	BCL2 like 11	Homo sapiens	4-11
23053257-1	2013	PURPOSE: To evaluate the efficacy and safety of 2-year adjuvant imatinib for patients at high risk of recurrence after complete resection of localized gastrointestinal stromal tumor with KIT exon 11 mutation.	imatinib	64-72	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	187-190
23053257-12	2013	CONCLUSIONS: Postoperative adjuvant imatinib for 2 years was safe and could prolong the recurrence-free survival in patients with a high risk of recurrence after complete resection of localized KIT exon 11 mutated gastrointestinal stromal tumor.	imatinib	36-44	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	194-197
24109527-3	2013	A case of e19a2 BCR-ABL1 CML is described in whom imatinib resistance, associated with a Q252H ABL1 kinase domain mutation, became apparent soon after initiation of TKI therapy.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-24
24109527-3	2013	A case of e19a2 BCR-ABL1 CML is described in whom imatinib resistance, associated with a Q252H ABL1 kinase domain mutation, became apparent soon after initiation of TKI therapy.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-99
23278880-14	2013	The effects of SCF on mediator release from mast cells were reversed by the c-kit inhibitor imatinib.	imatinib	92-100	KIT ligand	Homo sapiens	15-18
23569448-1	2013	BACKGROUND: Imatinib mesylate (IM) is the standard treatment for BCR-ABL-positive chronic myelogenous leukemia (CML) and is the first-line adjuvant and palliative treatment for metastatic and inoperable gastrointestinal stromal tumor (GIST).	imatinib	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
23983708-8	2013	Since pediatric GISTs are typically resistant to imatinib, we performed genotype analysis of the operative specimen that revealed KIT mutations associated with imatinib sensitivity and resistance.	imatinib	160-168	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	130-133
23278880-14	2013	The effects of SCF on mediator release from mast cells were reversed by the c-kit inhibitor imatinib.	imatinib	92-100	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	76-81
23092325-0	2013	Nuclear translocation of heme oxygenase-1 confers resistance to imatinib in chronic myeloid leukemia cells.	imatinib	64-72	heme oxygenase 1	Homo sapiens	25-41
23092325-5	2013	The aim of the present study was to investigate the effect of HO-1 expression on cell proliferation and apoptosis in chronic myeloid leukemia cells, K562 and LAMA-84 cell lines following imatinib treatment.	imatinib	187-195	heme oxygenase 1	Homo sapiens	62-66
23092343-6	2013	Imatinib, a KIT receptor inhibitor, was developed to treat GIST patients by inactivating signaling pathways.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	12-15
23092325-6	2013	Cells were incubated for 24h with Imatinib (1 muM) alone or in combination with Hemin (10muM), an inducer of HO-1.	imatinib	34-42	latexin	Homo sapiens	46-49
23092343-7	2013	However, some GISTs, especially cases with mutations in exon 13 and 17 of KIT, are resistant to imatinib treatment.	imatinib	96-104	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	74-77
23092325-6	2013	Cells were incubated for 24h with Imatinib (1 muM) alone or in combination with Hemin (10muM), an inducer of HO-1.	imatinib	34-42	heme oxygenase 1	Homo sapiens	109-113
23092325-8	2013	Pharmacological induction of HO-1 was able to overcome the effect of imatinib.	imatinib	69-77	heme oxygenase 1	Homo sapiens	29-33
23092325-12	2013	Finally, imatinib was able to increase the formation of cellular reactive oxygen species (ROS) and this effect was reversed by HO-1 induction or the addition of N-acetylcisteine (NAC).	imatinib	9-17	heme oxygenase 1	Homo sapiens	127-131
23092325-12	2013	Finally, imatinib was able to increase the formation of cellular reactive oxygen species (ROS) and this effect was reversed by HO-1 induction or the addition of N-acetylcisteine (NAC).	imatinib	9-17	X-linked Kx blood group	Homo sapiens	161-183
23092325-13	2013	In conclusion, the protective effect of HO-1 on imatinib-induced cytotoxicity does not involve its enzymatic byproducts, but rather the nuclear translocation of HO-1 following proteolytic cleavage.	imatinib	48-56	heme oxygenase 1	Homo sapiens	40-44
23092325-13	2013	In conclusion, the protective effect of HO-1 on imatinib-induced cytotoxicity does not involve its enzymatic byproducts, but rather the nuclear translocation of HO-1 following proteolytic cleavage.	imatinib	48-56	heme oxygenase 1	Homo sapiens	161-165
23762150-5	2013	The upregulated expression of alpha -MSH signaling-related molecules beta -catenin, c-Kit, and MITF was suppressed by resveratrol and/or STI571 treatment.	imatinib	137-143	pro-opiomelanocortin-alpha	Mus musculus	30-40
23028140-0	2013	Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.	imatinib	62-70	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	18-24
23028140-0	2013	Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.	imatinib	62-70	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	52-58
23028140-0	2013	Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.	imatinib	62-70	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	98-104
23028140-1	2013	Recent data suggest that the role of CYP3A4 in imatinib metabolism is smaller than presumed.	imatinib	47-55	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	37-43
23028140-5	2013	In vitro, CYP2C8 inhibitors and CYP3A4 inhibitors inhibited the depletion of 0.1 microM imatinib by 45 and 80%, respectively, and the formation of the main metabolite of imatinib, N-desmethylimatinib, by >50%.	imatinib	88-96	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	10-16
23028140-5	2013	In vitro, CYP2C8 inhibitors and CYP3A4 inhibitors inhibited the depletion of 0.1 microM imatinib by 45 and 80%, respectively, and the formation of the main metabolite of imatinib, N-desmethylimatinib, by >50%.	imatinib	88-96	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	32-38
23028140-5	2013	In vitro, CYP2C8 inhibitors and CYP3A4 inhibitors inhibited the depletion of 0.1 microM imatinib by 45 and 80%, respectively, and the formation of the main metabolite of imatinib, N-desmethylimatinib, by >50%.	imatinib	170-178	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	10-16
23028140-5	2013	In vitro, CYP2C8 inhibitors and CYP3A4 inhibitors inhibited the depletion of 0.1 microM imatinib by 45 and 80%, respectively, and the formation of the main metabolite of imatinib, N-desmethylimatinib, by >50%.	imatinib	170-178	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	32-38
23028140-6	2013	Likewise, recombinant CYP2C8 and CYP3A4 metabolized imatinib extensively, whereas other isoforms had minor effect on imatinib concentrations.	imatinib	52-60	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	22-28
23028140-6	2013	Likewise, recombinant CYP2C8 and CYP3A4 metabolized imatinib extensively, whereas other isoforms had minor effect on imatinib concentrations.	imatinib	52-60	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	33-39
23028140-7	2013	In the beginning of imatinib treatment, the fractions of its hepatic clearance mediated by CYP2C8 and CYP3A4 were predicted to approximate 40 and 60%, respectively.	imatinib	20-28	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	91-97
23028140-7	2013	In the beginning of imatinib treatment, the fractions of its hepatic clearance mediated by CYP2C8 and CYP3A4 were predicted to approximate 40 and 60%, respectively.	imatinib	20-28	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	102-108
23028140-8	2013	During long-term treatment with imatinib 400 mg once or twice daily, up to 65 or 75% of its hepatic elimination was predicted to occur via CYP2C8, and only about 35 or 25% by CYP3A4, due to dose- and time-dependent autoinactivation of CYP3A4 by imatinib.	imatinib	32-40	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	139-145
23028140-8	2013	During long-term treatment with imatinib 400 mg once or twice daily, up to 65 or 75% of its hepatic elimination was predicted to occur via CYP2C8, and only about 35 or 25% by CYP3A4, due to dose- and time-dependent autoinactivation of CYP3A4 by imatinib.	imatinib	32-40	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	175-181
23028140-8	2013	During long-term treatment with imatinib 400 mg once or twice daily, up to 65 or 75% of its hepatic elimination was predicted to occur via CYP2C8, and only about 35 or 25% by CYP3A4, due to dose- and time-dependent autoinactivation of CYP3A4 by imatinib.	imatinib	32-40	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	235-241
23028140-9	2013	Thus, although CYP2C8 and CYP3A4 are the main enzymes in imatinib metabolism in vitro, in silico predictions indicate that imatinib inhibits its own CYP3A4-mediated metabolism, assigning a key role for CYP2C8.	imatinib	57-65	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	15-21
23028140-9	2013	Thus, although CYP2C8 and CYP3A4 are the main enzymes in imatinib metabolism in vitro, in silico predictions indicate that imatinib inhibits its own CYP3A4-mediated metabolism, assigning a key role for CYP2C8.	imatinib	57-65	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	26-32
23028140-9	2013	Thus, although CYP2C8 and CYP3A4 are the main enzymes in imatinib metabolism in vitro, in silico predictions indicate that imatinib inhibits its own CYP3A4-mediated metabolism, assigning a key role for CYP2C8.	imatinib	123-131	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	149-155
23028140-9	2013	Thus, although CYP2C8 and CYP3A4 are the main enzymes in imatinib metabolism in vitro, in silico predictions indicate that imatinib inhibits its own CYP3A4-mediated metabolism, assigning a key role for CYP2C8.	imatinib	123-131	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	202-208
23028140-10	2013	During multiple dosing, pharmacogenetic polymorphisms and drug interactions affecting CYP2C8 activity may cause marked interindividual variation in the exposure and response to imatinib.	imatinib	177-185	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	86-92
23762150-5	2013	The upregulated expression of alpha -MSH signaling-related molecules beta -catenin, c-Kit, and MITF was suppressed by resveratrol and/or STI571 treatment.	imatinib	137-143	catenin (cadherin associated protein), beta 1	Mus musculus	69-82
23762150-5	2013	The upregulated expression of alpha -MSH signaling-related molecules beta -catenin, c-Kit, and MITF was suppressed by resveratrol and/or STI571 treatment.	imatinib	137-143	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	84-89
23762150-5	2013	The upregulated expression of alpha -MSH signaling-related molecules beta -catenin, c-Kit, and MITF was suppressed by resveratrol and/or STI571 treatment.	imatinib	137-143	melanogenesis associated transcription factor	Mus musculus	95-99
23762150-6	2013	Nuclear translocation of MITF, a hallmark of alpha -MSH signaling activation, was inhibited by combined treatment of resveratrol and STI571.	imatinib	133-139	melanogenesis associated transcription factor	Mus musculus	25-29
23762150-6	2013	Nuclear translocation of MITF, a hallmark of alpha -MSH signaling activation, was inhibited by combined treatment of resveratrol and STI571.	imatinib	133-139	pro-opiomelanocortin-alpha	Mus musculus	45-55
23762150-7	2013	At effective concentration, resveratrol and/or STI571 inhibited cell viability and alpha -MSH-activated matrix metalloproteinase- (MMP-)9 expression and invasion capacity of B16 melanoma cells.	imatinib	47-53	matrix metallopeptidase 9	Mus musculus	83-137
23762150-8	2013	In conclusion, resveratrol enhances STI571 effect on suppressing the alpha -MSH signaling, viability, and invasiveness in melanoma cells.	imatinib	36-42	pro-opiomelanocortin-alpha	Mus musculus	69-79
23853621-16	2013	To our knowledge, this is the first case of NF1 associated with clinical and biochemical features of Cushing"s secondary to ectopic ACTH due to MPNST in a plexiform neurofibroma and its resolution on treatment with imatinib.	imatinib	215-223	neurofibromin 1	Homo sapiens	44-47
23127174-2	2013	While benefits have been obtained from use of inhibitors of KIT kinase activity such as imatinib, especially in gastrointestinal stromal tumours (GIST), primary resistance occurs with certain oncogenic mutations.	imatinib	88-96	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	60-63
23127174-6	2013	The action of KIT kinase inhibitors, especially imatinib, sunitinib, dasatinib and PKC412, on different primary and secondary mutants is discussed.	imatinib	48-56	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-17
23423603-7	2013	Two patients with a KIT stop codon mutation did not respond to imatinib therapy and died shortly after treatment.	imatinib	63-71	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	20-23
23479771-7	2013	The imatinib-resistant tumor cells in the progressing metastases showed marked pleomorphism which proved to be rhabdomyoblastic differentiation with Desmin and Myogenin immunopositivity.	imatinib	4-12	desmin	Homo sapiens	149-155
23479771-7	2013	The imatinib-resistant tumor cells in the progressing metastases showed marked pleomorphism which proved to be rhabdomyoblastic differentiation with Desmin and Myogenin immunopositivity.	imatinib	4-12	myogenin	Homo sapiens	160-168
23041331-9	2013	RESULTS: Loss of Ptch from lysozyme M-expressing cells resulted in the development of tumors of GIST-like localization and histology; these were reduced when mice were given imatinib, a drug that targets KIT and PDGFRA.	imatinib	174-182	patched 1	Mus musculus	17-21
23041331-9	2013	RESULTS: Loss of Ptch from lysozyme M-expressing cells resulted in the development of tumors of GIST-like localization and histology; these were reduced when mice were given imatinib, a drug that targets KIT and PDGFRA.	imatinib	174-182	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	204-207
23041331-9	2013	RESULTS: Loss of Ptch from lysozyme M-expressing cells resulted in the development of tumors of GIST-like localization and histology; these were reduced when mice were given imatinib, a drug that targets KIT and PDGFRA.	imatinib	174-182	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	212-218
23221606-11	2013	CONCLUSIONS: In patients with LGESS, c-kit and PDGFR were expressed in higher portions of patients, suggesting that imatinib mesylate should be investigated as a potential targeting agent.	imatinib	116-133	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	37-42
23221606-11	2013	CONCLUSIONS: In patients with LGESS, c-kit and PDGFR were expressed in higher portions of patients, suggesting that imatinib mesylate should be investigated as a potential targeting agent.	imatinib	116-133	platelet derived growth factor receptor beta	Homo sapiens	47-52
23853621-16	2013	To our knowledge, this is the first case of NF1 associated with clinical and biochemical features of Cushing"s secondary to ectopic ACTH due to MPNST in a plexiform neurofibroma and its resolution on treatment with imatinib.	imatinib	215-223	proopiomelanocortin	Homo sapiens	132-136
23151973-4	2013	Among these phenyl amino pyrimidine derivatives, NRC-AN-019 has             been found to be a promising new lead compound for the therapy of imatinib mesylate-resistant             chronic myeloid leukemia.	imatinib	142-159	nuclear receptor coactivator 6	Homo sapiens	49-52
22858987-4	2013	We show for the first time that Gab2 signaling protects CML cells from various Bcr-Abl inhibitors (imatinib, nilotinib, dasatinib and GNF-2), whereas Gab2 knockdown or haploinsufficiency leads to increased TKI sensitivity.	imatinib	99-107	GRB2 associated binding protein 2	Homo sapiens	32-36
22691121-3	2013	Conversely, ABL1 mutations occur in 25% of imatinib-naive patients with CML-BP but are not described in patients with AML.	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-16
22712835-0	2013	Hyperpigmentation of the hard palate associated with imatinib therapy for chronic myeloid leukemia with a genetic variation in the proto-oncogene c-KIT.	imatinib	53-61	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	131-151
23069194-3	2013	Treatment with imatinib, a KIT inhibitor, resulted in resolution of the lesions and were well tolerated by the patients.	imatinib	15-23	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	27-30
23040543-1	2013	Targeted therapies, such as those using imatinib and rituximab, have revolutionized the treatment of Philadelphia chromosome-positive and CD20-positive acute lymphoblastic leukemia (ALL) respectively, yet these therapies are effective in only a subset of patients and remission is generally not durable.	imatinib	40-48	keratin 20	Homo sapiens	138-142
22898683-1	2013	INTRODUCTION: The purpose of the study was to evaluate the efficacy of imatinib mesylate in the treatment of nephrogenic systemic fibrosis (NSF) in a rat model administered high-dose gadodiamide, erythropoietin (Epo) and intravenous iron (IV iron).	imatinib	71-88	erythropoietin	Rattus norvegicus	212-215
23099235-1	2013	Since BCR-ABL plays an essential role in the growth factor-independent proliferation of Philadelphia chromosome (Ph)+ leukemia cells, imatinib treatment of Ph+ leukemia cells inactivates signaling pathways of BCR-ABL, and subsequent addition of growth factors (GFs) could restore the signaling pathways without reactivating BCR-ABL.	imatinib	134-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-13
23099235-1	2013	Since BCR-ABL plays an essential role in the growth factor-independent proliferation of Philadelphia chromosome (Ph)+ leukemia cells, imatinib treatment of Ph+ leukemia cells inactivates signaling pathways of BCR-ABL, and subsequent addition of growth factors (GFs) could restore the signaling pathways without reactivating BCR-ABL.	imatinib	134-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-216
23099235-1	2013	Since BCR-ABL plays an essential role in the growth factor-independent proliferation of Philadelphia chromosome (Ph)+ leukemia cells, imatinib treatment of Ph+ leukemia cells inactivates signaling pathways of BCR-ABL, and subsequent addition of growth factors (GFs) could restore the signaling pathways without reactivating BCR-ABL.	imatinib	134-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-216
23062378-0	2013	Emerging kinetics of BCR-ABL1 mutations and their effect on disease outcomes in chronic myeloid leukemia patients with imatinib failure.	imatinib	119-127	BCR activator of RhoGEF and GTPase	Homo sapiens	21-29
23493838-2	2013	Bosutinib effectively inhibits wild-type BCR-ABL and most imatinib-resistant BCR-ABL mutations except for V299L and T315I.	imatinib	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
23062378-4	2013	Seminested polymerase chain reaction followed by denaturing high-performance liquid chromatography with sequence confirmation were used to detect BCR-ABL1 mutations in 202 CML patients with imatinib resistance at different CML phases.	imatinib	190-198	BCR activator of RhoGEF and GTPase	Homo sapiens	146-154
24136010-1	2013	The oral tyrosine kinase inhibitor (TKI) imatinib has revolutionized the treatment of gastrointestinal stromal tumors (GISTs), most of which harbor oncogenic mutation in genes that encode the receptor tyrosine kinases KIT or PDGFA.	imatinib	41-49	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	218-221
23666688-0	2013	Detection of BCR-ABL1 kinase domain mutations causing imatinib resistance in chronic myelogenous leukemia.	imatinib	54-62	BCR activator of RhoGEF and GTPase	Homo sapiens	13-21
23666688-5	2013	However, a significant minority of patients being treated with imatinib develop resistance to the drug as evidenced by rising BCR-ABL1 levels.	imatinib	63-71	BCR activator of RhoGEF and GTPase	Homo sapiens	126-134
23666688-6	2013	The most common mechanism of resistance in these patients is the development of mutations in the BCR-ABL1 kinase domain (KD) that abrogate binding of imatinib.	imatinib	150-158	BCR activator of RhoGEF and GTPase	Homo sapiens	97-105
23408993-11	2013	CONCLUSIONS/SIGNIFICANCE: CD133 mRNA expression levels in GIST patients measured by real time RT-PCR assay appeared to correlate with tumor response to surgery or imatinib and may be used to predict tumor progression.	imatinib	163-171	prominin 1	Homo sapiens	26-31
24330849-0	2013	Restoration of INK4a/ARF gene inhibits cell growth and cooperates with imatinib mesylate in Philadelphia chromosome-positive leukemias.	imatinib	71-79	cyclin dependent kinase inhibitor 2A	Homo sapiens	15-20
24330849-4	2013	Furthermore, upon viral transduction at low multiplicity of infection, INK4a/ARF potentiated the effect of imatinib mesylate on Ph-positive leukemia cell lines in an additive but not synergistic manner.	imatinib	107-124	cyclin dependent kinase inhibitor 2A	Homo sapiens	71-80
24330849-5	2013	These results suggest that INK4a/ARF protein-mimetic agents may be promising options for Ph-positive leukemias in combination with imatinib mesylate.	imatinib	131-148	cyclin dependent kinase inhibitor 2A	Homo sapiens	27-32
24136010-1	2013	The oral tyrosine kinase inhibitor (TKI) imatinib has revolutionized the treatment of gastrointestinal stromal tumors (GISTs), most of which harbor oncogenic mutation in genes that encode the receptor tyrosine kinases KIT or PDGFA.	imatinib	41-49	platelet derived growth factor subunit A	Homo sapiens	225-230
24136010-8	2013	In the adjuvant setting, final results of the trial by the Scandinavian Sarcoma Group and the Sarcoma Group of the Arbeitsgemeinschaft Internistische Onkologie demonstrate that 3 years of adjuvant imatinib, compared with 1 year, significantly reduces the risk of recurrence and improves overall survival of patients with KIT-positive GIST at high risk of recurrence.	imatinib	197-205	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	321-324
23409026-0	2013	Sensitive detection of pre-existing BCR-ABL kinase domain mutations in CD34+ cells of newly diagnosed chronic-phase chronic myeloid leukemia patients is associated with imatinib resistance: implications in the post-imatinib era.	imatinib	169-177	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
23409026-0	2013	Sensitive detection of pre-existing BCR-ABL kinase domain mutations in CD34+ cells of newly diagnosed chronic-phase chronic myeloid leukemia patients is associated with imatinib resistance: implications in the post-imatinib era.	imatinib	169-177	CD34 molecule	Homo sapiens	71-75
23409026-0	2013	Sensitive detection of pre-existing BCR-ABL kinase domain mutations in CD34+ cells of newly diagnosed chronic-phase chronic myeloid leukemia patients is associated with imatinib resistance: implications in the post-imatinib era.	imatinib	215-223	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
23409026-0	2013	Sensitive detection of pre-existing BCR-ABL kinase domain mutations in CD34+ cells of newly diagnosed chronic-phase chronic myeloid leukemia patients is associated with imatinib resistance: implications in the post-imatinib era.	imatinib	215-223	CD34 molecule	Homo sapiens	71-75
23409026-2	2013	Recent studies indicate the presence of pre-existing BCR-ABL mutations in a higher percentage of CML patients when CD34+ stem/progenitor cells are investigated using sensitive techniques, and these mutations are associated with imatinib resistance and disease progression.	imatinib	228-236	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
23409026-2	2013	Recent studies indicate the presence of pre-existing BCR-ABL mutations in a higher percentage of CML patients when CD34+ stem/progenitor cells are investigated using sensitive techniques, and these mutations are associated with imatinib resistance and disease progression.	imatinib	228-236	CD34 molecule	Homo sapiens	115-119
23437189-4	2013	Accordingly, sensitive assays for detecting Bcr-Abl kinase activity compatible with small amounts of patient material are desirable as potential companion diagnostics for imatinib.	imatinib	171-179	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
23409026-7	2013	After a median follow-up of 30 months (range 8-48), all patients with pre-existing BCR-ABL mutations exhibited imatinib resistance.	imatinib	111-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
23409026-9	2013	All 32 patients with pre-existing BCR-ABL mutations had the same mutations after manifestation of imatinib-resistance.	imatinib	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
23409026-10	2013	In imatinib-resistant patients without pre-existing BCR-ABL mutations, we detected F311L, M351T, Y253F, and T315I mutations.	imatinib	3-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
23409026-14	2013	After the recent approval of nilotinib, dasatinib, bosutinib and ponatinib for treatment of chronic myeloid leukemia along with imatinib, all of which vary in their effectiveness against mutated BCR-ABL forms, detection of pre-existing BCR-ABL mutations can help in selection of appropriate first-line drug therapy.	imatinib	128-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	195-202
23409026-14	2013	After the recent approval of nilotinib, dasatinib, bosutinib and ponatinib for treatment of chronic myeloid leukemia along with imatinib, all of which vary in their effectiveness against mutated BCR-ABL forms, detection of pre-existing BCR-ABL mutations can help in selection of appropriate first-line drug therapy.	imatinib	128-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	236-243
23383209-0	2013	Imatinib reverses doxorubicin resistance by affecting activation of STAT3-dependent NF-kappaB and HSP27/p38/AKT pathways and by inhibiting ABCB1.	imatinib	0-8	signal transducer and activator of transcription 3	Homo sapiens	68-73
23372733-0	2013	ZNF-mediated resistance to imatinib mesylate in gastrointestinal stromal tumor.	imatinib	27-35	zinc finger protein 763	Homo sapiens	0-3
23383209-0	2013	Imatinib reverses doxorubicin resistance by affecting activation of STAT3-dependent NF-kappaB and HSP27/p38/AKT pathways and by inhibiting ABCB1.	imatinib	0-8	nuclear factor kappa B subunit 1	Homo sapiens	84-93
23383209-0	2013	Imatinib reverses doxorubicin resistance by affecting activation of STAT3-dependent NF-kappaB and HSP27/p38/AKT pathways and by inhibiting ABCB1.	imatinib	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	139-144
23383209-0	2013	Imatinib reverses doxorubicin resistance by affecting activation of STAT3-dependent NF-kappaB and HSP27/p38/AKT pathways and by inhibiting ABCB1.	imatinib	0-8	heat shock protein family B (small) member 1	Homo sapiens	98-103
23383209-4	2013	In this report, we demonstrate that the c-Abl/Arg inhibitor, imatinib (imatinib mesylate, STI571, Gleevec), reverses intrinsic and acquired resistance to the anthracycline, doxorubicin, by inducing G2/M arrest and promoting apoptosis in cancer cells expressing highly active c-Abl and Arg.	imatinib	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-45
23383209-4	2013	In this report, we demonstrate that the c-Abl/Arg inhibitor, imatinib (imatinib mesylate, STI571, Gleevec), reverses intrinsic and acquired resistance to the anthracycline, doxorubicin, by inducing G2/M arrest and promoting apoptosis in cancer cells expressing highly active c-Abl and Arg.	imatinib	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	275-280
23383209-4	2013	In this report, we demonstrate that the c-Abl/Arg inhibitor, imatinib (imatinib mesylate, STI571, Gleevec), reverses intrinsic and acquired resistance to the anthracycline, doxorubicin, by inducing G2/M arrest and promoting apoptosis in cancer cells expressing highly active c-Abl and Arg.	imatinib	71-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-45
23383209-0	2013	Imatinib reverses doxorubicin resistance by affecting activation of STAT3-dependent NF-kappaB and HSP27/p38/AKT pathways and by inhibiting ABCB1.	imatinib	0-8	mitogen-activated protein kinase 14	Homo sapiens	104-107
23383209-4	2013	In this report, we demonstrate that the c-Abl/Arg inhibitor, imatinib (imatinib mesylate, STI571, Gleevec), reverses intrinsic and acquired resistance to the anthracycline, doxorubicin, by inducing G2/M arrest and promoting apoptosis in cancer cells expressing highly active c-Abl and Arg.	imatinib	71-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	275-280
23383209-4	2013	In this report, we demonstrate that the c-Abl/Arg inhibitor, imatinib (imatinib mesylate, STI571, Gleevec), reverses intrinsic and acquired resistance to the anthracycline, doxorubicin, by inducing G2/M arrest and promoting apoptosis in cancer cells expressing highly active c-Abl and Arg.	imatinib	90-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-45
23383209-0	2013	Imatinib reverses doxorubicin resistance by affecting activation of STAT3-dependent NF-kappaB and HSP27/p38/AKT pathways and by inhibiting ABCB1.	imatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	108-111
23383209-4	2013	In this report, we demonstrate that the c-Abl/Arg inhibitor, imatinib (imatinib mesylate, STI571, Gleevec), reverses intrinsic and acquired resistance to the anthracycline, doxorubicin, by inducing G2/M arrest and promoting apoptosis in cancer cells expressing highly active c-Abl and Arg.	imatinib	90-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	275-280
23383209-5	2013	Significantly, imatinib prevents intrinsic resistance by promoting doxorubicin-mediated NF-kappaB/p65 nuclear localization and repression of NF-kappaB targets in a STAT3-dependent manner, and by preventing activation of a novel STAT3/HSP27/p38/Akt survival pathway.	imatinib	15-23	nuclear factor kappa B subunit 1	Homo sapiens	88-97
23300967-2	2013	In this paper we report that Gleevec (Imatinib), an Abl family kinase inhibitor, produces a profound change in the shape and migration of rat bladder tumor cells (NBTII) plated on collagen-coated substrates.	imatinib	29-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Rattus norvegicus	52-55
23383209-5	2013	Significantly, imatinib prevents intrinsic resistance by promoting doxorubicin-mediated NF-kappaB/p65 nuclear localization and repression of NF-kappaB targets in a STAT3-dependent manner, and by preventing activation of a novel STAT3/HSP27/p38/Akt survival pathway.	imatinib	15-23	RELA proto-oncogene, NF-kB subunit	Homo sapiens	98-101
23383209-5	2013	Significantly, imatinib prevents intrinsic resistance by promoting doxorubicin-mediated NF-kappaB/p65 nuclear localization and repression of NF-kappaB targets in a STAT3-dependent manner, and by preventing activation of a novel STAT3/HSP27/p38/Akt survival pathway.	imatinib	15-23	nuclear factor kappa B subunit 1	Homo sapiens	141-150
23383209-5	2013	Significantly, imatinib prevents intrinsic resistance by promoting doxorubicin-mediated NF-kappaB/p65 nuclear localization and repression of NF-kappaB targets in a STAT3-dependent manner, and by preventing activation of a novel STAT3/HSP27/p38/Akt survival pathway.	imatinib	15-23	signal transducer and activator of transcription 3	Homo sapiens	164-169
23383209-5	2013	Significantly, imatinib prevents intrinsic resistance by promoting doxorubicin-mediated NF-kappaB/p65 nuclear localization and repression of NF-kappaB targets in a STAT3-dependent manner, and by preventing activation of a novel STAT3/HSP27/p38/Akt survival pathway.	imatinib	15-23	signal transducer and activator of transcription 3	Homo sapiens	228-233
23383209-5	2013	Significantly, imatinib prevents intrinsic resistance by promoting doxorubicin-mediated NF-kappaB/p65 nuclear localization and repression of NF-kappaB targets in a STAT3-dependent manner, and by preventing activation of a novel STAT3/HSP27/p38/Akt survival pathway.	imatinib	15-23	heat shock protein family B (small) member 1	Homo sapiens	234-239
23383209-5	2013	Significantly, imatinib prevents intrinsic resistance by promoting doxorubicin-mediated NF-kappaB/p65 nuclear localization and repression of NF-kappaB targets in a STAT3-dependent manner, and by preventing activation of a novel STAT3/HSP27/p38/Akt survival pathway.	imatinib	15-23	mitogen-activated protein kinase 14	Homo sapiens	240-243
23383209-5	2013	Significantly, imatinib prevents intrinsic resistance by promoting doxorubicin-mediated NF-kappaB/p65 nuclear localization and repression of NF-kappaB targets in a STAT3-dependent manner, and by preventing activation of a novel STAT3/HSP27/p38/Akt survival pathway.	imatinib	15-23	AKT serine/threonine kinase 1	Homo sapiens	244-247
23383209-6	2013	In contrast, imatinib prevents acquired resistance by inhibiting upregulation of the ABC drug transporter, ABCB1, directly inhibiting ABCB1 function, and abrogating survival signaling.	imatinib	13-21	ATP binding cassette subfamily B member 1	Homo sapiens	107-112
23383209-6	2013	In contrast, imatinib prevents acquired resistance by inhibiting upregulation of the ABC drug transporter, ABCB1, directly inhibiting ABCB1 function, and abrogating survival signaling.	imatinib	13-21	ATP binding cassette subfamily B member 1	Homo sapiens	134-139
23383209-7	2013	Thus, imatinib inhibits multiple novel chemoresistance pathways, which indicates that it may be effective in reversing intrinsic and acquired resistance in cancers containing highly active c-Abl and Arg, a critical step in effectively treating metastatic disease.	imatinib	6-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	189-194
23383209-8	2013	Furthermore, since imatinib converts a master survival regulator, NF-kappaB, from a pro-survival into a pro-apoptotic factor, our data suggest that NF-kappaB inhibitors may be ineffective in sensitizing tumors containing activated c-Abl/Arg to anthracyclines, and instead might antagonize anthracycline-induced apoptosis.	imatinib	19-27	nuclear factor kappa B subunit 1	Homo sapiens	66-75
23437178-6	2013	We have previously shown that imatinib reduces BBB disruption and stroke volume after experimentally induced ischemic stroke by targeting platelet-derived growth factor receptor -alpha (PDGFR-alpha) signaling.	imatinib	30-38	platelet derived growth factor receptor alpha	Rattus norvegicus	138-184
23437178-6	2013	We have previously shown that imatinib reduces BBB disruption and stroke volume after experimentally induced ischemic stroke by targeting platelet-derived growth factor receptor -alpha (PDGFR-alpha) signaling.	imatinib	30-38	platelet derived growth factor receptor alpha	Rattus norvegicus	186-197
23437178-7	2013	Here we demonstrate that PDGFR-alpha signaling is a central regulator of BBB integrity during neuroinflammation and therefore imatinib should be considered as a potentially effective treatment for MS.	imatinib	126-134	platelet derived growth factor receptor alpha	Rattus norvegicus	25-36
23437189-1	2013	The protein kinase Bcr-Abl plays a major role in the pathogenesis of chronic myelogenous leukemia (CML), and is the target of the breakthrough drug imatinib (Gleevec ).	imatinib	148-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
23300967-2	2013	In this paper we report that Gleevec (Imatinib), an Abl family kinase inhibitor, produces a profound change in the shape and migration of rat bladder tumor cells (NBTII) plated on collagen-coated substrates.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Rattus norvegicus	52-55
23099479-5	2012	In human macro- and microvascular endothelial monolayers, imatinib attenuated endothelial barrier dysfunction induced by thrombin and histamine.	imatinib	58-66	coagulation factor II, thrombin	Homo sapiens	121-129
24137941-6	2013	Among the BCR-ABL TK inhibitors (TKI) registered in the Russian Federation and recommended for the treatment of chronic myeloid leukemia, there are 3 medications: imatinib, nilotinib, and dasatinib.	imatinib	163-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
23904814-1	2013	We report here on a rare case of BCR-ABL1-negative atypical chronic myeloid leukemia with a t(9;22)(p24;q11.2)translocation and a BCR-JAK2 fusion gene, with resistance to the tyrosine kinase inhibitors imatinib and dasatinib.At two years of follow-up, the patient showed no hematologic response and was submitted to an allogeneic bonemarrow transplantation.	imatinib	202-210	BCR activator of RhoGEF and GTPase	Homo sapiens	33-41
23904814-1	2013	We report here on a rare case of BCR-ABL1-negative atypical chronic myeloid leukemia with a t(9;22)(p24;q11.2)translocation and a BCR-JAK2 fusion gene, with resistance to the tyrosine kinase inhibitors imatinib and dasatinib.At two years of follow-up, the patient showed no hematologic response and was submitted to an allogeneic bonemarrow transplantation.	imatinib	202-210	BCR activator of RhoGEF and GTPase	Homo sapiens	33-36
23904814-1	2013	We report here on a rare case of BCR-ABL1-negative atypical chronic myeloid leukemia with a t(9;22)(p24;q11.2)translocation and a BCR-JAK2 fusion gene, with resistance to the tyrosine kinase inhibitors imatinib and dasatinib.At two years of follow-up, the patient showed no hematologic response and was submitted to an allogeneic bonemarrow transplantation.	imatinib	202-210	Janus kinase 2	Homo sapiens	134-138
23228190-2	2012	Targeted inhibition of platelet derived growth factor receptor (PDGFR) by imatinib may influence tumor growth and amplify chemotherapeutic effects.	imatinib	74-82	platelet derived growth factor receptor beta	Homo sapiens	23-62
23228190-2	2012	Targeted inhibition of platelet derived growth factor receptor (PDGFR) by imatinib may influence tumor growth and amplify chemotherapeutic effects.	imatinib	74-82	platelet derived growth factor receptor beta	Homo sapiens	64-69
23099479-6	2012	Small interfering RNA knock-downs of the imatinib-sensitive kinases revealed that imatinib attenuates endothelial barrier dysfunction via inhibition of Abl-related gene kinase (Arg/Abl2), a previously unknown mediator of endothelial barrier dysfunction.	imatinib	82-90	v-abl Abelson murine leukemia viral oncogene 2 (arg, Abelson-related gene)	Mus musculus	181-185
23099479-8	2012	Imatinib limited Arg-mediated endothelial barrier dysfunction by enhancing Rac1 activity and enforcing adhesion of endothelial cells to the extracellular matrix.	imatinib	0-8	Rac family small GTPase 1	Mus musculus	75-79
22736149-6	2012	In addition, a CD117 (c-kit) gene mutation has been identified in cutaneous melanomas, indicating that there may be potential therapeutic benefits of tyrosine kinase inhibitors, such as Imatinib.	imatinib	186-194	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	15-20
22965919-8	2012	We conclude that the differences and correlations of BCR-ABL mRNA between PB and BM assays depend on the depth of the molecular response in BM for CML during imatinib therapy.	imatinib	158-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
23184075-11	2012	CONCLUSION: Imatinib can exert inhibitory effects on myocardial fibrosis in DOCA/salt induced hypertensive rats, which may be attributed to the inhibition of PDGFR-alpha activity.	imatinib	12-20	platelet derived growth factor receptor alpha	Rattus norvegicus	158-169
23184075-0	2012	Imatinib attenuates myocardial fibrosis in association with inhibition of the PDGFRalpha activity.	imatinib	0-8	platelet derived growth factor receptor alpha	Rattus norvegicus	78-88
23184075-1	2012	BACKGROUND: Imatinib is a tyrosine kinase receptor inhibitor that has been confirmed to exert inhibitory effect on the platelet derived growth factor PDGF receptor (PDGFRalpha and PDGFRbeta) activity.	imatinib	12-20	platelet derived growth factor receptor alpha	Rattus norvegicus	165-175
23184075-1	2012	BACKGROUND: Imatinib is a tyrosine kinase receptor inhibitor that has been confirmed to exert inhibitory effect on the platelet derived growth factor PDGF receptor (PDGFRalpha and PDGFRbeta) activity.	imatinib	12-20	platelet derived growth factor receptor beta	Rattus norvegicus	180-189
23209150-4	2012	Accordingly, direct targeting of BCR-ABL through agents such as imatinib have profound antitumor effects.	imatinib	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
22736149-6	2012	In addition, a CD117 (c-kit) gene mutation has been identified in cutaneous melanomas, indicating that there may be potential therapeutic benefits of tyrosine kinase inhibitors, such as Imatinib.	imatinib	186-194	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	22-27
22748304-4	2012	Recently, some cases of Langerhans cell histiocytosis were reported to express platelet-derived growth factor receptors alpha and beta or c-KIT by immunohistochemistry, and some of these patients had a clinical response to imatinib mesylate.	imatinib	223-240	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	138-143
23100514-5	2012	Treatment with the Abl kinase inhibitors imatinib and GNF-2 or overexpression of kinase-inactive forms of the Abl family kinases also impairs particle internalization in murine macrophages, indicating Abl kinase activity is required for efficient phagocytosis.	imatinib	41-49	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	19-22
22748304-5	2012	Other hematologic disorders with PDGFRalpha or PDGFRbeta gene rearrangements also have responded to imatinib mesylate.	imatinib	100-117	platelet derived growth factor receptor alpha	Homo sapiens	33-43
22748304-5	2012	Other hematologic disorders with PDGFRalpha or PDGFRbeta gene rearrangements also have responded to imatinib mesylate.	imatinib	100-117	platelet derived growth factor receptor beta	Homo sapiens	47-56
25998099-0	2012	K356dup--an in-frame insertion in the BCR-ABL gene in an imatinib-resistant chronic myeloid leukemia.	imatinib	57-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
22415796-1	2012	Effective inhibition of BCR-ABL tyrosine kinase activity with Imatinib represents a breakthrough in the treatment of patients with chronic myeloid leukemia (CML).	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
22415796-4	2012	We recently reported downregulation of eukaryotic initiation factor 5A (eIF5A) in Imatinib treated K562 cells.	imatinib	82-90	eukaryotic translation initiation factor 5A	Homo sapiens	39-70
22415796-4	2012	We recently reported downregulation of eukaryotic initiation factor 5A (eIF5A) in Imatinib treated K562 cells.	imatinib	82-90	eukaryotic translation initiation factor 5A	Homo sapiens	72-77
22415796-5	2012	Furthermore, the inhibition of eIF5A by siRNA in combination with Imatinib has been shown to exert synergistic cytotoxic effects on BCR-ABL positive cell lines.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
23205316-0	2012	Extra Gastrointestinal Stromal Tumor treated with imatinib in a patient with Neurofibromatosis type 1.	imatinib	50-58	neurofibromin 1	Homo sapiens	77-101
22399151-1	2012	Nilotinib is a potent tyrosine kinase inhibitor of breakpoint cluster region-abelson (BCR-ABL), which has been approved as front-line therapy for newly diagnosed chronic myeloid leukemia in chronic phase and as second-line therapy after imatinib failure in chronic or accelerated phase chronic myeloid leukemia.	imatinib	237-245	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-84
22399151-1	2012	Nilotinib is a potent tyrosine kinase inhibitor of breakpoint cluster region-abelson (BCR-ABL), which has been approved as front-line therapy for newly diagnosed chronic myeloid leukemia in chronic phase and as second-line therapy after imatinib failure in chronic or accelerated phase chronic myeloid leukemia.	imatinib	237-245	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
23099009-0	2012	Imatinib mesylate for plexiform neurofibromas in patients with neurofibromatosis type 1: a phase 2 trial.	imatinib	0-17	neurofibromin 1	Homo sapiens	63-87
23099009-3	2012	We undertook an open-label phase 2 trial to test whether treatment with imatinib mesylate can decrease the volume burden of clinically significant plexiform neurofibromas in patients with NF1.	imatinib	72-89	neurofibromin 1	Homo sapiens	188-191
23099009-13	2012	INTERPRETATION: Imatinib mesylate could be used to treat plexiform neurofibromas in patients with NF1.	imatinib	16-33	neurofibromin 1	Homo sapiens	98-101
22616642-1	2012	In patients with chronic myeloid leukemia (CML), use of the BCR-ABL1-specific tyrosine kinase inhibitors (TKIs) imatinib, nilotinib and dasatinib has greatly improved patient survival and prolonged disease remission.	imatinib	112-120	BCR activator of RhoGEF and GTPase	Homo sapiens	60-68
22815156-0	2012	C-KIT mutations were closely associated with the response to Imatinib in Chinese advanced gastrointestinal stromal tumor patients.	imatinib	61-69	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-5
22815156-1	2012	To investigate the correlation between C-KIT/PDGFRalpha mutations and Imatinib response or survival in Chinese advanced gastrointestinal stromal tumor (GIST) patients.	imatinib	70-78	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	39-44
22815156-1	2012	To investigate the correlation between C-KIT/PDGFRalpha mutations and Imatinib response or survival in Chinese advanced gastrointestinal stromal tumor (GIST) patients.	imatinib	70-78	platelet derived growth factor receptor alpha	Homo sapiens	45-55
22815156-9	2012	C-KIT mutations were closely associated with Imatinib response and progression-free survival of Chinese advanced GIST patients.	imatinib	45-53	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-5
23238683-2	2012	Indeed, inhibition of BCR-ABL by imatinib, dasatinib or nilotinib triggers durable responses in most patients suffering from this disease.	imatinib	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
23355941-0	2012	Contribution of BCR-ABL kinase domain mutations to imatinib mesylate resistance in Philadelphia chromosome positive Malaysian chronic myeloid leukemia patients.	imatinib	51-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
23257431-4	2012	Lyn expression in imatinib-resistant patients was significantly higher than that in normal persons, newly diagnosed patients and imatinib-effective patients (P < 0.05).	imatinib	129-137	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	0-3
23257431-12	2012	Lyn is over-expressed in imatinib-resistant CML.	imatinib	25-33	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	0-3
23257463-3	2012	It has been confirmed that imatinib not only inhibits BCR-ABL mutations, but also suppresses other tyrosine kinase receptor genes such as PDGFR, JAK2V617F and C-KIT mutations, providing an important potential of targeted therapy for myeloproliferative disease.	imatinib	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
23257463-3	2012	It has been confirmed that imatinib not only inhibits BCR-ABL mutations, but also suppresses other tyrosine kinase receptor genes such as PDGFR, JAK2V617F and C-KIT mutations, providing an important potential of targeted therapy for myeloproliferative disease.	imatinib	27-35	platelet derived growth factor receptor beta	Homo sapiens	138-143
23257463-3	2012	It has been confirmed that imatinib not only inhibits BCR-ABL mutations, but also suppresses other tyrosine kinase receptor genes such as PDGFR, JAK2V617F and C-KIT mutations, providing an important potential of targeted therapy for myeloproliferative disease.	imatinib	27-35	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	159-164
23257463-4	2012	As the PDGFR, JAK2 and C-KIT play important roles in the regulation of hematopoiesis, suggesting that imatinib may block the phosphorylation of PDGFR, JAK2V617F and C-KIT receptors, interrupt the signal transduction cascades, disrupt cell differentiation and proliferation.	imatinib	102-110	platelet derived growth factor receptor beta	Homo sapiens	7-12
23257463-4	2012	As the PDGFR, JAK2 and C-KIT play important roles in the regulation of hematopoiesis, suggesting that imatinib may block the phosphorylation of PDGFR, JAK2V617F and C-KIT receptors, interrupt the signal transduction cascades, disrupt cell differentiation and proliferation.	imatinib	102-110	Janus kinase 2	Homo sapiens	14-18
23257463-4	2012	As the PDGFR, JAK2 and C-KIT play important roles in the regulation of hematopoiesis, suggesting that imatinib may block the phosphorylation of PDGFR, JAK2V617F and C-KIT receptors, interrupt the signal transduction cascades, disrupt cell differentiation and proliferation.	imatinib	102-110	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	23-28
23257463-4	2012	As the PDGFR, JAK2 and C-KIT play important roles in the regulation of hematopoiesis, suggesting that imatinib may block the phosphorylation of PDGFR, JAK2V617F and C-KIT receptors, interrupt the signal transduction cascades, disrupt cell differentiation and proliferation.	imatinib	102-110	platelet derived growth factor receptor beta	Homo sapiens	144-149
23257463-4	2012	As the PDGFR, JAK2 and C-KIT play important roles in the regulation of hematopoiesis, suggesting that imatinib may block the phosphorylation of PDGFR, JAK2V617F and C-KIT receptors, interrupt the signal transduction cascades, disrupt cell differentiation and proliferation.	imatinib	102-110	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	165-170
23257429-0	2012	[Increasing sensitivity of leukemia cells to imatinib by inhibiting NHE1 and p38MAPK signaling pathway].	imatinib	45-53	solute carrier family 9 member A1	Homo sapiens	68-72
23257429-1	2012	This study was aimed to investigate whether the inhibition of NHE1 activity and intracellular acidification can reverse resistance of leukemia cells to the imatinib and to explore downstream signal molecule networks of BCR/ABL in the cells of chronic myelocytic leukemia (CML) patients.	imatinib	156-164	solute carrier family 9 member A1	Homo sapiens	62-66
23257429-1	2012	This study was aimed to investigate whether the inhibition of NHE1 activity and intracellular acidification can reverse resistance of leukemia cells to the imatinib and to explore downstream signal molecule networks of BCR/ABL in the cells of chronic myelocytic leukemia (CML) patients.	imatinib	156-164	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	219-226
23257429-4	2012	The results showed that the intracellular concentration of drugs in the advanced patients increased and the sensitivity of K562/DOX and K562/G01 cells to imatinib was enhanced after intracellular acidification or treatment with NHE1 inhibitor cariporide.	imatinib	154-162	solute carrier family 9 member A1	Homo sapiens	228-232
23257429-7	2012	It is concluded that the inhibiton of NHE1 can significantly decrease the protein expression of Pgp in K562/DOX and K562/G01 cells, increase the accumulation of Rhodamine123 and doxorubicin in the cells of advanced patients and enhance the sensitivity of cells to imatinib in which the p38 MAPK signal transduction pathways involves.	imatinib	264-272	solute carrier family 9 member A1	Homo sapiens	38-42
23257429-7	2012	It is concluded that the inhibiton of NHE1 can significantly decrease the protein expression of Pgp in K562/DOX and K562/G01 cells, increase the accumulation of Rhodamine123 and doxorubicin in the cells of advanced patients and enhance the sensitivity of cells to imatinib in which the p38 MAPK signal transduction pathways involves.	imatinib	264-272	ATP binding cassette subfamily B member 1	Homo sapiens	96-99
23257431-0	2012	[Role of Lyn kinase in imatinib-resistant chronic myelogenous leukemia].	imatinib	23-31	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	9-12
23257431-1	2012	This study was aimed to explore the role of Lyn kinase in imatinib-resistant CML.	imatinib	58-66	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	44-47
23257431-4	2012	Lyn expression in imatinib-resistant patients was significantly higher than that in normal persons, newly diagnosed patients and imatinib-effective patients (P < 0.05).	imatinib	18-26	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	0-3
23088644-5	2012	These compounds may serve as lead compounds for further development of new Bcr-Abl inhibitors capable of overcoming clinical acquired resistance against imatinib.	imatinib	153-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
23355941-1	2012	Development of resistance to imatinib mesylate (IM) in chronic myeloid leukemia (CML) patients is mediated by different mechanisms that can be classified as BCR-ABL dependent or BCR-ABL independent pathways.	imatinib	29-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-164
23355941-1	2012	Development of resistance to imatinib mesylate (IM) in chronic myeloid leukemia (CML) patients is mediated by different mechanisms that can be classified as BCR-ABL dependent or BCR-ABL independent pathways.	imatinib	29-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185
22971013-3	2012	A classic example is chronic myeloid leukemia (CML) caused by BCR-ABL fusion protein, wherein a BCR-ABL kinase inhibitor, imatinib (IM), was highly successful in the early chronic phase of the disease, but failed in the advanced stages due to amplification of oncogene or point mutations in the drug-binding site of kinase domain.	imatinib	122-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
22915637-1	2012	Tyrosine kinase inhibitor therapy with imatinib (IM), dasatinib (DAS), or nilotinib is very effective in chronic-phase chronic myeloid leukemia.	imatinib	39-47	TXK tyrosine kinase	Homo sapiens	0-15
23162799-0	2012	Shiga toxin 2-induced intestinal pathology in infant rabbits is A-subunit dependent and responsive to the tyrosine kinase and potential ZAK inhibitor imatinib.	imatinib	150-158	mitogen-activated protein kinase kinase kinase 20	Homo sapiens	136-139
23162799-8	2012	While the p38 inhibitor SB203580 and the ZAK inhibitor DHP-2 were ineffective at preventing Shiga toxin-mediated damage to the colon, pretreatment of infant rabbits with the drug imatinib resulted in a decrease of Shiga toxin-mediated heterophil infiltration of the colon.	imatinib	179-187	mitogen-activated protein kinase 14	Homo sapiens	10-13
22971013-3	2012	A classic example is chronic myeloid leukemia (CML) caused by BCR-ABL fusion protein, wherein a BCR-ABL kinase inhibitor, imatinib (IM), was highly successful in the early chronic phase of the disease, but failed in the advanced stages due to amplification of oncogene or point mutations in the drug-binding site of kinase domain.	imatinib	122-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
22517301-2	2012	Earlier studies demonstrated that clusters of differentiation 34-positive, Philadelphia chromosome-positive (CD34(+) Ph(+) ) cells are detectable in about 45% of patients with CML, despite being on long-term imatinib therapy and having achieved sustained CCyR.	imatinib	208-216	CD34 molecule	Homo sapiens	109-113
23010596-1	2012	RNA-cleaving DNAzymes were constructed to target the point mutation in the BCR-ABL transcript that causes imatinib resistance in leukemic cells.	imatinib	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
22940072-4	2012	Treatment using imatinib or nilotinib abolished the aberrant activation of c-Abl and PDGFR and protected against experimental cGvHD.	imatinib	16-24	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	75-80
22940072-4	2012	Treatment using imatinib or nilotinib abolished the aberrant activation of c-Abl and PDGFR and protected against experimental cGvHD.	imatinib	16-24	platelet derived growth factor receptor, beta polypeptide	Mus musculus	85-90
22940072-9	2012	Considering the high morbidity associated with cGvHD, the lack of efficient molecular therapies for clinical use, and first positive signals from uncontrolled studies of imatinib, combined inhibition of c-Abl and PDGFR might be a promising future strategy for treatment of sclerodermatous cGvHD.	imatinib	170-178	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	203-208
22940072-9	2012	Considering the high morbidity associated with cGvHD, the lack of efficient molecular therapies for clinical use, and first positive signals from uncontrolled studies of imatinib, combined inhibition of c-Abl and PDGFR might be a promising future strategy for treatment of sclerodermatous cGvHD.	imatinib	170-178	platelet derived growth factor receptor, beta polypeptide	Mus musculus	213-218
22591006-9	2012	CONCLUSIONS: Constitutive activation of the c-Abl/PKC-delta/Fli1 pathway at least partially contributes to the establishment of the profibrotic phenotype in LSc dermal fibroblasts, which provides a novel molecular basis to explain the efficacy of imatinib against skin sclerosis in a certain subset of LSc.	imatinib	247-255	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-49
22591006-9	2012	CONCLUSIONS: Constitutive activation of the c-Abl/PKC-delta/Fli1 pathway at least partially contributes to the establishment of the profibrotic phenotype in LSc dermal fibroblasts, which provides a novel molecular basis to explain the efficacy of imatinib against skin sclerosis in a certain subset of LSc.	imatinib	247-255	protein kinase C delta	Homo sapiens	50-59
22591006-9	2012	CONCLUSIONS: Constitutive activation of the c-Abl/PKC-delta/Fli1 pathway at least partially contributes to the establishment of the profibrotic phenotype in LSc dermal fibroblasts, which provides a novel molecular basis to explain the efficacy of imatinib against skin sclerosis in a certain subset of LSc.	imatinib	247-255	Fli-1 proto-oncogene, ETS transcription factor	Homo sapiens	60-64
22795573-0	2012	KIT mutations in a series of melanomas and their impact on treatment with imatinib.	imatinib	74-82	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
23095523-0	2012	The PERK-eIF2alpha phosphorylation arm is a pro-survival pathway of BCR-ABL signaling and confers resistance to imatinib treatment in chronic myeloid leukemia cells.	imatinib	112-120	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	4-8
22895079-2	2012	The BCR-ABL tyrosine kinase inhibitor imatinib is the standard treatment for Ph+ leukemia and plays efficacious role in CML.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
22895079-9	2012	Oridonin plus imatinib exerted synergetic effects by overcoming imatinib defect of upregulating Akt/mTOR and LYN signaling.	imatinib	14-22	AKT serine/threonine kinase 1	Homo sapiens	96-99
22895079-9	2012	Oridonin plus imatinib exerted synergetic effects by overcoming imatinib defect of upregulating Akt/mTOR and LYN signaling.	imatinib	14-22	mechanistic target of rapamycin kinase	Homo sapiens	100-104
22895079-9	2012	Oridonin plus imatinib exerted synergetic effects by overcoming imatinib defect of upregulating Akt/mTOR and LYN signaling.	imatinib	14-22	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	109-112
22895079-9	2012	Oridonin plus imatinib exerted synergetic effects by overcoming imatinib defect of upregulating Akt/mTOR and LYN signaling.	imatinib	64-72	AKT serine/threonine kinase 1	Homo sapiens	96-99
22895079-9	2012	Oridonin plus imatinib exerted synergetic effects by overcoming imatinib defect of upregulating Akt/mTOR and LYN signaling.	imatinib	64-72	mechanistic target of rapamycin kinase	Homo sapiens	100-104
22895079-9	2012	Oridonin plus imatinib exerted synergetic effects by overcoming imatinib defect of upregulating Akt/mTOR and LYN signaling.	imatinib	64-72	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	109-112
22895079-11	2012	Our data showed that oridonin remarkably suppressed activations of Akt/mTOR, Raf/MEK and STAT5 pathway in these primary specimens and oridonin with imatinib exerted synergetic suppressive effects on mTOR, STAT5 and LYN signaling in one imatinib resistant patient specimen.	imatinib	148-156	mechanistic target of rapamycin kinase	Homo sapiens	199-203
22895079-11	2012	Our data showed that oridonin remarkably suppressed activations of Akt/mTOR, Raf/MEK and STAT5 pathway in these primary specimens and oridonin with imatinib exerted synergetic suppressive effects on mTOR, STAT5 and LYN signaling in one imatinib resistant patient specimen.	imatinib	148-156	signal transducer and activator of transcription 5A	Homo sapiens	205-210
22895079-0	2012	Oridonin in combination with imatinib exerts synergetic anti-leukemia effect in Ph+ acute lymphoblastic leukemia cells in vitro by inhibiting activation of LYN/mTOR signaling pathway.	imatinib	29-37	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	156-159
22895079-0	2012	Oridonin in combination with imatinib exerts synergetic anti-leukemia effect in Ph+ acute lymphoblastic leukemia cells in vitro by inhibiting activation of LYN/mTOR signaling pathway.	imatinib	29-37	mechanistic target of rapamycin kinase	Homo sapiens	160-164
22992064-4	2012	Dasatinib is also effective against most BCR-ABL1 mutations that arise during therapy with imatinib.	imatinib	91-99	BCR activator of RhoGEF and GTPase	Homo sapiens	41-49
23267948-6	2012	Because a duplication mutation in KIT exon 9 was found in the primary tumor, we decided to increase the dose of imatinib to 800 mg/day.	imatinib	112-120	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	34-37
23095523-0	2012	The PERK-eIF2alpha phosphorylation arm is a pro-survival pathway of BCR-ABL signaling and confers resistance to imatinib treatment in chronic myeloid leukemia cells.	imatinib	112-120	eukaryotic translation initiation factor 2A	Homo sapiens	9-18
23095523-0	2012	The PERK-eIF2alpha phosphorylation arm is a pro-survival pathway of BCR-ABL signaling and confers resistance to imatinib treatment in chronic myeloid leukemia cells.	imatinib	112-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
23095523-5	2012	Herein, we demonstrate that the PERK-eIF2alpha phosphorylation pathway is upregulated in CML cell lines and CD34+ cells from CML patients and is associated with CML progression and imatinib resistance.	imatinib	181-189	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	32-36
23095523-5	2012	Herein, we demonstrate that the PERK-eIF2alpha phosphorylation pathway is upregulated in CML cell lines and CD34+ cells from CML patients and is associated with CML progression and imatinib resistance.	imatinib	181-189	eukaryotic translation initiation factor 2A	Homo sapiens	37-46
23095523-6	2012	We also show that induction of apoptosis by imatinib results in the downregulation of the PERK-eIF2alpha phosphorylation arm.	imatinib	44-52	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	90-94
23095523-6	2012	We also show that induction of apoptosis by imatinib results in the downregulation of the PERK-eIF2alpha phosphorylation arm.	imatinib	44-52	eukaryotic translation initiation factor 2A	Homo sapiens	95-104
23095523-7	2012	Furthermore, we demonstrate that inactivation of the PERK-eIF2alpha phosphorylation arm decreases the clonogenic and proliferative capacities of CML cells and sensitizes them to death by imatinib.	imatinib	187-195	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	53-57
23095523-7	2012	Furthermore, we demonstrate that inactivation of the PERK-eIF2alpha phosphorylation arm decreases the clonogenic and proliferative capacities of CML cells and sensitizes them to death by imatinib.	imatinib	187-195	eukaryotic translation initiation factor 2A	Homo sapiens	58-67
23095523-8	2012	These findings provide evidence for a pro-survival role of PERK-eIF2alpha phosphorylation arm that contributes to CML progression and development of imatinib resistance.	imatinib	149-157	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	59-63
23095523-8	2012	These findings provide evidence for a pro-survival role of PERK-eIF2alpha phosphorylation arm that contributes to CML progression and development of imatinib resistance.	imatinib	149-157	eukaryotic translation initiation factor 2A	Homo sapiens	64-73
23125079-0	2012	Tetrandrine citrate eliminates imatinib-resistant chronic myeloid leukemia cells in vitro and in vivo by inhibiting Bcr-Abl/beta-catenin axis.	imatinib	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
22516345-5	2012	Insulin-like growth factor 1, total PKCtheta, phosphorylated PKCtheta, and RKIP immunohistochemical expression were correlated with objective response to imatinib treatment and progression-free and overall survival.	imatinib	154-162	phosphatidylethanolamine binding protein 1	Homo sapiens	75-79
22516345-7	2012	There was a statistically significant association between IGF1R expression and type of response to imatinib treatment (P = 0.05)-that is, higher IGF1R expression was related to lower objective response.	imatinib	99-107	insulin like growth factor 1 receptor	Homo sapiens	58-63
22516345-7	2012	There was a statistically significant association between IGF1R expression and type of response to imatinib treatment (P = 0.05)-that is, higher IGF1R expression was related to lower objective response.	imatinib	99-107	insulin like growth factor 1 receptor	Homo sapiens	145-150
23125079-0	2012	Tetrandrine citrate eliminates imatinib-resistant chronic myeloid leukemia cells in vitro and in vivo by inhibiting Bcr-Abl/beta-catenin axis.	imatinib	31-39	catenin beta 1	Homo sapiens	124-136
22516345-9	2012	Insulin-like growth factor 1, but not PKCtheta and RKIP, emerges as a potential biomarker for prediction of response to imatinib treatment in metastatic GISTs.	imatinib	120-128	insulin like growth factor 1	Homo sapiens	0-28
23127398-0	2012	[Effect of tyrosine kinase inhibitor imatinib mesylate   on K562 cell invasion by PTEN pathway].	imatinib	37-54	phosphatase and tensin homolog	Homo sapiens	82-86
22952296-0	2012	The lack of CD34 expression in gastrointestinal stromal tumors is related to cystic degeneration following imatinib use.	imatinib	107-115	CD34 molecule	Homo sapiens	12-16
22952296-8	2012	A lack of CD34 expression in tumors was found to be related to cystic degeneration after imatinib treatment (P=0.001).	imatinib	89-97	CD34 molecule	Homo sapiens	10-14
22829019-3	2012	This study demonstrated that long-term culture with imatinib mesylate, the tyrosine kinase inhibitor against PDGFR and c-Kit resulted in reduced cancer stem cell ability in glioblastoma cells through cell differentiation.	imatinib	52-69	platelet derived growth factor receptor beta	Homo sapiens	109-114
22829019-3	2012	This study demonstrated that long-term culture with imatinib mesylate, the tyrosine kinase inhibitor against PDGFR and c-Kit resulted in reduced cancer stem cell ability in glioblastoma cells through cell differentiation.	imatinib	52-69	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	119-124
22968735-8	2012	In KIT exon 9 mutations, a doubled daily dose of 800 mg imatinib is now standard.	imatinib	56-64	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	3-6
23127398-1	2012	AIM: To investigate the effect of tyrosine kinase inhibitor imatinib mesylate on the PTEN signaling pathway and the cell invasion in K562 cells.	imatinib	60-77	phosphatase and tensin homolog	Homo sapiens	85-89
23127398-6	2012	RESULTS: In the initial 36 h,  the expression level of PTEN mRNA was up-regulated and the FAK mRNA was down-regulated with the reduction of BCR/ABL fusion gene expression and the cell invasive ability of K562 cells was inhibited by 2 mug/mL imatinib mesylate.	imatinib	241-258	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
23127398-9	2012	CONCLUSION: Tyrosine kinase inhibitor imatinib mesylate can regulate PTEN/FAK pathway and inhibit the leukemia K562 cell invasive ability via restraining BCR/ABL fusion gene.	imatinib	38-55	phosphatase and tensin homolog	Homo sapiens	69-73
23127398-9	2012	CONCLUSION: Tyrosine kinase inhibitor imatinib mesylate can regulate PTEN/FAK pathway and inhibit the leukemia K562 cell invasive ability via restraining BCR/ABL fusion gene.	imatinib	38-55	protein tyrosine kinase 2	Homo sapiens	74-77
23127398-9	2012	CONCLUSION: Tyrosine kinase inhibitor imatinib mesylate can regulate PTEN/FAK pathway and inhibit the leukemia K562 cell invasive ability via restraining BCR/ABL fusion gene.	imatinib	38-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-161
22912393-2	2012	EXPERIMENTAL DESIGN: We assessed whether leukemia neoantigens could be generated from drug-resistant mutations in BCR-ABL after imatinib relapse in patients with chronic myelogenous leukemia (CML).	imatinib	128-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
22988110-2	2012	We show that immunoprecipitation (IP)-tandem mass spectrometry (LC-MS/MS) in H929 multiple myeloma (MM) cancer cells led to the discovery of a rare and unexpected BCR-ABL fusion, informing a therapeutic intervention using imatinib (Gleevec).	imatinib	222-230	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
22231445-6	2012	The interaction between STAP-2 and BCR-ABL plays a crucial role in conferring a growth advantage and resistance to imatinib, a BCR-ABL inhibitor, as well as tumor progression.	imatinib	115-123	signal transducing adaptor family member 2	Mus musculus	24-30
22231445-6	2012	The interaction between STAP-2 and BCR-ABL plays a crucial role in conferring a growth advantage and resistance to imatinib, a BCR-ABL inhibitor, as well as tumor progression.	imatinib	115-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
22231445-6	2012	The interaction between STAP-2 and BCR-ABL plays a crucial role in conferring a growth advantage and resistance to imatinib, a BCR-ABL inhibitor, as well as tumor progression.	imatinib	115-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
23036227-2	2012	Small molecule inhibitors such as imatinib and sunitinib are known to inhibit the aberrantly activated KIT and PDGFRA receptor signaling and can lead to excellent clinical outcomes for patients with GIST.	imatinib	34-42	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	103-106
23036227-2	2012	Small molecule inhibitors such as imatinib and sunitinib are known to inhibit the aberrantly activated KIT and PDGFRA receptor signaling and can lead to excellent clinical outcomes for patients with GIST.	imatinib	34-42	platelet derived growth factor receptor alpha	Homo sapiens	111-117
22988110-8	2012	The comparative treatment of tyrosine kinase inhibitor (TKI) drugs revealed only imatinib, the standard of care in CML, was inhibitory to BCR-ABL leading to down-regulation of pERK and pS6K and inhibiting cell proliferation.	imatinib	81-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
22988110-8	2012	The comparative treatment of tyrosine kinase inhibitor (TKI) drugs revealed only imatinib, the standard of care in CML, was inhibitory to BCR-ABL leading to down-regulation of pERK and pS6K and inhibiting cell proliferation.	imatinib	81-89	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	176-180
22988110-8	2012	The comparative treatment of tyrosine kinase inhibitor (TKI) drugs revealed only imatinib, the standard of care in CML, was inhibitory to BCR-ABL leading to down-regulation of pERK and pS6K and inhibiting cell proliferation.	imatinib	81-89	ribosomal protein S6 kinase B1	Homo sapiens	185-189
22798315-7	2012	We found that daily treatment with the EGF-R inhibitor gefitinib, the FGF-R inhibitor dovitinib, and the PDGF-R inhibitor imatinib started 2 weeks after a subcutaneous monocrotaline injection substantially attenuated the abnormal increase in p130(Cas) and ERK1/2 activation and regressed established pulmonary hypertension.	imatinib	122-130	nucleolar and coiled-body phosphoprotein 1	Homo sapiens	242-246
22798315-7	2012	We found that daily treatment with the EGF-R inhibitor gefitinib, the FGF-R inhibitor dovitinib, and the PDGF-R inhibitor imatinib started 2 weeks after a subcutaneous monocrotaline injection substantially attenuated the abnormal increase in p130(Cas) and ERK1/2 activation and regressed established pulmonary hypertension.	imatinib	122-130	BCAR1 scaffold protein, Cas family member	Homo sapiens	247-250
22798315-7	2012	We found that daily treatment with the EGF-R inhibitor gefitinib, the FGF-R inhibitor dovitinib, and the PDGF-R inhibitor imatinib started 2 weeks after a subcutaneous monocrotaline injection substantially attenuated the abnormal increase in p130(Cas) and ERK1/2 activation and regressed established pulmonary hypertension.	imatinib	122-130	mitogen-activated protein kinase 3	Homo sapiens	256-262
22733220-3	2012	Silencing of Abl expression in bone marrow-derived macrophages and monocyte-derived macrophages by siRNA or Abl enzymatic inhibition with imatinib resulted in the disassembly of macrophage podosomes and the reduction of their capacity to degrade an extracellular matrix and migrate through matrigel matrices and endothelial cell monolayers.	imatinib	138-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
23187745-3	2012	Four BCR-ABL TKIs are now commercially available for the treatment of CML: the first-generation TKI imatinib, and the second-generation TKIs dasatinib, nilotinib, and bosutinib.	imatinib	100-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	5-12
22633167-6	2012	An improved topologic fit to the ABL1 protein-binding surface contributes to its increased potency over imatinib.	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-37
22733220-3	2012	Silencing of Abl expression in bone marrow-derived macrophages and monocyte-derived macrophages by siRNA or Abl enzymatic inhibition with imatinib resulted in the disassembly of macrophage podosomes and the reduction of their capacity to degrade an extracellular matrix and migrate through matrigel matrices and endothelial cell monolayers.	imatinib	138-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-111
23073628-7	2012	The observation that gain-of-function mutations in c-Kit can promote tumor formation and progression has stimulated the development of therapeutics agents targeting this receptor, e.g., the clinically used inhibitor imatinib mesylate.	imatinib	216-233	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	51-56
22677017-1	2012	Low pretreatment expression of the imatinib uptake transporter human organic cation transporter 1 (hOCT1) is associated with inferior complete cytogenetic response rates, progression-free survival, and overall survival in imatinib-treated chronic myeloid leukemia (CML).	imatinib	35-43	solute carrier family 22 member 1	Homo sapiens	69-97
22677017-1	2012	Low pretreatment expression of the imatinib uptake transporter human organic cation transporter 1 (hOCT1) is associated with inferior complete cytogenetic response rates, progression-free survival, and overall survival in imatinib-treated chronic myeloid leukemia (CML).	imatinib	35-43	solute carrier family 22 member 1	Homo sapiens	99-104
22677017-2	2012	Upregulation of hOCT1 can therefore increase the uptake of imatinib.	imatinib	59-67	solute carrier family 22 member 1	Homo sapiens	16-21
22677017-6	2012	PPARalpha agonist treatment increased imatinib killing of CML KCL22 cells and primitive CD34(+) cells, and also upregulates hOCT1 gene expression and increases imatinib uptake into KCL22 cells and primary cells.	imatinib	38-46	peroxisome proliferator activated receptor alpha	Homo sapiens	0-9
22677017-6	2012	PPARalpha agonist treatment increased imatinib killing of CML KCL22 cells and primitive CD34(+) cells, and also upregulates hOCT1 gene expression and increases imatinib uptake into KCL22 cells and primary cells.	imatinib	160-168	peroxisome proliferator activated receptor alpha	Homo sapiens	0-9
22998385-0	2012	C-kit-positive acute myelogenous leukemia effectively treated with imatinib: a case report and review of the literature.	imatinib	67-75	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-5
22677017-7	2012	PPARalpha agonists might potentially be of clinical use in CML patients failing imatinib.	imatinib	80-88	peroxisome proliferator activated receptor alpha	Homo sapiens	0-9
22900848-2	2012	The purpose of this study was to test whether imatinib mesylate (Gleevec), a PDGF receptor (PDGFR) blocker, reduces angiogenic capacity in sporadic VS and in VS associated with neurofibromatosis Type 2 (NF2) using a corneal angiogenesis assay.	imatinib	46-54	platelet derived growth factor receptor beta	Homo sapiens	77-90
22900848-2	2012	The purpose of this study was to test whether imatinib mesylate (Gleevec), a PDGF receptor (PDGFR) blocker, reduces angiogenic capacity in sporadic VS and in VS associated with neurofibromatosis Type 2 (NF2) using a corneal angiogenesis assay.	imatinib	46-54	platelet derived growth factor receptor beta	Homo sapiens	92-97
22900848-2	2012	The purpose of this study was to test whether imatinib mesylate (Gleevec), a PDGF receptor (PDGFR) blocker, reduces angiogenic capacity in sporadic VS and in VS associated with neurofibromatosis Type 2 (NF2) using a corneal angiogenesis assay.	imatinib	46-54	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	177-201
22900848-2	2012	The purpose of this study was to test whether imatinib mesylate (Gleevec), a PDGF receptor (PDGFR) blocker, reduces angiogenic capacity in sporadic VS and in VS associated with neurofibromatosis Type 2 (NF2) using a corneal angiogenesis assay.	imatinib	46-54	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	203-206
22900848-8	2012	Imatinib treatment significantly reduced the angiogenic potential in both the sporadic VS and the NF2-associated VS groups.	imatinib	0-8	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	98-101
22900848-12	2012	Additionally, imatinib reduces the angiogenic activity of both sporadic and NF2-associated VS.	imatinib	14-22	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	76-79
22900848-13	2012	The authors conclude that imatinib may be a potential treatment for VS, especially for NF2-associated lesions that cannot be cured with resection or radiosurgery.	imatinib	26-34	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	87-90
22722872-0	2012	Marrow signal changes observed in follow-up whole-body MRI studies in children and young adults with neurofibromatosis type 1 treated with imatinib mesylate (Gleevec) for plexiform neurofibromas.	imatinib	139-156	neurofibromin 1	Homo sapiens	101-125
22722872-0	2012	Marrow signal changes observed in follow-up whole-body MRI studies in children and young adults with neurofibromatosis type 1 treated with imatinib mesylate (Gleevec) for plexiform neurofibromas.	imatinib	158-165	neurofibromin 1	Homo sapiens	101-125
22722872-12	2012	CONCLUSION: BMSC appeared in most patients with neurofibromatosis type 1 following treatment with imatinib mesylate.	imatinib	98-115	neurofibromin 1	Homo sapiens	48-72
22314612-7	2012	Administration of imatinib mesylate dose-dependently inhibited cell proliferation of PrSC with downregulation of JAK2 and STAT1, which are the main pathways downstream of SCF/KIT signal.	imatinib	18-35	Janus kinase 2	Homo sapiens	113-117
22314612-7	2012	Administration of imatinib mesylate dose-dependently inhibited cell proliferation of PrSC with downregulation of JAK2 and STAT1, which are the main pathways downstream of SCF/KIT signal.	imatinib	18-35	signal transducer and activator of transcription 1	Homo sapiens	122-127
22314612-7	2012	Administration of imatinib mesylate dose-dependently inhibited cell proliferation of PrSC with downregulation of JAK2 and STAT1, which are the main pathways downstream of SCF/KIT signal.	imatinib	18-35	KIT ligand	Homo sapiens	171-174
22314612-7	2012	Administration of imatinib mesylate dose-dependently inhibited cell proliferation of PrSC with downregulation of JAK2 and STAT1, which are the main pathways downstream of SCF/KIT signal.	imatinib	18-35	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	175-178
22787122-6	2012	Tumor biopsy analyses from a synovial sarcoma patient treated with the mTORC1 inhibitor everolimus and PDGFRA inhibitor imatinib mesylate confirmed that this drug combination can impact both mTORC1 and Akt signals in vivo.	imatinib	120-137	platelet derived growth factor receptor alpha	Homo sapiens	103-109
22926771-8	2012	Identification of rearranged PDGFRA or PDGFRB is critical because of the exquisite responsiveness of these diseases to imatinib.	imatinib	119-127	platelet derived growth factor receptor alpha	Homo sapiens	29-35
22926771-8	2012	Identification of rearranged PDGFRA or PDGFRB is critical because of the exquisite responsiveness of these diseases to imatinib.	imatinib	119-127	platelet derived growth factor receptor beta	Homo sapiens	39-45
23114125-2	2012	Small molecule inhibitors, such as imatinib, are effective for P210(bcr/abl) gene mediated CML, but drug resistance may occur.	imatinib	35-43	BCR activator of RhoGEF and GTPase	Mus musculus	63-75
23114125-6	2012	The results found that stable expression of the P210(bcr/abl) shRNA resulted in obvious inhibition of P210(bcr/abl) mRNA and protein expression and increased sensitivity of these P210(bcr/abl) gene transformed Ba/F3 cells to imatinib.	imatinib	225-233	BCR activator of RhoGEF and GTPase	Mus musculus	48-60
22995644-5	2012	Inhibition of BCR-ABL signalling either by Imatinib or by RNAi silencing BCR-ABL reduces PRL-3 and increases cleavage of PARP.	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
22995644-6	2012	In contrast, the amount of PRL-3 protein remains constant or even increased in response to Imatinib treatment in drug resistant cells expressing P210 T315I.	imatinib	91-99	protein tyrosine phosphatase 4A3	Homo sapiens	27-32
22985168-3	2012	The ABL-kinase inhibitors (AKIs) Imatinib, Nilotinib or Dasatinib, which target the ATP-binding site, are effective in Ph + leukemia.	imatinib	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
22950685-0	2012	Recombinant erythropoietin for the anaemia of patients with advanced Gastrointestinal Stromal Tumours (GIST) receiving imatinib: an active agent only in non progressive patients.	imatinib	119-127	erythropoietin	Homo sapiens	12-26
22950685-1	2012	UNLABELLED: Recombinant erythropoietin for the anaemia of patients with advanced Gastrointestinal Stromal Tumours (GIST) receiving imatinib : an active agent only in non progressive patients.	imatinib	131-139	erythropoietin	Homo sapiens	24-38
22950685-4	2012	Whether EPO treatment is useful in the management of GIST patients receiving imatinib treatment is unknown.	imatinib	77-85	erythropoietin	Homo sapiens	8-11
22950685-5	2012	METHODS: A retrospective study of EPO treatment in GIST patients receiving imatinib was undertaken in 4 centres.	imatinib	75-83	erythropoietin	Homo sapiens	34-37
22950685-6	2012	Thirty four patients received EPO treatment among the 319 GIST patients treated with imatinib in clinical trials or with compassionate use between 2001 and 2003.	imatinib	85-93	erythropoietin	Homo sapiens	30-33
22950685-7	2012	The efficacy of EPO on the anaemia of patients with GIST treated with imatinib was analyzed.	imatinib	70-78	erythropoietin	Homo sapiens	16-19
22950685-12	2012	The median delay between the initiation of imatinib treatment and EPO was 58 days (range 0-553).	imatinib	43-51	erythropoietin	Homo sapiens	66-69
22950685-17	2012	Response to EPO was observed in 2/11 patients receiving high-dose imatinib (800 mg/day) vs 16/23 of others.	imatinib	66-74	erythropoietin	Homo sapiens	12-15
22950685-19	2012	CONCLUSION: EPO enables to increase Hb in most anaemic GIST patients who do not progress under imatinib, but not in patients with progressive disease.	imatinib	95-103	erythropoietin	Homo sapiens	12-15
22787122-6	2012	Tumor biopsy analyses from a synovial sarcoma patient treated with the mTORC1 inhibitor everolimus and PDGFRA inhibitor imatinib mesylate confirmed that this drug combination can impact both mTORC1 and Akt signals in vivo.	imatinib	120-137	CREB regulated transcription coactivator 1	Mus musculus	191-197
22787122-6	2012	Tumor biopsy analyses from a synovial sarcoma patient treated with the mTORC1 inhibitor everolimus and PDGFRA inhibitor imatinib mesylate confirmed that this drug combination can impact both mTORC1 and Akt signals in vivo.	imatinib	120-137	AKT serine/threonine kinase 1	Homo sapiens	202-205
22743761-9	2012	Targeted therapies such as vemurafenib or imatinib can be offered to patients whose melanomas express the BRAF V600E or C-Kit mutations.	imatinib	42-50	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	106-110
22743761-9	2012	Targeted therapies such as vemurafenib or imatinib can be offered to patients whose melanomas express the BRAF V600E or C-Kit mutations.	imatinib	42-50	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	120-125
22806436-11	2012	Using of low-dose imatinib mesylate (100 mg/day) a hematological and molecular remission in all patients displaying the FIP1L1-PDGFRA fusion gene was observed.	imatinib	18-35	factor interacting with PAPOLA and CPSF1	Homo sapiens	120-126
22634393-0	2012	CML cells expressing the TEL/MDS1/EVI1 fusion are resistant to imatinib-induced apoptosis through inhibition of BAD, but are resensitized with ABT-737.	imatinib	63-71	ETS variant transcription factor 6	Homo sapiens	25-28
22634393-0	2012	CML cells expressing the TEL/MDS1/EVI1 fusion are resistant to imatinib-induced apoptosis through inhibition of BAD, but are resensitized with ABT-737.	imatinib	63-71	MDS1 and EVI1 complex locus	Homo sapiens	29-33
22634393-0	2012	CML cells expressing the TEL/MDS1/EVI1 fusion are resistant to imatinib-induced apoptosis through inhibition of BAD, but are resensitized with ABT-737.	imatinib	63-71	MDS1 and EVI1 complex locus	Homo sapiens	34-38
22634393-6	2012	In addition, application of EVI1-specific small interfering RNA decreased expression of the TEL/MDS1/EVI1 fusion, reduced resistance to imatinib, and increased sensitivity to ABT-737.	imatinib	136-144	MDS1 and EVI1 complex locus	Homo sapiens	28-32
22806436-11	2012	Using of low-dose imatinib mesylate (100 mg/day) a hematological and molecular remission in all patients displaying the FIP1L1-PDGFRA fusion gene was observed.	imatinib	18-35	platelet derived growth factor receptor alpha	Homo sapiens	127-133
22821389-0	2012	Polymorphisms of ERCC1 genotype associated with response to imatinib therapy in chronic phase chronic myeloid leukemia.	imatinib	60-68	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	17-22
22821389-2	2012	We examined the association between the single nucleotide polymorphism (SNP) markers involved in the DNA repair enzyme pathway (ERCC1/2/4/5, XRCC1/2/4/5) and the clinical outcomes following an imatinib therapy in chronic phase chronic myeloid leukemia (CML) patients.	imatinib	193-201	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	128-139
22821389-5	2012	This suggests that SNP markers on ERCC1 may predict the response to imatinib therapy, which proposes the potential involvement of the DNA repair machinery in the mechanism of imatinib action in chronic phase CML.	imatinib	68-76	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	34-39
22821389-5	2012	This suggests that SNP markers on ERCC1 may predict the response to imatinib therapy, which proposes the potential involvement of the DNA repair machinery in the mechanism of imatinib action in chronic phase CML.	imatinib	175-183	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	34-39
22425893-0	2012	Retention of CD34+ CML stem/progenitor cells during imatinib treatment and rapid decline after treatment with second-generation BCR-ABL inhibitors.	imatinib	52-60	CD34 molecule	Homo sapiens	13-17
22570081-0	2012	Molecular interactions of c-ABL mutants in complex with imatinib/nilotinib: a computational study using linear interaction energy (LIE) calculations.	imatinib	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-31
22570081-1	2012	In spite of the effectiveness of Imatinib for chronic myeloid leukemia (CML) treatment, resistance has repeatedly been reported and is associated with point mutations in the BCR-ABL chimeric gene.	imatinib	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-181
22570081-4	2012	Herein, we report a comparative molecular dynamics analysis of the interaction between two tyrosine kinase inhibitors (imatinib or nilotinib) against wild type c-ABL protein and 12 mutants, using the semi-empirical linear interaction energy (LIE) method, to assess the feasibility of this approach for studying resistance against the inhibitory activity of these drugs.	imatinib	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-165
22570081-6	2012	Experimental IC50 values for the interaction between imatinib, wild type c-ABL, and 12 mutants were used to obtain the proper LIE coefficients (alpha, beta and gamma) to estimate the free energy of the binding of imatinib with wild-type and mutant proteins, and values were extrapolated for the analysis of the nilotinib/c-ABL interaction.	imatinib	213-221	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-78
22570081-6	2012	Experimental IC50 values for the interaction between imatinib, wild type c-ABL, and 12 mutants were used to obtain the proper LIE coefficients (alpha, beta and gamma) to estimate the free energy of the binding of imatinib with wild-type and mutant proteins, and values were extrapolated for the analysis of the nilotinib/c-ABL interaction.	imatinib	213-221	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	321-326
22570081-8	2012	Additionally, for c-ABL mutants, the observed number of water molecules being turned over while interacting with amino acids Glu286, Lys271 and Asp381 was associated with resistance to imatinib, resulting in a less effective inhibition of the kinase activity.	imatinib	185-193	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-23
23230732-8	2012	CONCLUSION: The overexpression of MDR1 mRNA and higher activity of P-gp is partially responsible for acquiring of imatinib resistance in SUP-B15/RI cell line.	imatinib	114-122	ATP binding cassette subfamily B member 1	Homo sapiens	34-38
22038725-1	2012	In chronic myeloid leukemia (CML), the best characterized imatinib resistance mechanisms are BCR-ABL tyrosine kinase domain mutations and clonal evolution, but recently alternative splicing of BCR-ABL was also proposed as a mechanism for imatinib resistance.	imatinib	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
22038725-1	2012	In chronic myeloid leukemia (CML), the best characterized imatinib resistance mechanisms are BCR-ABL tyrosine kinase domain mutations and clonal evolution, but recently alternative splicing of BCR-ABL was also proposed as a mechanism for imatinib resistance.	imatinib	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	193-200
22038725-1	2012	In chronic myeloid leukemia (CML), the best characterized imatinib resistance mechanisms are BCR-ABL tyrosine kinase domain mutations and clonal evolution, but recently alternative splicing of BCR-ABL was also proposed as a mechanism for imatinib resistance.	imatinib	238-246	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	193-200
22038725-5	2012	The Deltaexon7 was abundantly detected with similar frequency in healthy controls, in imatinib naive and resistant CML patients on BCR-ABL and also on the nontranslocated ABL.	imatinib	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
22038725-5	2012	The Deltaexon7 was abundantly detected with similar frequency in healthy controls, in imatinib naive and resistant CML patients on BCR-ABL and also on the nontranslocated ABL.	imatinib	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-138
22161019-0	2012	Imatinib has the potential to exert its antileukemia effects by down-regulating hERG1 K+ channels in chronic myelogenous leukemia.	imatinib	0-8	potassium voltage-gated channel subfamily H member 2	Homo sapiens	80-85
22161019-1	2012	Imatinib is a powerful protein tyrosine kinase (PTK) inhibitor that specifically targets BCR-ABL, KIT, and PDGFR kinases, has become the current first-line therapy for all newly diagnosed chronic myeloid leukemia (CML).	imatinib	0-8	protein tyrosine kinase 2 beta	Homo sapiens	48-51
22161019-1	2012	Imatinib is a powerful protein tyrosine kinase (PTK) inhibitor that specifically targets BCR-ABL, KIT, and PDGFR kinases, has become the current first-line therapy for all newly diagnosed chronic myeloid leukemia (CML).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
22161019-1	2012	Imatinib is a powerful protein tyrosine kinase (PTK) inhibitor that specifically targets BCR-ABL, KIT, and PDGFR kinases, has become the current first-line therapy for all newly diagnosed chronic myeloid leukemia (CML).	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	98-101
22161019-1	2012	Imatinib is a powerful protein tyrosine kinase (PTK) inhibitor that specifically targets BCR-ABL, KIT, and PDGFR kinases, has become the current first-line therapy for all newly diagnosed chronic myeloid leukemia (CML).	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	107-112
22161019-4	2012	The present study explored a possible regulatory effect of imatinib upon hERG1 K(+) channels as a means to uncover new molecular events involved in the antileukemic activity of this PTK inhibitor in CML.	imatinib	59-67	potassium voltage-gated channel subfamily H member 2	Homo sapiens	73-78
22161019-4	2012	The present study explored a possible regulatory effect of imatinib upon hERG1 K(+) channels as a means to uncover new molecular events involved in the antileukemic activity of this PTK inhibitor in CML.	imatinib	59-67	protein tyrosine kinase 2 beta	Homo sapiens	182-185
22161019-5	2012	The results demonstrated that hERG1 was highly detected in K562 cells and primary CML cells, and down-regulated by imatinib at mRNA and protein levels.	imatinib	115-123	potassium voltage-gated channel subfamily H member 2	Homo sapiens	30-35
22161019-6	2012	Furthermore, imatinib markedly reduced hERG currents in HEK293T-hERG cells, this effect was accompanied by inhibition of CML cell proliferation and apoptosis, as well as suppression of vascular endothelial growth factor (VEGF) secretion.	imatinib	13-21	vascular endothelial growth factor A	Homo sapiens	185-219
22161019-6	2012	Furthermore, imatinib markedly reduced hERG currents in HEK293T-hERG cells, this effect was accompanied by inhibition of CML cell proliferation and apoptosis, as well as suppression of vascular endothelial growth factor (VEGF) secretion.	imatinib	13-21	vascular endothelial growth factor A	Homo sapiens	221-225
22161019-7	2012	Moreover, these antileukemia effects of imatinib were potentiated by E-4031, a specific hERG1 inhibitor.	imatinib	40-48	potassium voltage-gated channel subfamily H member 2	Homo sapiens	88-93
22161019-8	2012	Together, these results provide evidence of a novel potential molecular mechanism of antileukemic activities by imatinib which, independent of targeting tyrosine kinase, highlight hERG1 K(+) channels as a therapeutic target for CML treatment.	imatinib	112-120	potassium voltage-gated channel subfamily H member 2	Homo sapiens	180-185
22772337-7	2012	Validating the hybridization-mediated multiplexed kinase assay, when three peptide substrate-oligonucleotide conjugates were mixed with the tyrosine kinase c-Abl and ATP, we readily observed their differential phosphorylation yet measured a common IC(50) for the Abl kinase inhibitor imatinib.	imatinib	284-292	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-161
23230732-0	2012	[Multidrug resistant gene MDR1 contributes to development of imatinib-resistance in Ph (+) acute lymphoblastic leukemia cell line SUP-BS15RI].	imatinib	61-69	ATP binding cassette subfamily B member 1	Homo sapiens	26-30
23230732-1	2012	OBJECTIVE: To investigate the contribution of multidrug-resistant gene MDR1 to development of imatinib-resistance in Ph(+) acute lymphoblastic leukemia cell line SUP-B15/RI.	imatinib	94-102	ATP binding cassette subfamily B member 1	Homo sapiens	71-75
23230732-8	2012	CONCLUSION: The overexpression of MDR1 mRNA and higher activity of P-gp is partially responsible for acquiring of imatinib resistance in SUP-B15/RI cell line.	imatinib	114-122	phosphoglycolate phosphatase	Homo sapiens	67-71
22641616-3	2012	To investigate the specific role of Abelson oncogene 1 (c-Abl) in imatinib-induced cardiac toxicity, we performed targeted gene inhibition of c-Abl by RNA interference in neonatal cardiomyocytes (NCMs).	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-61
22942908-1	2012	Since its approval by the US Food and Drug Administration in February 2002, the tyrosine kinase inhibitor, imatinib, has become the standard of care for patients with metastatic or unresectable KIT-positive gastrointestinal stromal tumors (GISTs).	imatinib	107-115	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	194-197
22942908-2	2012	Imatinib functions by blocking the adenosine triphosphate binding site of the constitutively activated mutant KIT or platelet-derived growth factor receptor alpha, effectively shutting down the oncogenic signal that drives up to 90% of these tumors.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	110-113
22942908-2	2012	Imatinib functions by blocking the adenosine triphosphate binding site of the constitutively activated mutant KIT or platelet-derived growth factor receptor alpha, effectively shutting down the oncogenic signal that drives up to 90% of these tumors.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	117-162
22641616-6	2012	The c-Abl inactive analogs induced cytotoxicity and ER stress, at similar or greater potencies and magnitudes as imatinib.	imatinib	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-9
21376411-10	2012	PDGF-BB induced phosphorylation of Akt at 15 min, and Akt phosphorylation was inhibited by imatinib in IPAH-PASMCs.	imatinib	91-99	AKT serine/threonine kinase 1	Homo sapiens	54-57
23086637-0	2012	[Synergistic effect of histone deacetylase inhibitor suberoylanilide hydroxamic acid with imatinib on K562 cells].	imatinib	90-98	histone deacetylase 9	Homo sapiens	23-42
23086637-6	2012	RESULTS: SAHA synergized the cytotoxicity of imatinib against leukemia K562 cells, concomitantly with increased apoptosis and enhanced activation of Caspase-3, -8 and PRAP.	imatinib	45-53	src kinase associated phosphoprotein 2	Homo sapiens	167-171
23086637-10	2012	CONCLUSION: Combining HDAC inhibitor SAHA with imatinib can kill CML cells synergistically by inhibiting cell growth and inducing apoptosis, which is associated with activation of Caspase pathway and regulation of anti-apoptotic proteins.	imatinib	47-55	caspase 8	Homo sapiens	180-187
22842456-0	2012	Myc induced miR-144/451 contributes to the acquired imatinib resistance in chronic myelogenous leukemia cell K562.	imatinib	52-60	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	0-3
22842456-0	2012	Myc induced miR-144/451 contributes to the acquired imatinib resistance in chronic myelogenous leukemia cell K562.	imatinib	52-60	microRNA 144	Homo sapiens	12-19
22842456-3	2012	In this study, we first found that c-myc expression is upregulated in imatinib resistant K562R cells, which in turn enhances the expression of miR-144/451.	imatinib	70-78	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	35-40
22842456-3	2012	In this study, we first found that c-myc expression is upregulated in imatinib resistant K562R cells, which in turn enhances the expression of miR-144/451.	imatinib	70-78	microRNA 144	Homo sapiens	143-150
22842456-4	2012	Knockdown of c-myc or restoration of miR-144/451 in the K562R cells sensitizes K562R cells to imatinib therapy.	imatinib	94-102	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	13-18
22842456-4	2012	Knockdown of c-myc or restoration of miR-144/451 in the K562R cells sensitizes K562R cells to imatinib therapy.	imatinib	94-102	microRNA 144	Homo sapiens	37-44
21376411-12	2012	Thus, Akt-I-1/2 could mimic the effects of imatinib on PASMCs.	imatinib	43-51	AKT serine/threonine kinase 1	Homo sapiens	6-9
22842456-5	2012	Our study here reveals an regulatory pathway between myc and miR-144/451 and highlights that targeting either myc or miR-144/451 might be valuable for eliminating the imatinib resistant CML cells.	imatinib	167-175	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	53-56
22842456-5	2012	Our study here reveals an regulatory pathway between myc and miR-144/451 and highlights that targeting either myc or miR-144/451 might be valuable for eliminating the imatinib resistant CML cells.	imatinib	167-175	microRNA 144	Homo sapiens	61-68
21376411-14	2012	The inhibitory effect of imatinib on Akt phosphorylation induced by PDGF plays an important role in the pro-apoptotic effect.	imatinib	25-33	AKT serine/threonine kinase 1	Homo sapiens	37-40
22842456-5	2012	Our study here reveals an regulatory pathway between myc and miR-144/451 and highlights that targeting either myc or miR-144/451 might be valuable for eliminating the imatinib resistant CML cells.	imatinib	167-175	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	110-113
22718859-3	2012	EXPERIMENTAL DESIGN: We conducted an international survey among GIST referral centers to collect clinical data on patients with advanced PDGFRA-mutant GISTs treated with imatinib for advanced disease.	imatinib	170-178	platelet derived growth factor receptor alpha	Homo sapiens	137-143
22842456-5	2012	Our study here reveals an regulatory pathway between myc and miR-144/451 and highlights that targeting either myc or miR-144/451 might be valuable for eliminating the imatinib resistant CML cells.	imatinib	167-175	microRNA 144	Homo sapiens	117-124
22901309-0	2012	A novel dic (17;18) (p13.1;q11.2) with loss of TP53 and BCR/ABL rearrangement in an Imatinib resistant chronic myeloid leukemia.	imatinib	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
22898871-2	2012	Analysis of imatinib-treated K562 cells reveals a cell population with cell cycle arrest, p27 increase and senescence-associated beta galactosidase (SA-beta-Gal) staining.	imatinib	12-20	dynactin subunit 6	Homo sapiens	90-93
22898871-6	2012	The inhibition of autophagy by silencing the expression of the proteins ATG7 or Beclin-1 prevents the increase of SA-beta-Gal staining in response to imatinib plus Z-Vad.	imatinib	150-158	autophagy related 7	Homo sapiens	72-76
22898871-6	2012	The inhibition of autophagy by silencing the expression of the proteins ATG7 or Beclin-1 prevents the increase of SA-beta-Gal staining in response to imatinib plus Z-Vad.	imatinib	150-158	beclin 1	Homo sapiens	80-88
22745105-0	2012	Crenolanib inhibits the drug-resistant PDGFRA D842V mutation associated with imatinib-resistant gastrointestinal stromal tumors.	imatinib	77-85	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	39-45
22745105-4	2012	RESULTS: Crenolanib was significantly more potent than imatinib in inhibiting the kinase activity of imatinib-resistant PDGFRA kinases (D842I, D842V, D842Y, DI842-843IM, and deletion I843).	imatinib	55-63	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	120-126
22745105-4	2012	RESULTS: Crenolanib was significantly more potent than imatinib in inhibiting the kinase activity of imatinib-resistant PDGFRA kinases (D842I, D842V, D842Y, DI842-843IM, and deletion I843).	imatinib	101-109	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	120-126
22745105-9	2012	CONCLUSIONS: Crenolanib is a potent inhibitor of imatinib-resistant PDGFRA kinases associated with GIST, including the PDGFRA D842V mutation found in approximately 5% of GISTs.	imatinib	49-57	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	68-74
22862946-6	2012	Targeting GABPbeta1L/beta2 also impairs LSC self-renewal in p210(BCR-ABL)-induced chronic myelogenous leukemia (CML) and exhibits synergistic effects with tyrosine kinase inhibitor imatinib therapy in inhibiting CML propagation.	imatinib	181-189	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	21-26
22641468-0	2012	Early landmark analysis of imatinib treatment in CML chronic phase: less than 10% BCR-ABL by FISH at 3 months associated with improved long-term clinical outcome.	imatinib	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
22718859-11	2012	CONCLUSIONS: This study is the largest reported to date on patients with advanced PDGFRA-mutant GISTs treated with imatinib.	imatinib	115-123	platelet derived growth factor receptor alpha	Homo sapiens	82-88
22855146-0	2012	Tyrosine-kinase mutations in c-KIT and PDGFR-alpha genes of imatinib naive adult patients with gastrointestinal stromal tumours (GISTs) of the stomach and small intestine: relation to tumour-biological risk-profile and long-term outcome.	imatinib	60-68	TXK tyrosine kinase	Homo sapiens	0-15
22855146-0	2012	Tyrosine-kinase mutations in c-KIT and PDGFR-alpha genes of imatinib naive adult patients with gastrointestinal stromal tumours (GISTs) of the stomach and small intestine: relation to tumour-biological risk-profile and long-term outcome.	imatinib	60-68	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	29-34
22855146-0	2012	Tyrosine-kinase mutations in c-KIT and PDGFR-alpha genes of imatinib naive adult patients with gastrointestinal stromal tumours (GISTs) of the stomach and small intestine: relation to tumour-biological risk-profile and long-term outcome.	imatinib	60-68	platelet derived growth factor receptor alpha	Homo sapiens	39-50
22855146-2	2012	The aim of this study was to investigate the role of c-KIT and PDGFRA gene mutations in primary resectable, imatinib naive GISTs located in the stomach and small intestine.	imatinib	108-116	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	53-58
22855146-2	2012	The aim of this study was to investigate the role of c-KIT and PDGFRA gene mutations in primary resectable, imatinib naive GISTs located in the stomach and small intestine.	imatinib	108-116	platelet derived growth factor receptor alpha	Homo sapiens	63-69
22712502-9	2012	Furthermore, knockdown of EDAG in K562 cells led to increased cell apoptosis induced by imatinib, and re-expression of NPM1 attenuated the increased apoptosis.	imatinib	88-96	hemogen	Homo sapiens	26-30
22875343-4	2012	Resistance of K562 cells to DQA-induced apoptosis could be eliminated by inhibition of the kinase activity of the Bcr-Abl protein with imatinib.	imatinib	135-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
22875343-7	2012	Moreover, inhibition of ERK1/2 with U0126 enhanced the ability of DQA to potentiate imatinib-induced apoptosis, suggesting a role of the Raf/MEK/ERK pathway and the Bcr-Abl tyrosine kinase in the K562 cell survival.	imatinib	84-92	mitogen-activated protein kinase 3	Homo sapiens	24-30
22875343-7	2012	Moreover, inhibition of ERK1/2 with U0126 enhanced the ability of DQA to potentiate imatinib-induced apoptosis, suggesting a role of the Raf/MEK/ERK pathway and the Bcr-Abl tyrosine kinase in the K562 cell survival.	imatinib	84-92	zinc fingers and homeoboxes 2	Homo sapiens	137-140
22875343-7	2012	Moreover, inhibition of ERK1/2 with U0126 enhanced the ability of DQA to potentiate imatinib-induced apoptosis, suggesting a role of the Raf/MEK/ERK pathway and the Bcr-Abl tyrosine kinase in the K562 cell survival.	imatinib	84-92	mitogen-activated protein kinase kinase 7	Homo sapiens	141-144
22875343-7	2012	Moreover, inhibition of ERK1/2 with U0126 enhanced the ability of DQA to potentiate imatinib-induced apoptosis, suggesting a role of the Raf/MEK/ERK pathway and the Bcr-Abl tyrosine kinase in the K562 cell survival.	imatinib	84-92	mitogen-activated protein kinase 1	Homo sapiens	24-27
22875343-7	2012	Moreover, inhibition of ERK1/2 with U0126 enhanced the ability of DQA to potentiate imatinib-induced apoptosis, suggesting a role of the Raf/MEK/ERK pathway and the Bcr-Abl tyrosine kinase in the K562 cell survival.	imatinib	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	165-172
22233112-0	2012	BCR-ABL activity measured by 50% inhibitory concentration for imatinib, p-CrkL/CrkL ratio or p-CrkL ratio in CD34+ cells of patients with chronic myeloid leukemia does not predict treatment response.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
22251158-3	2012	NME2 protein was highly overexpressed in the cytoplasm of peripheral blood mononuclear cells from 29/30 patients with CML at diagnosis and 10/10 patients resistant to imatinib.	imatinib	167-175	NME/NM23 nucleoside diphosphate kinase 2	Homo sapiens	0-4
22395361-4	2012	Here, we show that imatinib markedly inhibits expression of miR-30a in human CML cells.	imatinib	19-27	microRNA 30a	Homo sapiens	60-67
22395361-6	2012	miR-30a mimic or knockdown of autophagy genes (ATGs) such as Beclin 1 and ATG5 by short hairpin RNA enhances imatinib-induced cytotoxicity and promotes mitochondria-dependent intrinsic apoptosis.	imatinib	109-117	microRNA 30a	Homo sapiens	0-7
22395361-6	2012	miR-30a mimic or knockdown of autophagy genes (ATGs) such as Beclin 1 and ATG5 by short hairpin RNA enhances imatinib-induced cytotoxicity and promotes mitochondria-dependent intrinsic apoptosis.	imatinib	109-117	beclin 1	Homo sapiens	61-69
22521726-1	2012	The advantage of Aurora kinase (AK) inhibitors in chronic myeloid leukemia (CML) therapy mostly arises from "off-target" effects on tyrosine kinase (TK) activity of wild type (wt) or mutated Bcr-Abl proteins which drive the disease resistance to imatinib (IM).	imatinib	246-254	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	191-198
22395361-6	2012	miR-30a mimic or knockdown of autophagy genes (ATGs) such as Beclin 1 and ATG5 by short hairpin RNA enhances imatinib-induced cytotoxicity and promotes mitochondria-dependent intrinsic apoptosis.	imatinib	109-117	autophagy related 5	Homo sapiens	74-78
22395361-7	2012	In contrast, knockdown of miR-30a by antagomir-30a increases the expression of Beclin 1 and ATG5, and inhibits imatinib-induced cytotoxicity.	imatinib	111-119	microRNA 30a	Homo sapiens	26-33
22395361-8	2012	These findings indicate that dysregulation of miR-30a may interfere with the effectiveness of imatinib-mediated apoptosis by an autophagy-dependent pathway, thus representing a novel potential therapeutic target in CML.	imatinib	94-102	microRNA 30a	Homo sapiens	46-53
22714264-0	2012	The HSP90 inhibitor, AT13387, is effective against imatinib-sensitive and -resistant gastrointestinal stromal tumor models.	imatinib	51-59	heat shock protein 90 alpha family class A member 1	Homo sapiens	4-9
22665498-5	2012	Imatinib, an Abl/Arg kinase inhibitor, decreases opsonized polystyrene bead phagocytosis and Leishmania uptake.	imatinib	0-8	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	13-16
22665524-7	2012	Notably our data indicate that sorafenib is more effective than imatinib or sunitinib for inhibiting the kinase activity of drug-resistant KIT mutants (as assessed by biochemical IC(50)).	imatinib	64-72	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	139-142
22714264-2	2012	Further secondary resistance mutations within KIT limit clinical responses to tyrosine kinase inhibitors, such as imatinib.	imatinib	114-122	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	46-49
22714264-3	2012	The dependence of KIT and its mutated forms on HSP90 suggests that HSP90 inhibition might be a valuable treatment option for GIST, which would be equally effective on imatinib-sensitive and -resistant clones.	imatinib	167-175	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	18-21
22708678-0	2012	Sulforaphane potentiates the efficacy of imatinib against chronic leukemia cancer stem cells through enhanced abrogation of Wnt/beta-catenin function.	imatinib	41-49	catenin beta 1	Homo sapiens	128-140
22467682-2	2012	Imatinib, an inhibitor of BCR-ABL, has emerged as the leading compound to treat CML patients.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
22467682-6	2012	Overexpression of several EMT markers was observed in this CML subpopulation, as well as in CD34(+) CML primary cells from patients who responded poorly to imatinib treatment.	imatinib	156-164	CD34 molecule	Homo sapiens	92-96
22467682-7	2012	In response to imatinib, this CD44(high)/CD24(low) IM-R Adh subpopulation exhibited increased adhesion, transmigration and invasion in vitro and in vivo through specific overexpression of the alphaVbeta3 receptor.	imatinib	15-23	CD44 molecule (Indian blood group)	Homo sapiens	30-34
22467682-7	2012	In response to imatinib, this CD44(high)/CD24(low) IM-R Adh subpopulation exhibited increased adhesion, transmigration and invasion in vitro and in vivo through specific overexpression of the alphaVbeta3 receptor.	imatinib	15-23	CD24 molecule	Homo sapiens	41-45
22467682-8	2012	FAK/Akt pathway activation following integrin beta3 (ITGbeta3) engagement mediated the migration and invasion of IM-R Adh cells, whereas persistent activation of ERK counteracted BCR-ABL inhibition by imatinib, promoting cell adhesion-mediated resistance.	imatinib	201-209	protein tyrosine kinase 2	Homo sapiens	0-3
22467682-8	2012	FAK/Akt pathway activation following integrin beta3 (ITGbeta3) engagement mediated the migration and invasion of IM-R Adh cells, whereas persistent activation of ERK counteracted BCR-ABL inhibition by imatinib, promoting cell adhesion-mediated resistance.	imatinib	201-209	AKT serine/threonine kinase 1	Homo sapiens	4-7
22467682-8	2012	FAK/Akt pathway activation following integrin beta3 (ITGbeta3) engagement mediated the migration and invasion of IM-R Adh cells, whereas persistent activation of ERK counteracted BCR-ABL inhibition by imatinib, promoting cell adhesion-mediated resistance.	imatinib	201-209	mitogen-activated protein kinase 1	Homo sapiens	162-165
22467682-8	2012	FAK/Akt pathway activation following integrin beta3 (ITGbeta3) engagement mediated the migration and invasion of IM-R Adh cells, whereas persistent activation of ERK counteracted BCR-ABL inhibition by imatinib, promoting cell adhesion-mediated resistance.	imatinib	201-209	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	179-186
22708678-5	2012	Differentially, CD34(+)/CD38(-) LSCs demonstrated higher BCR-ABL and beta-catenin expression and imatinib (IM) resistance than CD34(+)/CD38(+) counterparts.	imatinib	97-105	CD34 molecule	Homo sapiens	16-20
22708678-5	2012	Differentially, CD34(+)/CD38(-) LSCs demonstrated higher BCR-ABL and beta-catenin expression and imatinib (IM) resistance than CD34(+)/CD38(+) counterparts.	imatinib	97-105	CD38 molecule	Homo sapiens	24-28
22301675-0	2012	Ponatinib is active against imatinib-resistant mutants of FIP1L1-PDGFRA and KIT, and against FGFR1-derived fusion kinases.	imatinib	28-36	factor interacting with PAPOLA and CPSF1	Homo sapiens	58-64
22658485-4	2012	The imatinib-sensitive GIST882 and imatinib-resistant GIST48 cell lines secrete high levels of big-IGF-II as demonstrated by ELISA and Western blotting analyses.	imatinib	4-12	insulin like growth factor 2	Homo sapiens	99-105
22658485-4	2012	The imatinib-sensitive GIST882 and imatinib-resistant GIST48 cell lines secrete high levels of big-IGF-II as demonstrated by ELISA and Western blotting analyses.	imatinib	35-43	insulin like growth factor 2	Homo sapiens	99-105
22397755-2	2012	Imatinib (IM) effectively targets Bcr-Abl tyrosine kinase, but development of resistance to IM occurs with varying frequency.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
22510939-6	2012	This molecular pathway is the target of our current drug therapy for DFSP, imatinib, a tyrosine kinase inhibitor that interferes with the phosphorylation and activation of PDGFRbeta.	imatinib	75-83	platelet derived growth factor receptor beta	Homo sapiens	172-181
22612599-9	2012	Along the same way shown by imatinib in chronic myeloid leukemia, compounds that selectively target ALK are bringing a revolution in the treatment of ALK-positive tumors.	imatinib	28-36	ALK receptor tyrosine kinase	Homo sapiens	100-103
22612599-9	2012	Along the same way shown by imatinib in chronic myeloid leukemia, compounds that selectively target ALK are bringing a revolution in the treatment of ALK-positive tumors.	imatinib	28-36	ALK receptor tyrosine kinase	Homo sapiens	150-153
22684027-0	2012	Pretreatment with IFN-alpha increases resistance to imatinib mesylate in patients with chronic myelocytic leukemia.	imatinib	52-69	interferon alpha 1	Homo sapiens	18-27
23156891-1	2012	Chronic myeloid neoplasm with eosinophilia and abnormality of platelet-derived growth factor receptor alpha (PDGFRA), referred as chronic eosinophilic leukemia, is an extremely rare neoplasm where long-term prognosis is uncertain though a high grade of responsiveness to Imatinib has been reported.	imatinib	271-279	platelet derived growth factor receptor alpha	Homo sapiens	62-107
23156891-1	2012	Chronic myeloid neoplasm with eosinophilia and abnormality of platelet-derived growth factor receptor alpha (PDGFRA), referred as chronic eosinophilic leukemia, is an extremely rare neoplasm where long-term prognosis is uncertain though a high grade of responsiveness to Imatinib has been reported.	imatinib	271-279	platelet derived growth factor receptor alpha	Homo sapiens	109-115
22572726-4	2012	RECENT FINDINGS: Imatinib, a tyrosine kinase inhibitor, blocks expression of colony stimulating factor 1 (CSF1) by a small subpopulation of tumor cells that recruit CSF1-bearing nonneoplastic cells.	imatinib	17-25	colony stimulating factor 1	Homo sapiens	77-104
22572726-4	2012	RECENT FINDINGS: Imatinib, a tyrosine kinase inhibitor, blocks expression of colony stimulating factor 1 (CSF1) by a small subpopulation of tumor cells that recruit CSF1-bearing nonneoplastic cells.	imatinib	17-25	colony stimulating factor 1	Homo sapiens	106-110
22572726-4	2012	RECENT FINDINGS: Imatinib, a tyrosine kinase inhibitor, blocks expression of colony stimulating factor 1 (CSF1) by a small subpopulation of tumor cells that recruit CSF1-bearing nonneoplastic cells.	imatinib	17-25	colony stimulating factor 1	Homo sapiens	165-169
22587685-11	2012	The efficacy of imatinib therapy in patients showing PDGFRB rearrangement is high.	imatinib	16-24	platelet derived growth factor receptor beta	Homo sapiens	53-59
22271894-13	2012	These results suggest new treatment possibilities for imatinib-resistant myeloid neoplasms associated with PDGFR mutations.	imatinib	54-62	platelet derived growth factor receptor beta	Homo sapiens	107-112
22230800-0	2012	Prevalence and dynamics of bcr-abl kinase domain mutations during imatinib treatment differ in patients with newly diagnosed and recurrent bcr-abl positive acute lymphoblastic leukemia.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
22230800-0	2012	Prevalence and dynamics of bcr-abl kinase domain mutations during imatinib treatment differ in patients with newly diagnosed and recurrent bcr-abl positive acute lymphoblastic leukemia.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-146
22230800-2	2012	BCR-ABL tyrosine kinase domain (TKD) mutations are associated with acquired imatinib resistance, but their role in primary resistance is uncertain.	imatinib	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
22230800-4	2012	Within 4 weeks of starting the imatinib treatment, absolute levels of mutant bcr-abl transcripts increased significantly in patients with advanced, but not with de novo, Ph+ ALL.	imatinib	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
22230800-7	2012	The profoundly different outgrowth dynamics of leukemic clones with bcr-abl mutations in imatinib-treated patients who differ in their disease history, provides clinical-translational evidence for a contributory role of non-mutational resistance mechanisms, possibly induced by prior chemotherapy.	imatinib	89-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
22507133-0	2012	Anti-fibrotic activity and enhanced interleukin-6 production by hepatic stellate cells in response to imatinib mesylate.	imatinib	102-119	interleukin 6	Homo sapiens	36-49
22507133-7	2012	cDNA microarray uncovered up-regulation of 29 genes in response to imatinib, including interleukin-6 (IL-6) mRNA, which was correlated with progressive IL-6 secretion.	imatinib	67-75	interleukin 6	Homo sapiens	87-100
22507133-7	2012	cDNA microarray uncovered up-regulation of 29 genes in response to imatinib, including interleukin-6 (IL-6) mRNA, which was correlated with progressive IL-6 secretion.	imatinib	67-75	interleukin 6	Homo sapiens	102-106
22507133-7	2012	cDNA microarray uncovered up-regulation of 29 genes in response to imatinib, including interleukin-6 (IL-6) mRNA, which was correlated with progressive IL-6 secretion.	imatinib	67-75	interleukin 6	Homo sapiens	152-156
22507133-10	2012	Importantly, hepatic IL-6 mRNA levels were significantly increased in TAA-treated animals receiving imatinib.	imatinib	100-108	interleukin 6	Homo sapiens	21-25
22301675-0	2012	Ponatinib is active against imatinib-resistant mutants of FIP1L1-PDGFRA and KIT, and against FGFR1-derived fusion kinases.	imatinib	28-36	platelet derived growth factor receptor alpha	Homo sapiens	65-71
22301675-0	2012	Ponatinib is active against imatinib-resistant mutants of FIP1L1-PDGFRA and KIT, and against FGFR1-derived fusion kinases.	imatinib	28-36	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	76-79
22807968-4	2012	The activity of imatinib mesylate is correlated with the mutation of c-kit gene exons 9 and 11 in gastrointestinal stromal tumors.	imatinib	16-33	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	69-74
22709239-7	2012	Treatment with imatinib reduced the incidence of diarrhea, inhibited the development of mastocytosis and jejunal mRNA expression of IL-13, CCL1, CCL17 and CCL22.	imatinib	15-23	interleukin 13	Mus musculus	132-137
22709239-7	2012	Treatment with imatinib reduced the incidence of diarrhea, inhibited the development of mastocytosis and jejunal mRNA expression of IL-13, CCL1, CCL17 and CCL22.	imatinib	15-23	chemokine (C-C motif) ligand 1	Mus musculus	139-143
22709239-7	2012	Treatment with imatinib reduced the incidence of diarrhea, inhibited the development of mastocytosis and jejunal mRNA expression of IL-13, CCL1, CCL17 and CCL22.	imatinib	15-23	chemokine (C-C motif) ligand 17	Mus musculus	145-150
22709239-7	2012	Treatment with imatinib reduced the incidence of diarrhea, inhibited the development of mastocytosis and jejunal mRNA expression of IL-13, CCL1, CCL17 and CCL22.	imatinib	15-23	chemokine (C-C motif) ligand 22	Mus musculus	155-160
22709239-11	2012	Imatinib inhibited the development of intestinal mastocytosis, reduced the incidence of diarrhea, and reduced the expression of IL-13, CCL1, and CCL17.	imatinib	0-8	interleukin 13	Mus musculus	128-133
22709239-11	2012	Imatinib inhibited the development of intestinal mastocytosis, reduced the incidence of diarrhea, and reduced the expression of IL-13, CCL1, and CCL17.	imatinib	0-8	chemokine (C-C motif) ligand 1	Mus musculus	135-139
22709239-11	2012	Imatinib inhibited the development of intestinal mastocytosis, reduced the incidence of diarrhea, and reduced the expression of IL-13, CCL1, and CCL17.	imatinib	0-8	chemokine (C-C motif) ligand 17	Mus musculus	145-150
22576800-0	2012	Alteration of MMP-2 and -14 expression by imatinib in HPV-positive and             -negative squamous cell carcinoma.	imatinib	42-50	matrix metallopeptidase 2	Homo sapiens	14-27
22612329-2	2012	Although inhibiting BCR-Abl activity with imatinib shows great clinical success, many patients acquire secondary mutations that result in resistance to imatinib.	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
22576800-13	2012	Our results indicate that the expression of MMP-2 and -14 is suppressed             in the presence of imatinib.	imatinib	103-111	matrix metallopeptidase 2	Homo sapiens	44-57
22807968-3	2012	With the success of imatinib mesylate in the treatment of gastrointestinal stromal tumors expressing c-kit, its use in SCLC serves as a novel molecular therapeutic approach.	imatinib	20-37	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	101-106
22650230-0	2012	Imatinib enhances docetaxel-induced apoptosis through inhibition of nuclear factor-kappaB activation in anaplastic thyroid carcinoma cells.	imatinib	0-8	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	68-89
22681044-3	2012	A newly described protein, the gamma-secretase activating protein (GSAP), has been proposed to promote elevated levels of amyloid-beta production, an activity that seems to be inhibited using the well-establish cancer drug, imatinib (Gleevec).	imatinib	224-232	gamma-secretase activating protein	Homo sapiens	31-65
22681044-3	2012	A newly described protein, the gamma-secretase activating protein (GSAP), has been proposed to promote elevated levels of amyloid-beta production, an activity that seems to be inhibited using the well-establish cancer drug, imatinib (Gleevec).	imatinib	224-232	gamma-secretase activating protein	Homo sapiens	67-71
22414727-0	2012	Investigation of imatinib and other approved drugs as starting points for antidiabetic drug discovery with FXR modulating activity.	imatinib	17-25	nuclear receptor subfamily 1 group H member 4	Homo sapiens	107-110
22414727-6	2012	In this article, we report the successful identification of six approved drugs out of the Drugbank as FXR modulators (ketoconazole, pentamidine, dobutamine, imatinib, papaverine and montelukast) by using a SOM for screening of the DrugBank database.	imatinib	157-165	nuclear receptor subfamily 1 group H member 4	Homo sapiens	102-105
22682059-5	2012	Imatinib therapy was initiated if patient neutrophil counts were > 1.0 x 10(9)/L and platelet counts were > 50.0 x 10(9)/L, or if they displayed either elevated BCR-ABL transcript levels in two consecutive tests, or a BCR-ABL transcript level >= 10(-2) after initial engraftment.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-174
22682059-5	2012	Imatinib therapy was initiated if patient neutrophil counts were > 1.0 x 10(9)/L and platelet counts were > 50.0 x 10(9)/L, or if they displayed either elevated BCR-ABL transcript levels in two consecutive tests, or a BCR-ABL transcript level >= 10(-2) after initial engraftment.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	224-231
22682059-7	2012	The imatinib treatment was scheduled for 3-12 months, until BCR-ABL transcript levels were negative at least for three consecutive tests or complete molecular remission was sustained for at least 3 months.	imatinib	4-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
22153896-0	2012	Canine intestinal mast cell tumor with c-kit exon 8 mutation responsive to imatinib therapy.	imatinib	75-83	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	39-44
22153896-5	2012	This mutation caused ligand-independent phosphorylation of KIT, which was suppressed by imatinib.	imatinib	88-96	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	59-62
22153896-6	2012	Inhibition of constitutively activated mutant KIT with imatinib could underlie the tumor response in this dog.	imatinib	55-63	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	46-49
22327338-4	2012	By treating HUVEC with the specific tyrosine kinase inhibitor STI571 and over-expressing a dominant negative c-ABL mutant, we show that the VEGF-A-activated c-ABL reduces the amplitude of Mitogen-Activated Protein Kinases (ERK1/2, JNKs and p38) activation in a dose-dependent manner by a negative feedback mechanism.	imatinib	62-68	vascular endothelial growth factor A	Homo sapiens	140-146
22447953-14	2012	PDGFR-alpha remained unchanged in CDH but was significantly downregulated by imatinib.	imatinib	77-85	platelet derived growth factor receptor alpha	Rattus norvegicus	0-11
22430048-1	2012	KIT/PDGFRA wild-type (WT) gastrointestinal stromal tumours (GISTs) showed a response rate to imatinib ranging from 0 to 25%.	imatinib	93-101	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
22327338-4	2012	By treating HUVEC with the specific tyrosine kinase inhibitor STI571 and over-expressing a dominant negative c-ABL mutant, we show that the VEGF-A-activated c-ABL reduces the amplitude of Mitogen-Activated Protein Kinases (ERK1/2, JNKs and p38) activation in a dose-dependent manner by a negative feedback mechanism.	imatinib	62-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-162
22430048-1	2012	KIT/PDGFRA wild-type (WT) gastrointestinal stromal tumours (GISTs) showed a response rate to imatinib ranging from 0 to 25%.	imatinib	93-101	platelet derived growth factor receptor alpha	Homo sapiens	4-10
22327338-4	2012	By treating HUVEC with the specific tyrosine kinase inhibitor STI571 and over-expressing a dominant negative c-ABL mutant, we show that the VEGF-A-activated c-ABL reduces the amplitude of Mitogen-Activated Protein Kinases (ERK1/2, JNKs and p38) activation in a dose-dependent manner by a negative feedback mechanism.	imatinib	62-68	mitogen-activated protein kinase 3	Homo sapiens	223-229
22327338-4	2012	By treating HUVEC with the specific tyrosine kinase inhibitor STI571 and over-expressing a dominant negative c-ABL mutant, we show that the VEGF-A-activated c-ABL reduces the amplitude of Mitogen-Activated Protein Kinases (ERK1/2, JNKs and p38) activation in a dose-dependent manner by a negative feedback mechanism.	imatinib	62-68	mitogen-activated protein kinase 1	Homo sapiens	240-243
22516066-5	2012	Dasatinib (0.03 mumol/L), nilotinib (0.3 mumol/L), and imatinib (1 mumol/L) potently inhibited PDGF-induced signal transducer and activator of transcription 3 and Akt phosphorylation.	imatinib	55-63	signal transducer and activator of transcription 3	Homo sapiens	108-158
22713591-7	2012	A radical surgery was rejected by the patient and adjuvant therapy with imatinib at an initial dose of 400 mg/day was considered, with the intention of increasing the dose to 800 mg/day because of the presence of mutation in c-KIT exon 9 related to a poor response to imatinib.	imatinib	72-80	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	225-230
22713591-7	2012	A radical surgery was rejected by the patient and adjuvant therapy with imatinib at an initial dose of 400 mg/day was considered, with the intention of increasing the dose to 800 mg/day because of the presence of mutation in c-KIT exon 9 related to a poor response to imatinib.	imatinib	268-276	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	225-230
22516066-5	2012	Dasatinib (0.03 mumol/L), nilotinib (0.3 mumol/L), and imatinib (1 mumol/L) potently inhibited PDGF-induced signal transducer and activator of transcription 3 and Akt phosphorylation.	imatinib	55-63	AKT serine/threonine kinase 1	Homo sapiens	163-166
22328017-2	2012	Patients in CML-CP usually respond to treatment with ABL1 tyrosine kinase inhibitors (TKIs) such as imatinib, though some patients who respond initially may become resistant later.	imatinib	100-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-57
22349810-0	2012	Phase I trial of the combination of flavopiridol and imatinib mesylate in patients with Bcr-Abl+ hematological malignancies.	imatinib	53-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
22349810-1	2012	PURPOSE: Imatinib is an inhibitor of the Bcr-Abl tyrosine kinase; however, resistance is common.	imatinib	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
22154054-10	2012	These results indicate that a subset of anorectal melanomas have activating c-kit mutations, which suggests that kinase inhibitors such as imatinib may be used to treat this subset of melanoma patients.	imatinib	139-147	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	76-81
22483154-3	2012	Approximately 20-25% of patients initially treated with imatinib will need alternative therapy, due to drug resistance which is often caused by the appearance of clones expressing mutant forms of BCR-ABL.	imatinib	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	196-203
22207690-1	2012	BACKGROUND: The functional activity of the organic cation transporter 1 (OCT-1) protein (OCT-1 activity) is an excellent predictor of molecular response and progression-free survival in patients with newly diagnosed chronic phase chronic myeloid leukemia treated with imatinib as front-line therapy.	imatinib	268-276	solute carrier family 22 member 1	Homo sapiens	43-71
22207690-1	2012	BACKGROUND: The functional activity of the organic cation transporter 1 (OCT-1) protein (OCT-1 activity) is an excellent predictor of molecular response and progression-free survival in patients with newly diagnosed chronic phase chronic myeloid leukemia treated with imatinib as front-line therapy.	imatinib	268-276	solute carrier family 22 member 1	Homo sapiens	73-78
22207690-1	2012	BACKGROUND: The functional activity of the organic cation transporter 1 (OCT-1) protein (OCT-1 activity) is an excellent predictor of molecular response and progression-free survival in patients with newly diagnosed chronic phase chronic myeloid leukemia treated with imatinib as front-line therapy.	imatinib	268-276	solute carrier family 22 member 1	Homo sapiens	89-94
22207690-2	2012	DESIGN AND METHODS: In this study the predictive value of OCT-1 activity in patients treated with imatinib 400 mg/day or 800 mg/day was evaluated in relation to trough imatinib plasma levels assessed in 100 patients enrolled in the Tyrosine Kinase Inhibitor Optimization and Selectivity (TOPS) trial.	imatinib	98-106	solute carrier family 22 member 1	Homo sapiens	58-63
22207690-2	2012	DESIGN AND METHODS: In this study the predictive value of OCT-1 activity in patients treated with imatinib 400 mg/day or 800 mg/day was evaluated in relation to trough imatinib plasma levels assessed in 100 patients enrolled in the Tyrosine Kinase Inhibitor Optimization and Selectivity (TOPS) trial.	imatinib	168-176	solute carrier family 22 member 1	Homo sapiens	58-63
22207690-3	2012	RESULTS: The rate of major molecular responses by 24 months in patients on imatinib 400 mg/day was significantly higher in those with high OCT-1 activity than in those with low OCT-1 activity (low OCT-1 activity, 57% of patients; high OCT-1 activity, 100%; P < 0.001); the corresponding difference in patients treated with imatinib 800 mg/day did not reach statistical significance (low OCT-1 activity, 68%; high OCT-1 activity, 95%; P = 0.073).	imatinib	75-83	solute carrier family 22 member 1	Homo sapiens	139-144
22207690-3	2012	RESULTS: The rate of major molecular responses by 24 months in patients on imatinib 400 mg/day was significantly higher in those with high OCT-1 activity than in those with low OCT-1 activity (low OCT-1 activity, 57% of patients; high OCT-1 activity, 100%; P < 0.001); the corresponding difference in patients treated with imatinib 800 mg/day did not reach statistical significance (low OCT-1 activity, 68%; high OCT-1 activity, 95%; P = 0.073).	imatinib	75-83	solute carrier family 22 member 1	Homo sapiens	177-182
22207690-3	2012	RESULTS: The rate of major molecular responses by 24 months in patients on imatinib 400 mg/day was significantly higher in those with high OCT-1 activity than in those with low OCT-1 activity (low OCT-1 activity, 57% of patients; high OCT-1 activity, 100%; P < 0.001); the corresponding difference in patients treated with imatinib 800 mg/day did not reach statistical significance (low OCT-1 activity, 68%; high OCT-1 activity, 95%; P = 0.073).	imatinib	75-83	solute carrier family 22 member 1	Homo sapiens	177-182
22207690-9	2012	Hence OCT-1 activity determined prior to the start of therapy in newly diagnosed CML patients provides a valuable prognostic tool to determine the optimal up-front dose of imatinib in patients with newly diagnosed chronic phase chronic myeloid leukemia.	imatinib	172-180	solute carrier family 22 member 1	Homo sapiens	6-11
22207690-3	2012	RESULTS: The rate of major molecular responses by 24 months in patients on imatinib 400 mg/day was significantly higher in those with high OCT-1 activity than in those with low OCT-1 activity (low OCT-1 activity, 57% of patients; high OCT-1 activity, 100%; P < 0.001); the corresponding difference in patients treated with imatinib 800 mg/day did not reach statistical significance (low OCT-1 activity, 68%; high OCT-1 activity, 95%; P = 0.073).	imatinib	75-83	solute carrier family 22 member 1	Homo sapiens	177-182
22124674-3	2012	DISCUSSION: Besides surgery, therapy with imatinib mesylate, which inhibits KIT kinase activity, represents the other cornerstone for the treatment of GIST.	imatinib	42-59	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	76-79
22207690-3	2012	RESULTS: The rate of major molecular responses by 24 months in patients on imatinib 400 mg/day was significantly higher in those with high OCT-1 activity than in those with low OCT-1 activity (low OCT-1 activity, 57% of patients; high OCT-1 activity, 100%; P < 0.001); the corresponding difference in patients treated with imatinib 800 mg/day did not reach statistical significance (low OCT-1 activity, 68%; high OCT-1 activity, 95%; P = 0.073).	imatinib	75-83	solute carrier family 22 member 1	Homo sapiens	177-182
22207690-3	2012	RESULTS: The rate of major molecular responses by 24 months in patients on imatinib 400 mg/day was significantly higher in those with high OCT-1 activity than in those with low OCT-1 activity (low OCT-1 activity, 57% of patients; high OCT-1 activity, 100%; P < 0.001); the corresponding difference in patients treated with imatinib 800 mg/day did not reach statistical significance (low OCT-1 activity, 68%; high OCT-1 activity, 95%; P = 0.073).	imatinib	75-83	solute carrier family 22 member 1	Homo sapiens	177-182
22207690-6	2012	CONCLUSIONS: High-dose imatinib leads to superior molecular responses in patients with low OCT-1 activity.	imatinib	23-31	solute carrier family 22 member 1	Homo sapiens	91-96
25436685-3	2012	Indirect strategies have yielded potent agents, such as imatinib, AC2207, and EXEL823 which effectively silence STAT5 activity but which suffer from off-target effects and toxicity.	imatinib	56-64	signal transducer and activator of transcription 5A	Homo sapiens	112-117
21938724-0	2012	Imatinib treatment inhibit IL-6, IL-8, NF-KB and AP-1 production and modulate intracellular calcium in CML patients.	imatinib	0-8	interleukin 6	Homo sapiens	27-31
21938724-0	2012	Imatinib treatment inhibit IL-6, IL-8, NF-KB and AP-1 production and modulate intracellular calcium in CML patients.	imatinib	0-8	C-X-C motif chemokine ligand 8	Homo sapiens	33-37
21938724-0	2012	Imatinib treatment inhibit IL-6, IL-8, NF-KB and AP-1 production and modulate intracellular calcium in CML patients.	imatinib	0-8	JunD proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	49-53
21938724-7	2012	Our results demonstrated a significant down-regulation in IL-6 and IL-8 release as well as NF-kB and AP-1 activation in lymphomonocytes from Imatinib-treated patients, compared to samples from untreated patients.	imatinib	141-149	interleukin 6	Homo sapiens	58-62
21938724-7	2012	Our results demonstrated a significant down-regulation in IL-6 and IL-8 release as well as NF-kB and AP-1 activation in lymphomonocytes from Imatinib-treated patients, compared to samples from untreated patients.	imatinib	141-149	C-X-C motif chemokine ligand 8	Homo sapiens	67-71
21938724-7	2012	Our results demonstrated a significant down-regulation in IL-6 and IL-8 release as well as NF-kB and AP-1 activation in lymphomonocytes from Imatinib-treated patients, compared to samples from untreated patients.	imatinib	141-149	JunD proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	101-105
21938724-9	2012	The results of this study show that measurements of NF-kB, AP-1, IL-6, IL-8, and intracellular calcium in CML patients treated with Imatinib may give important information to the hematologist on diagnostic criteria and are highly predictive in patients with newly diagnosed CML.	imatinib	132-140	JunD proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	59-63
21938724-9	2012	The results of this study show that measurements of NF-kB, AP-1, IL-6, IL-8, and intracellular calcium in CML patients treated with Imatinib may give important information to the hematologist on diagnostic criteria and are highly predictive in patients with newly diagnosed CML.	imatinib	132-140	interleukin 6	Homo sapiens	65-69
21938724-9	2012	The results of this study show that measurements of NF-kB, AP-1, IL-6, IL-8, and intracellular calcium in CML patients treated with Imatinib may give important information to the hematologist on diagnostic criteria and are highly predictive in patients with newly diagnosed CML.	imatinib	132-140	C-X-C motif chemokine ligand 8	Homo sapiens	71-75
22289991-2	2012	Kinase mutations of BCR-ABL and cytokine-mediated modulation of response to tyrosine kinase inhibitors (TKIs) are key mechanisms governing clinical response to imatinib and second generation TKIs.	imatinib	160-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
22643209-1	2012	BACKGROUND: Imatinib therapy has been successful in gastrointestinal stromal tumours containing mutation of the KIT gene.	imatinib	12-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	112-115
22643209-2	2012	However, there are few reported cases of successful imatinib therapy in patients with melanoma containing KIT gene mutation or c-kit protein expression.	imatinib	52-60	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	106-109
22643209-2	2012	However, there are few reported cases of successful imatinib therapy in patients with melanoma containing KIT gene mutation or c-kit protein expression.	imatinib	52-60	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	127-132
22009701-2	2012	Although it has been described only in one patient with testicular hydrocele and gynecomastia in the literature, several cases of male gynecomastia have been reported with the use of imatinib mesylate in chronic myeloid leukemia (GML).	imatinib	183-200	glycosylphosphatidylinositol anchored molecule like	Homo sapiens	230-233
22883199-0	2012	[Effects of hOCT1 and ABCB1 gene on the efficacy of imatinib mesylate in chronic myelocytic leukemia].	imatinib	52-69	solute carrier family 22 member 1	Homo sapiens	12-17
21258876-0	2012	Imatinib mesylate may induce long-term clinical response in FIP1L1-PDGFRalpha-negative hypereosinophilic syndrome.	imatinib	0-17	factor interacting with PAPOLA and CPSF1	Homo sapiens	60-66
21258876-0	2012	Imatinib mesylate may induce long-term clinical response in FIP1L1-PDGFRalpha-negative hypereosinophilic syndrome.	imatinib	0-17	platelet derived growth factor receptor alpha	Homo sapiens	67-77
21258876-2	2012	Eight patients with a median age at diagnosis of 42 years (range 19-67) received imatinib mesylate (IM) for FIP1L1-PDGFRalpha-negative HES resistant to previous conventional treatment.	imatinib	81-98	factor interacting with PAPOLA and CPSF1	Homo sapiens	108-114
21258876-2	2012	Eight patients with a median age at diagnosis of 42 years (range 19-67) received imatinib mesylate (IM) for FIP1L1-PDGFRalpha-negative HES resistant to previous conventional treatment.	imatinib	81-98	platelet derived growth factor receptor alpha	Homo sapiens	115-125
22350755-0	2012	BGP-15, a PARP-inhibitor, prevents imatinib-induced cardiotoxicity by activating Akt and suppressing JNK and p38 MAP kinases.	imatinib	35-43	AKT serine/threonine kinase 1	Rattus norvegicus	81-84
22350755-0	2012	BGP-15, a PARP-inhibitor, prevents imatinib-induced cardiotoxicity by activating Akt and suppressing JNK and p38 MAP kinases.	imatinib	35-43	mitogen-activated protein kinase 8	Rattus norvegicus	101-104
22350755-0	2012	BGP-15, a PARP-inhibitor, prevents imatinib-induced cardiotoxicity by activating Akt and suppressing JNK and p38 MAP kinases.	imatinib	35-43	mitogen activated protein kinase 14	Rattus norvegicus	109-112
22350755-6	2012	Imatinib mesylate treatment-induced activation of MAP kinases (including ERK1/2, p38, and JNK) and the phosphorylation of Akt and GSK-3beta.	imatinib	0-17	mitogen activated protein kinase 3	Rattus norvegicus	73-79
22350755-6	2012	Imatinib mesylate treatment-induced activation of MAP kinases (including ERK1/2, p38, and JNK) and the phosphorylation of Akt and GSK-3beta.	imatinib	0-17	mitogen activated protein kinase 14	Rattus norvegicus	81-84
22350755-6	2012	Imatinib mesylate treatment-induced activation of MAP kinases (including ERK1/2, p38, and JNK) and the phosphorylation of Akt and GSK-3beta.	imatinib	0-17	mitogen-activated protein kinase 8	Rattus norvegicus	90-93
22350755-6	2012	Imatinib mesylate treatment-induced activation of MAP kinases (including ERK1/2, p38, and JNK) and the phosphorylation of Akt and GSK-3beta.	imatinib	0-17	AKT serine/threonine kinase 1	Rattus norvegicus	122-125
22350755-6	2012	Imatinib mesylate treatment-induced activation of MAP kinases (including ERK1/2, p38, and JNK) and the phosphorylation of Akt and GSK-3beta.	imatinib	0-17	glycogen synthase kinase 3 beta	Rattus norvegicus	130-139
22350755-7	2012	BGP-15 (200 muM) prevented the imatinib mesylate-induced oxidative damages, attenuated the depletion of high-energy phosphates, altered the signaling effect of imatinib mesylate by preventing p38 MAP kinase and JNK activation, and induced the phosphorylation of Akt and GSK-3beta.	imatinib	160-177	mitogen activated protein kinase 14	Rattus norvegicus	192-195
22932406-0	2012	[Secondary mutation of c-kit/PDGFRalpha genotypes after imatinib mesylate therapy and its relationship with efficacy of sunitinib].	imatinib	56-64	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	23-28
22932406-0	2012	[Secondary mutation of c-kit/PDGFRalpha genotypes after imatinib mesylate therapy and its relationship with efficacy of sunitinib].	imatinib	56-64	platelet derived growth factor receptor alpha	Homo sapiens	29-39
22932406-1	2012	OBJECTIVE: To investigate the relationship between secondary mutations of c-kit/PDGFRalpha resistance to imatinib mesylate and the efficacy of sunitinib in patients with gastrointestinal stromal tumor (GIST).	imatinib	105-122	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	74-79
22932406-1	2012	OBJECTIVE: To investigate the relationship between secondary mutations of c-kit/PDGFRalpha resistance to imatinib mesylate and the efficacy of sunitinib in patients with gastrointestinal stromal tumor (GIST).	imatinib	105-122	platelet derived growth factor receptor alpha	Homo sapiens	80-90
22932406-6	2012	C-kit exon 11 mutations were detected in 3 patients, which were all acquired mutations, including c-kit exon 13 V654A, c-kit exon 13 V654E and c-kit exon 17 N822K, after imatinib mesylate resistance.	imatinib	170-187	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-5
22932406-8	2012	C-kit exon 9 mutations were detected in 2 patients with no acquired mutations after imatinib mesylate resistance.	imatinib	84-92	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-5
22932406-10	2012	CONCLUSION: The c-kit/PDGFRalpha genotypes after imatinib mesylate resistance may both relate to primary mutations and efficacy of sunitinib treatment.	imatinib	49-57	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	16-21
22932406-10	2012	CONCLUSION: The c-kit/PDGFRalpha genotypes after imatinib mesylate resistance may both relate to primary mutations and efficacy of sunitinib treatment.	imatinib	49-57	platelet derived growth factor receptor alpha	Homo sapiens	22-32
22883199-0	2012	[Effects of hOCT1 and ABCB1 gene on the efficacy of imatinib mesylate in chronic myelocytic leukemia].	imatinib	52-69	ATP binding cassette subfamily B member 1	Homo sapiens	22-27
22229850-7	2012	Patients whose tumors harbor a KIT exon 11 mutation benefit the most from imatinib mesylate therapy, in terms of response rate, progression-free survival, and overall survival.	imatinib	74-91	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	31-34
22474082-0	2012	Suppression of PDGF-induced PI3 kinase activity by imatinib promotes adipogenesis and adiponectin secretion.	imatinib	51-59	adiponectin, C1Q and collagen domain containing	Homo sapiens	86-97
22474082-2	2012	We recently reported that plasma levels of adiponectin, an important regulator of insulin sensitivity, are elevated following imatinib therapy in CML patients, which could account for these improved metabolic outcomes.	imatinib	126-134	adiponectin, C1Q and collagen domain containing	Homo sapiens	43-54
22474082-3	2012	Adiponectin is secreted exclusively from adipocytes, suggesting that imatinib modulates adiponectin levels directly, by transcriptional upregulation of adiponectin in pre-existing adipocytes, and/or indirectly, by stimulating adipogenesis.	imatinib	69-77	adiponectin, C1Q and collagen domain containing	Homo sapiens	0-11
22474082-3	2012	Adiponectin is secreted exclusively from adipocytes, suggesting that imatinib modulates adiponectin levels directly, by transcriptional upregulation of adiponectin in pre-existing adipocytes, and/or indirectly, by stimulating adipogenesis.	imatinib	69-77	adiponectin, C1Q and collagen domain containing	Homo sapiens	88-99
22474082-3	2012	Adiponectin is secreted exclusively from adipocytes, suggesting that imatinib modulates adiponectin levels directly, by transcriptional upregulation of adiponectin in pre-existing adipocytes, and/or indirectly, by stimulating adipogenesis.	imatinib	69-77	adiponectin, C1Q and collagen domain containing	Homo sapiens	152-163
22474082-4	2012	In this report, we have demonstrated that imatinib promotes adipogenic differentiation of human mesenchymal stromal cells (MSCs), which in turn secrete high-molecular-weight adiponectin.	imatinib	42-50	adiponectin, C1Q and collagen domain containing	Homo sapiens	174-185
22474082-6	2012	We hypothesise that inhibition of PDGFRalpha (PDGFRA) and PDGFRbeta (PDGFRB) is the mechanism by which imatinib promotes adipogenesis.	imatinib	103-111	platelet derived growth factor receptor alpha	Homo sapiens	34-44
22474082-6	2012	We hypothesise that inhibition of PDGFRalpha (PDGFRA) and PDGFRbeta (PDGFRB) is the mechanism by which imatinib promotes adipogenesis.	imatinib	103-111	platelet derived growth factor receptor alpha	Homo sapiens	46-52
22474082-6	2012	We hypothesise that inhibition of PDGFRalpha (PDGFRA) and PDGFRbeta (PDGFRB) is the mechanism by which imatinib promotes adipogenesis.	imatinib	103-111	platelet derived growth factor receptor beta	Homo sapiens	58-67
22474082-6	2012	We hypothesise that inhibition of PDGFRalpha (PDGFRA) and PDGFRbeta (PDGFRB) is the mechanism by which imatinib promotes adipogenesis.	imatinib	103-111	platelet derived growth factor receptor beta	Homo sapiens	69-75
22474082-8	2012	We have shown that imatinib is a potent inhibitor of PDGF-induced PI3 kinase activation and, using a PI3 kinase p110alpha-specific inhibitor (PIK-75), we have demonstrated that suppression of this pathway recapitulates the effects of imatinib on MSC differentiation.	imatinib	19-27	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	112-121
22474082-9	2012	Furthermore, using mitogens that activate the PI3 kinase pathway, or MSCs expressing constitutively activated Akt, we have shown that activation of the PI3 kinase pathway negates the pro-adipogenic effects of imatinib.	imatinib	209-217	AKT serine/threonine kinase 1	Homo sapiens	110-113
22474082-10	2012	Taken together, our results suggest that imatinib increases plasma adiponectin levels by promoting adipogenesis through the suppression of PI3 kinase signalling downstream of PDGFR.	imatinib	41-49	adiponectin, C1Q and collagen domain containing	Homo sapiens	67-78
22474082-10	2012	Taken together, our results suggest that imatinib increases plasma adiponectin levels by promoting adipogenesis through the suppression of PI3 kinase signalling downstream of PDGFR.	imatinib	41-49	platelet derived growth factor receptor beta	Homo sapiens	175-180
22431575-1	2012	Rising BCR-ABL1 transcripts indicate potential loss of imatinib response in CML.	imatinib	55-63	BCR activator of RhoGEF and GTPase	Homo sapiens	7-15
22531634-1	2012	BACKGROUND: The human organic cation transporter-1 (OCT-1) is the primary active protein for imatinib uptake into target BCR-ABL-positive cells.	imatinib	93-101	solute carrier family 22 member 1	Homo sapiens	22-50
22531634-1	2012	BACKGROUND: The human organic cation transporter-1 (OCT-1) is the primary active protein for imatinib uptake into target BCR-ABL-positive cells.	imatinib	93-101	solute carrier family 22 member 1	Homo sapiens	52-57
22531634-1	2012	BACKGROUND: The human organic cation transporter-1 (OCT-1) is the primary active protein for imatinib uptake into target BCR-ABL-positive cells.	imatinib	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
22617440-5	2012	We demonstrate that MIR30A-mediated autophagy enhances imatinib resistance against CML including primary stem and progenitor cells.	imatinib	55-63	microRNA 30a	Homo sapiens	20-26
22225474-0	2012	Undetectable molecular residual disease after omacetaxine and nilotinib combination therapy in an imatinib-resistant chronic myeloid leukaemia patient harbouring the BCR-ABL1 T315I gatekeeper mutation.	imatinib	98-106	BCR activator of RhoGEF and GTPase	Homo sapiens	166-174
22829973-6	2012	Ectopic expression of p(c-Mybex9b) enhanced proliferation and colony formation and reduced imatinib (IM) sensitivity of K562 cells; conversely, specific downregulation of p(c-Mybex9b) reduced proliferation and colony formation, enhanced IM sensitivity of K562 cells and markedly suppressed colony formation of CML CD34(+) cells, without affecting the levels of p75(c-Myb).	imatinib	91-99	MYB proto-oncogene, transcription factor	Homo sapiens	24-29
22829974-0	2012	Prognostic factors influencing clinical outcome of allogeneic hematopoietic stem cell transplantation following imatinib-based therapy in BCR-ABL-positive ALL.	imatinib	112-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
22299775-0	2012	Imatinib resistant BCR-ABL1 mutations at relapse in children with Ph+ ALL: a Children"s Oncology Group (COG) study.	imatinib	0-8	BCR activator of RhoGEF and GTPase	Homo sapiens	19-27
22005789-0	2012	Role of stromal microenvironment in nonpharmacological resistance of CML to imatinib through Lyn/CXCR4 interactions in lipid rafts.	imatinib	76-84	C-X-C motif chemokine receptor 4	Homo sapiens	97-102
22372463-4	2012	Furthermore, MECOM mRNA and protein expression were repressed by imatinib mesylate treatment of CML-CP CD34(+)  cells, K562 and KY01 cell lines whereas imatinib had no effect in non-CML BCR-ABL1 -ve CD34(+)  cells.	imatinib	65-73	MDS1 and EVI1 complex locus	Homo sapiens	13-18
22372463-4	2012	Furthermore, MECOM mRNA and protein expression were repressed by imatinib mesylate treatment of CML-CP CD34(+)  cells, K562 and KY01 cell lines whereas imatinib had no effect in non-CML BCR-ABL1 -ve CD34(+)  cells.	imatinib	65-73	CD34 molecule	Homo sapiens	103-107
22372463-4	2012	Furthermore, MECOM mRNA and protein expression were repressed by imatinib mesylate treatment of CML-CP CD34(+)  cells, K562 and KY01 cell lines whereas imatinib had no effect in non-CML BCR-ABL1 -ve CD34(+)  cells.	imatinib	65-73	BCR activator of RhoGEF and GTPase	Homo sapiens	186-194
22372463-4	2012	Furthermore, MECOM mRNA and protein expression were repressed by imatinib mesylate treatment of CML-CP CD34(+)  cells, K562 and KY01 cell lines whereas imatinib had no effect in non-CML BCR-ABL1 -ve CD34(+)  cells.	imatinib	65-73	CD34 molecule	Homo sapiens	199-203
23226581-4	2012	In parallel, Abl oncoproteins have become prime molecular targets for cancer therapy, using adenosine triphosphate (ATP)-competitive kinase inhibitors, such as imatinib.	imatinib	160-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
25031941-3	2012	The tyrosine kinase inhibitors imatinib, nilotinib, and dasatinib block the BCR-ABL protein and prevent activation of the transformation pathways.	imatinib	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
22157807-1	2012	Nilotinib is a selective inhibitor of BCR-ABL approved for use in newly diagnosed and imatinib-resistant or -intolerant patients with chronic myeloid leukemia (CML) in chronic phase.	imatinib	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
22643838-0	2012	A novel co-operative mechanism linking TGFbeta and Lyn kinase activation to imatinib resistance in chronic myeloid leukaemia cells.	imatinib	76-84	transforming growth factor beta 1	Homo sapiens	39-46
22643838-0	2012	A novel co-operative mechanism linking TGFbeta and Lyn kinase activation to imatinib resistance in chronic myeloid leukaemia cells.	imatinib	76-84	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	51-54
22643838-2	2012	However, resistance to imatinib is common in patients and has recently been linked to both transforming growth factor-beta (TGFbeta) and elevated Lyn kinase activity, although molecular mechanisms remain largely unknown.	imatinib	23-31	transforming growth factor beta 1	Homo sapiens	91-122
22783407-0	2012	A novel PDGFRA mutation in gastrointestinal stromal tumours, L839P, is sensitive to imatinib in vitro.	imatinib	84-92	platelet-derived growth factor receptor alpha	Cricetulus griseus	8-14
22783407-5	2012	Reults of the MTT assay revealed that the growth rate of CHO(PDGFRA(L839P)) cells decreased to approximately 60% when exposed to 1 muM imatinib and to approximately 50% with 5 muM imatinib.	imatinib	135-143	platelet-derived growth factor receptor alpha	Cricetulus griseus	61-67
22643838-2	2012	However, resistance to imatinib is common in patients and has recently been linked to both transforming growth factor-beta (TGFbeta) and elevated Lyn kinase activity, although molecular mechanisms remain largely unknown.	imatinib	23-31	transforming growth factor beta 1	Homo sapiens	124-131
22783407-5	2012	Reults of the MTT assay revealed that the growth rate of CHO(PDGFRA(L839P)) cells decreased to approximately 60% when exposed to 1 muM imatinib and to approximately 50% with 5 muM imatinib.	imatinib	180-188	platelet-derived growth factor receptor alpha	Cricetulus griseus	61-67
22643838-2	2012	However, resistance to imatinib is common in patients and has recently been linked to both transforming growth factor-beta (TGFbeta) and elevated Lyn kinase activity, although molecular mechanisms remain largely unknown.	imatinib	23-31	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	146-149
22783407-7	2012	Western blot analysis indicated that 1 muM imatinib completely blocked the phosphorylation of PDGFRA(L839P), but did not affect PDGFRA(D842V) phosphorylation.	imatinib	43-51	platelet-derived growth factor receptor alpha	Cricetulus griseus	94-100
22643838-3	2012	Here, using leukaemic MYL cell lines derived from CML patients, we show that TGFbeta plays a key role in imatinib-resistance via direct effects on Lyn ubiquitination and turnover that results in bursts of Lyn kinase activity, and identify c-cbl is a candidate E3 ubiquitin ligase.	imatinib	105-113	transforming growth factor beta 1	Homo sapiens	77-84
22783407-8	2012	Apoptosis analysis suggested that the percentage of apoptotic CHO(PDGFRA(L839P)) cells increased approximately 4-fold (from 5.90 to 25.2%) with 1 muM imatinib.	imatinib	150-158	platelet-derived growth factor receptor alpha	Cricetulus griseus	66-72
22643838-3	2012	Here, using leukaemic MYL cell lines derived from CML patients, we show that TGFbeta plays a key role in imatinib-resistance via direct effects on Lyn ubiquitination and turnover that results in bursts of Lyn kinase activity, and identify c-cbl is a candidate E3 ubiquitin ligase.	imatinib	105-113	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	147-150
22783407-9	2012	Although the treatment of CHO(PDGFRA(D842V)) and CHO(PDGFRA(Wild)) cells with 5 muM imatinib resulted in a slight increase in the number of apoptotic cells, the percentage of apoptotic cells remained approximately 10% of the total population.	imatinib	84-92	platelet-derived growth factor receptor alpha	Cricetulus griseus	30-36
22783407-9	2012	Although the treatment of CHO(PDGFRA(D842V)) and CHO(PDGFRA(Wild)) cells with 5 muM imatinib resulted in a slight increase in the number of apoptotic cells, the percentage of apoptotic cells remained approximately 10% of the total population.	imatinib	84-92	platelet-derived growth factor receptor alpha	Cricetulus griseus	53-59
22783407-2	2012	The purpose of this study was to explore the sensitivity of the PDGFRA(L839P) mutant, a novel gain-of-function mutation isoform related to GISTs, to imatinib in vitro.	imatinib	149-157	platelet-derived growth factor receptor alpha	Cricetulus griseus	64-70
22783407-4	2012	The responses of cells with PDGFRA(Wild), PDGFRA(L839P) and PDGFRA(D842V) mutants to imatinib were determined by methyl thiazolyl tetrazolium (MTT) assay, western blotting and apoptosis assays.	imatinib	85-93	platelet-derived growth factor receptor alpha	Cricetulus griseus	28-34
22643838-3	2012	Here, using leukaemic MYL cell lines derived from CML patients, we show that TGFbeta plays a key role in imatinib-resistance via direct effects on Lyn ubiquitination and turnover that results in bursts of Lyn kinase activity, and identify c-cbl is a candidate E3 ubiquitin ligase.	imatinib	105-113	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	205-208
22783407-10	2012	Our findings showed that the PDGFRA gene mutation isoform L839P is sensitive to inhibition by imatinib.	imatinib	94-102	platelet-derived growth factor receptor alpha	Cricetulus griseus	29-35
22783407-11	2012	Screening for PDGFRA mutations in GISTs is essential to identify the response to treatment with imatinib.	imatinib	96-104	platelet-derived growth factor receptor alpha	Cricetulus griseus	14-20
22643838-3	2012	Here, using leukaemic MYL cell lines derived from CML patients, we show that TGFbeta plays a key role in imatinib-resistance via direct effects on Lyn ubiquitination and turnover that results in bursts of Lyn kinase activity, and identify c-cbl is a candidate E3 ubiquitin ligase.	imatinib	105-113	Cbl proto-oncogene	Homo sapiens	239-244
22643838-4	2012	Furthermore, blockade of TGFbeta signalling activity with the TGFbeta receptor kinase inhibitor SB431542 significantly reduces Lyn turnover and activation, and subsequently enhances imatinib-mediated CML cell death in a proteasomal-dependent manner.	imatinib	182-190	transforming growth factor beta 1	Homo sapiens	25-32
22643838-4	2012	Furthermore, blockade of TGFbeta signalling activity with the TGFbeta receptor kinase inhibitor SB431542 significantly reduces Lyn turnover and activation, and subsequently enhances imatinib-mediated CML cell death in a proteasomal-dependent manner.	imatinib	182-190	transforming growth factor beta 1	Homo sapiens	62-69
22643838-5	2012	Collectively, our data reveals novel co-operative mechanisms in CML involving TGFbeta and Lyn kinase linked to proteasome function and ubiquitination, and thus supports therapeutic approaches that target TGFbeta pathway activity as a strategy for overcoming imatinib-resistance in CML.	imatinib	258-266	transforming growth factor beta 1	Homo sapiens	78-85
22643838-5	2012	Collectively, our data reveals novel co-operative mechanisms in CML involving TGFbeta and Lyn kinase linked to proteasome function and ubiquitination, and thus supports therapeutic approaches that target TGFbeta pathway activity as a strategy for overcoming imatinib-resistance in CML.	imatinib	258-266	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	90-93
22643838-5	2012	Collectively, our data reveals novel co-operative mechanisms in CML involving TGFbeta and Lyn kinase linked to proteasome function and ubiquitination, and thus supports therapeutic approaches that target TGFbeta pathway activity as a strategy for overcoming imatinib-resistance in CML.	imatinib	258-266	transforming growth factor beta 1	Homo sapiens	204-211
22461388-8	2012	Attenuation of PAR-2 expression was also observed in smooth muscle cells of pulmonary vessels of mice exposed to hypoxia and rats challenged with MCT in response to Imatinib treatment.	imatinib	165-173	pulmonary adenoma resistance 2	Mus musculus	15-20
22388797-5	2012	Imatinib mesylate targets the oncogenic kinase activity of BCR-ABL.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
22388797-9	2012	CONCLUSION: The blockade of oncoprotein Bcr-Abl by imatinib could cause a decrease in the expression of key DNA repair genes and substantially modify the expression profile of the bone marrow cells in the first days of therapy.	imatinib	51-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
22482506-0	2012	Genetic and pharmacologic inhibition of beta-catenin targets imatinib-resistant leukemia stem cells in CML.	imatinib	61-69	catenin (cadherin associated protein), beta 1	Mus musculus	40-52
22388075-0	2012	Imatinib induces H2AX phosphorylation and apoptosis in chronic myelogenous leukemia cells in vitro via caspase-3/Mst1 pathway.	imatinib	0-8	H2A.X variant histone	Homo sapiens	17-21
22388075-0	2012	Imatinib induces H2AX phosphorylation and apoptosis in chronic myelogenous leukemia cells in vitro via caspase-3/Mst1 pathway.	imatinib	0-8	caspase 3	Homo sapiens	103-112
22388075-0	2012	Imatinib induces H2AX phosphorylation and apoptosis in chronic myelogenous leukemia cells in vitro via caspase-3/Mst1 pathway.	imatinib	0-8	macrophage stimulating 1	Homo sapiens	113-117
22388075-2	2012	The aim of the present study was to elucidate the mechanisms underlying imatinib-induced C-terminal phosphorylation of H2AX in chronic myelogenous leukemia cells in vitro.	imatinib	72-80	H2A.X variant histone	Homo sapiens	119-123
22388075-4	2012	Microscopy, Western blotting and flow cytometry were used to study the signaling pathways that regulate imatinib-induced H2AX phosphorylation and the apoptotic mechanisms.	imatinib	104-112	H2A.X variant histone	Homo sapiens	121-125
22388075-5	2012	RESULTS: Treatment of K562 cells with imatinib (1-8 mumol/L) induced phosphorylation of H2AX at Ser139 and Tyr142 in time- and dose-dependent manners.	imatinib	38-46	H2A.X variant histone	Homo sapiens	88-92
22388075-7	2012	Meanwhile, imatinib (1-8 mumol/L) activated caspase-3 and its downstream mammalian STE20-like kinase 1 (Mst1), and induced apoptosis of K562 cells.	imatinib	11-19	caspase 3	Homo sapiens	44-53
22388075-7	2012	Meanwhile, imatinib (1-8 mumol/L) activated caspase-3 and its downstream mammalian STE20-like kinase 1 (Mst1), and induced apoptosis of K562 cells.	imatinib	11-19	macrophage stimulating 1	Homo sapiens	104-108
22388075-8	2012	The caspase-3 inhibitor Z-VAD (40 mumol/L) reduced imatinib-induced H2AX phosphorylation at Ser139 and Tyr142 and blocked imatinib-induced apoptosis of K562 cells.	imatinib	51-59	caspase 3	Homo sapiens	4-13
22388075-8	2012	The caspase-3 inhibitor Z-VAD (40 mumol/L) reduced imatinib-induced H2AX phosphorylation at Ser139 and Tyr142 and blocked imatinib-induced apoptosis of K562 cells.	imatinib	51-59	H2A.X variant histone	Homo sapiens	68-72
22388075-8	2012	The caspase-3 inhibitor Z-VAD (40 mumol/L) reduced imatinib-induced H2AX phosphorylation at Ser139 and Tyr142 and blocked imatinib-induced apoptosis of K562 cells.	imatinib	122-130	caspase 3	Homo sapiens	4-13
22388075-9	2012	Imatinib (4 mumol/L) induced expression of Williams-Beuren syndrome transcription factor (WSTF), but not wild-type p53-induced phosphatase 1 (Wip1) in K562 cells.	imatinib	0-8	bromodomain adjacent to zinc finger domain 1B	Homo sapiens	43-88
22388075-9	2012	Imatinib (4 mumol/L) induced expression of Williams-Beuren syndrome transcription factor (WSTF), but not wild-type p53-induced phosphatase 1 (Wip1) in K562 cells.	imatinib	0-8	bromodomain adjacent to zinc finger domain 1B	Homo sapiens	90-94
22388075-10	2012	CONCLUSION: The caspase-3/Mst1 pathway is required for H2AX C-terminal phosphorylation at Ser139 and Tyr142 and subsequent apoptosis in Bcr-Abl-positive K562 cells induced by imatinib.	imatinib	175-183	caspase 3	Homo sapiens	16-25
22388075-10	2012	CONCLUSION: The caspase-3/Mst1 pathway is required for H2AX C-terminal phosphorylation at Ser139 and Tyr142 and subsequent apoptosis in Bcr-Abl-positive K562 cells induced by imatinib.	imatinib	175-183	macrophage stimulating 1	Homo sapiens	26-30
22388075-10	2012	CONCLUSION: The caspase-3/Mst1 pathway is required for H2AX C-terminal phosphorylation at Ser139 and Tyr142 and subsequent apoptosis in Bcr-Abl-positive K562 cells induced by imatinib.	imatinib	175-183	H2A.X variant histone	Homo sapiens	55-59
21750117-2	2012	This study aimed to define safe doses of gemcitabine plus oxaliplatin when combined with imatinib (potent PDGFR-beta inhibitor) in patients with advanced gemcitabine-refractory pancreatic cancer (PC).	imatinib	89-97	platelet derived growth factor receptor beta	Homo sapiens	106-116
22203182-1	2012	BACKGROUND: Imatinib inhibits the KIT and PDGFR tyrosine kinases, resulting in its notable antitumor activity in gastrointestinal stromal tumor (GIST).	imatinib	12-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	34-37
22410759-10	2012	Imatinib has a therapeutic role in the presence of an imatinib-sensitive KIT mutation or in KITD816-unmutated patients.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
22410759-10	2012	Imatinib has a therapeutic role in the presence of an imatinib-sensitive KIT mutation or in KITD816-unmutated patients.	imatinib	54-62	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
22493373-2	2012	Imatinib mesylate (Gleevec( ), ST1571, Novartis Pharmaceuticals, Basel, Switzerland) is a selective inhibitor of break point cluster-Ableson (BCR-ABL), c-Kit, and platelet-derived growth factor receptor alpha (PDGFRalpha) tyrosine kinases.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	152-157
22493373-3	2012	Imatinib has been approved in the U.S. for the treatment of Philadelphia-chromosome positive chronic myeloid leukemia, KIT (CD117)-positive unresectable and metastatic malignant GIST and adjuvant treatment of adult patients following resection.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	119-122
22493373-3	2012	Imatinib has been approved in the U.S. for the treatment of Philadelphia-chromosome positive chronic myeloid leukemia, KIT (CD117)-positive unresectable and metastatic malignant GIST and adjuvant treatment of adult patients following resection.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	124-129
22482506-5	2012	However, deletion of beta-catenin synergizes with imatinib (IM) to delay disease recurrence after imatinib discontinuation and to abrogate CML stem cells.	imatinib	98-106	catenin (cadherin associated protein), beta 1	Mus musculus	21-33
22482506-8	2012	In conclusion, inhibiting beta-catenin by genetic inactivation or pharmacologic modulation is an effective combination therapy with imatinib and targets CML stem cells.	imatinib	132-140	catenin (cadherin associated protein), beta 1	Mus musculus	26-38
22014153-0	2012	Potent mechanism-based inhibition of CYP3A4 by imatinib explains its liability to interact with CYP3A4 substrates.	imatinib	47-55	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	37-43
22069079-7	2012	This device was also capable of quantifying inhibition of Bcr-Abl activity by imatinib mesylate, which demonstrates the potential to predict the biochemical response to drug inhibitors.	imatinib	78-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
22014153-7	2012	The time-dependent inhibition effect of imatinib was predicted to cause up to 90% inhibition of hepatic CYP3A4 activity with clinically relevant imatinib concentrations, whereas the direct inhibition was predicted to be negligible in vivo.	imatinib	40-48	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	104-110
22014153-7	2012	The time-dependent inhibition effect of imatinib was predicted to cause up to 90% inhibition of hepatic CYP3A4 activity with clinically relevant imatinib concentrations, whereas the direct inhibition was predicted to be negligible in vivo.	imatinib	145-153	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	104-110
22077498-0	2012	Increased natural killer cells and decreased CD3(+)CD8(+)CD62L(+) T cells in CML patients who sustained complete molecular remission after discontinuation of imatinib.	imatinib	158-166	CD8a molecule	Homo sapiens	51-54
22014153-0	2012	Potent mechanism-based inhibition of CYP3A4 by imatinib explains its liability to interact with CYP3A4 substrates.	imatinib	47-55	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	96-102
22077498-0	2012	Increased natural killer cells and decreased CD3(+)CD8(+)CD62L(+) T cells in CML patients who sustained complete molecular remission after discontinuation of imatinib.	imatinib	158-166	selectin L	Homo sapiens	57-62
22014153-8	2012	CONCLUSIONS AND IMPLICATIONS: Imatinib is a potent mechanism-based inhibitor of CYP3A4 in vitro and this finding explains the imatinib-simvastatin interaction and suggests that imatinib could markedly increase plasma concentrations of other CYP3A4 substrates.	imatinib	30-38	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	80-86
22014153-8	2012	CONCLUSIONS AND IMPLICATIONS: Imatinib is a potent mechanism-based inhibitor of CYP3A4 in vitro and this finding explains the imatinib-simvastatin interaction and suggests that imatinib could markedly increase plasma concentrations of other CYP3A4 substrates.	imatinib	30-38	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	241-247
22014153-8	2012	CONCLUSIONS AND IMPLICATIONS: Imatinib is a potent mechanism-based inhibitor of CYP3A4 in vitro and this finding explains the imatinib-simvastatin interaction and suggests that imatinib could markedly increase plasma concentrations of other CYP3A4 substrates.	imatinib	126-134	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	80-86
22014153-9	2012	Our results also suggest a possibility of autoinhibition of CYP3A4-mediated imatinib metabolism leading to a less significant role for CYP3A4 in imatinib biotransformation in vivo than previously proposed.	imatinib	76-84	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	60-66
22014153-1	2012	BACKGROUND AND PURPOSE: Imatinib, a cytochrome P450 2C8 (CYP2C8) and CYP3A4 substrate, markedly increases plasma concentrations of the CYP3A4/5 substrate simvastatin and reduces hepatic CYP3A4/5 activity in humans.	imatinib	24-32	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	36-55
22014153-1	2012	BACKGROUND AND PURPOSE: Imatinib, a cytochrome P450 2C8 (CYP2C8) and CYP3A4 substrate, markedly increases plasma concentrations of the CYP3A4/5 substrate simvastatin and reduces hepatic CYP3A4/5 activity in humans.	imatinib	24-32	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	57-63
22014153-1	2012	BACKGROUND AND PURPOSE: Imatinib, a cytochrome P450 2C8 (CYP2C8) and CYP3A4 substrate, markedly increases plasma concentrations of the CYP3A4/5 substrate simvastatin and reduces hepatic CYP3A4/5 activity in humans.	imatinib	24-32	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	69-75
22014153-1	2012	BACKGROUND AND PURPOSE: Imatinib, a cytochrome P450 2C8 (CYP2C8) and CYP3A4 substrate, markedly increases plasma concentrations of the CYP3A4/5 substrate simvastatin and reduces hepatic CYP3A4/5 activity in humans.	imatinib	24-32	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	135-141
22014153-9	2012	Our results also suggest a possibility of autoinhibition of CYP3A4-mediated imatinib metabolism leading to a less significant role for CYP3A4 in imatinib biotransformation in vivo than previously proposed.	imatinib	145-153	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	60-66
22014153-9	2012	Our results also suggest a possibility of autoinhibition of CYP3A4-mediated imatinib metabolism leading to a less significant role for CYP3A4 in imatinib biotransformation in vivo than previously proposed.	imatinib	145-153	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	135-141
23550446-8	2012	For example, patients with metastatic GIST and a duplication of KIT exon 9 should receive twice the usual dose of imatinib, while GIST with the PDGFRA p. D842 V mutation are resistant to imatinib.	imatinib	114-122	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	64-67
22014153-1	2012	BACKGROUND AND PURPOSE: Imatinib, a cytochrome P450 2C8 (CYP2C8) and CYP3A4 substrate, markedly increases plasma concentrations of the CYP3A4/5 substrate simvastatin and reduces hepatic CYP3A4/5 activity in humans.	imatinib	24-32	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	135-141
22014153-5	2012	KEY RESULTS: Inhibition of CYP3A4 activity by imatinib was pre-incubation time-, concentration- and NADPH-dependent, and the time-dependent inactivation variables K(I) and k(inact) were 14.3 microM and 0.072 in(-1) respectively.	imatinib	46-54	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	27-33
22285607-8	2012	These agents have demonstrated activity in patients harboring imatinib-resistant BCR-ABL mutations, except for the T315I substitution.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
22354538-6	2012	Here, we investigated seven different TKIs, gefitinib, erlotinib, AG1478, PD158780, PD153035, nilotinib and imatinib, for their potential to restore ABCG2 sensitivity to cells.	imatinib	108-116	ATP binding cassette subfamily G member 2	Canis lupus familiaris	149-154
22286373-3	2012	Some clinical trials have been conducted showing the ability of targeted therapies able to inhibit RET(sorafenib, imatinib, vandetanib) in stabilizing the course of the disease.	imatinib	114-122	ret proto-oncogene	Homo sapiens	99-102
22447844-1	2012	PURPOSE: The "gate-keeper" mutations T674I platelet-derived growth factor receptor alpha (PDGFRalpha) in hypereosinophilic syndrome (HES) and T315I Bcr-Abl in chronic myeloid leukemia (CML) are resistant to imatinib and the second-generation small-molecule tyrosine kinase inhibitors (TKI).	imatinib	207-215	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	90-100
21986839-0	2012	Development of acute myeloid leukemia with NPM1 mutation, in Ph-negative clone, during treatment of CML with imatinib.	imatinib	109-117	nucleophosmin 1	Homo sapiens	43-47
22211240-2	2012	In these patients, imatinib has been shown to induce an apoptotic response specifically in cells expressing the oncogenic fusion protein BCR-ABL.	imatinib	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-144
22211240-3	2012	Previous studies in our lab revealed that imatinib-induced apoptosis in K562 cells involves a shift in production of Bcl-x splice isoforms towards the pro-apoptotic Bcl-xs splice variant.	imatinib	42-50	BCL2 like 1	Homo sapiens	117-122
22381410-12	2012	Immunohistochemistry data suggest that GLUT4 may play a role in (18)F-FDG uptake in gastrointestinal stromal tumor, GLUT4 levels decrease after imatinib mesylate therapy in most patients with PMR, and the biologic action of imatinib mesylate interacts with glycolysis and GLUT4 expression.	imatinib	144-161	solute carrier family 2 member 4	Homo sapiens	39-44
22381410-12	2012	Immunohistochemistry data suggest that GLUT4 may play a role in (18)F-FDG uptake in gastrointestinal stromal tumor, GLUT4 levels decrease after imatinib mesylate therapy in most patients with PMR, and the biologic action of imatinib mesylate interacts with glycolysis and GLUT4 expression.	imatinib	144-161	solute carrier family 2 member 4	Homo sapiens	116-121
22381410-12	2012	Immunohistochemistry data suggest that GLUT4 may play a role in (18)F-FDG uptake in gastrointestinal stromal tumor, GLUT4 levels decrease after imatinib mesylate therapy in most patients with PMR, and the biologic action of imatinib mesylate interacts with glycolysis and GLUT4 expression.	imatinib	144-161	solute carrier family 2 member 4	Homo sapiens	116-121
22381410-12	2012	Immunohistochemistry data suggest that GLUT4 may play a role in (18)F-FDG uptake in gastrointestinal stromal tumor, GLUT4 levels decrease after imatinib mesylate therapy in most patients with PMR, and the biologic action of imatinib mesylate interacts with glycolysis and GLUT4 expression.	imatinib	224-241	solute carrier family 2 member 4	Homo sapiens	39-44
22033489-5	2012	Combination of ABT-737 with imatinib (which decreases Mcl-1 levels) or triptolide (which decreases Mcl-1 and XIAP) synergistically induced death of both proliferating and quiescent CD34(+) progenitor cells obtained from TKI-resistant BC CML patients.	imatinib	28-36	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	54-59
22033489-5	2012	Combination of ABT-737 with imatinib (which decreases Mcl-1 levels) or triptolide (which decreases Mcl-1 and XIAP) synergistically induced death of both proliferating and quiescent CD34(+) progenitor cells obtained from TKI-resistant BC CML patients.	imatinib	28-36	CD34 molecule	Homo sapiens	181-185
22462553-0	2012	STI571 reduces TRAIL-induced apoptosis in colon cancer cells: c-Abl activation by the death receptor leads to stress kinase-dependent cell death.	imatinib	0-6	TNF superfamily member 10	Homo sapiens	15-20
22300707-0	2012	Imatinib mesylate prevents cerebral vasospasm after subarachnoid hemorrhage via inhibiting tenascin-C expression in rats.	imatinib	0-17	tenascin C	Rattus norvegicus	91-101
22300707-2	2012	The purpose of this study was to assess whether imatinib mesylate (imatinib), an inhibitor of the tyrosine kinases of PDGF receptors (PDGFRs), prevents cerebral vasospasm after SAH in rats, and to elucidate if tenascin-C (TNC), a matricellular protein, is involved in the mechanism.	imatinib	48-65	tenascin C	Rattus norvegicus	210-220
22300707-2	2012	The purpose of this study was to assess whether imatinib mesylate (imatinib), an inhibitor of the tyrosine kinases of PDGF receptors (PDGFRs), prevents cerebral vasospasm after SAH in rats, and to elucidate if tenascin-C (TNC), a matricellular protein, is involved in the mechanism.	imatinib	48-65	tenascin C	Rattus norvegicus	222-225
22300707-2	2012	The purpose of this study was to assess whether imatinib mesylate (imatinib), an inhibitor of the tyrosine kinases of PDGF receptors (PDGFRs), prevents cerebral vasospasm after SAH in rats, and to elucidate if tenascin-C (TNC), a matricellular protein, is involved in the mechanism.	imatinib	48-56	tenascin C	Rattus norvegicus	210-220
22300707-2	2012	The purpose of this study was to assess whether imatinib mesylate (imatinib), an inhibitor of the tyrosine kinases of PDGF receptors (PDGFRs), prevents cerebral vasospasm after SAH in rats, and to elucidate if tenascin-C (TNC), a matricellular protein, is involved in the mechanism.	imatinib	48-56	tenascin C	Rattus norvegicus	222-225
22300707-5	2012	Recombinant TNC was administered intracisternally to imatinib-treated SAH rats, and the effects were evaluated by neurobehavioral tests, India-ink angiography and immunohistochemistry at 24 h post-SAH.	imatinib	53-61	tenascin C	Rattus norvegicus	12-15
22300707-6	2012	Both dosages of imatinib significantly prevented post-SAH neurological impairments and vasospasm at 24-72 h. SAH caused PDGFR-beta upregulation, PDGFR activation, mitogen-activated protein kinase activation, and TNC upregulation in the spastic cerebral arteries, all of which were significantly suppressed by imatinib treatment.	imatinib	16-24	platelet derived growth factor receptor beta	Rattus norvegicus	120-130
22300707-6	2012	Both dosages of imatinib significantly prevented post-SAH neurological impairments and vasospasm at 24-72 h. SAH caused PDGFR-beta upregulation, PDGFR activation, mitogen-activated protein kinase activation, and TNC upregulation in the spastic cerebral arteries, all of which were significantly suppressed by imatinib treatment.	imatinib	16-24	tenascin C	Rattus norvegicus	212-215
22300707-7	2012	Recombinant TNC reversed the anti-vasospastic effects and protein expression changes by imatinib.	imatinib	88-96	tenascin C	Rattus norvegicus	12-15
22300707-8	2012	This study suggests that imatinib prevents cerebral vasospasm at least partly via inhibiting the upregulation of TNC, implying that TNC may be a new therapeutic target for post-SAH vasospasm.	imatinib	25-33	tenascin C	Rattus norvegicus	113-116
22300707-8	2012	This study suggests that imatinib prevents cerebral vasospasm at least partly via inhibiting the upregulation of TNC, implying that TNC may be a new therapeutic target for post-SAH vasospasm.	imatinib	25-33	tenascin C	Rattus norvegicus	132-135
22880266-8	2012	Biological therapy with imatinib mesylate is recommended in patients with newly diagnosed, locally advanced, inoperable, or metastasizing gastrointestinal GISTs that express the c-KIT protein.	imatinib	24-41	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	178-183
22541073-0	2012	[Suppression of NAMPT expression enhances the sensitivity of K562 cells to imatinib and its relative mechanism].	imatinib	75-83	nicotinamide phosphoribosyltransferase	Homo sapiens	16-21
22541073-1	2012	The aim of this study was to investigate the effect of suppression of nicotinamide phosphoribosyltransferase (NAMPT) expression on imatinib-sensitivity in chronic myelogenous leukemia (CML) cell line K562 and its mechanisms, NAMPT siRNA was synthesized and transfected into K562 cells.	imatinib	131-139	nicotinamide phosphoribosyltransferase	Homo sapiens	70-108
22541073-1	2012	The aim of this study was to investigate the effect of suppression of nicotinamide phosphoribosyltransferase (NAMPT) expression on imatinib-sensitivity in chronic myelogenous leukemia (CML) cell line K562 and its mechanisms, NAMPT siRNA was synthesized and transfected into K562 cells.	imatinib	131-139	nicotinamide phosphoribosyltransferase	Homo sapiens	110-115
22541073-1	2012	The aim of this study was to investigate the effect of suppression of nicotinamide phosphoribosyltransferase (NAMPT) expression on imatinib-sensitivity in chronic myelogenous leukemia (CML) cell line K562 and its mechanisms, NAMPT siRNA was synthesized and transfected into K562 cells.	imatinib	131-139	nicotinamide phosphoribosyltransferase	Homo sapiens	225-230
22541073-4	2012	Expression of NAMPT at 3rd-48th hour after exposure to 1 micromol/L imatinib was determined by Western blot.	imatinib	68-76	nicotinamide phosphoribosyltransferase	Homo sapiens	14-19
22541073-9	2012	After exposure to 1 micromol/L of imatinib for 48 h, the survival rate of NAMPT-siRNA interference group was lower than that of negative control group (P < 0.05), indicating that suppression of NAMPT expression can increase the sensitivity of K562 cells to imatinib and enhance the killing effect of imatinib on K562 cells.	imatinib	34-42	nicotinamide phosphoribosyltransferase	Homo sapiens	74-79
22541073-9	2012	After exposure to 1 micromol/L of imatinib for 48 h, the survival rate of NAMPT-siRNA interference group was lower than that of negative control group (P < 0.05), indicating that suppression of NAMPT expression can increase the sensitivity of K562 cells to imatinib and enhance the killing effect of imatinib on K562 cells.	imatinib	34-42	nicotinamide phosphoribosyltransferase	Homo sapiens	197-202
22541073-9	2012	After exposure to 1 micromol/L of imatinib for 48 h, the survival rate of NAMPT-siRNA interference group was lower than that of negative control group (P < 0.05), indicating that suppression of NAMPT expression can increase the sensitivity of K562 cells to imatinib and enhance the killing effect of imatinib on K562 cells.	imatinib	260-268	nicotinamide phosphoribosyltransferase	Homo sapiens	74-79
22541073-9	2012	After exposure to 1 micromol/L of imatinib for 48 h, the survival rate of NAMPT-siRNA interference group was lower than that of negative control group (P < 0.05), indicating that suppression of NAMPT expression can increase the sensitivity of K562 cells to imatinib and enhance the killing effect of imatinib on K562 cells.	imatinib	260-268	nicotinamide phosphoribosyltransferase	Homo sapiens	197-202
22541073-9	2012	After exposure to 1 micromol/L of imatinib for 48 h, the survival rate of NAMPT-siRNA interference group was lower than that of negative control group (P < 0.05), indicating that suppression of NAMPT expression can increase the sensitivity of K562 cells to imatinib and enhance the killing effect of imatinib on K562 cells.	imatinib	260-268	nicotinamide phosphoribosyltransferase	Homo sapiens	74-79
22541073-9	2012	After exposure to 1 micromol/L of imatinib for 48 h, the survival rate of NAMPT-siRNA interference group was lower than that of negative control group (P < 0.05), indicating that suppression of NAMPT expression can increase the sensitivity of K562 cells to imatinib and enhance the killing effect of imatinib on K562 cells.	imatinib	260-268	nicotinamide phosphoribosyltransferase	Homo sapiens	197-202
22541073-10	2012	The IC(50) of imatinib in NAMPT-siRNA interference group was the lowest compared with that of control group (P < 0.05) after exposure to different concentrations of imatinib for 48 h, the fitted survival curves showed that the slope of NAMPT-siRNA interference group was the largest ranging between 0.01 - 0.1 micromol/L of imatinib.	imatinib	14-22	nicotinamide phosphoribosyltransferase	Homo sapiens	26-31
22541073-10	2012	The IC(50) of imatinib in NAMPT-siRNA interference group was the lowest compared with that of control group (P < 0.05) after exposure to different concentrations of imatinib for 48 h, the fitted survival curves showed that the slope of NAMPT-siRNA interference group was the largest ranging between 0.01 - 0.1 micromol/L of imatinib.	imatinib	14-22	nicotinamide phosphoribosyltransferase	Homo sapiens	239-244
22541073-10	2012	The IC(50) of imatinib in NAMPT-siRNA interference group was the lowest compared with that of control group (P < 0.05) after exposure to different concentrations of imatinib for 48 h, the fitted survival curves showed that the slope of NAMPT-siRNA interference group was the largest ranging between 0.01 - 0.1 micromol/L of imatinib.	imatinib	168-176	nicotinamide phosphoribosyltransferase	Homo sapiens	26-31
22541073-10	2012	The IC(50) of imatinib in NAMPT-siRNA interference group was the lowest compared with that of control group (P < 0.05) after exposure to different concentrations of imatinib for 48 h, the fitted survival curves showed that the slope of NAMPT-siRNA interference group was the largest ranging between 0.01 - 0.1 micromol/L of imatinib.	imatinib	168-176	nicotinamide phosphoribosyltransferase	Homo sapiens	26-31
22541073-11	2012	Data mining of expression profiling indicated that the anti-apoptotic factor Bcl-2 decreased in K562 cells treated with either NAMPT-siRNA or imatinib, which was confirmed by Western blot.	imatinib	142-150	BCL2 apoptosis regulator	Homo sapiens	77-82
22541073-16	2012	When expression of NAMPT decreases, the K562 cells are more sensitive to imatinib, this may be related with the decreased transcriptional activity of NF-kappaB and its downstream effector Bcl-2.	imatinib	73-81	nicotinamide phosphoribosyltransferase	Homo sapiens	19-24
22541073-16	2012	When expression of NAMPT decreases, the K562 cells are more sensitive to imatinib, this may be related with the decreased transcriptional activity of NF-kappaB and its downstream effector Bcl-2.	imatinib	73-81	BCL2 apoptosis regulator	Homo sapiens	188-193
22462553-0	2012	STI571 reduces TRAIL-induced apoptosis in colon cancer cells: c-Abl activation by the death receptor leads to stress kinase-dependent cell death.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-67
22462553-1	2012	BACKGROUND: In an effort to achieve better cancer therapies, we elucidated the combination cancer therapy of STI571 (an inhibitor of Bcr-Abl and clinically used for chronic myelogenous leukemia) and TNF-related apoptosis-inducing ligand (TRAIL, a developing antitumor agent) in leukemia, colon, and prostate cancer cells.	imatinib	109-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
22462553-1	2012	BACKGROUND: In an effort to achieve better cancer therapies, we elucidated the combination cancer therapy of STI571 (an inhibitor of Bcr-Abl and clinically used for chronic myelogenous leukemia) and TNF-related apoptosis-inducing ligand (TRAIL, a developing antitumor agent) in leukemia, colon, and prostate cancer cells.	imatinib	109-115	TNF superfamily member 10	Homo sapiens	238-243
22462553-11	2012	Next, we found that STI571 could attenuate TRAIL-induced c-Abl, JNK and p38 activation in HCT116 cells.	imatinib	20-26	TNF superfamily member 10	Homo sapiens	43-48
22462553-11	2012	Next, we found that STI571 could attenuate TRAIL-induced c-Abl, JNK and p38 activation in HCT116 cells.	imatinib	20-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-62
22462553-11	2012	Next, we found that STI571 could attenuate TRAIL-induced c-Abl, JNK and p38 activation in HCT116 cells.	imatinib	20-26	mitogen-activated protein kinase 8	Homo sapiens	64-67
22458888-0	2012	A comparative proteomic study identified LRPPRC and MCM7 as putative actors in imatinib mesylate cross-resistance in Lucena cell line.	imatinib	79-87	leucine rich pentatricopeptide repeat containing	Homo sapiens	41-47
22462553-11	2012	Next, we found that STI571 could attenuate TRAIL-induced c-Abl, JNK and p38 activation in HCT116 cells.	imatinib	20-26	CRK proto-oncogene, adaptor protein	Homo sapiens	72-75
22462553-12	2012	In addition, siRNA targeting knockdown of c-Abl and p73 also reduced TRAIL-induced cytotoxicity, rendering HCT116 cells less responsive to stress kinase activation, and masking the cytoprotective effect of STI571.	imatinib	206-212	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-47
22458888-0	2012	A comparative proteomic study identified LRPPRC and MCM7 as putative actors in imatinib mesylate cross-resistance in Lucena cell line.	imatinib	79-87	minichromosome maintenance complex component 7	Homo sapiens	52-56
22462553-12	2012	In addition, siRNA targeting knockdown of c-Abl and p73 also reduced TRAIL-induced cytotoxicity, rendering HCT116 cells less responsive to stress kinase activation, and masking the cytoprotective effect of STI571.	imatinib	206-212	tumor protein p73	Homo sapiens	52-55
22337716-0	2012	Imatinib mesylate directly impairs class switch recombination through down-regulation of AID: its potential efficacy as an AID suppressor.	imatinib	0-17	activation induced cytidine deaminase	Homo sapiens	89-92
22337716-0	2012	Imatinib mesylate directly impairs class switch recombination through down-regulation of AID: its potential efficacy as an AID suppressor.	imatinib	0-17	activation induced cytidine deaminase	Homo sapiens	123-126
22462553-12	2012	In addition, siRNA targeting knockdown of c-Abl and p73 also reduced TRAIL-induced cytotoxicity, rendering HCT116 cells less responsive to stress kinase activation, and masking the cytoprotective effect of STI571.	imatinib	206-212	TNF superfamily member 10	Homo sapiens	69-74
22462553-15	2012	Through the inhibition of c-Abl-mediated apoptotic p73 signaling, STI571 reduces the antitumor activity of TRAIL in colon cancer cells.	imatinib	66-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-31
22462553-15	2012	Through the inhibition of c-Abl-mediated apoptotic p73 signaling, STI571 reduces the antitumor activity of TRAIL in colon cancer cells.	imatinib	66-72	tumor protein p73	Homo sapiens	51-54
22462553-15	2012	Through the inhibition of c-Abl-mediated apoptotic p73 signaling, STI571 reduces the antitumor activity of TRAIL in colon cancer cells.	imatinib	66-72	TNF superfamily member 10	Homo sapiens	107-112
21823110-4	2012	METHODS: Imatinib mesylate (IM) blocks CSF1R, and previous case reports indicated that it also exerts antitumor activity in PVNS.	imatinib	9-26	colony stimulating factor 1 receptor	Homo sapiens	39-44
22331945-1	2012	PURPOSE: To explore the antitumor activity of imatinib in patients with advanced platelet-derived growth factor beta (PDGFB)/PDGF receptor beta (PDGFRB)-positive chordomas.	imatinib	46-54	platelet derived growth factor subunit B	Homo sapiens	118-123
22331945-1	2012	PURPOSE: To explore the antitumor activity of imatinib in patients with advanced platelet-derived growth factor beta (PDGFB)/PDGF receptor beta (PDGFRB)-positive chordomas.	imatinib	46-54	platelet derived growth factor receptor beta	Homo sapiens	145-151
22282465-0	2012	KRAS and BRAF mutations predict primary resistance to imatinib in gastrointestinal stromal tumors.	imatinib	54-62	KRAS proto-oncogene, GTPase	Homo sapiens	0-4
22282465-0	2012	KRAS and BRAF mutations predict primary resistance to imatinib in gastrointestinal stromal tumors.	imatinib	54-62	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	9-13
22282465-1	2012	PURPOSE: Gastrointestinal stromal tumors (GIST) are characterized by gain-of-function mutations in KIT/PDGFRA genes leading to a constitutive receptor activation which is well counteracted by imatinib.	imatinib	192-200	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	99-102
22282465-1	2012	PURPOSE: Gastrointestinal stromal tumors (GIST) are characterized by gain-of-function mutations in KIT/PDGFRA genes leading to a constitutive receptor activation which is well counteracted by imatinib.	imatinib	192-200	platelet derived growth factor receptor alpha	Homo sapiens	103-109
22282465-5	2012	Cell lines expressing a constitutively activated and imatinib-responding KIT, alone or in combination with activated KRAS and BRAF, were produced and treated with imatinib.	imatinib	53-61	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
22282465-5	2012	Cell lines expressing a constitutively activated and imatinib-responding KIT, alone or in combination with activated KRAS and BRAF, were produced and treated with imatinib.	imatinib	163-171	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
21804606-4	2012	Here, we show that the glucocorticoid-induced leucine zipper protein (GILZ) modulates imatinib and dasatinib resistance and suppresses tumor growth by inactivating the mammalian target of rapamycin complex-2 (mTORC2)/AKT signaling pathway.	imatinib	86-94	TSC22 domain family member 3	Homo sapiens	23-68
21804606-4	2012	Here, we show that the glucocorticoid-induced leucine zipper protein (GILZ) modulates imatinib and dasatinib resistance and suppresses tumor growth by inactivating the mammalian target of rapamycin complex-2 (mTORC2)/AKT signaling pathway.	imatinib	86-94	TSC22 domain family member 3	Homo sapiens	70-74
22282465-8	2012	In vitro experiments showed that imatinib was able to switch off the mutated receptor KIT but not the downstream signaling triggered by RAS-RAF effectors.	imatinib	33-41	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	86-89
21804606-4	2012	Here, we show that the glucocorticoid-induced leucine zipper protein (GILZ) modulates imatinib and dasatinib resistance and suppresses tumor growth by inactivating the mammalian target of rapamycin complex-2 (mTORC2)/AKT signaling pathway.	imatinib	86-94	CREB regulated transcription coactivator 2	Mus musculus	209-215
22285130-9	2012	Increased EGFR expression was associated with gefitinib response; increased PDGFR-alpha expression was associated with imatinib response.	imatinib	119-127	platelet derived growth factor receptor alpha	Homo sapiens	76-87
21804606-4	2012	Here, we show that the glucocorticoid-induced leucine zipper protein (GILZ) modulates imatinib and dasatinib resistance and suppresses tumor growth by inactivating the mammalian target of rapamycin complex-2 (mTORC2)/AKT signaling pathway.	imatinib	86-94	AKT serine/threonine kinase 1	Homo sapiens	217-220
21804606-6	2012	Furthermore, CD34(+) stem cells isolated from relapsing CML patients underwent apoptosis and showed inhibition of mTORC2 after incubation with glucocorticoids and imatinib.	imatinib	163-171	CD34 molecule	Homo sapiens	13-17
21804606-6	2012	Furthermore, CD34(+) stem cells isolated from relapsing CML patients underwent apoptosis and showed inhibition of mTORC2 after incubation with glucocorticoids and imatinib.	imatinib	163-171	CREB regulated transcription coactivator 2	Mus musculus	114-120
21544849-1	2012	The BCR-ABL inhibitor imatinib is a standard first-line therapy for patients with chronic myeloid leukemia.	imatinib	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
22210874-1	2012	Specific imatinib-resistant BCR-ABL1 mutations (Y253H, E255K/V, T315I, F317L, and F359V/C) predict failure of second-line nilotinib or dasatinib therapy in patients with chronic myeloid leukemia; however, such therapy also fails in approximately 40% of patients in the chronic phase of this disease who do not have these resistant mutations.	imatinib	9-17	BCR activator of RhoGEF and GTPase	Homo sapiens	28-36
22266405-1	2012	OBJECTIVES: Within the laboratory protocols, used for the study of BCR-ABL resistance mutations in chronic myeloid leukemia patients treated with Imatinib, direct sequencing remains the reference method.	imatinib	146-154	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
22691216-2	2012	An important downstream target of TGF-beta is the Abelson (c-Abl) tyrosine kinase, and its inhibition by imatinib mesylate (Gleevec) attenuates fibrosis in mice.	imatinib	105-122	transforming growth factor, beta 1	Mus musculus	34-42
22691216-2	2012	An important downstream target of TGF-beta is the Abelson (c-Abl) tyrosine kinase, and its inhibition by imatinib mesylate (Gleevec) attenuates fibrosis in mice.	imatinib	105-122	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	59-64
22691216-6	2012	RESULTS: Treatment of control fibroblasts with TGF-beta resulted in activation of c-Abl and stimulation of fibrotic gene expression that was prevented by imatinib.	imatinib	154-162	transforming growth factor beta 1	Homo sapiens	47-55
22691216-6	2012	RESULTS: Treatment of control fibroblasts with TGF-beta resulted in activation of c-Abl and stimulation of fibrotic gene expression that was prevented by imatinib.	imatinib	154-162	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-87
22262776-0	2012	Targeting of GSK3beta promotes imatinib-mediated apoptosis in quiescent CD34+ chronic myeloid leukemia progenitors, preserving normal stem cells.	imatinib	31-39	glycogen synthase kinase 3 beta	Homo sapiens	13-21
22262776-0	2012	Targeting of GSK3beta promotes imatinib-mediated apoptosis in quiescent CD34+ chronic myeloid leukemia progenitors, preserving normal stem cells.	imatinib	31-39	CD34 molecule	Homo sapiens	72-76
22262776-5	2012	Specifically, GSK3beta activity and nuclear import were increased by imatinib mesylate (IM), a selective ABL inhibitor, but prevented by dasatinib that targets both BCR-ABL- and cytokine-dependent MAPK/p60-SRC activity.	imatinib	69-86	glycogen synthase kinase 3 beta	Homo sapiens	14-22
22262776-5	2012	Specifically, GSK3beta activity and nuclear import were increased by imatinib mesylate (IM), a selective ABL inhibitor, but prevented by dasatinib that targets both BCR-ABL- and cytokine-dependent MAPK/p60-SRC activity.	imatinib	69-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-108
22262776-5	2012	Specifically, GSK3beta activity and nuclear import were increased by imatinib mesylate (IM), a selective ABL inhibitor, but prevented by dasatinib that targets both BCR-ABL- and cytokine-dependent MAPK/p60-SRC activity.	imatinib	69-86	sequestosome 1	Homo sapiens	202-205
22369443-6	2012	In addition, patients with documented KIT exon 9 mutations are likely to derive benefit from initial treatment with high-dose imatinib to improve clinical outcomes.	imatinib	126-134	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	38-41
22369443-8	2012	However, the decision to use either high-dose imatinib or sunitinib should be based on the underlying cause of failure on imatinib, KIT mutational status and on whether the patient is intolerant of or has developed a resistance to imatinib.	imatinib	46-54	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	132-135
22453014-5	2012	Nevertheless, case reports continued to surface that demonstrated the remarkable efficacy of imatinib for patients with specific KIT genetic aberrations.	imatinib	93-101	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	129-132
22453014-6	2012	Recently, trials of imatinib have selected patients with KIT genetic aberrations and have shown promising results.	imatinib	20-28	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	57-60
21773872-6	2012	K562/CCN3 cells exposed to Imatinib (1 muM and 5 muM) showed an increase in events within the subG(0) phase of cell cycle over 96 h and mirrored the enhanced cell kill demonstrated by Annexin staining.	imatinib	27-35	cellular communication network factor 3	Homo sapiens	5-9
21773872-6	2012	K562/CCN3 cells exposed to Imatinib (1 muM and 5 muM) showed an increase in events within the subG(0) phase of cell cycle over 96 h and mirrored the enhanced cell kill demonstrated by Annexin staining.	imatinib	27-35	latexin	Homo sapiens	39-42
21773872-6	2012	K562/CCN3 cells exposed to Imatinib (1 muM and 5 muM) showed an increase in events within the subG(0) phase of cell cycle over 96 h and mirrored the enhanced cell kill demonstrated by Annexin staining.	imatinib	27-35	latexin	Homo sapiens	49-52
21773872-7	2012	Wild type K562 cells treated with recombinant human Ccn3 (10 nM) in combination with Imatinib (5 muM) also displayed enhanced cell kill (p = 0.008).	imatinib	85-93	latexin	Homo sapiens	97-100
21773872-9	2012	CCN3 restores cellular growth regulatory properties that are absent in CML and sensitises CML cells to imatinib induced apoptosis.	imatinib	103-111	cellular communication network factor 3	Homo sapiens	0-4
22083669-5	2012	Imatinib, a small molecule of tyrosine kinase inhibitor, effectively inhibited autophosphorylation of KIT-Tyr552Cys.	imatinib	0-8	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	102-105
22238384-10	2012	Finally, in particular imatinib mesylate and PDGF-BB-neutralizing antibodies reduced IL-6 and hyaluronan production by whole orbital tissue cultures from GO patients.	imatinib	23-40	interleukin 6	Homo sapiens	85-89
22083669-7	2012	In fact, proliferation of Ba/F3 cells expressing KIT-Tyr552Cys was effectively inhibited by both imatinib and nilotinib.	imatinib	97-105	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	49-52
21886172-1	2012	Imatinib is a substrate for hOCT1 (SLC22A1) and inhibitors of this influx transporter, such as amantadine and prazosin, have previously been shown to decrease cellular imatinib uptake.	imatinib	0-8	solute carrier family 22 member 1	Homo sapiens	28-33
21221851-0	2012	BCR-ABL isoforms associated with intrinsic or acquired resistance to imatinib: more heterogeneous than just ABL kinase domain point mutations?	imatinib	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
22083669-8	2012	These findings indicate that the novel type human KIT-Tyr553Cys mutation is the cause of the present familial and multiple GISTs, and that both imatinib and nilotinib might effectively inhibit the growth of GISTs developing in the patients of this family.	imatinib	144-152	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	50-53
21221851-0	2012	BCR-ABL isoforms associated with intrinsic or acquired resistance to imatinib: more heterogeneous than just ABL kinase domain point mutations?	imatinib	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
21221851-1	2012	Imatinib, a small molecule inhibitor of ABL, PDGFR and C-KIT, has revolutionized treatment of chronic myeloid leukaemia (CML).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-43
21886172-1	2012	Imatinib is a substrate for hOCT1 (SLC22A1) and inhibitors of this influx transporter, such as amantadine and prazosin, have previously been shown to decrease cellular imatinib uptake.	imatinib	0-8	solute carrier family 22 member 1	Homo sapiens	35-42
21886172-1	2012	Imatinib is a substrate for hOCT1 (SLC22A1) and inhibitors of this influx transporter, such as amantadine and prazosin, have previously been shown to decrease cellular imatinib uptake.	imatinib	168-176	solute carrier family 22 member 1	Homo sapiens	28-33
22781602-21	2012	Imatinib concentration was regulated by AGP and the activities of hOCT1 and ABCB1.	imatinib	0-8	solute carrier family 22 member 1	Homo sapiens	66-71
21886172-1	2012	Imatinib is a substrate for hOCT1 (SLC22A1) and inhibitors of this influx transporter, such as amantadine and prazosin, have previously been shown to decrease cellular imatinib uptake.	imatinib	168-176	solute carrier family 22 member 1	Homo sapiens	35-42
22133064-8	2012	Co-culturing CCA cells with PDGF-BB-secreting MFBs significantly decreased TRAIL-induced CCA cell apoptosis when compared with monoculture conditions; this cytoprotective effect was abrogated in the presence of the tyrosine kinase inhibitors imatinib mesylate or linifanib, which inhibit PDGFR-beta.	imatinib	242-259	TNF superfamily member 10	Homo sapiens	75-80
22241070-5	2012	RESULTS: Although ABCB1 protein was not expressed, ABCG2 protein was 7.2-fold elevated after long-term treatment with 0.3 micromol/l imatinib and decreased gradually at higher concentrations.	imatinib	133-141	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	51-56
22241070-10	2012	CONCLUSION: Our study suggests an association of imatinib treatment, miRNA downregulation and ABCG2 overexpression, possibly contributing to the mechanisms involved in imatinib distribution and response in CML therapy.	imatinib	49-57	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	94-99
22241070-10	2012	CONCLUSION: Our study suggests an association of imatinib treatment, miRNA downregulation and ABCG2 overexpression, possibly contributing to the mechanisms involved in imatinib distribution and response in CML therapy.	imatinib	168-176	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	94-99
21221851-1	2012	Imatinib, a small molecule inhibitor of ABL, PDGFR and C-KIT, has revolutionized treatment of chronic myeloid leukaemia (CML).	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	45-50
21221851-1	2012	Imatinib, a small molecule inhibitor of ABL, PDGFR and C-KIT, has revolutionized treatment of chronic myeloid leukaemia (CML).	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	55-60
21221851-9	2012	We conclude that Abl KD point mutations represent a major mechanism of imatinib resistance.	imatinib	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-20
21221851-11	2012	Diagnostic strategies looking for imatinib-resistant clones should be designed to detect a broader profile of BCR-ABL variants than just point mutations.	imatinib	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
22678007-0	2012	High-risk CD117-positive gastrointestinal stromal tumor of the colon in a 12-year-old girl:  adjuvant treatment with imatinib mesylate.	imatinib	117-134	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	10-15
22800481-10	2012	CONCLUSIONS: Human GIST xenografts with mutation in c-kit have been established from imatinib-resistant GIST lines.	imatinib	85-93	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	52-57
22454169-10	2012	CONCLUSION: Imatinib is effective in treating patients with advanced GIST, c-kit exon 9 mutations and poor performance status predict an adverse survival benefit of imatinib therapy.	imatinib	165-173	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	75-80
22780968-2	2012	METHODS: Different methylation status of PU.1 promoter region containing 20 CpG islands in normal individuals, CML chronic phase and blast crisis patients, complete cytogenetic remission patients after imatinib treatment, and blast crisis bone marrow K562 CML cells was detected by bisulfite sequencing.	imatinib	202-210	Spi-1 proto-oncogene	Homo sapiens	41-45
22781602-21	2012	Imatinib concentration was regulated by AGP and the activities of hOCT1 and ABCB1.	imatinib	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	76-81
22134106-0	2012	ABCB1 haplotype is associated with major molecular response in chronic myeloid leukemia patients treated with standard-dose of imatinib.	imatinib	127-135	ATP binding cassette subfamily B member 1	Homo sapiens	0-5
22100984-7	2012	Imatinib, a PDGFR inhibitor, significantly enhanced the anti-proliferative effect of ZM447439, an Aurora B specific inhibitor, and PHA-739358, a pan-Aurora kinase inhibitor.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	12-17
22100984-7	2012	Imatinib, a PDGFR inhibitor, significantly enhanced the anti-proliferative effect of ZM447439, an Aurora B specific inhibitor, and PHA-739358, a pan-Aurora kinase inhibitor.	imatinib	0-8	aurora kinase B	Homo sapiens	98-106
22207735-5	2012	Imatinib-mediated inhibition of BCR-ABL kinase activity partially reduces SIRT1 expression and SIRT1 inhibition further sensitizes CML cells to imatinib-induced apoptosis.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
22207735-5	2012	Imatinib-mediated inhibition of BCR-ABL kinase activity partially reduces SIRT1 expression and SIRT1 inhibition further sensitizes CML cells to imatinib-induced apoptosis.	imatinib	0-8	sirtuin 1	Mus musculus	74-79
22207735-5	2012	Imatinib-mediated inhibition of BCR-ABL kinase activity partially reduces SIRT1 expression and SIRT1 inhibition further sensitizes CML cells to imatinib-induced apoptosis.	imatinib	0-8	sirtuin 1	Mus musculus	95-100
22207735-5	2012	Imatinib-mediated inhibition of BCR-ABL kinase activity partially reduces SIRT1 expression and SIRT1 inhibition further sensitizes CML cells to imatinib-induced apoptosis.	imatinib	144-152	sirtuin 1	Mus musculus	95-100
22280319-4	2012	On the basis of the reconstruction of the free energy surfaces for the DFG-in to DFG-out conformational changes of c-Src and c-Abl, we propose that the different flexibility of the two kinases results in a different stability of the DFG-out conformation and might be the main determinant of imatinib selectivity.	imatinib	291-299	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	115-120
22340598-0	2012	Activation of p53 by SIRT1 inhibition enhances elimination of CML leukemia stem cells in combination with imatinib.	imatinib	106-114	tumor protein p53	Homo sapiens	14-17
22340598-5	2012	SIRT1 effects were enhanced in combination with the BCR-ABL TKI imatinib.	imatinib	64-72	sirtuin 1	Homo sapiens	0-5
22340598-5	2012	SIRT1 effects were enhanced in combination with the BCR-ABL TKI imatinib.	imatinib	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
21911014-1	2012	The anticancer drug imatinib is an inhibitor of the platelet-derived growth factor receptor (PDGFR) kinases, which are involved in the pathogenesis of fibrotic diseases.	imatinib	20-28	platelet derived growth factor receptor, beta polypeptide	Mus musculus	52-91
21911014-1	2012	The anticancer drug imatinib is an inhibitor of the platelet-derived growth factor receptor (PDGFR) kinases, which are involved in the pathogenesis of fibrotic diseases.	imatinib	20-28	platelet derived growth factor receptor, beta polypeptide	Mus musculus	93-98
21911014-11	2012	Further evaluation of imatinib mesylate and imatinib-ULS-lysozyme is therefore warranted in an animal model of renal disease in which the activation of PDGFR-beta is more pronounced.	imatinib	22-30	platelet derived growth factor receptor, beta polypeptide	Mus musculus	152-162
22280319-4	2012	On the basis of the reconstruction of the free energy surfaces for the DFG-in to DFG-out conformational changes of c-Src and c-Abl, we propose that the different flexibility of the two kinases results in a different stability of the DFG-out conformation and might be the main determinant of imatinib selectivity.	imatinib	291-299	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-130
22160483-1	2012	Dasatinib is a highly potent BCR-ABL inhibitor with established efficacy and safety in imatinib-resistant/-intolerant patients with chronic myeloid leukemia (CML).	imatinib	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
22160483-5	2012	Cumulative response rates by 24 months in dasatinib and imatinib arms were: CCyR in 86% versus 82%, MMR in 64% versus 46%, and BCR-ABL reduction to <= 0.0032% (4.5-log reduction) in 17% versus 8%.	imatinib	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
22233429-1	2012	Dasatinib (Sprycel ) is an orally administered small molecule inhibitor of multiple tyrosine kinases, including BCR-ABL and SRC family kinases, which is indicated for the treatment of adults with newly diagnosed chronic-phase chronic myeloid leukemia (CML), CML (chronic-, accelerated- or blast-phase) with resistance or intolerance to prior therapy, including imatinib, or Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL) with resistance or intolerance to prior therapy.	imatinib	361-369	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
22233429-2	2012	Dasatinib is  325-fold more active than imatinib in inhibiting wild-type BCR-ABL kinase in vitro and is active against a wide variety of imatinib-resistant BCR-ABL mutants, except for T315I.	imatinib	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
22233429-2	2012	Dasatinib is  325-fold more active than imatinib in inhibiting wild-type BCR-ABL kinase in vitro and is active against a wide variety of imatinib-resistant BCR-ABL mutants, except for T315I.	imatinib	137-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
21874302-4	2012	We here report that exposure of developing human monocyte-derived dendritic cells to the BCR-ABL inhibitors imatinib, dasatinib, and nilotinib results in profound upregulation of the transmembrane glycoprotein osteoactivin that has recently been characterized as a negative regulator of T-cell activation.	imatinib	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
21710245-3	2012	On the basis of the radiographic response obtained with imatinib (Novartis Pharma, Basel, Switzerland) in a patient with thymic carcinoma harboring the V560del c-KIT mutation, a phase II trial was initiated at the Department of Molecular and Clinical Oncology and Endocrinology of University "Federico II of Naples" with the purpose to test imatinib in TETs.	imatinib	56-64	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	160-165
21874302-4	2012	We here report that exposure of developing human monocyte-derived dendritic cells to the BCR-ABL inhibitors imatinib, dasatinib, and nilotinib results in profound upregulation of the transmembrane glycoprotein osteoactivin that has recently been characterized as a negative regulator of T-cell activation.	imatinib	108-116	glycoprotein nmb	Homo sapiens	210-222
21710245-19	2012	Nevertheless, imatinib may represent a valuable option in selected patients with TETs, such as those harboring the V560del c-KIT mutation.	imatinib	14-22	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	123-128
22285209-2	2012	Second-generation BCR-ABL inhibitors have shorter onset times and higher rates of complete cytogenetic response (CCyR) than imatinib.	imatinib	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
22098951-0	2012	Overexpression of P-glycoprotein induces acquired resistance to imatinib in chronic myelogenous leukemia cells.	imatinib	64-72	ATP binding cassette subfamily B member 1	Homo sapiens	18-32
22098951-1	2012	Imatinib, a breakpoint cluster region (BCR)-Abelson murine leukemia(ABL) tyrosine kinase inhibitor (TKI), has revolutionized the treatment of chronic myelogenous leukemia (CML).	imatinib	0-8	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	68-71
22098951-7	2012	Western blot analysis and reverse transcription-polymerase chain reaction(RT-PCR) demonstrated that P-glycoprotein(P-gp) and MDR1 mRNA levels were increased in K562-imatinib cells.	imatinib	165-173	ATP binding cassette subfamily B member 1	Homo sapiens	100-114
22098951-7	2012	Western blot analysis and reverse transcription-polymerase chain reaction(RT-PCR) demonstrated that P-glycoprotein(P-gp) and MDR1 mRNA levels were increased in K562-imatinib cells.	imatinib	165-173	phosphoglycolate phosphatase	Homo sapiens	115-119
22098951-7	2012	Western blot analysis and reverse transcription-polymerase chain reaction(RT-PCR) demonstrated that P-glycoprotein(P-gp) and MDR1 mRNA levels were increased in K562-imatinib cells.	imatinib	165-173	ATP binding cassette subfamily B member 1	Homo sapiens	125-129
22098951-9	2012	These data suggest that the overexpression of P-gp may play a crucial role in acquired resistance to imatinib in CML K562-imatinib cells.	imatinib	101-109	phosphoglycolate phosphatase	Homo sapiens	46-50
22098951-9	2012	These data suggest that the overexpression of P-gp may play a crucial role in acquired resistance to imatinib in CML K562-imatinib cells.	imatinib	122-130	phosphoglycolate phosphatase	Homo sapiens	46-50
22116466-3	2012	Using the KCL-22 cell culture model we have recently developed for studying mechanisms of CML acquired resistance, we found that Aurora A expression was partially reduced in these cells upon treatment with the tyrosine kinase inhibitor imatinib, which accompanied the acquisition of BCR-ABL mutation for imatinib resistance.	imatinib	236-244	aurora kinase A	Homo sapiens	129-137
22116466-3	2012	Using the KCL-22 cell culture model we have recently developed for studying mechanisms of CML acquired resistance, we found that Aurora A expression was partially reduced in these cells upon treatment with the tyrosine kinase inhibitor imatinib, which accompanied the acquisition of BCR-ABL mutation for imatinib resistance.	imatinib	236-244	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	283-290
22116466-3	2012	Using the KCL-22 cell culture model we have recently developed for studying mechanisms of CML acquired resistance, we found that Aurora A expression was partially reduced in these cells upon treatment with the tyrosine kinase inhibitor imatinib, which accompanied the acquisition of BCR-ABL mutation for imatinib resistance.	imatinib	304-312	aurora kinase A	Homo sapiens	129-137
22116466-3	2012	Using the KCL-22 cell culture model we have recently developed for studying mechanisms of CML acquired resistance, we found that Aurora A expression was partially reduced in these cells upon treatment with the tyrosine kinase inhibitor imatinib, which accompanied the acquisition of BCR-ABL mutation for imatinib resistance.	imatinib	304-312	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	283-290
22116466-6	2012	Inhibition of Aurora A by gene knockdown or a highly specific small molecule inhibitor sensitized CML cells to imatinib treatment and effectively blocked acquisition of BCR-ABL mutations and KCL-22 cell relapse on imatinib, nilotinib or dasatinib.	imatinib	111-119	aurora kinase A	Homo sapiens	14-22
22116466-6	2012	Inhibition of Aurora A by gene knockdown or a highly specific small molecule inhibitor sensitized CML cells to imatinib treatment and effectively blocked acquisition of BCR-ABL mutations and KCL-22 cell relapse on imatinib, nilotinib or dasatinib.	imatinib	214-222	aurora kinase A	Homo sapiens	14-22
22285209-3	2012	Dasatinib has a half-maximal inhibitory concentration 325 times lower than imatinib for BCR-ABL substrate phosphorylation in vitro and is less susceptible to most known molecular mechanisms of BCR-ABL imatinib resistance.	imatinib	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
22262141-2	2012	This mutation confers resistance not only to imatinib, but also to second-generation BCR-ABL tyrosine kinases, such as nilotinib and dasatinib.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
22076958-11	2012	CD133 expression was also detected in the two imatinib-sensitive GIST cell lines, while was absent in the imatinib-resistant lines.	imatinib	46-54	prominin 1	Homo sapiens	0-5
22002244-0	2012	Imatinib and bortezomib induce the expression and distribution of anaphase-promoting             complex adaptor protein Cdh1 in blast crisis of chronic myeloid leukemia.	imatinib	0-8	cadherin 1	Homo sapiens	121-125
22002244-7	2012	Our study revealed that Cdh1 was expressed             at lower levels in imatinib-resistant CML blast crisis (BC) patients than imatinib-sensitive             ones.	imatinib	74-82	cadherin 1	Homo sapiens	24-28
22002244-7	2012	Our study revealed that Cdh1 was expressed             at lower levels in imatinib-resistant CML blast crisis (BC) patients than imatinib-sensitive             ones.	imatinib	129-137	cadherin 1	Homo sapiens	24-28
22002244-8	2012	Moreover, imatinib and bortezomib induced cell cycle quiescence or arrest,             upregulation and nuclear relocation of Cdh1 in CML cells.	imatinib	10-18	cadherin 1	Homo sapiens	126-130
22002244-9	2012	Furthermore, nilotinib             and bortezomib resulted in upregulation of Cdh1 in imatinib-resistant CML cells.	imatinib	86-94	cadherin 1	Homo sapiens	78-82
22002244-11	2012	Our study shows             that TKIs and bortezomib can regulate the cell cycle and cell apoptosis via regulation             of the expression and redistribution of Cdh1 in CML-BC, which sheds light on the             orchestration of crosstalk between TKIs and bortezomib in imatinib-resistant CML-BC.	imatinib	278-286	cadherin 1	Homo sapiens	167-171
22262141-9	2012	To our knowledge, this is the first case report showing the effectiveness of imatinib/IFNalpha combination therapy for CML patients bearing the T315I BCR-ABL mutation.	imatinib	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
21854543-10	2012	The selective inhibition of the tyrosine kinase activity by adenosine-5"-triphosphate competitors, such as imatinib, is a major therapeutic success.	imatinib	107-115	TXK tyrosine kinase	Homo sapiens	32-47
21503882-7	2012	Finally, Gleevec (STI571) a pharmacological inhibitor of p73, a master gene controlling apoptosis induced by etoposide, prevented the increase of TACE/ADAM17 levels.	imatinib	18-24	tumor protein p73	Rattus norvegicus	57-60
22089930-8	2012	RESULTS: The ABL-inhibitors imatinib and nilotinib activate MAPKs in CD34+ chronic myelogenous leukemia progenitor cells, whereas treatment with the SRC/ABL-inhibitor dasatinib does not affect MAPK-activation at clinically relevant concentrations.	imatinib	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
22089930-8	2012	RESULTS: The ABL-inhibitors imatinib and nilotinib activate MAPKs in CD34+ chronic myelogenous leukemia progenitor cells, whereas treatment with the SRC/ABL-inhibitor dasatinib does not affect MAPK-activation at clinically relevant concentrations.	imatinib	28-36	CD34 molecule	Homo sapiens	69-73
22089930-8	2012	RESULTS: The ABL-inhibitors imatinib and nilotinib activate MAPKs in CD34+ chronic myelogenous leukemia progenitor cells, whereas treatment with the SRC/ABL-inhibitor dasatinib does not affect MAPK-activation at clinically relevant concentrations.	imatinib	28-36	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	149-152
22089930-8	2012	RESULTS: The ABL-inhibitors imatinib and nilotinib activate MAPKs in CD34+ chronic myelogenous leukemia progenitor cells, whereas treatment with the SRC/ABL-inhibitor dasatinib does not affect MAPK-activation at clinically relevant concentrations.	imatinib	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-156
21854543-11	2012	Imatinib induces remission in leukaemia patients that are positive for BCR-ABL or PDGFR fusions.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
21503882-7	2012	Finally, Gleevec (STI571) a pharmacological inhibitor of p73, a master gene controlling apoptosis induced by etoposide, prevented the increase of TACE/ADAM17 levels.	imatinib	18-24	ADAM metallopeptidase domain 17	Rattus norvegicus	146-150
21503882-7	2012	Finally, Gleevec (STI571) a pharmacological inhibitor of p73, a master gene controlling apoptosis induced by etoposide, prevented the increase of TACE/ADAM17 levels.	imatinib	18-24	ADAM metallopeptidase domain 17	Rattus norvegicus	151-157
21854543-11	2012	Imatinib induces remission in leukaemia patients that are positive for BCR-ABL or PDGFR fusions.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	82-87
22306903-0	2012	Imatinib sensitizes T-cell lymphocytes from chronic myeloid leukemia patients to FasL-induced cell death: a brief communication.	imatinib	0-8	Fas ligand	Homo sapiens	81-85
22068968-0	2012	Imatinib mesylate improves liver regeneration and attenuates liver fibrogenesis in CCL4-treated mice.	imatinib	0-17	chemokine (C-C motif) ligand 4	Mus musculus	83-87
22068968-7	2012	Further, increased apoptosis and a reduced proliferation were observed in the CCL(4)-treated mice after STI-571 treatment based on the immunohistochemical staining of Annexin V, phosphorylated STAT3, and PCNA.	imatinib	104-111	annexin A5	Mus musculus	167-176
22068968-7	2012	Further, increased apoptosis and a reduced proliferation were observed in the CCL(4)-treated mice after STI-571 treatment based on the immunohistochemical staining of Annexin V, phosphorylated STAT3, and PCNA.	imatinib	104-111	signal transducer and activator of transcription 3	Mus musculus	193-198
22306903-4	2012	In comparison with healthy controls, we found not only a mild blood lymphopenia but also impairment of phytohemagglutinin activation in CD4Fas and CD8Fas lymphocytes of imatinib-treated patients.	imatinib	169-177	CD8a molecule	Homo sapiens	147-150
22068968-7	2012	Further, increased apoptosis and a reduced proliferation were observed in the CCL(4)-treated mice after STI-571 treatment based on the immunohistochemical staining of Annexin V, phosphorylated STAT3, and PCNA.	imatinib	104-111	proliferating cell nuclear antigen	Mus musculus	204-208
23264790-3	2012	Treatment with thyrosin kinase inhibitors (e.g., Imatinib) is useful in CD117- positive GISTs.	imatinib	49-57	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	72-77
22173128-6	2012	Treatment of HMC-cells with the c-Kit inhibitor STI571 blocked the IL-1beta-induced activation of Erk1/2 and JNK1/2 but not p38 and NFkappaB.	imatinib	48-54	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	32-37
21724255-0	2012	Functional polymorphisms in SOCS1 and PTPN22 genes correlate with the response to imatinib treatment in newly diagnosed chronic-phase chronic myeloid leukemia.	imatinib	82-90	suppressor of cytokine signaling 1	Homo sapiens	28-33
21724255-0	2012	Functional polymorphisms in SOCS1 and PTPN22 genes correlate with the response to imatinib treatment in newly diagnosed chronic-phase chronic myeloid leukemia.	imatinib	82-90	protein tyrosine phosphatase non-receptor type 22	Homo sapiens	38-44
21724255-1	2012	The function of the natural modulators of BCR-ABL-induced signaling pathways could influence the results to imatinib treatment.	imatinib	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
21724255-3	2012	SNPs in SOCS1 (rs243327) and PTPN22 (rs2476601) genes correlated with the risk of primary resistance to imatinib.	imatinib	104-112	suppressor of cytokine signaling 1	Homo sapiens	8-13
21724255-3	2012	SNPs in SOCS1 (rs243327) and PTPN22 (rs2476601) genes correlated with the risk of primary resistance to imatinib.	imatinib	104-112	protein tyrosine phosphatase non-receptor type 22	Homo sapiens	29-35
21993902-2	2012	However, some patients with CML are less likely             to respond to imatinib, the inhibitor of Bcr-Abl kinase.	imatinib	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
21993902-3	2012	Recent studies showed             that mTOR pathway can increase responses to imatinib.	imatinib	78-86	mechanistic target of rapamycin kinase	Homo sapiens	39-43
22213031-1	2012	KIT protein expression and mutational status of KIT gene in different types of tumours have been intensively studied since Imatinib Mesylate, KIT/PDGFRA tyrosine kinase inhibitor became available.	imatinib	123-131	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
22213031-11	2012	Our results may suggest a role of KIT in the pathogenesis of a subset of pituitary adenomas and point out the need for further research to find out if KIT-reactive adenomas could be sensitive to Imatinib Mesylate.	imatinib	195-212	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	151-154
21844872-2	2012	Imatinib, a tyrosine kinase inhibitor of BCR-ABL, has been the mainstay of first-line therapy for CML for 10 years.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
21844874-0	2012	KIR2DS1 genotype predicts for complete cytogenetic response and survival in newly diagnosed chronic myeloid leukemia patients treated with imatinib.	imatinib	139-147	killer cell immunoglobulin like receptor, two Ig domains and short cytoplasmic tail 1	Homo sapiens	0-7
22173128-6	2012	Treatment of HMC-cells with the c-Kit inhibitor STI571 blocked the IL-1beta-induced activation of Erk1/2 and JNK1/2 but not p38 and NFkappaB.	imatinib	48-54	interleukin 1 beta	Homo sapiens	67-75
22173128-6	2012	Treatment of HMC-cells with the c-Kit inhibitor STI571 blocked the IL-1beta-induced activation of Erk1/2 and JNK1/2 but not p38 and NFkappaB.	imatinib	48-54	mitogen-activated protein kinase 3	Homo sapiens	98-104
22173128-6	2012	Treatment of HMC-cells with the c-Kit inhibitor STI571 blocked the IL-1beta-induced activation of Erk1/2 and JNK1/2 but not p38 and NFkappaB.	imatinib	48-54	mitogen-activated protein kinase 8	Homo sapiens	109-115
22508387-0	2012	Pretherapeutic expression of the hOCT1 gene predicts a complete molecular response to imatinib mesylate in chronic-phase chronic myeloid leukemia.	imatinib	86-103	solute carrier family 22 member 1	Homo sapiens	33-38
22005133-5	2012	In 27 of 74 imatinib-resistant patients (36%), 15 different BCR-ABL TKD mutations were detected.	imatinib	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
21685944-7	2012	Additionally, imatinib mesylate that inhibits release of VEGF induces nuclear export of beta-arrestin1-HIF-1alpha complexes.	imatinib	14-31	vascular endothelial growth factor A	Homo sapiens	57-61
21685944-7	2012	Additionally, imatinib mesylate that inhibits release of VEGF induces nuclear export of beta-arrestin1-HIF-1alpha complexes.	imatinib	14-31	arrestin beta 1	Homo sapiens	88-102
21685944-7	2012	Additionally, imatinib mesylate that inhibits release of VEGF induces nuclear export of beta-arrestin1-HIF-1alpha complexes.	imatinib	14-31	hypoxia inducible factor 1 subunit alpha	Homo sapiens	103-113
21986252-0	2012	Imatinib mesylate therapy induces reduction in neutrophil gelatinase-associated lipocalin serum levels and increase in leptin concentrations in chronic myeloid leukemia patients in molecular remission.	imatinib	0-17	lipocalin 2	Homo sapiens	47-89
22508387-1	2012	In this retrospective study we evaluated the pretherapeutic mRNA expression of the hOCT1 (human organic cation transporter 1) gene in patients with chronic-phase (CP) chronic myeloid leukemia (CML) who varied in terms of their response to imatinib (IM).	imatinib	239-247	solute carrier family 22 member 1	Homo sapiens	83-88
21986252-0	2012	Imatinib mesylate therapy induces reduction in neutrophil gelatinase-associated lipocalin serum levels and increase in leptin concentrations in chronic myeloid leukemia patients in molecular remission.	imatinib	0-17	leptin	Homo sapiens	119-125
21986252-1	2012	The aim of the present study was to determine serum levels of neutrophil gelatinase-associated lipocalin (NGAL) and leptin in patients with chronic myeloid leukemia (CML) at diagnosis and after imatinib therapy when patients achieved a complete molecular remission.	imatinib	194-202	lipocalin 2	Homo sapiens	62-104
22508387-1	2012	In this retrospective study we evaluated the pretherapeutic mRNA expression of the hOCT1 (human organic cation transporter 1) gene in patients with chronic-phase (CP) chronic myeloid leukemia (CML) who varied in terms of their response to imatinib (IM).	imatinib	239-247	solute carrier family 22 member 1	Homo sapiens	96-124
21986252-4	2012	After imatinib therapy, all patients achieved complete molecular remission and NGAL levels decreased and were found significantly lower with respect to the baseline.	imatinib	6-14	lipocalin 2	Homo sapiens	79-83
21986252-7	2012	After therapy with imatinib, all patients in molecular remission presented an increase in leptin levels.	imatinib	19-27	leptin	Homo sapiens	90-96
22722648-0	2012	Complete response of myeloid sarcoma with FIP1L1-PDGFRA -associated myeloproliferative neoplasms to imatinib mesylate monotherapy.	imatinib	100-117	factor interacting with PAPOLA and CPSF1	Homo sapiens	42-48
22722648-0	2012	Complete response of myeloid sarcoma with FIP1L1-PDGFRA -associated myeloproliferative neoplasms to imatinib mesylate monotherapy.	imatinib	100-117	platelet derived growth factor receptor alpha	Homo sapiens	49-55
24451813-1	2012	The identification of KIT as a critical driver in the pathogenesis of GI stromal tumor (GIST), and its subsequent inhibition with imatinib, have resulted in tremendous efforts to identify other potential therapeutic targets for the heterogeneous group of diseases known as sarcomas.	imatinib	130-138	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	22-25
24451731-2	2012	Imatinib mesylate, a selective Bcr-Abl tyrosine kinase inhibitor (TKI), transformed the course of CML from a rapidly fatal disease (median survival, 3 to 6 years) to a functionally curable, indolent disease with an estimated median survival of more than 25 years.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
22922489-9	2012	Our experience reveals that IM is an effective rescue therapy in most CML LCP patients who are intolerant or in whom IFN-alpha therapy fails.	imatinib	28-30	interferon alpha 2	Homo sapiens	117-126
21975872-0	2012	Imatinib ameliorates renal morphological changes in Cyp1a1-Ren2 transgenic rats with inducible ANG II-dependent malignant hypertension.	imatinib	0-8	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	52-58
21975872-0	2012	Imatinib ameliorates renal morphological changes in Cyp1a1-Ren2 transgenic rats with inducible ANG II-dependent malignant hypertension.	imatinib	0-8	angiotensinogen	Rattus norvegicus	95-101
24451731-3	2012	This transformation can be attributed to several key factors: the identification of a causal and actionable molecular aberration-BCR-ABL; the development of a potent and selective Bcr-Abl TKI-imatinib; and, importantly the application of imatinib in the earliest phase of CML.	imatinib	192-200	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
21943109-1	2012	Alcoholic extract of Piper betle (Piper betle L.) leaves was recently found to induce apoptosis of CML cells expressing wild type and mutated Bcr-Abl with imatinib resistance phenotype.	imatinib	155-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
24451731-3	2012	This transformation can be attributed to several key factors: the identification of a causal and actionable molecular aberration-BCR-ABL; the development of a potent and selective Bcr-Abl TKI-imatinib; and, importantly the application of imatinib in the earliest phase of CML.	imatinib	192-200	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	180-187
24451731-3	2012	This transformation can be attributed to several key factors: the identification of a causal and actionable molecular aberration-BCR-ABL; the development of a potent and selective Bcr-Abl TKI-imatinib; and, importantly the application of imatinib in the earliest phase of CML.	imatinib	238-246	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
24451731-3	2012	This transformation can be attributed to several key factors: the identification of a causal and actionable molecular aberration-BCR-ABL; the development of a potent and selective Bcr-Abl TKI-imatinib; and, importantly the application of imatinib in the earliest phase of CML.	imatinib	238-246	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	180-187
24451733-6	2012	Positron Emission Tomography in patients with GI stromal tumors or genotyping of c-kit in chronic myelogenous leukemia cells can guide the use of imatinib, these scenarios represent a minority of patients.	imatinib	146-154	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	81-86
21717109-1	2012	Imatinib mesylate is considered the standard first-line systemic treatment for patients with chronic myeloid leukaemia (CML) and gastrointestinal stromal tumour (GIST) by targeting BCR-ABL and c-KIT tyrosine kinases, respectively.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	181-188
22103975-0	2012	Histone H3 covalent modifications driving response of BCR-ABL1+ cells sensitive and resistant to imatinib to Aurora kinase inhibitor MK-0457.	imatinib	97-105	BCR activator of RhoGEF and GTPase	Homo sapiens	54-62
21857502-0	2012	Methyl-beta-cyclodextrin induces programmed cell death in chronic myeloid leukemia cells and, combined with imatinib, produces a synergistic downregulation of ERK/SPK1 signaling.	imatinib	108-116	mitogen-activated protein kinase 1	Homo sapiens	159-162
21857502-0	2012	Methyl-beta-cyclodextrin induces programmed cell death in chronic myeloid leukemia cells and, combined with imatinib, produces a synergistic downregulation of ERK/SPK1 signaling.	imatinib	108-116	sphingosine kinase 1	Homo sapiens	163-167
21857502-6	2012	Extracellular signal-regulated kinase/sphingosine kinase 1 signaling downstream of lipid raft-activated signaling pathways was significantly inhibited by treatment of cells with a combination of MbetaCD and imatinib compared with treatment with either agent alone.	imatinib	207-215	sphingosine kinase 1	Homo sapiens	38-58
21968742-10	2012	Ex vivo targeting of synovial mast cells with the c-Kit inhibitor imatinib mesylate significantly decreased the production of IL-17 as well as other proinflammatory cytokines in synovial tissue cultures.	imatinib	66-83	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	50-55
21968742-10	2012	Ex vivo targeting of synovial mast cells with the c-Kit inhibitor imatinib mesylate significantly decreased the production of IL-17 as well as other proinflammatory cytokines in synovial tissue cultures.	imatinib	66-83	interleukin 17A	Homo sapiens	126-131
22015552-4	2012	Indeed, imatinib mesylate inhibits KIT kinase activity and represents the front line drug for the treatment of unresectable and advanced GISTs, achieving a partial response or stable disease in about 80% of patients with metastatic GIST.	imatinib	8-25	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	35-38
22855636-2	2012	Early events in GIST development are activating mutations in KIT or PDGFRA, which occur in most GISTs and encode for mutated tyrosine receptor kinases that are therapeutic targets for tyrosine kinase inhibitors, including imatinib and sunitinib.	imatinib	222-230	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	61-64
22855636-2	2012	Early events in GIST development are activating mutations in KIT or PDGFRA, which occur in most GISTs and encode for mutated tyrosine receptor kinases that are therapeutic targets for tyrosine kinase inhibitors, including imatinib and sunitinib.	imatinib	222-230	platelet derived growth factor receptor alpha	Homo sapiens	68-74
22015552-6	2012	Patients with the most common exon 11 mutation experience higher rates of tumor shrinkage and prolonged survival, as tumors with an exon 9 mutation or wild-type KIT are less likely to respond to imatinib.	imatinib	195-203	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	161-164
22846208-2	2012	Its product, CD117, is a specific immunohistochemical (IHQ) marker that is associated with response to a potent tyrosine kinase inhibitor therapy with STI-571 (Gleevec ) in chronic myelogenous leukemia and GISTs.	imatinib	151-158	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	13-18
22447116-1	2012	FB2 is a promising Abl/Src dual tyrosine kinase inhibitor which is designed to overcome imatinib resistance.	imatinib	88-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Rattus norvegicus	19-22
22447116-1	2012	FB2 is a promising Abl/Src dual tyrosine kinase inhibitor which is designed to overcome imatinib resistance.	imatinib	88-96	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	23-26
21938754-4	2012	Here, we developed version 2.0 of a genomically based systematic kinase fusion screen and used it to detect a novel imatinib-sensitive C6orf204-PDGFRB fusion in a patient with precursor T lymphoblastic lymphoma (T-ALL) and an associated myeloproliferative neoplasm with eosinophilia.	imatinib	116-124	centrosomal protein 85 like	Homo sapiens	135-143
21938754-4	2012	Here, we developed version 2.0 of a genomically based systematic kinase fusion screen and used it to detect a novel imatinib-sensitive C6orf204-PDGFRB fusion in a patient with precursor T lymphoblastic lymphoma (T-ALL) and an associated myeloproliferative neoplasm with eosinophilia.	imatinib	116-124	platelet derived growth factor receptor beta	Homo sapiens	144-150
21993629-7	2012	When we measured the relative mRNA expression levels of Runx2, we found that Runx2 expression was higher in imatinib-treated (5 muM) cultures at early time points during differentiation.	imatinib	108-116	RUNX family transcription factor 2	Homo sapiens	56-61
21993629-7	2012	When we measured the relative mRNA expression levels of Runx2, we found that Runx2 expression was higher in imatinib-treated (5 muM) cultures at early time points during differentiation.	imatinib	108-116	RUNX family transcription factor 2	Homo sapiens	77-82
21993629-7	2012	When we measured the relative mRNA expression levels of Runx2, we found that Runx2 expression was higher in imatinib-treated (5 muM) cultures at early time points during differentiation.	imatinib	108-116	latexin	Homo sapiens	128-131
21993629-8	2012	On the other hand, the expression of Osterix late during differentiation was lower in imatinib-treated (5 muM) cultures, corresponding to the ARS results.	imatinib	86-94	Sp7 transcription factor	Homo sapiens	37-44
21993629-8	2012	On the other hand, the expression of Osterix late during differentiation was lower in imatinib-treated (5 muM) cultures, corresponding to the ARS results.	imatinib	86-94	latexin	Homo sapiens	106-109
23226701-2	2012	In particular, the availability of imatinib mesylate, a tyrosine kinase inhibitor targeting BCR-ABL, has led to profound and durable remissions in the majority of patients.	imatinib	35-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
23259070-3	2012	The BCR-ABL kinase inhibitor, imatinib, is the front-line treatment for CML, but the emergence of imatinib resistance and other tyrosine kinase inhibitors (TKIs) has called attention for additional resistance mechanisms and has led to the search for alternative drug treatments.	imatinib	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
23037633-0	2012	Disappearance of both the BCR/ABL1 fusion gene and the JAK2V617F mutation with dasatinib therapy in a patient with imatinib-resistant chronic myelogenous leukemia.	imatinib	115-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-34
21947613-1	2012	The interaction of an anti-leukemic drug, imatinib mesylate (IMT) with human serum albumin (HSA) was investigated by fluorescence, synchronous fluorescence, three-dimensional fluorescence, circular dichroism and UV-vis absorption techniques under physiological condition.	imatinib	42-59	albumin	Homo sapiens	77-96
23102192-5	2012	Tumors with C-KIT mutation respond to therapy with C-KIT kinase inhibitor imatinib and the ones characterized by BRAF mutations respond to BRAF kinase inhibitor vemurafenib.	imatinib	74-82	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	12-17
23102192-5	2012	Tumors with C-KIT mutation respond to therapy with C-KIT kinase inhibitor imatinib and the ones characterized by BRAF mutations respond to BRAF kinase inhibitor vemurafenib.	imatinib	74-82	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	51-56
21993766-0	2012	Chemotherapeutic alteration of beta-catenin and c-kit expression by imatinib             in p16-positive squamous cell carcinoma compared to HPV-negative HNSCC cells in             vitro.	imatinib	68-76	catenin beta 1	Homo sapiens	31-43
22956142-2	2012	As exemplified by Imatinib (Gleevec), a specific inhibitor of the Chronic Myeloid Leukemia-associated BCR/ABL kinase, these agents promise impressive activity in clinical trials, with low levels of clinical toxicity.	imatinib	18-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
22956142-2	2012	As exemplified by Imatinib (Gleevec), a specific inhibitor of the Chronic Myeloid Leukemia-associated BCR/ABL kinase, these agents promise impressive activity in clinical trials, with low levels of clinical toxicity.	imatinib	28-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
22956142-5	2012	Using Imatinib and BCR/ABL as a paradigm for a drug-target pair, we reported a retroviral vector-based screening strategy to identify the spectrum of resistance-conferring mutations, which has helped in designing the next-generation BCR/ABL inhibitors such as Nilotinib, Dasatinib, and Ponatinib.	imatinib	6-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	233-240
21993766-0	2012	Chemotherapeutic alteration of beta-catenin and c-kit expression by imatinib             in p16-positive squamous cell carcinoma compared to HPV-negative HNSCC cells in             vitro.	imatinib	68-76	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	48-53
21993766-0	2012	Chemotherapeutic alteration of beta-catenin and c-kit expression by imatinib             in p16-positive squamous cell carcinoma compared to HPV-negative HNSCC cells in             vitro.	imatinib	68-76	cyclin dependent kinase inhibitor 2A	Homo sapiens	92-95
21993766-8	2012	ELISA and immunohistochemical methods were carried out after 48, 72, 120, 192             and 240 h. We detected a reliable trend towards significantly decreased cytosolic             and nuclear beta-catenin and c-kit expression levels in p16-positive SCC and non-HPV             HNSCC cells induced by imatinib exposure for an extended incubation period, whereas             platinum-based agents had no or, at best, a slight influence.	imatinib	304-312	catenin beta 1	Homo sapiens	196-208
21993766-8	2012	ELISA and immunohistochemical methods were carried out after 48, 72, 120, 192             and 240 h. We detected a reliable trend towards significantly decreased cytosolic             and nuclear beta-catenin and c-kit expression levels in p16-positive SCC and non-HPV             HNSCC cells induced by imatinib exposure for an extended incubation period, whereas             platinum-based agents had no or, at best, a slight influence.	imatinib	304-312	cyclin dependent kinase inhibitor 2A	Homo sapiens	240-243
21993766-9	2012	Virus-transformed             squamous cell carcinoma (CERV196) cells were characterized by a reduced susceptibility             to an imatinib-altered beta-catenin expression.	imatinib	135-143	catenin beta 1	Homo sapiens	152-164
23285214-6	2012	The effect of imatinib on CD117(high)/KIT+ tumors was determined on first passage cells; absolute cell counts and flow cytometry were readouts for drug sensitivity of cell subsets.	imatinib	14-22	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	26-31
23285088-2	2012	The BCR-ABL inhibitor imatinib is also known to inhibit the tyrosine kinase of the stem cell factor receptor, c-Kit.	imatinib	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
23285088-2	2012	The BCR-ABL inhibitor imatinib is also known to inhibit the tyrosine kinase of the stem cell factor receptor, c-Kit.	imatinib	22-30	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	110-115
23285088-3	2012	Nilotinib is 30 times more potent than imatinib towards BCR-ABL in vitro.	imatinib	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
23285088-5	2012	The aim of this study was to compare the inhibitory effects of imatinib and nilotinib on proliferation, differentiation, adhesion, migration and engraftment capacities of human cord blood CD34(+) cells.	imatinib	63-71	CD34 molecule	Homo sapiens	188-192
23285088-9	2012	Adhesion of CD34(+) cells to retronectin was reduced in the presence of either imatinib or nilotinib but only at high concentrations.	imatinib	79-87	CD34 molecule	Homo sapiens	12-16
22286586-4	2012	With the advent of imatinib mesylate, a new era in the management of patients with BCR-ABL+ chronic myelogenous leukemia (CML), gastrointestinal stromal tumors, and myeloproliferative neoplasms including chronic myelomonocytic leukemia with PDGFRB gene rearrangements and hypereosinophilic syndrome has begun.	imatinib	19-36	platelet derived growth factor receptor beta	Homo sapiens	241-247
23284953-6	2012	In transfection experiments, hMATE1 showed the highest apparent affinity for Imatinib among all known Imatinib transporters.	imatinib	77-85	solute carrier family 47 member 1	Homo sapiens	29-35
23284953-7	2012	Experiments quantifying the Imatinib uptake in the presence of specific transporter inhibitors and after siRNA knockdown of hMATE1 indeed identified hMATE1 to mediate Imatinib transport in hRASF.	imatinib	28-36	solute carrier family 47 member 1	Homo sapiens	149-155
23284953-7	2012	Experiments quantifying the Imatinib uptake in the presence of specific transporter inhibitors and after siRNA knockdown of hMATE1 indeed identified hMATE1 to mediate Imatinib transport in hRASF.	imatinib	167-175	solute carrier family 47 member 1	Homo sapiens	124-130
23284953-7	2012	Experiments quantifying the Imatinib uptake in the presence of specific transporter inhibitors and after siRNA knockdown of hMATE1 indeed identified hMATE1 to mediate Imatinib transport in hRASF.	imatinib	167-175	solute carrier family 47 member 1	Homo sapiens	149-155
23284953-8	2012	The anti-proliferative effect of Imatinib on PDGF stimulated hRASF was quantified by cell counting and directly correlated with the uptake activity of hMATE1.	imatinib	33-41	solute carrier family 47 member 1	Homo sapiens	151-157
23284953-12	2012	CONCLUSION/SIGNIFICANCE: The regulation of Imatinib uptake via hMATE1 in hRASF and resulting effects on their proliferation may explain moderate in vivo effects on RA.	imatinib	43-51	solute carrier family 47 member 1	Homo sapiens	63-69
23285214-6	2012	The effect of imatinib on CD117(high)/KIT+ tumors was determined on first passage cells; absolute cell counts and flow cytometry were readouts for drug sensitivity of cell subsets.	imatinib	14-22	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	38-41
23285214-10	2012	Primary cultures of CD117(high) tumors were sensitive to imatinib (5 microM) in short term culture.	imatinib	57-65	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	20-25
23272163-0	2012	SLC22A1-ABCB1 haplotype profiles predict imatinib pharmacokinetics in Asian patients with chronic myeloid leukemia.	imatinib	41-49	solute carrier family 22 member 1	Homo sapiens	0-7
23272163-0	2012	SLC22A1-ABCB1 haplotype profiles predict imatinib pharmacokinetics in Asian patients with chronic myeloid leukemia.	imatinib	41-49	ATP binding cassette subfamily B member 1	Homo sapiens	8-13
23272163-1	2012	OBJECTIVE: This study aimed to explore the influence of SLC22A1, PXR, ABCG2, ABCB1 and CYP3A5 3 genetic polymorphisms on imatinib mesylate (IM) pharmacokinetics in Asian patients with chronic myeloid leukemia (CML).	imatinib	121-138	solute carrier family 22 member 1	Homo sapiens	56-63
23272163-1	2012	OBJECTIVE: This study aimed to explore the influence of SLC22A1, PXR, ABCG2, ABCB1 and CYP3A5 3 genetic polymorphisms on imatinib mesylate (IM) pharmacokinetics in Asian patients with chronic myeloid leukemia (CML).	imatinib	121-138	nuclear receptor subfamily 1 group I member 2	Homo sapiens	65-68
23272163-1	2012	OBJECTIVE: This study aimed to explore the influence of SLC22A1, PXR, ABCG2, ABCB1 and CYP3A5 3 genetic polymorphisms on imatinib mesylate (IM) pharmacokinetics in Asian patients with chronic myeloid leukemia (CML).	imatinib	121-138	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	70-75
23272163-1	2012	OBJECTIVE: This study aimed to explore the influence of SLC22A1, PXR, ABCG2, ABCB1 and CYP3A5 3 genetic polymorphisms on imatinib mesylate (IM) pharmacokinetics in Asian patients with chronic myeloid leukemia (CML).	imatinib	121-138	ATP binding cassette subfamily B member 1	Homo sapiens	77-82
23272163-1	2012	OBJECTIVE: This study aimed to explore the influence of SLC22A1, PXR, ABCG2, ABCB1 and CYP3A5 3 genetic polymorphisms on imatinib mesylate (IM) pharmacokinetics in Asian patients with chronic myeloid leukemia (CML).	imatinib	121-138	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	87-93
22693568-3	2012	Inhibition of the oncogenic Abl kinase with imatinib reverses transformation, allowing progression to the next stage of B cell development.	imatinib	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-31
23071680-6	2012	In marked contrast, the alpha6 integrin(high+)/CD44(+) cells were sensitive to apoptosis induced by the cross-linking agent cisplatin, and imatinib inhibition of c-Abl blocked the ability of cisplatin to kill alpha6 integrin(high+)/CD44(+) cells.	imatinib	139-147	CD44 molecule (Indian blood group)	Homo sapiens	47-51
23071680-6	2012	In marked contrast, the alpha6 integrin(high+)/CD44(+) cells were sensitive to apoptosis induced by the cross-linking agent cisplatin, and imatinib inhibition of c-Abl blocked the ability of cisplatin to kill alpha6 integrin(high+)/CD44(+) cells.	imatinib	139-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-167
23071680-6	2012	In marked contrast, the alpha6 integrin(high+)/CD44(+) cells were sensitive to apoptosis induced by the cross-linking agent cisplatin, and imatinib inhibition of c-Abl blocked the ability of cisplatin to kill alpha6 integrin(high+)/CD44(+) cells.	imatinib	139-147	CD44 molecule (Indian blood group)	Homo sapiens	232-236
22957062-6	2012	Knocking down LMW-PTP in Lucena-1 cells reverted chemoresistance to vincristine and imatinib mesylate, followed by a decrease of Src and Bcr-Abl phosphorylation at the activating sites, inactivating both kinases.	imatinib	84-101	acid phosphatase 1	Homo sapiens	14-21
22879933-7	2012	Here we show that STI-571 (imatinib, inhibitor of c-Abl) inhibited RGDfV-induced ASM activity.	imatinib	18-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-55
22879933-7	2012	Here we show that STI-571 (imatinib, inhibitor of c-Abl) inhibited RGDfV-induced ASM activity.	imatinib	18-25	sphingomyelin phosphodiesterase 1	Homo sapiens	81-84
22879933-7	2012	Here we show that STI-571 (imatinib, inhibitor of c-Abl) inhibited RGDfV-induced ASM activity.	imatinib	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-55
22879933-7	2012	Here we show that STI-571 (imatinib, inhibitor of c-Abl) inhibited RGDfV-induced ASM activity.	imatinib	27-35	sphingomyelin phosphodiesterase 1	Homo sapiens	81-84
22815843-3	2012	Here, we report a novel mechanism of prolonged intracellular TKI activity upon HD-TKI pulse-exposure (imatinib, dasatinib) in BCR-ABL-positive cells.	imatinib	102-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
23284724-4	2012	Our recent studies uncovered a role for Fyn in promoting BCR-ABL1 mediated cell growth and sensitivity to imatinib.	imatinib	106-114	Fyn proto-oncogene	Mus musculus	40-43
23284724-4	2012	Our recent studies uncovered a role for Fyn in promoting BCR-ABL1 mediated cell growth and sensitivity to imatinib.	imatinib	106-114	BCR activator of RhoGEF and GTPase	Mus musculus	57-65
22870341-0	2012	The proteolytic activity of separase in BCR-ABL-positive cells is increased by imatinib.	imatinib	79-87	extra spindle pole bodies like 1, separase	Homo sapiens	28-36
22870341-0	2012	The proteolytic activity of separase in BCR-ABL-positive cells is increased by imatinib.	imatinib	79-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
22204395-4	2011	Imatinib was used to control the activation of BCR-ABL and TEL-PDGFRB, and TEL-JAK2-mediated gene expression was examined 1 week after Ba/F3-TEL-JAK2 cells were switched to factor-independent conditions.	imatinib	0-8	ets variant 6	Mus musculus	59-62
22662219-8	2012	The commonly used imatinib-sensitive cell lines GIST882 and GIST-T1 were shown to harbor defective p53 and therefore failed to respond to nutlin-3 treatment.	imatinib	18-26	tumor protein p53	Homo sapiens	99-102
22493660-2	2012	The Abl inhibitors imatinib, nilotinib and dasatinib are currently used to treat CML, but resistance to these inhibitors is a significant clinical problem.	imatinib	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
22493660-4	2012	We present the 2.4 A structure of bosutinib bound to the kinase domain of Abl, which explains the inhibitor"s activity against several imatinib-resistant mutants, and reveals that similar inhibitors that lack a nitrile moiety could be effective against the common T315I mutant.	imatinib	135-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-77
22788088-1	2012	Gastrointestinal stromal tumors (GISTs) have been a topic of increasing interest since the discovery of their cellular activation pathway via the receptor for tyrosine kinase (KIT) leading to the possibility of targeted molecular therapy in the form of imatinib mesylate.	imatinib	253-270	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	176-179
22204395-4	2011	Imatinib was used to control the activation of BCR-ABL and TEL-PDGFRB, and TEL-JAK2-mediated gene expression was examined 1 week after Ba/F3-TEL-JAK2 cells were switched to factor-independent conditions.	imatinib	0-8	platelet derived growth factor receptor, beta polypeptide	Mus musculus	63-69
22169110-1	2011	We show that imatinib, nilotinib, and dasatinib possess weak off-target activity against RAF and, therefore, drive paradoxical activation of BRAF and CRAF in a RAS-dependent manner.	imatinib	13-21	zinc fingers and homeoboxes 2	Mus musculus	89-92
21890264-0	2011	Rapid automated detection of ABL kinase domain mutations in imatinib-resistant patients.	imatinib	60-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-32
21890264-1	2011	ABL tyrosine kinase inhibitor (TKI), imatinib is used for BCR-ABL(+) leukemias.	imatinib	37-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
21890264-1	2011	ABL tyrosine kinase inhibitor (TKI), imatinib is used for BCR-ABL(+) leukemias.	imatinib	37-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
22097958-2	2011	The classical kinase inhibitors imatinib and sorafenib as well as BI-1 and BIRB-796 were reported to bind in the DFG-out form of human p38alpha, known as type II or allosteric kinase inhibitors.	imatinib	32-40	mitogen-activated protein kinase 14	Homo sapiens	135-143
22097958-4	2011	As allosteric inhibition is important to the selectivity of kinase inhibitor, herein the binding modes of imatinib, sorafenib, BI-1 and BIRB-796 to p38alpha were investigated by molecular dynamics simulation.	imatinib	106-114	mitogen-activated protein kinase 14	Homo sapiens	148-156
21906872-0	2011	Growth inhibition of imatinib-resistant CML cells with the T315I mutation and hypoxia-adaptation by AV65--a novel Wnt/beta-catenin signaling inhibitor.	imatinib	21-29	catenin beta 1	Homo sapiens	118-130
22169110-1	2011	We show that imatinib, nilotinib, and dasatinib possess weak off-target activity against RAF and, therefore, drive paradoxical activation of BRAF and CRAF in a RAS-dependent manner.	imatinib	13-21	Braf transforming gene	Mus musculus	141-145
22169110-1	2011	We show that imatinib, nilotinib, and dasatinib possess weak off-target activity against RAF and, therefore, drive paradoxical activation of BRAF and CRAF in a RAS-dependent manner.	imatinib	13-21	v-raf-leukemia viral oncogene 1	Mus musculus	150-154
22169110-4	2011	Thus, we show that imatinib, nilotinib, and dasatinib drive paradoxical RAF/MEK/ERK pathway activation and have uncovered a synthetic lethal interaction that can be used to kill drug-resistant CML cells in vitro and in vivo.	imatinib	19-27	zinc fingers and homeoboxes 2	Mus musculus	72-75
22169110-4	2011	Thus, we show that imatinib, nilotinib, and dasatinib drive paradoxical RAF/MEK/ERK pathway activation and have uncovered a synthetic lethal interaction that can be used to kill drug-resistant CML cells in vitro and in vivo.	imatinib	19-27	midkine	Mus musculus	76-79
22169110-4	2011	Thus, we show that imatinib, nilotinib, and dasatinib drive paradoxical RAF/MEK/ERK pathway activation and have uncovered a synthetic lethal interaction that can be used to kill drug-resistant CML cells in vitro and in vivo.	imatinib	19-27	mitogen-activated protein kinase 1	Mus musculus	80-83
22013071-6	2011	Biochemical studies made in Xenopus oocytes using inhibitors against Src (herbimycin A) and Abl (imatinib) kinases exhibited a biochemical inhibition profile of SmTK6, which was intermediate of Src and Abl kinases.	imatinib	97-105	ABL proto-oncogene 1, non-receptor tyrosine kinase S homeolog	Xenopus laevis	92-95
21868503-8	2011	The direct profibrotic effects of T reg cells were abolished by the inhibitor of the PDGF-B/TGF-beta signaling pathway, imatinib mesylate.	imatinib	120-137	platelet derived growth factor, B polypeptide	Mus musculus	85-91
21868503-8	2011	The direct profibrotic effects of T reg cells were abolished by the inhibitor of the PDGF-B/TGF-beta signaling pathway, imatinib mesylate.	imatinib	120-137	transforming growth factor, beta 1	Mus musculus	92-100
22829096-0	2011	Imatinib causes epigenetic alterations of PTEN gene via upregulation of DNA methyltransferases and polycomb group proteins.	imatinib	0-8	phosphatase and tensin homolog	Homo sapiens	42-46
22346278-1	2011	Imatinib mesylate (Gleevec , STI571), a selective inhibitor of BCR-ABL, c-Kit, and platelet-derived factor receptor, has been used to treat chronic myelogenous leukemia (CML) and gastrointestinal stromal tumors.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
22346278-1	2011	Imatinib mesylate (Gleevec , STI571), a selective inhibitor of BCR-ABL, c-Kit, and platelet-derived factor receptor, has been used to treat chronic myelogenous leukemia (CML) and gastrointestinal stromal tumors.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	72-77
22346278-1	2011	Imatinib mesylate (Gleevec , STI571), a selective inhibitor of BCR-ABL, c-Kit, and platelet-derived factor receptor, has been used to treat chronic myelogenous leukemia (CML) and gastrointestinal stromal tumors.	imatinib	19-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
22346278-1	2011	Imatinib mesylate (Gleevec , STI571), a selective inhibitor of BCR-ABL, c-Kit, and platelet-derived factor receptor, has been used to treat chronic myelogenous leukemia (CML) and gastrointestinal stromal tumors.	imatinib	19-26	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	72-77
22346278-1	2011	Imatinib mesylate (Gleevec , STI571), a selective inhibitor of BCR-ABL, c-Kit, and platelet-derived factor receptor, has been used to treat chronic myelogenous leukemia (CML) and gastrointestinal stromal tumors.	imatinib	29-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
22346278-1	2011	Imatinib mesylate (Gleevec , STI571), a selective inhibitor of BCR-ABL, c-Kit, and platelet-derived factor receptor, has been used to treat chronic myelogenous leukemia (CML) and gastrointestinal stromal tumors.	imatinib	29-35	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	72-77
22033461-1	2011	Six analogs of imatinib, an Abl kinase inhibitor clinically used as a first-line therapeutic agent for chronic myeloid leukaemia (CML), have been synthesized and characterized.	imatinib	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-31
22033461-4	2011	And the H-bonds between imatinib analogs and Thr315 and Met318 residues in Abl kinase are shown to be crucial for achieving accurate poses and high binding affinities for the ATP-competitive kinase inhibitors.	imatinib	24-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-78
21931113-1	2011	Dasatinib is a potent BCR-ABL inhibitor effective in chronic myeloid leukemia and Ph(+) acute lymphoblastic leukemia (ALL) resistant/intolerant to imatinib.	imatinib	147-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
22829096-1	2011	We have recently reported the possible imatinib-resistant mechanism; long-term exposure of leukemia cells to imatinib downregulated levels of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) via hypermethylation of its promoter region (Leukemia 2010; 24: 1631).	imatinib	39-47	phosphatase and tensin homolog	Homo sapiens	199-203
22829096-1	2011	We have recently reported the possible imatinib-resistant mechanism; long-term exposure of leukemia cells to imatinib downregulated levels of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) via hypermethylation of its promoter region (Leukemia 2010; 24: 1631).	imatinib	109-117	phosphatase and tensin homolog	Homo sapiens	199-203
22829096-3	2011	Real-time reverse transcription PCR found that long-term exposure of chronic eosinophilic leukemia EOL-1 cells expressing FIP1L1/platelet-derived growth factor receptor-alpha to imatinib induced expression of DNA methyltransferase 3A (DNMT3A) and histone-methyltransferase enhancer of zeste homolog 2 (EZH2), a family of polycomb group, thereby increasing methylation of the gene.	imatinib	178-186	factor interacting with PAPOLA and CPSF1	Homo sapiens	122-128
21598241-2	2011	This dependency has led to the development of BCR-ABL1 inhibitors, such as imatinib, dasatinib, and nilotinib, which have proved to be highly efficacious treatments for CML.	imatinib	75-83	BCR activator of RhoGEF and GTPase	Homo sapiens	46-54
22829096-3	2011	Real-time reverse transcription PCR found that long-term exposure of chronic eosinophilic leukemia EOL-1 cells expressing FIP1L1/platelet-derived growth factor receptor-alpha to imatinib induced expression of DNA methyltransferase 3A (DNMT3A) and histone-methyltransferase enhancer of zeste homolog 2 (EZH2), a family of polycomb group, thereby increasing methylation of the gene.	imatinib	178-186	platelet derived growth factor receptor alpha	Homo sapiens	129-174
22829096-3	2011	Real-time reverse transcription PCR found that long-term exposure of chronic eosinophilic leukemia EOL-1 cells expressing FIP1L1/platelet-derived growth factor receptor-alpha to imatinib induced expression of DNA methyltransferase 3A (DNMT3A) and histone-methyltransferase enhancer of zeste homolog 2 (EZH2), a family of polycomb group, thereby increasing methylation of the gene.	imatinib	178-186	DNA methyltransferase 3 alpha	Homo sapiens	209-233
22829096-3	2011	Real-time reverse transcription PCR found that long-term exposure of chronic eosinophilic leukemia EOL-1 cells expressing FIP1L1/platelet-derived growth factor receptor-alpha to imatinib induced expression of DNA methyltransferase 3A (DNMT3A) and histone-methyltransferase enhancer of zeste homolog 2 (EZH2), a family of polycomb group, thereby increasing methylation of the gene.	imatinib	178-186	DNA methyltransferase 3 alpha	Homo sapiens	235-241
22829096-3	2011	Real-time reverse transcription PCR found that long-term exposure of chronic eosinophilic leukemia EOL-1 cells expressing FIP1L1/platelet-derived growth factor receptor-alpha to imatinib induced expression of DNA methyltransferase 3A (DNMT3A) and histone-methyltransferase enhancer of zeste homolog 2 (EZH2), a family of polycomb group, thereby increasing methylation of the gene.	imatinib	178-186	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	302-306
22829096-5	2011	Moreover, chromatin immunoprecipitation assay showed that amounts of both DNMT3A and EZH2 proteins bound around the promoter region of PTEN gene were increased in EOL-1 cells after exposure to imatinib.	imatinib	193-201	DNA methyltransferase 3 alpha	Homo sapiens	74-80
22829096-5	2011	Moreover, chromatin immunoprecipitation assay showed that amounts of both DNMT3A and EZH2 proteins bound around the promoter region of PTEN gene were increased in EOL-1 cells after exposure to imatinib.	imatinib	193-201	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	85-89
22829096-5	2011	Moreover, chromatin immunoprecipitation assay showed that amounts of both DNMT3A and EZH2 proteins bound around the promoter region of PTEN gene were increased in EOL-1 cells after exposure to imatinib.	imatinib	193-201	phosphatase and tensin homolog	Homo sapiens	135-139
22829096-6	2011	Furthermore, we found that levels of DNMT3A and EZH2 were strikingly increased in leukemia cells isolated from individuals with chronic myelogenous leukemia (n=1) and Philadelphia chromosome-positive acute lymphoblastic leukemia (n=2), who relapsed after treatment with imatinib compared with those isolated at their initial presentation.	imatinib	270-278	DNA methyltransferase 3 alpha	Homo sapiens	37-43
22829096-6	2011	Furthermore, we found that levels of DNMT3A and EZH2 were strikingly increased in leukemia cells isolated from individuals with chronic myelogenous leukemia (n=1) and Philadelphia chromosome-positive acute lymphoblastic leukemia (n=2), who relapsed after treatment with imatinib compared with those isolated at their initial presentation.	imatinib	270-278	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	48-52
22829096-7	2011	Taken together, imatinib could cause drug-resistance via recruitment of polycomb gene complex to the promoter region of the PTEN and downregulation of this gene"s transcripts in leukemia patients.	imatinib	16-24	phosphatase and tensin homolog	Homo sapiens	124-128
22015344-0	2011	Treatment with imatinib results in reduced IL-4-producing T cells, but increased CD4(+) T cells in the broncho-alveolar lavage of patients with systemic sclerosis.	imatinib	15-23	interleukin 4	Homo sapiens	43-47
22101339-5	2011	Either blocking the functional activity of the KIT protein with imatinib or knocking-down oncogene expression using lentiviral vectors producing shRNA against AML1-ETO or KIT eliminated the sensitivity of Kasumi-1 cells to binase toxic action and promoted their survival, even in the absence of KIT-dependent proliferation and antiapoptotic pathways.	imatinib	64-72	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	47-50
22015344-0	2011	Treatment with imatinib results in reduced IL-4-producing T cells, but increased CD4(+) T cells in the broncho-alveolar lavage of patients with systemic sclerosis.	imatinib	15-23	CD4 molecule	Homo sapiens	81-84
22015344-8	2011	Post-imatinib increase in CD4(+) T cells correlated with soluble ICAM-3 and PECAM-1 levels in BAL, which associated with the lack of worsening in SSc-ILD.	imatinib	5-13	CD4 molecule	Homo sapiens	26-29
22015344-8	2011	Post-imatinib increase in CD4(+) T cells correlated with soluble ICAM-3 and PECAM-1 levels in BAL, which associated with the lack of worsening in SSc-ILD.	imatinib	5-13	intercellular adhesion molecule 3	Homo sapiens	65-71
22015344-8	2011	Post-imatinib increase in CD4(+) T cells correlated with soluble ICAM-3 and PECAM-1 levels in BAL, which associated with the lack of worsening in SSc-ILD.	imatinib	5-13	platelet and endothelial cell adhesion molecule 1	Homo sapiens	76-83
22015344-9	2011	Thus, imatinib might confer its therapeutic effect in fibrosis via re-directing T cell responses from type 2 to other, non-type 2 cytokine producing CD4(+) T cells.	imatinib	6-14	CD4 molecule	Homo sapiens	149-152
21645124-10	2011	Irresectable or metastatic transformed DFSP harbouring the COL1A1-PDGFB fusion gene should be treated with imatinib in the palliative setting or as an adjunctive treatment before surgery, although responses may be short-lasting.	imatinib	107-115	collagen type I alpha 1 chain	Homo sapiens	59-65
21676437-7	2011	Because of the presumptive platelet-derived growth factor receptor alpha translocation and its sensitivity to tyrosine-kinase inhibitor, the patient was treated with imatinib mesylate, cytarabine, and idarubicin as induction and maintenance therapy; and she has remained free of disease for 5 months since the initial diagnosis.	imatinib	166-183	platelet derived growth factor receptor alpha	Homo sapiens	27-72
22057509-0	2011	Successful treatment of lymphoid blastic crisis in chronic myelogenous leukemia with the additional bcr/abl transcript using imatinib-combined chemotherapy and high-dose chemotherapy with allogeneic bone marrow stem cell transplantation.	imatinib	125-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
22204765-4	2011	These findings have been quite significant, as those individuals with a FIP1L1-PDGFRA fusion have an exquisite susceptibility to tyrosine kinase inhibitors (TKIs), such as imatinib mesylate.	imatinib	172-189	factor interacting with PAPOLA and CPSF1	Homo sapiens	72-78
22204765-4	2011	These findings have been quite significant, as those individuals with a FIP1L1-PDGFRA fusion have an exquisite susceptibility to tyrosine kinase inhibitors (TKIs), such as imatinib mesylate.	imatinib	172-189	platelet derived growth factor receptor alpha	Homo sapiens	79-85
22204765-6	2011	Unfortunately, TKIs have not been shown to be particularly active in the case of mastocytosis, although the majority of patients with mastocytosis carry a c-KIT alteration, a target of agents such as imatinib.	imatinib	200-208	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	155-160
21847523-5	2011	In vitro, imatinib and sorafenib inhibited astrocyte proliferation mediated by the tyrosine kinase platelet-derived growth factor receptor (PDGFR), whereas GW2580 and sorafenib inhibited macrophage tumor necrosis factor (TNF) production mediated by the tyrosine kinases c-Fms and PDGFR, respectively.	imatinib	10-18	platelet derived growth factor receptor, beta polypeptide	Mus musculus	99-138
21847523-5	2011	In vitro, imatinib and sorafenib inhibited astrocyte proliferation mediated by the tyrosine kinase platelet-derived growth factor receptor (PDGFR), whereas GW2580 and sorafenib inhibited macrophage tumor necrosis factor (TNF) production mediated by the tyrosine kinases c-Fms and PDGFR, respectively.	imatinib	10-18	platelet derived growth factor receptor, beta polypeptide	Mus musculus	140-145
21645124-10	2011	Irresectable or metastatic transformed DFSP harbouring the COL1A1-PDGFB fusion gene should be treated with imatinib in the palliative setting or as an adjunctive treatment before surgery, although responses may be short-lasting.	imatinib	107-115	platelet derived growth factor subunit B	Homo sapiens	66-71
21716259-8	2011	Imatinib, a PDGFR tyrosine kinase inhibitor, attenuated pericyte proliferation and kidney fibrosis in both fibrogenic models.	imatinib	0-8	platelet derived growth factor receptor, beta polypeptide	Mus musculus	12-17
21955167-5	2011	We report a case of a 60-year-old woman with a heavily pretreated recurrent, c-kit positive, GCT of the ovary who underwent an experimental therapy with imatinib, a tyrosine kinase inhibitor.	imatinib	153-161	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	77-82
21892101-2	2011	We hypothesized that imatinib mesylate would inhibit platelet-derived growth factor receptor (PDGFR) on pericytes and increase docetaxel uptake into tumor cells for an additive antitumor effect.	imatinib	21-38	platelet derived growth factor receptor beta	Homo sapiens	53-92
21892101-2	2011	We hypothesized that imatinib mesylate would inhibit platelet-derived growth factor receptor (PDGFR) on pericytes and increase docetaxel uptake into tumor cells for an additive antitumor effect.	imatinib	21-38	platelet derived growth factor receptor beta	Homo sapiens	94-99
22069175-1	2011	Progression on first-line therapy with imatinib in gastrointestinal stromal tumors (GIST) is caused by either initial resistance or more often a secondary mutation in tyrosine kinases KIT or PDGFR.	imatinib	39-47	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	184-187
22069175-1	2011	Progression on first-line therapy with imatinib in gastrointestinal stromal tumors (GIST) is caused by either initial resistance or more often a secondary mutation in tyrosine kinases KIT or PDGFR.	imatinib	39-47	platelet derived growth factor receptor beta	Homo sapiens	191-196
22069175-2	2011	Therapies in development for imatinib-resistant GIST include agents that target KIT/PDGFR with greater potency or possess broader kinase inhibition profiles including VEGFR.	imatinib	29-37	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	80-83
22069175-2	2011	Therapies in development for imatinib-resistant GIST include agents that target KIT/PDGFR with greater potency or possess broader kinase inhibition profiles including VEGFR.	imatinib	29-37	platelet derived growth factor receptor beta	Homo sapiens	84-89
22069175-2	2011	Therapies in development for imatinib-resistant GIST include agents that target KIT/PDGFR with greater potency or possess broader kinase inhibition profiles including VEGFR.	imatinib	29-37	kinase insert domain receptor	Homo sapiens	167-172
20799000-1	2011	Gastrointestinal stromal tumors lacking mutations in KIT or PDGFRalpha are known as wild type (WT) and are less responsive to imatinib.	imatinib	126-134	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	53-56
20799000-1	2011	Gastrointestinal stromal tumors lacking mutations in KIT or PDGFRalpha are known as wild type (WT) and are less responsive to imatinib.	imatinib	126-134	platelet derived growth factor receptor alpha	Homo sapiens	60-70
22190996-0	2011	Imatinib Mesylate for Patients with Recurrent or Metastatic Gastrointestinal Stromal Tumors Expressing KIT: A Decade Experience from Taiwan.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	103-106
21892628-5	2011	In vitro, BCR-ABL kinase inhibitor imatinib mesylate or siRNA specific to BCR-ABL upregulated SARI mRNA expression in human leukemia cells.	imatinib	35-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
21969494-0	2011	Impressive response with imatinib in a heavily pretreated patient with metastatic c-KIT mutated thymic carcinoma.	imatinib	25-33	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	82-87
21892628-5	2011	In vitro, BCR-ABL kinase inhibitor imatinib mesylate or siRNA specific to BCR-ABL upregulated SARI mRNA expression in human leukemia cells.	imatinib	35-52	basic leucine zipper ATF-like transcription factor 2	Homo sapiens	94-98
21892628-7	2011	Functionally, silencing of SARI in CML-derived cell line K562 partially decreased imatinib mesylate-induced apoptosis.	imatinib	82-99	basic leucine zipper ATF-like transcription factor 2	Homo sapiens	27-31
22169301-3	2011	The result showed that PDGFRalpha fusion gene was found in 6 out of the 146 bone marrow or peripheral blood samples, the positive rate was 4.11%, 4 from the 6 patients received treatment with imatinib and showed therapeutic effect.	imatinib	192-200	platelet derived growth factor receptor alpha	Homo sapiens	23-33
22100163-3	2011	In mice, the ABL family tyrosine kinase inhibitor, imatinib (Gleevec), when administered prophylactically or therapeutically, reduced both the number of granulomatous lesions and bacterial load in infected organs and was also effective against a rifampicin-resistant strain.	imatinib	51-59	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	13-16
21931114-3	2011	We have previously shown that residual BCR-ABL(+) progenitors can be detected in CML patients within the first 2 years of imatinib treatment.	imatinib	122-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
22100163-3	2011	In mice, the ABL family tyrosine kinase inhibitor, imatinib (Gleevec), when administered prophylactically or therapeutically, reduced both the number of granulomatous lesions and bacterial load in infected organs and was also effective against a rifampicin-resistant strain.	imatinib	61-68	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	13-16
21990409-0	2011	Sensitive detection of BCR-ABL1 mutations in patients with chronic myeloid leukemia after imatinib resistance is predictive of outcome during subsequent therapy.	imatinib	90-98	BCR activator of RhoGEF and GTPase	Homo sapiens	23-31
21763684-7	2011	Pharmacological inhibition of c-Abl by Imatinib (STI571) protects the ovarian reserve from the toxic effect of cisplatin.	imatinib	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-35
21763684-7	2011	Pharmacological inhibition of c-Abl by Imatinib (STI571) protects the ovarian reserve from the toxic effect of cisplatin.	imatinib	49-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-35
21990409-1	2011	PURPOSE: BCR-ABL1 mutation analysis is recommended to facilitate selection of appropriate therapy for patients with chronic myeloid leukemia after treatment with imatinib has failed, since some frequently occurring mutations confer clinical resistance to nilotinib and/or dasatinib.	imatinib	162-170	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-17
21769849-1	2011	OBJECTIVE: Transforming growth factor beta (TGFbeta) and platelet-derived growth factor (PDGF) may play a critical role in systemic sclerosis (SSc)-related interstitial lung disease (ILD), and imatinib is a potent inhibitor of TGFbeta and PDGF production.	imatinib	193-201	transforming growth factor beta 1	Homo sapiens	44-51
21990039-4	2011	One of the compounds obtained shows general activity similar to that of imatinib; in particular, it was observed to be more effective in decreasing the fundamental function of cdc25A phosphatases in the K-562 cell line.	imatinib	72-80	cell division cycle 25A	Homo sapiens	176-182
21982419-3	2011	Fortunately, CML has been the epicenter of exciting advances in cancer therapy with the discovery of the Bcr-Abl gene fusion and the subsequent development of imatinib mesylate, a small molecule tyrosine kinase inhibitor, to target the kinase activity of the bcr-abl protein product.	imatinib	159-176	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	259-266
21757001-11	2011	In the human GIST882 imatinib sensitive cell line, both PTEN and SHIP2 were expressed and showed, in part, a nuclear localization.	imatinib	21-29	phosphatase and tensin homolog	Homo sapiens	56-60
21757001-11	2011	In the human GIST882 imatinib sensitive cell line, both PTEN and SHIP2 were expressed and showed, in part, a nuclear localization.	imatinib	21-29	inositol polyphosphate phosphatase like 1	Homo sapiens	65-70
21805039-0	2011	Chemotherapeutic alteration of VEGF-/PDGF- and PDGF-Ralpha/beta expression by imatinib in HPV-transformed squamous cell carcinoma compared to HPV-negative HNSCC in vitro.	imatinib	78-86	vascular endothelial growth factor A	Homo sapiens	31-35
21948230-2	2011	Patients with chronic phase chronic myeloid leukemia who respond to imatinib have a rapid initial decrease in BCR-ABL transcript levels (alpha), followed by a slow decline (beta).	imatinib	68-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
21828123-5	2011	In these 2 patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to show that the leukemic clone remains detectable, as we have previously shown in imatinib-treated patients.	imatinib	162-170	BCR activator of RhoGEF and GTPase	Homo sapiens	62-70
21718141-5	2011	Two imatinib-resistant K562 lines both had increased BCR-ABL expression as the apparent mode of resistance.	imatinib	4-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
21903771-0	2011	BCR-ABL transcript dynamics support the hypothesis that leukemic stem cells are reduced during imatinib treatment.	imatinib	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
21903771-3	2011	EXPERIMENTAL DESIGN: Patients with at least 1 BCR-ABL transcript measurement on imatinib were included (N = 477).	imatinib	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
21903771-4	2011	Maximum likelihood methods were used to test 3 potential hypotheses of the dynamics of BCR-ABL transcripts on imatinib therapy: (i) monoexponential, in which there is little, if any, decline in BCR-ABL transcripts; (ii) biexponential, in which patients have a rapid initial decrease in BCR-ABL transcripts followed by a more gradual response; and (iii) triexponential, in which patients first exhibit a biphasic decline but then have a third phase when BCR-ABL transcripts increase rapidly.	imatinib	110-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
21903771-5	2011	RESULTS: We found that most patients treated with imatinib exhibit a biphasic decrease in BCR-ABL transcript levels, with a rapid decrease during the first few months of treatment, followed by a more gradual decrease that often continues over many years.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
22183070-5	2011	In the first 6 months of imatinib therapy, AHI1 expression was found to increase and then gradually decrease.	imatinib	25-33	Abelson helper integration site 1	Homo sapiens	43-47
21935931-2	2011	In this study, we show that inhibition of Bcr-Abl oncogene by imatinib induces down-regulation of Jab1 in Bcr-Abl-positive K562, Ku812, and MEG01 leukemia cells suggesting Bcr-Abl may regulate Jab1 expression.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
21935931-2	2011	In this study, we show that inhibition of Bcr-Abl oncogene by imatinib induces down-regulation of Jab1 in Bcr-Abl-positive K562, Ku812, and MEG01 leukemia cells suggesting Bcr-Abl may regulate Jab1 expression.	imatinib	62-70	COP9 signalosome subunit 5	Homo sapiens	98-102
21935931-2	2011	In this study, we show that inhibition of Bcr-Abl oncogene by imatinib induces down-regulation of Jab1 in Bcr-Abl-positive K562, Ku812, and MEG01 leukemia cells suggesting Bcr-Abl may regulate Jab1 expression.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
21935931-2	2011	In this study, we show that inhibition of Bcr-Abl oncogene by imatinib induces down-regulation of Jab1 in Bcr-Abl-positive K562, Ku812, and MEG01 leukemia cells suggesting Bcr-Abl may regulate Jab1 expression.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
21935931-2	2011	In this study, we show that inhibition of Bcr-Abl oncogene by imatinib induces down-regulation of Jab1 in Bcr-Abl-positive K562, Ku812, and MEG01 leukemia cells suggesting Bcr-Abl may regulate Jab1 expression.	imatinib	62-70	COP9 signalosome subunit 5	Homo sapiens	193-197
21718141-8	2011	In contrast, three imatinib-resistant K562 Dox lines exhibited only a further increase in ABCB1 expression.	imatinib	19-27	ATP binding cassette subfamily B member 1	Homo sapiens	90-95
21718141-9	2011	All TKI-resistant cell lines generated had increased IC(50) (dose of drug required to reduce phosphorylation of the adaptor protein p-Crkl by 50%) to imatinib, dasatinib, and nilotinib, regardless of which TKI was used to induce resistance.	imatinib	150-158	CRK like proto-oncogene, adaptor protein	Homo sapiens	134-138
21762985-1	2011	We investigated whether low-level Bcr-Abl kinase domain mutations can be detected in patients who have stable responses to first-line nilotinib-like it is known to happen in patients receiving imatinib.	imatinib	193-201	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
22141136-0	2011	Mechanisms of AXL overexpression and function in Imatinib-resistant chronic myeloid leukemia cells.	imatinib	49-57	AXL receptor tyrosine kinase	Homo sapiens	14-17
22141136-2	2011	We previously identified AXL overexpression in Imatinib (IM)-resistant CML cell lines and patients.	imatinib	47-55	AXL receptor tyrosine kinase	Homo sapiens	25-28
22141136-2	2011	We previously identified AXL overexpression in Imatinib (IM)-resistant CML cell lines and patients.	imatinib	57-59	AXL receptor tyrosine kinase	Homo sapiens	25-28
21805039-11	2011	ELISA immunohistochemical methods were carried out after 48, 72, 120, 192 and 240 h. We demonstrated a significant reduction of VEGF and PDGF-Ralpha/beta expression patterns after incubation of imatinib in ELISA and immunohistochemical methods, irrespective of the HPV status of the tumor cells, whereas the application of carboplatin had no impact on the expression of angiogenic peptides.	imatinib	194-202	vascular endothelial growth factor A	Homo sapiens	128-132
21805039-12	2011	Viral oncogen-transformed squamous cell carcinoma (CERV196) cells were characterized by a reduced susceptibility for an imatinib-altered VEGF expression.	imatinib	120-128	vascular endothelial growth factor A	Homo sapiens	137-141
21821707-2	2011	Inhibitors of Bcr-abl such as imatinib mesylate have replaced the cytokine IFNalpha as the primary treatment for the management of patients with this malignancy.	imatinib	30-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
22191306-1	2011	BACKGROUND/AIM: Imatinib mesylate, a selective Bcr-Abl tyrosine kinase inhibitor, has revolutionized the treatment of Bcr-Abl positive chronic myeloid leukemia and become the standard of care for this disease.	imatinib	16-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
22191306-1	2011	BACKGROUND/AIM: Imatinib mesylate, a selective Bcr-Abl tyrosine kinase inhibitor, has revolutionized the treatment of Bcr-Abl positive chronic myeloid leukemia and become the standard of care for this disease.	imatinib	16-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
21821707-3	2011	We found that pretreatment of CML cells with imatinib mesylate augments the antigrowth effects of IFNalpha.	imatinib	45-62	interferon alpha 1	Homo sapiens	98-106
21828142-12	2011	We conclude that cGVHD responds to imatinib through multiple pathways that may include PDGFRA signal transduction.	imatinib	35-43	platelet derived growth factor receptor alpha	Homo sapiens	87-93
21455220-2	2011	This discrepancy illustrates the limited success of RTK antagonists in solid tumor treatment compared with the impact of Imatinib in BCR-ABL-dependent leukemia.	imatinib	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
21970335-4	2011	CASE PRESENTATION: We report on a 76-year-old patient with EGFR-overexpressing advanced chordoma that progressed on imatinib and subsequently responded to erlotinib during 12 months.	imatinib	116-124	epidermal growth factor receptor	Homo sapiens	59-63
21970485-2	2011	They harbor specific activating mutations in the KIT or platelet-derived growth factor receptor alpha ( PDGFRA ) receptor tyrosine kinases, which makes them responsive to pharmacologic inhibitors, such as imatinib mesylate and sunitinib malate.	imatinib	205-222	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	49-52
21970485-2	2011	They harbor specific activating mutations in the KIT or platelet-derived growth factor receptor alpha ( PDGFRA ) receptor tyrosine kinases, which makes them responsive to pharmacologic inhibitors, such as imatinib mesylate and sunitinib malate.	imatinib	205-222	platelet derived growth factor receptor alpha	Homo sapiens	56-101
21970485-2	2011	They harbor specific activating mutations in the KIT or platelet-derived growth factor receptor alpha ( PDGFRA ) receptor tyrosine kinases, which makes them responsive to pharmacologic inhibitors, such as imatinib mesylate and sunitinib malate.	imatinib	205-222	platelet derived growth factor receptor alpha	Homo sapiens	104-110
21523440-0	2011	Backbone assignment of the tyrosine kinase Src catalytic domain in complex with imatinib.	imatinib	80-88	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	43-46
21523440-2	2011	The assignment of backbone (1)H(N), (13)C(alpha), (13)CO, and (15)N, and sidechain (13)C(beta) resonances of the catalytic domain of Src (283 residues) in complex with the anticancer drug Imatinib is reported here.	imatinib	188-196	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	133-136
21810089-2	2011	Targeted therapies, such as the anti-CD20 antibody rituximab, or the BCR-ABL1 inhibitor imatinib, have proven to be effective treatments in the management of some of these malignancies, though relapsing or refractory disease is still common.	imatinib	88-96	BCR activator of RhoGEF and GTPase	Homo sapiens	69-77
21723805-1	2011	The success of tyrosine kinase inhibition of the BCR-ABL fusion gene with imatinib in the treatment of chronic myeloid leukemia (CML) has resulted in the use of molecular detection techniques for routine clinical management.	imatinib	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
21705667-10	2011	Furthermore, PDMP sensitized the most clinical problematic drug-resistant CML T315I mutant to Bcr-Abl inhibitor GNF-2-, imatinib-, or nilotinib-induced apoptosis by >5-fold.	imatinib	120-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
21641899-2	2011	Indeed imatinib mesylate (Gleevec( )) treatment has dramatically improved the management of these tumors as they frequently express the c-kit oncogene.	imatinib	7-24	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	136-141
21934616-6	2011	SUMMARY: Gastric GISTs are relatively frequent and recent data indicate that imatinib-resistant PDGFRA-D842V mutation may be found in up to 10% of cases of localized gastric GISTs and this impacts the prescription of adjuvant imatinib.	imatinib	77-85	platelet derived growth factor receptor alpha	Homo sapiens	96-102
21934616-6	2011	SUMMARY: Gastric GISTs are relatively frequent and recent data indicate that imatinib-resistant PDGFRA-D842V mutation may be found in up to 10% of cases of localized gastric GISTs and this impacts the prescription of adjuvant imatinib.	imatinib	226-234	platelet derived growth factor receptor alpha	Homo sapiens	96-102
21934616-8	2011	Furthermore these tumors frequently harbor KIT exon 9 mutations for which the adequate dose of adjuvant imatinib is debated.	imatinib	104-112	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	43-46
21873591-7	2011	Their profiling shows surprisingly that imatinib has a preference for the active form of CSF1R and that Ki20227 has an unusually slow target dissociation rate.	imatinib	40-48	colony stimulating factor 1 receptor	Homo sapiens	89-94
22054731-4	2011	Over 100 point mutations coding for single amino acid substitutions in the BCR-ABL kinase domain have been isolated from CML patients resistant to imatinib treatment.	imatinib	147-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
22054731-6	2011	BCR-ABL mutations affect amino acids involved in imatinib binding or in regulatory regions of the BCR-ABL kinase domain, resulting in decreased sensitivity to imatinib while retaining aberrant kinase activity.	imatinib	49-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
22054731-6	2011	BCR-ABL mutations affect amino acids involved in imatinib binding or in regulatory regions of the BCR-ABL kinase domain, resulting in decreased sensitivity to imatinib while retaining aberrant kinase activity.	imatinib	159-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
22054731-6	2011	BCR-ABL mutations affect amino acids involved in imatinib binding or in regulatory regions of the BCR-ABL kinase domain, resulting in decreased sensitivity to imatinib while retaining aberrant kinase activity.	imatinib	159-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
21833718-0	2011	Targeting glucosylceramide synthase sensitizes imatinib-resistant chronic myeloid leukemia cells via endogenous ceramide accumulation.	imatinib	47-55	UDP-glucose ceramide glucosyltransferase	Homo sapiens	10-35
21833718-2	2011	Pro-apoptotic ceramide mediates imatinib-induced apoptosis, and metabolism of ceramide by glucosylceramide synthase (GCS) activity, converting ceramide to glucosyl ceramide, might contribute to imatinib resistance.	imatinib	194-202	UDP-glucose ceramide glucosyltransferase	Homo sapiens	90-115
21833718-2	2011	Pro-apoptotic ceramide mediates imatinib-induced apoptosis, and metabolism of ceramide by glucosylceramide synthase (GCS) activity, converting ceramide to glucosyl ceramide, might contribute to imatinib resistance.	imatinib	194-202	UDP-glucose ceramide glucosyltransferase	Homo sapiens	117-120
21833718-3	2011	In this study, we investigated the role of ceramide metabolism by GCS in the regulation of imatinib-induced apoptosis in drug-sensitive and drug-resistant K562 and K562/IMA-0.2 and K562/IMA-1 human CML cells, which exhibit about 2.3- and 19-fold imatinib resistance, respectively.	imatinib	91-99	UDP-glucose ceramide glucosyltransferase	Homo sapiens	66-69
21833718-10	2011	Next, forced expression of GCS in sensitive K562 cells conferred resistance to imatinib-induced apoptosis.	imatinib	79-87	UDP-glucose ceramide glucosyltransferase	Homo sapiens	27-30
21833718-11	2011	In reciprocal experiments, targeting GCS using its known inhibitor, PDMP, enhanced ceramide accumulation and increased cell death in response to imatinib in K562/IMA cells.	imatinib	145-153	UDP-glucose ceramide glucosyltransferase	Homo sapiens	37-40
21833718-12	2011	CONCLUSION: Our data suggest the involvement of GCS in resistance to imatinib-induced apoptosis, and that targeting GCS by PDMP increased imatinib-induced cell death in drug-sensitive and drug-resistant K562 cells via enhancing ceramide accumulation.	imatinib	138-146	UDP-glucose ceramide glucosyltransferase	Homo sapiens	116-119
21570118-0	2011	AID expression is correlated with Bcr-Abl expression in CML-LBC and can be down-regulated by As2O3 and/or imatinib.	imatinib	106-114	activation induced cytidine deaminase	Homo sapiens	0-3
21570118-0	2011	AID expression is correlated with Bcr-Abl expression in CML-LBC and can be down-regulated by As2O3 and/or imatinib.	imatinib	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
21570118-4	2011	AID expression was significantly decreased in CML-LBC cells after treated with arsenic trioxide, especially together with imatinib.	imatinib	122-130	activation induced cytidine deaminase	Homo sapiens	0-3
21663515-0	2011	Development of imatinib and dasatinib resistance: dynamics of expression of drug transporters ABCB1, ABCC1, ABCG2, MVP, and SLC22A1.	imatinib	15-23	ATP binding cassette subfamily B member 1	Homo sapiens	94-99
22040950-10	2011	It provides a possible explanation that blockage of PDGFR may reduce thrombopoiesis and play a role in imatinib mesylate-induced thrombocytopenia.	imatinib	103-120	platelet derived growth factor receptor beta	Homo sapiens	52-57
21663515-0	2011	Development of imatinib and dasatinib resistance: dynamics of expression of drug transporters ABCB1, ABCC1, ABCG2, MVP, and SLC22A1.	imatinib	15-23	ATP binding cassette subfamily C member 1	Homo sapiens	101-106
21663515-0	2011	Development of imatinib and dasatinib resistance: dynamics of expression of drug transporters ABCB1, ABCC1, ABCG2, MVP, and SLC22A1.	imatinib	15-23	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	108-113
21663515-0	2011	Development of imatinib and dasatinib resistance: dynamics of expression of drug transporters ABCB1, ABCC1, ABCG2, MVP, and SLC22A1.	imatinib	15-23	major vault protein	Homo sapiens	115-118
21663515-0	2011	Development of imatinib and dasatinib resistance: dynamics of expression of drug transporters ABCB1, ABCC1, ABCG2, MVP, and SLC22A1.	imatinib	15-23	solute carrier family 22 member 1	Homo sapiens	124-131
21903705-12	2011	Pfetin appears to be a novel clinically applicable prognostic factor, which may be useful for deciding whether to administer imatinib mesylate or not.	imatinib	125-142	potassium channel tetramerization domain containing 12	Homo sapiens	0-6
22040995-4	2011	It is suggested that imatinib may block the PDGF/PDGFR and PI3-K/Akt pathway, then inducing the apoptosis of megakaryocytes and developing thrombocytopenia in these patients.	imatinib	21-29	platelet derived growth factor receptor beta	Homo sapiens	49-54
22339825-0	2011	[Imatinib combined with modified hyper-CVAD/MA followed by allogeneic hematopoietic stem cell transplantation in CR1 as the front-line therapy for adult Ph(+) acute lymphoblastic leukemia].	imatinib	1-9	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	113-116
22040995-4	2011	It is suggested that imatinib may block the PDGF/PDGFR and PI3-K/Akt pathway, then inducing the apoptosis of megakaryocytes and developing thrombocytopenia in these patients.	imatinib	21-29	AKT serine/threonine kinase 1	Homo sapiens	65-68
22040995-5	2011	In this review, the potential molecular mechanism of imatinib-induced thrombocytopenia in the treatment of CML patients is discussed, including imatinib and thrombocytopenia, PDGF/PDGFR and thrombopoiesis, potential mechanism of imatinib-induced thrombocytopenia in treatment of patients with CML and so on.	imatinib	53-61	platelet derived growth factor receptor beta	Homo sapiens	180-185
22339825-1	2011	OBJECTIVE: To explore the efficacy of imatinib (IM)-based chemotherapy followed by allogeneic hematopoietic stem cell transplantation (allo-SCT) in first complete remission (CR1) for adult Ph(+) acute lymphoblastic leukemia \[Ph(+)-ALL\].	imatinib	38-46	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	174-177
22339825-1	2011	OBJECTIVE: To explore the efficacy of imatinib (IM)-based chemotherapy followed by allogeneic hematopoietic stem cell transplantation (allo-SCT) in first complete remission (CR1) for adult Ph(+) acute lymphoblastic leukemia \[Ph(+)-ALL\].	imatinib	48-50	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	174-177
21795709-7	2011	Furthermore, PTP1B inhibition reduces cell viability and the IC(50) of the Bcr-Abl inhibitor imatinib mesylate.	imatinib	93-110	protein tyrosine phosphatase non-receptor type 1	Homo sapiens	13-18
21821701-0	2011	SHP-1 expression accounts for resistance to imatinib treatment in Philadelphia chromosome-positive cells derived from patients with chronic myeloid leukemia.	imatinib	44-52	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	0-5
21821701-1	2011	We prove that the SH2-containing tyrosine phosphatase 1 (SHP-1) plays a prominent role as resistance determinant of imatinib (IMA) treatment response in chronic myelogenous leukemia cell lines (sensitive/KCL22-S and resistant/KCL22-R).	imatinib	116-124	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	18-55
21821701-1	2011	We prove that the SH2-containing tyrosine phosphatase 1 (SHP-1) plays a prominent role as resistance determinant of imatinib (IMA) treatment response in chronic myelogenous leukemia cell lines (sensitive/KCL22-S and resistant/KCL22-R).	imatinib	116-124	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	57-62
21821701-1	2011	We prove that the SH2-containing tyrosine phosphatase 1 (SHP-1) plays a prominent role as resistance determinant of imatinib (IMA) treatment response in chronic myelogenous leukemia cell lines (sensitive/KCL22-S and resistant/KCL22-R).	imatinib	126-129	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	18-55
21821701-1	2011	We prove that the SH2-containing tyrosine phosphatase 1 (SHP-1) plays a prominent role as resistance determinant of imatinib (IMA) treatment response in chronic myelogenous leukemia cell lines (sensitive/KCL22-S and resistant/KCL22-R).	imatinib	126-129	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	57-62
21821701-3	2011	In KCL22-R SHP-1 ectopic expression restores both SHP-1/SHP-2 interaction and IMA responsiveness; it also decreases SHP-2 activity after IMA treatment.	imatinib	78-81	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	11-16
21658383-7	2011	Cells were exposed to 0.1-100 muM imatinib for 24 and 48 h. Dose-dependent decreases in cell viability and morphological changes were observed.	imatinib	34-42	latexin	Homo sapiens	30-33
21658383-8	2011	Moreover, the apoptotic effect of imatinib (10 muM, 50 muM) after 24 h of exposure was demonstrated as evaluated by translocation of phosphatidylserine to external membrane leaflet and by increased activity of caspase-3.	imatinib	34-42	latexin	Homo sapiens	47-50
21658383-8	2011	Moreover, the apoptotic effect of imatinib (10 muM, 50 muM) after 24 h of exposure was demonstrated as evaluated by translocation of phosphatidylserine to external membrane leaflet and by increased activity of caspase-3.	imatinib	34-42	latexin	Homo sapiens	55-58
21658383-8	2011	Moreover, the apoptotic effect of imatinib (10 muM, 50 muM) after 24 h of exposure was demonstrated as evaluated by translocation of phosphatidylserine to external membrane leaflet and by increased activity of caspase-3.	imatinib	34-42	caspase 3	Homo sapiens	210-219
21943129-7	2011	RESULTS: Our proteomic results indicate an elevated concentration of Stem Cell Growth Factor (SCGF), a hematopoietic growth factor having a role in the development of erythroid and myeloid progenitors, in imatinib-responsive tumor areas.	imatinib	205-213	C-type lectin domain containing 11A	Homo sapiens	69-92
21943129-7	2011	RESULTS: Our proteomic results indicate an elevated concentration of Stem Cell Growth Factor (SCGF), a hematopoietic growth factor having a role in the development of erythroid and myeloid progenitors, in imatinib-responsive tumor areas.	imatinib	205-213	C-type lectin domain containing 11A	Homo sapiens	94-98
21795709-7	2011	Furthermore, PTP1B inhibition reduces cell viability and the IC(50) of the Bcr-Abl inhibitor imatinib mesylate.	imatinib	93-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
21795709-9	2011	These results suggest that inhibition of PTP1B may be a useful strategy to explore in the development of novel therapeutic agents for the treatment of CML, particularly because host drugs currently used in CML such as imatinib focus on inhibiting the kinase activity of Bcr-Abl.	imatinib	218-226	protein tyrosine phosphatase non-receptor type 1	Homo sapiens	41-46
21795709-9	2011	These results suggest that inhibition of PTP1B may be a useful strategy to explore in the development of novel therapeutic agents for the treatment of CML, particularly because host drugs currently used in CML such as imatinib focus on inhibiting the kinase activity of Bcr-Abl.	imatinib	218-226	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	270-277
21715304-6	2011	Previous studies have shown that the BCR-ABL inhibitor imatinib mesylate induces both apoptosis and autophagy, and that the resultant autophagy modulates the efficiency by which imatinib kills BCR-ABL-transformed cells.	imatinib	55-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
20609486-0	2011	Complete reversal of left ventricular mass in FIP1L1-PDGFRA-positive chronic eosinophilic leukemia after therapy with imatinib.	imatinib	118-126	factor interacting with PAPOLA and CPSF1	Homo sapiens	46-52
21902298-1	2011	Dasatinib (Sprycel ) is an orally administered small molecule inhibitor of multiple tyrosine kinases, including BCR-ABL and SRC family kinases, which is indicated for the treatment of adults with newly diagnosed chronic-phase chronic myeloid leukaemia (CML), CML (chronic-, accelerated- or blast-phase) with resistance or intolerance to prior therapy, including imatinib, or Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukaemia (ALL) with resistance or intolerance to prior therapy.	imatinib	362-370	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
21902298-2	2011	Dasatinib is  325-fold more active than imatinib in inhibiting wild-type ABL kinase in vitro and is active against a wide variety of imatinib-resistant BCR-ABL mutants, except for T315I.	imatinib	133-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-159
21715304-6	2011	Previous studies have shown that the BCR-ABL inhibitor imatinib mesylate induces both apoptosis and autophagy, and that the resultant autophagy modulates the efficiency by which imatinib kills BCR-ABL-transformed cells.	imatinib	55-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	193-200
21715304-6	2011	Previous studies have shown that the BCR-ABL inhibitor imatinib mesylate induces both apoptosis and autophagy, and that the resultant autophagy modulates the efficiency by which imatinib kills BCR-ABL-transformed cells.	imatinib	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
21715304-6	2011	Previous studies have shown that the BCR-ABL inhibitor imatinib mesylate induces both apoptosis and autophagy, and that the resultant autophagy modulates the efficiency by which imatinib kills BCR-ABL-transformed cells.	imatinib	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	193-200
21715304-7	2011	We demonstrate that imatinib-induced autophagy is because of inhibition of the BCR-ABL/PI3K/AKT/FOXO4/ATF5/mTOR pathway that we have identified in this study.	imatinib	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
21715304-7	2011	We demonstrate that imatinib-induced autophagy is because of inhibition of the BCR-ABL/PI3K/AKT/FOXO4/ATF5/mTOR pathway that we have identified in this study.	imatinib	20-28	AKT serine/threonine kinase 1	Homo sapiens	92-95
21715304-7	2011	We demonstrate that imatinib-induced autophagy is because of inhibition of the BCR-ABL/PI3K/AKT/FOXO4/ATF5/mTOR pathway that we have identified in this study.	imatinib	20-28	forkhead box O4	Homo sapiens	96-101
21715304-7	2011	We demonstrate that imatinib-induced autophagy is because of inhibition of the BCR-ABL/PI3K/AKT/FOXO4/ATF5/mTOR pathway that we have identified in this study.	imatinib	20-28	activating transcription factor 5	Homo sapiens	102-106
21715304-7	2011	We demonstrate that imatinib-induced autophagy is because of inhibition of the BCR-ABL/PI3K/AKT/FOXO4/ATF5/mTOR pathway that we have identified in this study.	imatinib	20-28	mechanistic target of rapamycin kinase	Homo sapiens	107-111
21310760-7	2011	Estimated GFR decreased significantly with imatinib treatment duration; the mean decrease per year was 2.77 ml/min/1.73 m(2) (P < 0.001); 12% of patients developed chronic renal failure.	imatinib	43-51	CD59 molecule (CD59 blood group)	Homo sapiens	111-116
21763682-7	2011	In the orthotopic model, tumor formation by MSTO-211H and Y-Meso-14 cells was significantly inhibited by TSU-68, an inhibitor of FGF, VEGF, and PDGF receptors; imatinib, an inhibitor of PDGF receptors; and NK4, an antagonist of HGF.	imatinib	160-168	fibroblast growth factor 2	Homo sapiens	129-132
21763682-7	2011	In the orthotopic model, tumor formation by MSTO-211H and Y-Meso-14 cells was significantly inhibited by TSU-68, an inhibitor of FGF, VEGF, and PDGF receptors; imatinib, an inhibitor of PDGF receptors; and NK4, an antagonist of HGF.	imatinib	160-168	vascular endothelial growth factor A	Homo sapiens	134-138
21763682-7	2011	In the orthotopic model, tumor formation by MSTO-211H and Y-Meso-14 cells was significantly inhibited by TSU-68, an inhibitor of FGF, VEGF, and PDGF receptors; imatinib, an inhibitor of PDGF receptors; and NK4, an antagonist of HGF.	imatinib	160-168	interleukin 32	Homo sapiens	206-209
21763682-7	2011	In the orthotopic model, tumor formation by MSTO-211H and Y-Meso-14 cells was significantly inhibited by TSU-68, an inhibitor of FGF, VEGF, and PDGF receptors; imatinib, an inhibitor of PDGF receptors; and NK4, an antagonist of HGF.	imatinib	160-168	hepatocyte growth factor	Homo sapiens	228-231
21924129-0	2011	[Durable efficacity and remission after treatment with imatinib mesylate for FIP1L1-PDGFRA transcript negative associated eosinophilic cardiomyopathy].	imatinib	55-72	factor interacting with PAPOLA and CPSF1	Homo sapiens	77-83
21924129-0	2011	[Durable efficacity and remission after treatment with imatinib mesylate for FIP1L1-PDGFRA transcript negative associated eosinophilic cardiomyopathy].	imatinib	55-72	platelet derived growth factor receptor alpha	Homo sapiens	84-90
21924129-3	2011	Since the discovery of the involvement of deregulated tyrosine kinases in the pathophysiology of these diseases, and particularly the identification of the fusion gene FIP1L1-PDGFRA, new molecules inhibiting specifically this signaling pathway (imatinib) were individualized, leading to dramatic therapeutic benefits in proliferative forms of HES considered before that of very poor prognosis.	imatinib	245-253	factor interacting with PAPOLA and CPSF1	Homo sapiens	168-174
21660654-4	2011	Small-molecule tyrosine kinase inhibitors, such as imatinib and dasatinib, directly inhibit the BCR-ABL kinase, offering a targeted approach as a therapeutic option.	imatinib	51-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
21924129-3	2011	Since the discovery of the involvement of deregulated tyrosine kinases in the pathophysiology of these diseases, and particularly the identification of the fusion gene FIP1L1-PDGFRA, new molecules inhibiting specifically this signaling pathway (imatinib) were individualized, leading to dramatic therapeutic benefits in proliferative forms of HES considered before that of very poor prognosis.	imatinib	245-253	platelet derived growth factor receptor alpha	Homo sapiens	175-181
21924129-4	2011	CASE REPORT: We report here the dramatic effectiveness of imatinib used as second line therapy for dilated cardiomyopathy revealing a hypereosinophilic syndrome in a patient in whom the search for FIP1-L1-PDGFRA fusion gene was negative.	imatinib	58-66	factor interacting with PAPOLA and CPSF1	Homo sapiens	197-204
21924129-4	2011	CASE REPORT: We report here the dramatic effectiveness of imatinib used as second line therapy for dilated cardiomyopathy revealing a hypereosinophilic syndrome in a patient in whom the search for FIP1-L1-PDGFRA fusion gene was negative.	imatinib	58-66	platelet derived growth factor receptor alpha	Homo sapiens	205-211
21924129-6	2011	We report here a case of HES lacking the FIP1-L1-PDGFRA fusion gene showing that despite the absence of this molecular defect, imatinib mesylate may have therapeutic interest in those cases of HES resistant to first line therapies.	imatinib	127-144	factor interacting with PAPOLA and CPSF1	Homo sapiens	41-48
21924129-6	2011	We report here a case of HES lacking the FIP1-L1-PDGFRA fusion gene showing that despite the absence of this molecular defect, imatinib mesylate may have therapeutic interest in those cases of HES resistant to first line therapies.	imatinib	127-144	platelet derived growth factor receptor alpha	Homo sapiens	49-55
21576001-0	2011	Reversal of Imatinib resistance in BCR-ABL-positive leukemia after inhibition of the Na+/H+ exchanger.	imatinib	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
21737509-2	2011	Imatinib (IMA) and sunitinib (SUN) are very effective KIT-inhibitors in patients with advanced GIST but have no curative potential.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	54-57
21737509-2	2011	Imatinib (IMA) and sunitinib (SUN) are very effective KIT-inhibitors in patients with advanced GIST but have no curative potential.	imatinib	10-13	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	54-57
21440936-3	2011	When the remaining phosphorylated Crkl after treatment with imatinib was evaluated as the "residual index (RI)", high values were found in accordance with imatinib resistance.	imatinib	60-68	CRK like proto-oncogene, adaptor protein	Homo sapiens	34-38
21863287-7	2011	Tyrosine kinase inhibitors, imatinib and dasatinib, coadministered with dexamethasone achieved transient clinical effects in the present RCSD1-ABL1-positive ALL.	imatinib	28-36	RCSD domain containing 1	Homo sapiens	137-142
21863287-7	2011	Tyrosine kinase inhibitors, imatinib and dasatinib, coadministered with dexamethasone achieved transient clinical effects in the present RCSD1-ABL1-positive ALL.	imatinib	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-147
20860069-0	2011	The duration of the use of imatinib mesylate is only weakly related to elevated BNP levels in chronic myeloid leukaemia patients.	imatinib	27-44	natriuretic peptide B	Homo sapiens	80-83
20860069-11	2011	A weak relation was observed between log BNP and imatinib treatment duration and dose.	imatinib	49-57	natriuretic peptide B	Homo sapiens	41-44
21637917-0	2011	BCR-ABL- and Ras-independent activation of Raf as a novel mechanism of Imatinib resistance in CML.	imatinib	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-16
21637917-0	2011	BCR-ABL- and Ras-independent activation of Raf as a novel mechanism of Imatinib resistance in CML.	imatinib	71-79	zinc fingers and homeoboxes 2	Homo sapiens	43-46
21637917-1	2011	Although the BCR-ABL tyrosine kinase inhibitor Imatinib has undoubtedly revolutionized the therapy of chronic myeloid leukaemia (CML), acquired drug resistance remains a common problem in CML therapy.	imatinib	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
21637917-3	2011	Imatinib-resistant CML cell lines have been widely used for comparative proteome/genome-wide expression screens in order to decipher resistance mechanisms but a clearcut molecular mechanism or molecular player in BCR-ABL-independent resistance to Imatinib has not yet evolved from those studies.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	213-220
21637917-3	2011	Imatinib-resistant CML cell lines have been widely used for comparative proteome/genome-wide expression screens in order to decipher resistance mechanisms but a clearcut molecular mechanism or molecular player in BCR-ABL-independent resistance to Imatinib has not yet evolved from those studies.	imatinib	247-255	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	213-220
21637917-5	2011	Pharmacological analysis evidenced a constitutive, Imatinib-insensitive activation of the Erk-MAPK pathway in resistant cells.	imatinib	51-59	mitogen-activated protein kinase 1	Homo sapiens	90-93
21637917-8	2011	Collectively, these findings highlight a novel mechanism of acquired Imatinib resistance based on the BCR-ABL and Ras-independent constitutive activation of the Erk-MAPK pathway through activated c-Raf, which could prove helpful for a better functional classification of the causes of Imatinib resistance in CML.	imatinib	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
21637917-8	2011	Collectively, these findings highlight a novel mechanism of acquired Imatinib resistance based on the BCR-ABL and Ras-independent constitutive activation of the Erk-MAPK pathway through activated c-Raf, which could prove helpful for a better functional classification of the causes of Imatinib resistance in CML.	imatinib	69-77	mitogen-activated protein kinase 1	Homo sapiens	161-164
21637917-8	2011	Collectively, these findings highlight a novel mechanism of acquired Imatinib resistance based on the BCR-ABL and Ras-independent constitutive activation of the Erk-MAPK pathway through activated c-Raf, which could prove helpful for a better functional classification of the causes of Imatinib resistance in CML.	imatinib	69-77	mitogen-activated protein kinase 1	Homo sapiens	165-169
21637917-8	2011	Collectively, these findings highlight a novel mechanism of acquired Imatinib resistance based on the BCR-ABL and Ras-independent constitutive activation of the Erk-MAPK pathway through activated c-Raf, which could prove helpful for a better functional classification of the causes of Imatinib resistance in CML.	imatinib	69-77	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	196-201
21637917-8	2011	Collectively, these findings highlight a novel mechanism of acquired Imatinib resistance based on the BCR-ABL and Ras-independent constitutive activation of the Erk-MAPK pathway through activated c-Raf, which could prove helpful for a better functional classification of the causes of Imatinib resistance in CML.	imatinib	285-293	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
21637917-8	2011	Collectively, these findings highlight a novel mechanism of acquired Imatinib resistance based on the BCR-ABL and Ras-independent constitutive activation of the Erk-MAPK pathway through activated c-Raf, which could prove helpful for a better functional classification of the causes of Imatinib resistance in CML.	imatinib	285-293	mitogen-activated protein kinase 1	Homo sapiens	161-164
21637917-8	2011	Collectively, these findings highlight a novel mechanism of acquired Imatinib resistance based on the BCR-ABL and Ras-independent constitutive activation of the Erk-MAPK pathway through activated c-Raf, which could prove helpful for a better functional classification of the causes of Imatinib resistance in CML.	imatinib	285-293	mitogen-activated protein kinase 1	Homo sapiens	165-169
21637917-8	2011	Collectively, these findings highlight a novel mechanism of acquired Imatinib resistance based on the BCR-ABL and Ras-independent constitutive activation of the Erk-MAPK pathway through activated c-Raf, which could prove helpful for a better functional classification of the causes of Imatinib resistance in CML.	imatinib	285-293	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	196-201
22052279-1	2011	Imatinib mesylate (STI 571; Gleevec; Novartis Pharmaceuticals, Basel, Switzerland) is an orally available tyrosine kinase inhibitor that targets a constitutively activated BCR-ABL tyrosine kinase with additional inhibitory effects on platelet derived growth factor (PDGF) receptors alpha and beta, and KIT.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	302-305
21641642-8	2011	Imatinib is effective in patients with increased mast cells and eosinophils associated with FIP1L1/PDGFRA+ (e.g., myeloid neoplasm with eosinophilia and rearrangement of PDGFRA) or rare patients with SM associated with KIT mutations outside of exon 17.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	219-222
21663510-0	2011	Clinical outcome of chronic myeloid leukemia imatinib-resistant patients: do BCR-ABL kinase domain mutations affect patient survival?	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
21663510-2	2011	In imatinib-treated patients with chronic myeloid leukemia (CML), BCR-ABL mutations are the most common mechanism of resistance.	imatinib	3-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
21641642-8	2011	Imatinib is effective in patients with increased mast cells and eosinophils associated with FIP1L1/PDGFRA+ (e.g., myeloid neoplasm with eosinophilia and rearrangement of PDGFRA) or rare patients with SM associated with KIT mutations outside of exon 17.	imatinib	0-8	factor interacting with PAPOLA and CPSF1	Homo sapiens	92-98
21641642-8	2011	Imatinib is effective in patients with increased mast cells and eosinophils associated with FIP1L1/PDGFRA+ (e.g., myeloid neoplasm with eosinophilia and rearrangement of PDGFRA) or rare patients with SM associated with KIT mutations outside of exon 17.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	99-105
21641642-8	2011	Imatinib is effective in patients with increased mast cells and eosinophils associated with FIP1L1/PDGFRA+ (e.g., myeloid neoplasm with eosinophilia and rearrangement of PDGFRA) or rare patients with SM associated with KIT mutations outside of exon 17.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	170-176
21440936-3	2011	When the remaining phosphorylated Crkl after treatment with imatinib was evaluated as the "residual index (RI)", high values were found in accordance with imatinib resistance.	imatinib	155-163	CRK like proto-oncogene, adaptor protein	Homo sapiens	34-38
20407854-0	2011	Knockdown of SOD1 sensitizes the CD34+ CML cells to imatinib therapy.	imatinib	52-60	superoxide dismutase 1	Homo sapiens	13-17
20407854-0	2011	Knockdown of SOD1 sensitizes the CD34+ CML cells to imatinib therapy.	imatinib	52-60	CD34 molecule	Homo sapiens	33-37
20407854-4	2011	Knockdown of SOD1 in CD34+ cells had no significant effects on cell survival and growth, while it sensitized the CD34+ cells to imatinib therapy.	imatinib	128-136	superoxide dismutase 1	Homo sapiens	13-17
20407854-4	2011	Knockdown of SOD1 in CD34+ cells had no significant effects on cell survival and growth, while it sensitized the CD34+ cells to imatinib therapy.	imatinib	128-136	CD34 molecule	Homo sapiens	113-117
20407854-5	2011	N-acetyl-L cysteine (NAC) blocked the pro-apoptotic effects of SOD1 knockdown, suggesting the antioxidant effects of SOD1 was essential for the resistance of CD34+ cells to imatinib therapy.	imatinib	173-181	X-linked Kx blood group	Homo sapiens	21-24
20407854-5	2011	N-acetyl-L cysteine (NAC) blocked the pro-apoptotic effects of SOD1 knockdown, suggesting the antioxidant effects of SOD1 was essential for the resistance of CD34+ cells to imatinib therapy.	imatinib	173-181	superoxide dismutase 1	Homo sapiens	63-67
20407854-5	2011	N-acetyl-L cysteine (NAC) blocked the pro-apoptotic effects of SOD1 knockdown, suggesting the antioxidant effects of SOD1 was essential for the resistance of CD34+ cells to imatinib therapy.	imatinib	173-181	superoxide dismutase 1	Homo sapiens	117-121
20407854-5	2011	N-acetyl-L cysteine (NAC) blocked the pro-apoptotic effects of SOD1 knockdown, suggesting the antioxidant effects of SOD1 was essential for the resistance of CD34+ cells to imatinib therapy.	imatinib	173-181	CD34 molecule	Homo sapiens	158-162
21279555-3	2011	The initial response to kinase inhibitors (imatinib mesylate, Gleevec, Novartis) usually is partial and depend on the mutational KIT or PDGFRA state.	imatinib	43-60	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	129-132
21279555-3	2011	The initial response to kinase inhibitors (imatinib mesylate, Gleevec, Novartis) usually is partial and depend on the mutational KIT or PDGFRA state.	imatinib	43-60	platelet derived growth factor receptor alpha	Homo sapiens	136-142
21705501-1	2011	Imatinib-resistant tyrosine kinase (TK) fusions involving FGFR1, JAK2, or FLT3 are rare but recurrent in patients with eosinophilia-associated neoplasms.	imatinib	0-8	TXK tyrosine kinase	Homo sapiens	19-34
21874433-7	2011	We speculate that the treatment might have triggered development of the imatinib mesylate-resistant clone, which may have existed in the primary lesion as a KIT gene mutant.	imatinib	72-89	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	157-160
21867983-2	2011	The most common and best-characterized mechanism of secondary imatinib resistance in CML is the development of kinase domain mutations in the BCR-ABL gene.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
21873989-0	2011	Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido.	imatinib	0-8	indoleamine 2,3-dioxygenase 1	Homo sapiens	108-111
21873989-1	2011	Imatinib mesylate targets mutated KIT oncoproteins in gastrointestinal stromal tumor (GIST) and produces a clinical response in 80% of patients.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	34-37
21873989-4	2011	Imatinib therapy activated CD8(+) T cells and induced regulatory T cell (T(reg) cell) apoptosis within the tumor by reducing tumor-cell expression of the immunosuppressive enzyme indoleamine 2,3-dioxygenase (Ido).	imatinib	0-8	indoleamine 2,3-dioxygenase 1	Homo sapiens	179-206
21873989-4	2011	Imatinib therapy activated CD8(+) T cells and induced regulatory T cell (T(reg) cell) apoptosis within the tumor by reducing tumor-cell expression of the immunosuppressive enzyme indoleamine 2,3-dioxygenase (Ido).	imatinib	0-8	indoleamine 2,3-dioxygenase 1	Homo sapiens	208-211
21705501-1	2011	Imatinib-resistant tyrosine kinase (TK) fusions involving FGFR1, JAK2, or FLT3 are rare but recurrent in patients with eosinophilia-associated neoplasms.	imatinib	0-8	TXK tyrosine kinase	Homo sapiens	36-38
21705501-1	2011	Imatinib-resistant tyrosine kinase (TK) fusions involving FGFR1, JAK2, or FLT3 are rare but recurrent in patients with eosinophilia-associated neoplasms.	imatinib	0-8	fibroblast growth factor receptor 1	Homo sapiens	58-63
21705501-1	2011	Imatinib-resistant tyrosine kinase (TK) fusions involving FGFR1, JAK2, or FLT3 are rare but recurrent in patients with eosinophilia-associated neoplasms.	imatinib	0-8	Janus kinase 2	Homo sapiens	65-69
21705501-1	2011	Imatinib-resistant tyrosine kinase (TK) fusions involving FGFR1, JAK2, or FLT3 are rare but recurrent in patients with eosinophilia-associated neoplasms.	imatinib	0-8	fms related receptor tyrosine kinase 3	Homo sapiens	74-78
21495997-1	2011	A comparison of in vitro and in vivo characteristics of tumour cells derived from patients with mucosal melanoma treated with imatinib was performed with respect to KIT mutations.	imatinib	126-134	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	165-168
21693657-0	2011	Imatinib sensitivity in BCR-ABL1-positive chronic myeloid leukemia cells is regulated by the remaining normal ABL1 allele.	imatinib	0-8	BCR activator of RhoGEF and GTPase	Homo sapiens	24-32
21693657-0	2011	Imatinib sensitivity in BCR-ABL1-positive chronic myeloid leukemia cells is regulated by the remaining normal ABL1 allele.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-32
21693657-1	2011	Chronic myeloid leukemia in chronic phase (CML-CP) cells that harbor oncogenic BCR-ABL1 and normal ABL1 allele often become resistant to the ABL1 kinase inhibitor imatinib.	imatinib	163-171	BCR activator of RhoGEF and GTPase	Homo sapiens	79-87
21693657-1	2011	Chronic myeloid leukemia in chronic phase (CML-CP) cells that harbor oncogenic BCR-ABL1 and normal ABL1 allele often become resistant to the ABL1 kinase inhibitor imatinib.	imatinib	163-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-87
21693657-1	2011	Chronic myeloid leukemia in chronic phase (CML-CP) cells that harbor oncogenic BCR-ABL1 and normal ABL1 allele often become resistant to the ABL1 kinase inhibitor imatinib.	imatinib	163-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-103
21693657-2	2011	Here, we report that loss of the remaining normal ABL1 allele in these tumors, which results from cryptic interstitial deletion in 9q34 in patients who did not achieve a complete cytogenetic remission (CCyR) during treatment, engenders a novel unexpected mechanism of imatinib resistance.	imatinib	268-276	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-54
21693657-3	2011	BCR-ABL1-positive Abl1(-/-) leukemia cells were refractory to imatinib as indicated by persistent BCR-ABL1-mediated tyrosine phosphorylation, lack of BCR-ABL1 protein degradation, increased cell survival, and clonogenic activity.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-8
21693657-3	2011	BCR-ABL1-positive Abl1(-/-) leukemia cells were refractory to imatinib as indicated by persistent BCR-ABL1-mediated tyrosine phosphorylation, lack of BCR-ABL1 protein degradation, increased cell survival, and clonogenic activity.	imatinib	62-70	BCR activator of RhoGEF and GTPase	Homo sapiens	0-8
21693657-4	2011	Expression of ABL1 kinase, but not a kinase-dead mutant, restored the antileukemic effects of imatinib in ABL1-negative chronic myelogenous leukemia (CML) cells and in BCR-ABL1-positive Abl1(-/-) murine leukemia cells.	imatinib	94-102	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	14-18
21693657-4	2011	Expression of ABL1 kinase, but not a kinase-dead mutant, restored the antileukemic effects of imatinib in ABL1-negative chronic myelogenous leukemia (CML) cells and in BCR-ABL1-positive Abl1(-/-) murine leukemia cells.	imatinib	94-102	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	106-110
21693657-4	2011	Expression of ABL1 kinase, but not a kinase-dead mutant, restored the antileukemic effects of imatinib in ABL1-negative chronic myelogenous leukemia (CML) cells and in BCR-ABL1-positive Abl1(-/-) murine leukemia cells.	imatinib	94-102	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	106-110
21693657-6	2011	Furthermore, 12 genes associated with imatinib resistance were favorably deregulated in Abl1(-/-) leukemia.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-92
21425122-8	2011	These effects were mediated by a marked increase in Snail-1 expression and were abolished by treatment with either the c-Abl tyrosine kinase inhibitor imatinib mesylate or the protein kinase Cdelta (PKCdelta) inhibitor rottlerin.	imatinib	151-168	snail family zinc finger 1	Mus musculus	52-59
21425122-8	2011	These effects were mediated by a marked increase in Snail-1 expression and were abolished by treatment with either the c-Abl tyrosine kinase inhibitor imatinib mesylate or the protein kinase Cdelta (PKCdelta) inhibitor rottlerin.	imatinib	151-168	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	119-124
21761433-8	2011	Identification of rearranged PDGFRA or PDGFRB is critical because of the exquisite responsiveness of these diseases to imatinib.	imatinib	119-127	platelet derived growth factor receptor alpha	Homo sapiens	29-35
21761433-8	2011	Identification of rearranged PDGFRA or PDGFRB is critical because of the exquisite responsiveness of these diseases to imatinib.	imatinib	119-127	platelet derived growth factor receptor beta	Homo sapiens	39-45
21495997-6	2011	Expression of KIT protein and KIT mutation was shown in two patients who responded to imatinib in vivo.	imatinib	86-94	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-17
22829191-3	2011	Microarray-based transcriptome profiling of resistant cells revealed that nilotinib- and imatinib-resistant cells showed the upregulation of kinase-encoding genes (AURKC, FYN, SYK, BTK and YES1).	imatinib	89-97	aurora kinase C	Homo sapiens	164-169
21495997-6	2011	Expression of KIT protein and KIT mutation was shown in two patients who responded to imatinib in vivo.	imatinib	86-94	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	30-33
22829191-3	2011	Microarray-based transcriptome profiling of resistant cells revealed that nilotinib- and imatinib-resistant cells showed the upregulation of kinase-encoding genes (AURKC, FYN, SYK, BTK and YES1).	imatinib	89-97	FYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	171-174
22829191-3	2011	Microarray-based transcriptome profiling of resistant cells revealed that nilotinib- and imatinib-resistant cells showed the upregulation of kinase-encoding genes (AURKC, FYN, SYK, BTK and YES1).	imatinib	89-97	spleen associated tyrosine kinase	Homo sapiens	176-179
21697284-1	2011	The emergence of drug resistance is a primary concern in any cancer treatment, including with targeted kinase inhibitors as exemplified by the appearance of Bcr-Abl point mutations in chronic myeloid leukemia (CML) patients treated with imatinib.	imatinib	237-245	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-164
22829191-3	2011	Microarray-based transcriptome profiling of resistant cells revealed that nilotinib- and imatinib-resistant cells showed the upregulation of kinase-encoding genes (AURKC, FYN, SYK, BTK and YES1).	imatinib	89-97	Bruton tyrosine kinase	Homo sapiens	181-184
22829191-3	2011	Microarray-based transcriptome profiling of resistant cells revealed that nilotinib- and imatinib-resistant cells showed the upregulation of kinase-encoding genes (AURKC, FYN, SYK, BTK and YES1).	imatinib	89-97	YES proto-oncogene 1, Src family tyrosine kinase	Homo sapiens	189-193
22829191-4	2011	Among them, the upregulation of AURKC and FYN was observed both in nilotinib- and imatinib-resistant cells irrespective of exposure doses, while SYK, BTK and YES1 showed dose-dependent upregulation of expression.	imatinib	82-90	aurora kinase C	Homo sapiens	32-37
22829191-4	2011	Among them, the upregulation of AURKC and FYN was observed both in nilotinib- and imatinib-resistant cells irrespective of exposure doses, while SYK, BTK and YES1 showed dose-dependent upregulation of expression.	imatinib	82-90	FYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	42-45
21534915-6	2011	Furthermore, as exemplary experiments, novel optimized assay protocols were used to study extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase (MAPK) activity after cell inhibition with imatinib in chronic myelocytic leukemia K562 cells, revealing the phosphorylation kinetics of ERK MAPK.	imatinib	210-218	mitogen-activated protein kinase 1	Homo sapiens	90-127
21443462-5	2011	Several anti-cancer drugs like paclitaxel, imatinib, and doxorubicin activate FOXO3a by counteracting those oncogenic pathways which restrain FOXOs functions.	imatinib	43-51	forkhead box O3	Homo sapiens	78-84
21534915-6	2011	Furthermore, as exemplary experiments, novel optimized assay protocols were used to study extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase (MAPK) activity after cell inhibition with imatinib in chronic myelocytic leukemia K562 cells, revealing the phosphorylation kinetics of ERK MAPK.	imatinib	210-218	mitogen-activated protein kinase 1	Homo sapiens	129-132
21534915-6	2011	Furthermore, as exemplary experiments, novel optimized assay protocols were used to study extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase (MAPK) activity after cell inhibition with imatinib in chronic myelocytic leukemia K562 cells, revealing the phosphorylation kinetics of ERK MAPK.	imatinib	210-218	mitogen-activated protein kinase 1	Homo sapiens	168-172
21659463-8	2011	Treatment of KNS42 with the PDGFR inhibitor imatinib showed additional effects targeting the mitogen-activated protein kinase pathway, and cotreatment of the PDGFR inhibitor imatinib with NVP-AEW541 resulted in a highly synergistic interaction in vitro and increased efficacy after 14 days therapy in vivo compared with either agent alone.	imatinib	44-52	platelet derived growth factor receptor beta	Homo sapiens	28-33
21689725-10	2011	In vitro assays on KIT-N822I-expressing Ba/F3 cells confirmed that the N822I mutant is resistant to imatinib mesylate.	imatinib	100-117	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	19-22
21689725-13	2011	In addition, we demonstrated that KIT-N822I is resistant to imatinib and sensitive to dasatinib.	imatinib	60-68	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	34-37
21185600-0	2011	Correlation between genetic polymorphisms of the hOCT1 and MDR1 genes and the response to imatinib in patients newly diagnosed with chronic-phase chronic myeloid leukemia.	imatinib	90-98	solute carrier family 22 member 1	Homo sapiens	49-54
21185600-0	2011	Correlation between genetic polymorphisms of the hOCT1 and MDR1 genes and the response to imatinib in patients newly diagnosed with chronic-phase chronic myeloid leukemia.	imatinib	90-98	ATP binding cassette subfamily B member 1	Homo sapiens	59-63
21185600-1	2011	The association between seven polymorphisms in the genes hOCT1 and MDR1, encoding for imatinib transporter proteins, and the response to imatinib 400mg/daily was investigated in 65 patients newly diagnosed with chronic-phase chronic myeloid leukemia.	imatinib	86-94	solute carrier family 22 member 1	Homo sapiens	57-62
21185600-1	2011	The association between seven polymorphisms in the genes hOCT1 and MDR1, encoding for imatinib transporter proteins, and the response to imatinib 400mg/daily was investigated in 65 patients newly diagnosed with chronic-phase chronic myeloid leukemia.	imatinib	86-94	ATP binding cassette subfamily B member 1	Homo sapiens	67-71
21185600-1	2011	The association between seven polymorphisms in the genes hOCT1 and MDR1, encoding for imatinib transporter proteins, and the response to imatinib 400mg/daily was investigated in 65 patients newly diagnosed with chronic-phase chronic myeloid leukemia.	imatinib	137-145	solute carrier family 22 member 1	Homo sapiens	57-62
21185600-1	2011	The association between seven polymorphisms in the genes hOCT1 and MDR1, encoding for imatinib transporter proteins, and the response to imatinib 400mg/daily was investigated in 65 patients newly diagnosed with chronic-phase chronic myeloid leukemia.	imatinib	137-145	ATP binding cassette subfamily B member 1	Homo sapiens	67-71
21185600-4	2011	Beside, the MDR1 haplotype 1236T-2677G-3435C was more frequently found in patients primarily resistant to imatinib.	imatinib	106-114	ATP binding cassette subfamily B member 1	Homo sapiens	12-16
21764785-2	2011	Imatinib is known to inhibit the dysregulated proliferation of chronic myeloid leukemia, which is associated with the Bcr-Abl kinase; in gastrointestinal stromal tumors, imatinib is known to act via c-Kit kinase inhibition.	imatinib	0-8	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	122-125
21764785-2	2011	Imatinib is known to inhibit the dysregulated proliferation of chronic myeloid leukemia, which is associated with the Bcr-Abl kinase; in gastrointestinal stromal tumors, imatinib is known to act via c-Kit kinase inhibition.	imatinib	0-8	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	199-204
21764785-2	2011	Imatinib is known to inhibit the dysregulated proliferation of chronic myeloid leukemia, which is associated with the Bcr-Abl kinase; in gastrointestinal stromal tumors, imatinib is known to act via c-Kit kinase inhibition.	imatinib	170-178	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	199-204
21764785-4	2011	METHODS: Molecular modeling studies based on the crystal structure of imatinib bound to the active site of Abl were performed for designing the fluorinated analog.	imatinib	70-78	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	107-110
21659463-8	2011	Treatment of KNS42 with the PDGFR inhibitor imatinib showed additional effects targeting the mitogen-activated protein kinase pathway, and cotreatment of the PDGFR inhibitor imatinib with NVP-AEW541 resulted in a highly synergistic interaction in vitro and increased efficacy after 14 days therapy in vivo compared with either agent alone.	imatinib	174-182	platelet derived growth factor receptor beta	Homo sapiens	158-163
21867603-3	2011	K562 cells were in vitro incubated with the BCR-ABL inhibitor STI571 (imatinib) at 37 C and 5% CO2 for 24 hours, then SARI expression was detected by using real-time quantitative PCR.	imatinib	62-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
21586300-2	2011	It has recently become evident that bone forming and bone resorbing cells are affected by the receptor tyrosine kinase (RTK) inhibitor imatinib mesylate (STI571, Gleevec ).	imatinib	135-152	ret proto-oncogene	Rattus norvegicus	94-118
21586300-2	2011	It has recently become evident that bone forming and bone resorbing cells are affected by the receptor tyrosine kinase (RTK) inhibitor imatinib mesylate (STI571, Gleevec ).	imatinib	135-152	ret proto-oncogene	Rattus norvegicus	120-123
21586300-2	2011	It has recently become evident that bone forming and bone resorbing cells are affected by the receptor tyrosine kinase (RTK) inhibitor imatinib mesylate (STI571, Gleevec ).	imatinib	154-160	ret proto-oncogene	Rattus norvegicus	94-118
21586300-2	2011	It has recently become evident that bone forming and bone resorbing cells are affected by the receptor tyrosine kinase (RTK) inhibitor imatinib mesylate (STI571, Gleevec ).	imatinib	154-160	ret proto-oncogene	Rattus norvegicus	120-123
21586300-3	2011	Imatinib targets PDGF, ABL-related gene, c-Abl, c-Kit and c-Fms receptors, many of which have multiple functions in the bone microenvironment.	imatinib	0-8	colony stimulating factor 1 receptor	Rattus norvegicus	58-63
21867603-3	2011	K562 cells were in vitro incubated with the BCR-ABL inhibitor STI571 (imatinib) at 37 C and 5% CO2 for 24 hours, then SARI expression was detected by using real-time quantitative PCR.	imatinib	70-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
21867603-6	2011	After exposure of K562 cells to STI571 (2.5 micromol/L) for 24 hours, the SARI expression was higher than that in K562 cells treated without STI571 (p < 0.001).	imatinib	32-38	basic leucine zipper ATF-like transcription factor 2	Homo sapiens	74-78
21863513-12	2011	Patients with mutations in KIT exon 9 should be treated with 800 mg imatinib/day, since they profit from a significantly longer progression-free survival.	imatinib	68-76	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	27-30
21867645-5	2011	Subsequently, because of need for the resistance or intolerance, novel agents are being explored and imatinib has now been extended to eosinophilia-associated myeloid neoplasms with PDGFRA, PDGFRB or FGFR1 gene mutations.	imatinib	101-109	platelet derived growth factor receptor alpha	Homo sapiens	182-188
21356308-0	2011	Activation of STAT5 confers imatinib resistance on leukemic cells through the transcription of TERT and MDR1.	imatinib	28-36	signal transducer and activator of transcription 5A	Homo sapiens	14-19
21653319-2	2011	These phenomena are often associated with the appearance of imatinib-resistant BCR-ABL1 kinase mutants (eg, T315I) and overexpression of BCR-ABL1.	imatinib	60-68	BCR activator of RhoGEF and GTPase	Homo sapiens	79-87
21690468-0	2011	Phase II, open-label, single-arm trial of imatinib mesylate in patients with metastatic melanoma harboring c-Kit mutation or amplification.	imatinib	42-59	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	107-112
21690468-2	2011	We tested the efficiency of the tyrosine kinase inhibitor imatinib in selected patients with metastatic melanoma harboring c-Kit mutations or amplifications.	imatinib	58-66	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	123-128
21690468-14	2011	CONCLUSION: Imatinib demonstrated significant activity in patients with metastatic melanoma harboring genetic c-Kit aberrations, with an overall response rate of 23.3%.	imatinib	12-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	110-115
21561667-0	2011	Imatinib elicited a favorable response in a dog with a mast cell tumor carrying a c-kit c.1523A>T mutation via suppression of constitutive KIT activation.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	82-87
21561667-0	2011	Imatinib elicited a favorable response in a dog with a mast cell tumor carrying a c-kit c.1523A>T mutation via suppression of constitutive KIT activation.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	142-145
21561667-2	2011	In the present report, we demonstrate a clinical response to imatinib in a dog with MCT carrying a c-kit c.1523A>T mutation.	imatinib	61-69	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	99-104
21561667-3	2011	Moreover, the effect of this mutation on the phosphorylation status of KIT and the inhibitory potency of imatinib on the phosphorylation of the mutant KIT were examined in vitro.	imatinib	105-113	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	151-154
21561667-8	2011	The mutant KIT expressed on 293 cells showed ligand-independent phosphorylation and imatinib suppressed this phosphorylation in a dose-dependent manner.	imatinib	84-92	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	11-14
21561667-9	2011	From these findings, imatinib was considered to elicit a clinical response in a canine case of MCT via inhibition of the constitutively activated KIT caused by a c-kit c.1523A>T mutation.	imatinib	21-29	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	146-149
21561667-9	2011	From these findings, imatinib was considered to elicit a clinical response in a canine case of MCT via inhibition of the constitutively activated KIT caused by a c-kit c.1523A>T mutation.	imatinib	21-29	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	162-167
21225261-0	2011	Interactions of N-desmethyl imatinib, an active metabolite of imatinib, with P-glycoprotein in human leukemia cells.	imatinib	28-36	ATP binding cassette subfamily B member 1	Homo sapiens	77-91
21225261-7	2011	Our results indicate that CGP74588 could hardly positively contribute to the treatment of chronic myeloid leukemia (CML) where ABCB1 gene overexpression represents a possible mechanism of resistance to imatinib in vivo.	imatinib	202-210	ATP binding cassette subfamily B member 1	Homo sapiens	127-132
21666577-13	2011	KIT and PDGFRalpha mutational analyses are important in confirming a diagnosis of GIST and predicting its response to imatinib therapy.	imatinib	118-126	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
21666577-13	2011	KIT and PDGFRalpha mutational analyses are important in confirming a diagnosis of GIST and predicting its response to imatinib therapy.	imatinib	118-126	platelet derived growth factor receptor alpha	Homo sapiens	8-18
21530604-7	2011	Moreover, PL3 also resensitized T315I-mutated Bcr-ABL+ BA/F3 cells to improve the cytotoxicity of Imatinib in Imatinib-resistant cell line.	imatinib	98-106	lethal, Chr 9, Russell 3	Mus musculus	10-13
21530604-7	2011	Moreover, PL3 also resensitized T315I-mutated Bcr-ABL+ BA/F3 cells to improve the cytotoxicity of Imatinib in Imatinib-resistant cell line.	imatinib	110-118	lethal, Chr 9, Russell 3	Mus musculus	10-13
21700550-2	2011	In Philadelphia chromosome-positive (Ph(+)) ALL, the optimal treatment requires the addition of BCR-ABL tyrosine kinase inhibitors, as imatinib.	imatinib	135-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
21356308-0	2011	Activation of STAT5 confers imatinib resistance on leukemic cells through the transcription of TERT and MDR1.	imatinib	28-36	telomerase reverse transcriptase	Homo sapiens	95-99
21356308-0	2011	Activation of STAT5 confers imatinib resistance on leukemic cells through the transcription of TERT and MDR1.	imatinib	28-36	ATP binding cassette subfamily B member 1	Homo sapiens	104-108
21356308-4	2011	Conversely, silencing of endogenous STAT5 expression by siRNA significantly reduced both the expression of P-glycoprotein and telomerase activity and resulted in the recovery of the imatinib sensitivity of K562-ADM cells.	imatinib	182-190	signal transducer and activator of transcription 5A	Homo sapiens	36-41
21599631-3	2011	Imatinib, first designed to competitively inhibit the ATP-binding pocket of the BCR-ABL tyrosin kinase exhibits inhibition also in the KIT and PDGFRalpha tyrosine kinases, which revolutionized the therapy of gastrointestinal stromal tumors, a disease without any systemic treatment options prior to imatinib.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	135-138
21633340-0	2011	Pharmacokinetic impact of SLCO1A2 polymorphisms on imatinib disposition in patients with chronic myeloid leukemia.	imatinib	51-59	solute carrier organic anion transporter family member 1A2	Homo sapiens	26-33
21633340-1	2011	The purpose of this study was to explore the role of the organic anion-transporting polypeptide (OATP) 1A2, which is encoded by SLCO1A2, in the cellular uptake of the Bcr-Abl tyrosine kinase inhibitor imatinib, and the relationship between SLCO1A2 polymorphisms and the pharmacokinetics of imatinib in patients with chronic myeloid leukemia (CML).	imatinib	201-209	solute carrier organic anion transporter family member 1A2	Homo sapiens	57-106
21633340-1	2011	The purpose of this study was to explore the role of the organic anion-transporting polypeptide (OATP) 1A2, which is encoded by SLCO1A2, in the cellular uptake of the Bcr-Abl tyrosine kinase inhibitor imatinib, and the relationship between SLCO1A2 polymorphisms and the pharmacokinetics of imatinib in patients with chronic myeloid leukemia (CML).	imatinib	201-209	solute carrier organic anion transporter family member 1A2	Homo sapiens	128-135
21633340-1	2011	The purpose of this study was to explore the role of the organic anion-transporting polypeptide (OATP) 1A2, which is encoded by SLCO1A2, in the cellular uptake of the Bcr-Abl tyrosine kinase inhibitor imatinib, and the relationship between SLCO1A2 polymorphisms and the pharmacokinetics of imatinib in patients with chronic myeloid leukemia (CML).	imatinib	201-209	solute carrier organic anion transporter family member 1A2	Homo sapiens	240-247
21599631-3	2011	Imatinib, first designed to competitively inhibit the ATP-binding pocket of the BCR-ABL tyrosin kinase exhibits inhibition also in the KIT and PDGFRalpha tyrosine kinases, which revolutionized the therapy of gastrointestinal stromal tumors, a disease without any systemic treatment options prior to imatinib.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	143-153
21633340-1	2011	The purpose of this study was to explore the role of the organic anion-transporting polypeptide (OATP) 1A2, which is encoded by SLCO1A2, in the cellular uptake of the Bcr-Abl tyrosine kinase inhibitor imatinib, and the relationship between SLCO1A2 polymorphisms and the pharmacokinetics of imatinib in patients with chronic myeloid leukemia (CML).	imatinib	290-298	solute carrier organic anion transporter family member 1A2	Homo sapiens	57-106
21633340-1	2011	The purpose of this study was to explore the role of the organic anion-transporting polypeptide (OATP) 1A2, which is encoded by SLCO1A2, in the cellular uptake of the Bcr-Abl tyrosine kinase inhibitor imatinib, and the relationship between SLCO1A2 polymorphisms and the pharmacokinetics of imatinib in patients with chronic myeloid leukemia (CML).	imatinib	290-298	solute carrier organic anion transporter family member 1A2	Homo sapiens	128-135
21462307-2	2011	Imatinib mesylate, which targets KIT and PDGFRA, is effective in treating GISTs, but 90% of GIST patients become imatinib-resistant as a result of acquiring secondary KIT mutations.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	33-36
21633340-2	2011	Imatinib uptake was significantly enhanced in OATP1A2-transfected human embryonic kidney (HEK) 293 cells (P = 0.002).	imatinib	0-8	solute carrier organic anion transporter family member 1A2	Homo sapiens	46-53
21633340-3	2011	Naringin, an OATP1A2 inhibitor, decreased the transport of imatinib in OATP1A2-transfected HEK293 cells, the human intestinal cell line Caco-2, and K562 CML cells.	imatinib	59-67	solute carrier organic anion transporter family member 1A2	Homo sapiens	13-20
21633340-3	2011	Naringin, an OATP1A2 inhibitor, decreased the transport of imatinib in OATP1A2-transfected HEK293 cells, the human intestinal cell line Caco-2, and K562 CML cells.	imatinib	59-67	solute carrier organic anion transporter family member 1A2	Homo sapiens	71-78
21633340-5	2011	Imatinib clearance in CML patients was influenced by the SLCO1A2 -1105G>A/-1032G>A genotype (P = 0.075) and the SLCO1A2 -361GG genotype (P = 0.005).	imatinib	0-8	solute carrier organic anion transporter family member 1A2	Homo sapiens	57-64
21633340-5	2011	Imatinib clearance in CML patients was influenced by the SLCO1A2 -1105G>A/-1032G>A genotype (P = 0.075) and the SLCO1A2 -361GG genotype (P = 0.005).	imatinib	0-8	solute carrier organic anion transporter family member 1A2	Homo sapiens	118-125
21633340-6	2011	These findings suggest that imatinib is transported into cells by OATP1A2, and that SLCO1A2 polymorphisms significantly affect imatinib pharmacokinetics.	imatinib	28-36	solute carrier organic anion transporter family member 1A2	Homo sapiens	66-73
21633340-6	2011	These findings suggest that imatinib is transported into cells by OATP1A2, and that SLCO1A2 polymorphisms significantly affect imatinib pharmacokinetics.	imatinib	127-135	solute carrier organic anion transporter family member 1A2	Homo sapiens	84-91
21462307-2	2011	Imatinib mesylate, which targets KIT and PDGFRA, is effective in treating GISTs, but 90% of GIST patients become imatinib-resistant as a result of acquiring secondary KIT mutations.	imatinib	0-17	platelet derived growth factor receptor alpha	Homo sapiens	41-47
21462307-2	2011	Imatinib mesylate, which targets KIT and PDGFRA, is effective in treating GISTs, but 90% of GIST patients become imatinib-resistant as a result of acquiring secondary KIT mutations.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	167-170
21462307-2	2011	Imatinib mesylate, which targets KIT and PDGFRA, is effective in treating GISTs, but 90% of GIST patients become imatinib-resistant as a result of acquiring secondary KIT mutations.	imatinib	113-121	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	167-170
21462307-4	2011	It is therefore possible that the acquisition of secondary KIT mutations during imatinib treatment may occur in putative GIST CSCs.	imatinib	80-88	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	59-62
21577109-4	2011	Inhibition of CSF1R using small molecule inhibitors such as imatinib, nilotinib or sunitinib can result in clinical, radiological and functional improvement in the affected joint.	imatinib	60-68	colony stimulating factor 1 receptor	Homo sapiens	14-19
21519258-4	2011	RECENT FINDINGS: The major mechanism of resistance toward imatinib and sunitinib is the development of secondary resistance mutations in the kinase domain of KIT.	imatinib	58-66	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	158-161
21534873-1	2011	Imatinib mesylate and other tyrosine kinase inhibitors (TKIs) that inhibit BCR-ABL have had a favorable impact on the treatment of Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
21244632-4	2011	An example of targeted therapies is the successful treatment of KIT-mutant melanoma with the kinase inhibitor imatinib.	imatinib	110-118	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	64-67
21323568-0	2011	Placental growth factor and soluble c-kit receptor dynamics characterize the cytokine signature of imatinib in prostate cancer and bone metastases.	imatinib	99-107	placental growth factor	Homo sapiens	0-23
21323568-0	2011	Placental growth factor and soluble c-kit receptor dynamics characterize the cytokine signature of imatinib in prostate cancer and bone metastases.	imatinib	99-107	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	36-41
21323568-1	2011	To assess the hypothesis that the dynamics of plasma angiogenic and inflammatory cytokines after docetaxel chemotherapy with or without the c-kit/abl/platelet-derived growth factor receptor (PDGFR) inhibitor imatinib mesylate for prostate cancer are associated with outcome, the kinetics of 17 plasma cytokines before versus after chemotherapy were assessed and associations with progression-free survival (PFS) examined.	imatinib	208-225	platelet derived growth factor receptor beta	Homo sapiens	140-189
21323568-1	2011	To assess the hypothesis that the dynamics of plasma angiogenic and inflammatory cytokines after docetaxel chemotherapy with or without the c-kit/abl/platelet-derived growth factor receptor (PDGFR) inhibitor imatinib mesylate for prostate cancer are associated with outcome, the kinetics of 17 plasma cytokines before versus after chemotherapy were assessed and associations with progression-free survival (PFS) examined.	imatinib	208-225	platelet derived growth factor receptor beta	Homo sapiens	191-196
21323568-2	2011	After adjusting for multiple tests, significantly different declines in placental growth factor (PIGF), soluble vascular endothelial growth factor receptor-1 (VEGFR1), VEGF, and soluble c-kit were observed with docetaxel plus imatinib (n=41) compared to docetaxel alone (n=47).	imatinib	226-234	placental growth factor	Homo sapiens	72-95
21323568-2	2011	After adjusting for multiple tests, significantly different declines in placental growth factor (PIGF), soluble vascular endothelial growth factor receptor-1 (VEGFR1), VEGF, and soluble c-kit were observed with docetaxel plus imatinib (n=41) compared to docetaxel alone (n=47).	imatinib	226-234	phosphatidylinositol glycan anchor biosynthesis class F	Homo sapiens	97-101
21323568-2	2011	After adjusting for multiple tests, significantly different declines in placental growth factor (PIGF), soluble vascular endothelial growth factor receptor-1 (VEGFR1), VEGF, and soluble c-kit were observed with docetaxel plus imatinib (n=41) compared to docetaxel alone (n=47).	imatinib	226-234	fms related receptor tyrosine kinase 1	Homo sapiens	159-165
21323568-2	2011	After adjusting for multiple tests, significantly different declines in placental growth factor (PIGF), soluble vascular endothelial growth factor receptor-1 (VEGFR1), VEGF, and soluble c-kit were observed with docetaxel plus imatinib (n=41) compared to docetaxel alone (n=47).	imatinib	226-234	vascular endothelial growth factor A	Homo sapiens	159-163
21323568-2	2011	After adjusting for multiple tests, significantly different declines in placental growth factor (PIGF), soluble vascular endothelial growth factor receptor-1 (VEGFR1), VEGF, and soluble c-kit were observed with docetaxel plus imatinib (n=41) compared to docetaxel alone (n=47).	imatinib	226-234	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	186-191
21323568-6	2011	Plasma PIGF and soluble c-kit kinetics are candidate biomarkers of imatinib effect.	imatinib	67-75	phosphatidylinositol glycan anchor biosynthesis class F	Homo sapiens	7-11
21323568-6	2011	Plasma PIGF and soluble c-kit kinetics are candidate biomarkers of imatinib effect.	imatinib	67-75	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	24-29
21382639-1	2011	Chronic myeloid leukaemia has a specific therapy: BCR/ABL inhibitor imatinib.	imatinib	68-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
21382639-4	2011	VPA plus imatinib significantly increased acetylation of HSP90 and hnRNP L and decreased phosphorylation of HSPs and hnRNPs in imatinib resistant cells.	imatinib	9-17	heat shock protein 90 alpha family class A member 1	Homo sapiens	57-62
21382639-4	2011	VPA plus imatinib significantly increased acetylation of HSP90 and hnRNP L and decreased phosphorylation of HSPs and hnRNPs in imatinib resistant cells.	imatinib	9-17	heterogeneous nuclear ribonucleoprotein L	Homo sapiens	67-74
21466892-2	2011	It has been reported that imatinib damaged cardiomyocytes by triggering endoplasmic reticulum (ER) stress and that ER stress inducers intensified TRAIL-sensitivity of some cancer cells by upregulating DR4/DR5 expression.	imatinib	26-34	TNFRSF10A	Sus scrofa	201-204
21466892-4	2011	In contrast, imatinib did not induce ER stress responses and unexpectedly downregulated DR4/DR5 expression, indicating that sensitization of Ph1-positive leukemia cells to TRAIL-mediated cellular immunity by imatinib through upregulation of DR4/DR5 expression is unlikely.	imatinib	13-21	TNFRSF10A	Sus scrofa	88-91
21466892-4	2011	In contrast, imatinib did not induce ER stress responses and unexpectedly downregulated DR4/DR5 expression, indicating that sensitization of Ph1-positive leukemia cells to TRAIL-mediated cellular immunity by imatinib through upregulation of DR4/DR5 expression is unlikely.	imatinib	13-21	tumor necrosis factor ligand superfamily member 10	Sus scrofa	172-177
21466892-4	2011	In contrast, imatinib did not induce ER stress responses and unexpectedly downregulated DR4/DR5 expression, indicating that sensitization of Ph1-positive leukemia cells to TRAIL-mediated cellular immunity by imatinib through upregulation of DR4/DR5 expression is unlikely.	imatinib	208-216	tumor necrosis factor ligand superfamily member 10	Sus scrofa	172-177
21534873-6	2011	Patients with Ph+ ALL receiving imatinib mesylate, and likely also dasatinib, in conjunction with systemic and intrathecal chemotherapy may be at increased risk of SDH, and should be closely monitored for subtle manifestations of this complication.	imatinib	32-49	serine dehydratase	Homo sapiens	164-167
21466892-4	2011	In contrast, imatinib did not induce ER stress responses and unexpectedly downregulated DR4/DR5 expression, indicating that sensitization of Ph1-positive leukemia cells to TRAIL-mediated cellular immunity by imatinib through upregulation of DR4/DR5 expression is unlikely.	imatinib	208-216	TNFRSF10A	Sus scrofa	241-244
21659960-7	2011	Using cultures of neonatal mouse LF, we showed that imatinib did not suppress PDGF-Ralpha gene expression but reduced PDGF-A-mediated Akt phosphorylation, potentially explaining the increase in apoptosis.	imatinib	52-60	platelet derived growth factor, alpha	Mus musculus	118-124
21502378-9	2011	Finally, because STI571 potently inhibits Abl kinase activity, the autonomic dysfunction side effects associated with its use as a chemotherapeutic agent may result from perturbed alpha3*- and/or alpha7-nAChR function.	imatinib	17-23	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	196-208
19700222-8	2011	Moreover, STI571 treatment decreased the phospho-Cdk5 levels.	imatinib	10-16	cyclin-dependent kinase 5	Mus musculus	49-53
21489623-0	2011	NUP214-ABL1 positive T-cell acute lymphoblastic leukemia patient shows an initial favorable response to imatinib therapy post relapse.	imatinib	104-112	nucleoporin 214	Homo sapiens	0-6
21489623-0	2011	NUP214-ABL1 positive T-cell acute lymphoblastic leukemia patient shows an initial favorable response to imatinib therapy post relapse.	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	7-11
21511335-2	2011	Despite of high efficiency of imatinib, selective BCR-ABL inhibitor, about 30% of patients develop resistance.	imatinib	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
21536647-0	2011	Forced expression of cyclin-dependent kinase 6 confers resistance of pro-B acute lymphocytic leukemia to Gleevec treatment.	imatinib	105-112	cyclin dependent kinase 6	Homo sapiens	21-46
21536647-7	2011	Finally, we show that the cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitor PD0332991 can act synergistically with STI571 to enhance leukemic cell death, suggesting a potential role for CDK6 inhibitors in the treatment of STI571-resistant CML or ALL.	imatinib	116-122	cyclin dependent kinase 4	Homo sapiens	26-57
21536647-7	2011	Finally, we show that the cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitor PD0332991 can act synergistically with STI571 to enhance leukemic cell death, suggesting a potential role for CDK6 inhibitors in the treatment of STI571-resistant CML or ALL.	imatinib	116-122	cyclin dependent kinase 4	Homo sapiens	59-65
21536647-7	2011	Finally, we show that the cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitor PD0332991 can act synergistically with STI571 to enhance leukemic cell death, suggesting a potential role for CDK6 inhibitors in the treatment of STI571-resistant CML or ALL.	imatinib	116-122	cyclin dependent kinase 6	Homo sapiens	187-191
21536647-7	2011	Finally, we show that the cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitor PD0332991 can act synergistically with STI571 to enhance leukemic cell death, suggesting a potential role for CDK6 inhibitors in the treatment of STI571-resistant CML or ALL.	imatinib	223-229	cyclin dependent kinase 4	Homo sapiens	26-57
21536647-7	2011	Finally, we show that the cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitor PD0332991 can act synergistically with STI571 to enhance leukemic cell death, suggesting a potential role for CDK6 inhibitors in the treatment of STI571-resistant CML or ALL.	imatinib	223-229	cyclin dependent kinase 4	Homo sapiens	59-65
21536647-7	2011	Finally, we show that the cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitor PD0332991 can act synergistically with STI571 to enhance leukemic cell death, suggesting a potential role for CDK6 inhibitors in the treatment of STI571-resistant CML or ALL.	imatinib	223-229	cyclin dependent kinase 6	Homo sapiens	187-191
21727212-7	2011	Imatinib and nilotinib inhibited PDGF-DD-mediated ERK1/2 activation, basal and PDGF-DD-mediated activation of PDGFR-beta and AKT, and schwannoma proliferation.	imatinib	0-8	mitogen-activated protein kinase 3	Homo sapiens	50-56
21727212-7	2011	Imatinib and nilotinib inhibited PDGF-DD-mediated ERK1/2 activation, basal and PDGF-DD-mediated activation of PDGFR-beta and AKT, and schwannoma proliferation.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	110-120
21727212-7	2011	Imatinib and nilotinib inhibited PDGF-DD-mediated ERK1/2 activation, basal and PDGF-DD-mediated activation of PDGFR-beta and AKT, and schwannoma proliferation.	imatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	125-128
22213863-1	2011	OBJECTIVE: To analyze the clinical efficacy of imatinib mesylate (IM) for Ph-positive or BCR-ABL positive chronic myeloid leukemia (CML) to couple the trough plasma concentrations (C mins) of IM with clinical responses and adverse events (AEs).	imatinib	47-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
21902100-12	2011	NF1-associated GISTs almost uniformly do not exhibit gain-of-function activation of KIT or PDGFA (pathogenesis is suggested to be from the loss of heterozygosity of the NF1 gene) and are not likely to respond to imatinib.	imatinib	212-220	neurofibromin 1	Homo sapiens	0-3
21641409-8	2011	Similarly, the PDGF receptor signaling inhibitor imatinib increased delivery of cyclophosphamide and reduced tumor burden in RIP-Tag2 mice, without evidence of tumor cell sensitization to chemotherapy.	imatinib	49-57	regulation of phenobarbitol-inducible P450	Mus musculus	125-128
21471107-11	2011	c-Kit inhibition with imatinib attenuated in vitro proliferation of cells expressing epithelial cell adhesion molecule.	imatinib	22-30	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	0-5
21642685-3	2011	OBJECTIVE: To assess clinical effects of imatinib mesylate in patients with melanoma harboring KIT alterations.	imatinib	41-58	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	95-98
21642685-11	2011	CONCLUSIONS: Among patients with advanced melanoma harboring KIT alterations, treatment with imatinib mesylate results in significant clinical responses in a subset of patients.	imatinib	93-101	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	61-64
20622642-11	2011	Concomitant treatment of CD117 positive tumors with imatinib leads to long-term survival.	imatinib	52-60	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	25-30
21140451-11	2011	The expression of MAGE-A3 (p = 0.018) and NY-ESO-1 (p = 0.001) were associated with tumor progression under imatinib treatment.	imatinib	108-116	MAGE family member A3	Homo sapiens	18-25
21140451-11	2011	The expression of MAGE-A3 (p = 0.018) and NY-ESO-1 (p = 0.001) were associated with tumor progression under imatinib treatment.	imatinib	108-116	cancer/testis antigen 1A	Homo sapiens	42-50
21665148-0	2011	Loss or inhibition of stromal-derived PlGF prolongs survival of mice with imatinib-resistant Bcr-Abl1(+) leukemia.	imatinib	74-82	placental growth factor	Mus musculus	38-42
21665148-4	2011	Anti-PlGF treatment prolongs survival of imatinib-sensitive and -resistant CML mice and adds to the anti-CML activity of imatinib.	imatinib	41-49	placental growth factor	Mus musculus	5-9
21665148-4	2011	Anti-PlGF treatment prolongs survival of imatinib-sensitive and -resistant CML mice and adds to the anti-CML activity of imatinib.	imatinib	121-129	placental growth factor	Mus musculus	5-9
21665148-5	2011	These results may warrant further investigation of the therapeutic potential of PlGF inhibition for (imatinib-resistant) CML.	imatinib	101-109	placental growth factor	Mus musculus	80-84
27264123-1	2011	OBJECTIVE: Despite the efficacy of the BCR-ABL tyrosine kinase inhibitor imatinib, the development of resistance against imatinib has been observed.	imatinib	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-46
27264123-1	2011	OBJECTIVE: Despite the efficacy of the BCR-ABL tyrosine kinase inhibitor imatinib, the development of resistance against imatinib has been observed.	imatinib	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-46
21527515-1	2011	The mechanisms by which sphingosine kinase-1 (SK-1)/sphingosine 1-phosphate (S1P) activation contributes to imatinib resistance in chronic myeloid leukemia (CML) are unknown.	imatinib	108-116	sphingosine kinase 1	Homo sapiens	24-44
21527515-1	2011	The mechanisms by which sphingosine kinase-1 (SK-1)/sphingosine 1-phosphate (S1P) activation contributes to imatinib resistance in chronic myeloid leukemia (CML) are unknown.	imatinib	108-116	sphingosine kinase 1	Homo sapiens	46-50
21527515-2	2011	We show herein that increased SK-1/S1P enhances Bcr-Abl1 protein stability, through inhibition of its proteasomal degradation in imatinib-resistant K562/IMA-3 and LAMA-4/IMA human CML cells.	imatinib	129-137	sphingosine kinase 1	Homo sapiens	30-38
21508937-0	2011	Environmental and genetic factors affecting transport of imatinib by OATP1A2.	imatinib	57-65	solute carrier organic anion transporter family member 1A2	Homo sapiens	69-76
21804629-10	2011	In vitro test of sensitivity of the patients" leukemic cells to imatinib demonstrated sensitivity of Bcr-Abl tyrosine kinase to imatinib, as assessed by a decrease in phosphorylated Crkl and the disappearance of P-SFK, suggesting that P-Src reflects only the Bcr-Abl-dependent Src activity.	imatinib	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
21804629-10	2011	In vitro test of sensitivity of the patients" leukemic cells to imatinib demonstrated sensitivity of Bcr-Abl tyrosine kinase to imatinib, as assessed by a decrease in phosphorylated Crkl and the disappearance of P-SFK, suggesting that P-Src reflects only the Bcr-Abl-dependent Src activity.	imatinib	64-72	CRK like proto-oncogene, adaptor protein	Homo sapiens	182-186
21804629-10	2011	In vitro test of sensitivity of the patients" leukemic cells to imatinib demonstrated sensitivity of Bcr-Abl tyrosine kinase to imatinib, as assessed by a decrease in phosphorylated Crkl and the disappearance of P-SFK, suggesting that P-Src reflects only the Bcr-Abl-dependent Src activity.	imatinib	64-72	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	237-240
21804629-10	2011	In vitro test of sensitivity of the patients" leukemic cells to imatinib demonstrated sensitivity of Bcr-Abl tyrosine kinase to imatinib, as assessed by a decrease in phosphorylated Crkl and the disappearance of P-SFK, suggesting that P-Src reflects only the Bcr-Abl-dependent Src activity.	imatinib	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	259-266
21804629-10	2011	In vitro test of sensitivity of the patients" leukemic cells to imatinib demonstrated sensitivity of Bcr-Abl tyrosine kinase to imatinib, as assessed by a decrease in phosphorylated Crkl and the disappearance of P-SFK, suggesting that P-Src reflects only the Bcr-Abl-dependent Src activity.	imatinib	64-72	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	277-280
21804629-10	2011	In vitro test of sensitivity of the patients" leukemic cells to imatinib demonstrated sensitivity of Bcr-Abl tyrosine kinase to imatinib, as assessed by a decrease in phosphorylated Crkl and the disappearance of P-SFK, suggesting that P-Src reflects only the Bcr-Abl-dependent Src activity.	imatinib	128-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
21804629-10	2011	In vitro test of sensitivity of the patients" leukemic cells to imatinib demonstrated sensitivity of Bcr-Abl tyrosine kinase to imatinib, as assessed by a decrease in phosphorylated Crkl and the disappearance of P-SFK, suggesting that P-Src reflects only the Bcr-Abl-dependent Src activity.	imatinib	128-136	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	237-240
21804629-10	2011	In vitro test of sensitivity of the patients" leukemic cells to imatinib demonstrated sensitivity of Bcr-Abl tyrosine kinase to imatinib, as assessed by a decrease in phosphorylated Crkl and the disappearance of P-SFK, suggesting that P-Src reflects only the Bcr-Abl-dependent Src activity.	imatinib	128-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	259-266
21804629-10	2011	In vitro test of sensitivity of the patients" leukemic cells to imatinib demonstrated sensitivity of Bcr-Abl tyrosine kinase to imatinib, as assessed by a decrease in phosphorylated Crkl and the disappearance of P-SFK, suggesting that P-Src reflects only the Bcr-Abl-dependent Src activity.	imatinib	128-136	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	277-280
21459800-6	2011	We also used short hairpin RNA interference (shRNAi) and imatinib to block PDGF-D/PDGFRbeta signaling.	imatinib	57-65	platelet derived growth factor D	Homo sapiens	75-81
21459800-6	2011	We also used short hairpin RNA interference (shRNAi) and imatinib to block PDGF-D/PDGFRbeta signaling.	imatinib	57-65	platelet derived growth factor receptor beta	Homo sapiens	82-91
21325637-11	2011	Pharmacological inhibition of PDGF receptor tyrosine kinase with imatinib prevented IRS-1/IRS-2 dysregulation and restored insulin receptor signaling.	imatinib	65-73	insulin receptor substrate 1	Homo sapiens	84-89
21325637-11	2011	Pharmacological inhibition of PDGF receptor tyrosine kinase with imatinib prevented IRS-1/IRS-2 dysregulation and restored insulin receptor signaling.	imatinib	65-73	insulin receptor substrate 2	Homo sapiens	90-95
21325637-11	2011	Pharmacological inhibition of PDGF receptor tyrosine kinase with imatinib prevented IRS-1/IRS-2 dysregulation and restored insulin receptor signaling.	imatinib	65-73	insulin	Homo sapiens	123-130
21321929-8	2011	Experiments using a constitutively activated form of c-Abl, small interfering RNA against c-Abl and the specific tyrosine kinase inhibitor imatinib, demonstrated the requirement of c-Abl for the TGFbeta-induced phosphorylation of Fli-1.	imatinib	139-147	transforming growth factor beta 1	Homo sapiens	195-202
21235620-7	2011	RESULTS: Sorafenib, dasatinib and imatinib exhibited mixed inhibition against paracetamol glucuronidation in pooled HLMs, and potent inhibition in UGT1A9 and UGT2B15.	imatinib	34-42	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	147-153
21235620-7	2011	RESULTS: Sorafenib, dasatinib and imatinib exhibited mixed inhibition against paracetamol glucuronidation in pooled HLMs, and potent inhibition in UGT1A9 and UGT2B15.	imatinib	34-42	UDP glucuronosyltransferase family 2 member B15	Homo sapiens	158-165
21235620-8	2011	Dasatinib and imatinib also inhibited UGT1A1-mediated paracetamol glucuronidation.	imatinib	14-22	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
22035739-1	2011	Mutations of BCR-ABL1 are observed in 50% of patients with imatinib-resistant chronic myeloid leukemia (CML).	imatinib	59-67	BCR activator of RhoGEF and GTPase	Homo sapiens	13-21
21508937-2	2011	In vitro, we found that imatinib is transported by the intestinal uptake carrier organic anion transporting polypeptide (OATP1A2) and that this process is sensitive to pH, rosuvastatin, and genetic variants.	imatinib	24-32	solute carrier organic anion transporter family member 1A2	Homo sapiens	121-128
21392556-0	2011	Sphingosine kinase 1 overexpression is regulated by signaling through PI3K, AKT2, and mTOR in imatinib-resistant chronic myeloid leukemia cells.	imatinib	94-102	sphingosine kinase 1	Homo sapiens	0-20
21392556-8	2011	The partial inhibition of SphK1 activity by N,N-dimethylsphingosine or expression by small interfering RNA increased sensitivity to imatinib-induced apoptosis in resistant cells and returned BCR-ABL to baseline levels.	imatinib	132-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	191-198
21392556-0	2011	Sphingosine kinase 1 overexpression is regulated by signaling through PI3K, AKT2, and mTOR in imatinib-resistant chronic myeloid leukemia cells.	imatinib	94-102	AKT serine/threonine kinase 2	Homo sapiens	76-80
21392556-10	2011	CONCLUSIONS: These results demonstrate that SphK1 is upregulated in imatinib-resistant K562 cells by a pathway contingent on a phosphoinositide 3-kinase/AKT2/mammalian target of rapamycin signaling pathway.	imatinib	68-76	sphingosine kinase 1	Homo sapiens	44-49
21392556-0	2011	Sphingosine kinase 1 overexpression is regulated by signaling through PI3K, AKT2, and mTOR in imatinib-resistant chronic myeloid leukemia cells.	imatinib	94-102	mechanistic target of rapamycin kinase	Homo sapiens	86-90
21392556-10	2011	CONCLUSIONS: These results demonstrate that SphK1 is upregulated in imatinib-resistant K562 cells by a pathway contingent on a phosphoinositide 3-kinase/AKT2/mammalian target of rapamycin signaling pathway.	imatinib	68-76	AKT serine/threonine kinase 2	Homo sapiens	153-157
21392556-10	2011	CONCLUSIONS: These results demonstrate that SphK1 is upregulated in imatinib-resistant K562 cells by a pathway contingent on a phosphoinositide 3-kinase/AKT2/mammalian target of rapamycin signaling pathway.	imatinib	68-76	mechanistic target of rapamycin kinase	Homo sapiens	158-187
21392556-5	2011	MATERIALS AND METHODS: In this study, we used continuous exposure to stepwise increasing concentrations of imatinib (0.6-1 muM) to select imatinib-resistant K562 cells.	imatinib	107-115	latexin	Homo sapiens	123-126
21392556-11	2011	We propose that SphK1 plays an important role in development of acquired resistance to imatinib in chronic myeloid leukemia cell lines.	imatinib	87-95	sphingosine kinase 1	Homo sapiens	16-21
21392556-5	2011	MATERIALS AND METHODS: In this study, we used continuous exposure to stepwise increasing concentrations of imatinib (0.6-1 muM) to select imatinib-resistant K562 cells.	imatinib	138-146	latexin	Homo sapiens	123-126
21392556-6	2011	RESULTS: Expression of BCR-ABL increased both at RNA and protein levels in imatinib-resistant cell lines.	imatinib	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
21392556-8	2011	The partial inhibition of SphK1 activity by N,N-dimethylsphingosine or expression by small interfering RNA increased sensitivity to imatinib-induced apoptosis in resistant cells and returned BCR-ABL to baseline levels.	imatinib	132-140	sphingosine kinase 1	Homo sapiens	26-31
21677482-2	2011	Imatinib mesylate, a tyrosine kinase inhibitor of KIT and platelet-derived growth factor receptor(PDGFR), has dramatically improved the prognosis ofpatients with advanced, recurrent, and/or metastatic GISTs.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	50-53
21622134-0	2011	NPB001-05 inhibits Bcr-Abl kinase leading to apoptosis of imatinib-resistant cells.	imatinib	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
21677482-2	2011	Imatinib mesylate, a tyrosine kinase inhibitor of KIT and platelet-derived growth factor receptor(PDGFR), has dramatically improved the prognosis ofpatients with advanced, recurrent, and/or metastatic GISTs.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	98-103
21677482-4	2011	Sunitinib malate, a multi-targeted tyrosine kinase inhibitor that shows activity against KIT and other receptor tyrosine kinases, including PDGFR and vascular endothelial growth factor receptor, is the only treatment for imatinib-resistant GISTs that is covered by national health insurance in Japan as ofthis writing.	imatinib	221-229	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	89-92
21677482-4	2011	Sunitinib malate, a multi-targeted tyrosine kinase inhibitor that shows activity against KIT and other receptor tyrosine kinases, including PDGFR and vascular endothelial growth factor receptor, is the only treatment for imatinib-resistant GISTs that is covered by national health insurance in Japan as ofthis writing.	imatinib	221-229	platelet derived growth factor receptor beta	Homo sapiens	140-145
20127176-6	2011	In addition, the relative concentration of BCR-ABL measured by PCR was in agreement with the patient"s response to the Imatinib treatment and bone marrow morphology remission.	imatinib	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
21403650-0	2011	A phase I/II study of imatinib plus reinduction therapy for c-kit-positive relapsed/refractory acute myeloid leukemia: inhibition of Akt activation correlates with complete response.	imatinib	22-30	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	60-65
21403650-0	2011	A phase I/II study of imatinib plus reinduction therapy for c-kit-positive relapsed/refractory acute myeloid leukemia: inhibition of Akt activation correlates with complete response.	imatinib	22-30	AKT serine/threonine kinase 1	Homo sapiens	133-136
21403650-1	2011	This phase I/II study evaluated imatinib as a c-kit inhibitor combined with mitoxantrone, etoposide and cytarabine therapy for patients with primary refractory or relapsed c-kit+ acute myeloid leukemia (AML).	imatinib	32-40	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	46-51
21403650-1	2011	This phase I/II study evaluated imatinib as a c-kit inhibitor combined with mitoxantrone, etoposide and cytarabine therapy for patients with primary refractory or relapsed c-kit+ acute myeloid leukemia (AML).	imatinib	32-40	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	172-177
21482077-8	2011	STI571-mediated a ROS-dependent apoptosis potentiated by JNK inhibitor SP600125 was first identified in melanoma B16F0 cells.	imatinib	0-6	mitogen-activated protein kinase 8	Mus musculus	57-60
21292323-0	2011	Changes in the activity of the GPx-1 anti-oxidant selenoenzyme in mononuclear cells following imatinib treatment.	imatinib	94-102	glutathione peroxidase 1	Homo sapiens	31-36
21292323-1	2011	Imatinib inhibits the ABL tyrosine kinase and is effective for the treatment of chronic myeloid leukemia (CML).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-25
20354828-0	2011	Combination of simvastatin and imatinib sensitizes the CD34+ cells in K562 to cell death.	imatinib	31-39	CD34 molecule	Homo sapiens	55-59
21188449-1	2011	Imatinib and nilotinib are inhibitors that selectively target a set of protein tyrosine kinases, including abelson kinase (Abl), together with the chimeric oncoprotein, breakpoint cluster region-abelson kinase (Bcr-Abl), as well as stem cell factor receptor (KIT), platelet-derived growth factor receptor (PDGFR), discoidin domain receptor (DDR), and colony stimulating factor-1 receptor (CSF-1R).	imatinib	0-8	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	259-262
20354828-4	2011	In this study, we identified a subpopulation of CD34+ cells in K562 were much more resistant to imatinib than the bulk cells.	imatinib	96-104	CD34 molecule	Homo sapiens	48-52
20354828-6	2011	In contrast, combination of simvastatin and imatinib induced a significant cell death in the subpopulation, which is dependent on the induced ROS by simvastatin as the effect was blocked by ROS scavenger N-acetyl-L: -cysteine (NAC).	imatinib	44-52	X-linked Kx blood group	Homo sapiens	227-230
21188449-1	2011	Imatinib and nilotinib are inhibitors that selectively target a set of protein tyrosine kinases, including abelson kinase (Abl), together with the chimeric oncoprotein, breakpoint cluster region-abelson kinase (Bcr-Abl), as well as stem cell factor receptor (KIT), platelet-derived growth factor receptor (PDGFR), discoidin domain receptor (DDR), and colony stimulating factor-1 receptor (CSF-1R).	imatinib	0-8	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	107-121
21188449-1	2011	Imatinib and nilotinib are inhibitors that selectively target a set of protein tyrosine kinases, including abelson kinase (Abl), together with the chimeric oncoprotein, breakpoint cluster region-abelson kinase (Bcr-Abl), as well as stem cell factor receptor (KIT), platelet-derived growth factor receptor (PDGFR), discoidin domain receptor (DDR), and colony stimulating factor-1 receptor (CSF-1R).	imatinib	0-8	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	123-126
21188449-1	2011	Imatinib and nilotinib are inhibitors that selectively target a set of protein tyrosine kinases, including abelson kinase (Abl), together with the chimeric oncoprotein, breakpoint cluster region-abelson kinase (Bcr-Abl), as well as stem cell factor receptor (KIT), platelet-derived growth factor receptor (PDGFR), discoidin domain receptor (DDR), and colony stimulating factor-1 receptor (CSF-1R).	imatinib	0-8	platelet derived growth factor receptor, beta polypeptide	Mus musculus	265-304
21188449-1	2011	Imatinib and nilotinib are inhibitors that selectively target a set of protein tyrosine kinases, including abelson kinase (Abl), together with the chimeric oncoprotein, breakpoint cluster region-abelson kinase (Bcr-Abl), as well as stem cell factor receptor (KIT), platelet-derived growth factor receptor (PDGFR), discoidin domain receptor (DDR), and colony stimulating factor-1 receptor (CSF-1R).	imatinib	0-8	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	195-209
21188449-1	2011	Imatinib and nilotinib are inhibitors that selectively target a set of protein tyrosine kinases, including abelson kinase (Abl), together with the chimeric oncoprotein, breakpoint cluster region-abelson kinase (Bcr-Abl), as well as stem cell factor receptor (KIT), platelet-derived growth factor receptor (PDGFR), discoidin domain receptor (DDR), and colony stimulating factor-1 receptor (CSF-1R).	imatinib	0-8	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	215-218
21188449-1	2011	Imatinib and nilotinib are inhibitors that selectively target a set of protein tyrosine kinases, including abelson kinase (Abl), together with the chimeric oncoprotein, breakpoint cluster region-abelson kinase (Bcr-Abl), as well as stem cell factor receptor (KIT), platelet-derived growth factor receptor (PDGFR), discoidin domain receptor (DDR), and colony stimulating factor-1 receptor (CSF-1R).	imatinib	0-8	platelet derived growth factor receptor, beta polypeptide	Mus musculus	306-311
21188449-1	2011	Imatinib and nilotinib are inhibitors that selectively target a set of protein tyrosine kinases, including abelson kinase (Abl), together with the chimeric oncoprotein, breakpoint cluster region-abelson kinase (Bcr-Abl), as well as stem cell factor receptor (KIT), platelet-derived growth factor receptor (PDGFR), discoidin domain receptor (DDR), and colony stimulating factor-1 receptor (CSF-1R).	imatinib	0-8	colony stimulating factor 1 receptor	Mus musculus	351-387
21188449-1	2011	Imatinib and nilotinib are inhibitors that selectively target a set of protein tyrosine kinases, including abelson kinase (Abl), together with the chimeric oncoprotein, breakpoint cluster region-abelson kinase (Bcr-Abl), as well as stem cell factor receptor (KIT), platelet-derived growth factor receptor (PDGFR), discoidin domain receptor (DDR), and colony stimulating factor-1 receptor (CSF-1R).	imatinib	0-8	colony stimulating factor 1 receptor	Mus musculus	389-395
21188449-2	2011	The aim of the present study was to investigate whether imatinib or nilotinib was effective against arthritis in the glucose-6-phosphate isomerase (GPI)-induced arthritis mouse model.	imatinib	56-64	glucose-6-phosphate isomerase 1	Mus musculus	117-146
21188449-2	2011	The aim of the present study was to investigate whether imatinib or nilotinib was effective against arthritis in the glucose-6-phosphate isomerase (GPI)-induced arthritis mouse model.	imatinib	56-64	glucose-6-phosphate isomerase 1	Mus musculus	148-151
21188449-5	2011	Splenocytes from the arthritic mice were cultured with GPI in the presence of imatinib or nilotinib in vitro, and cytokine levels in the culture supernatants were analyzed.	imatinib	78-86	glucose-6-phosphate isomerase 1	Mus musculus	55-58
21188449-9	2011	A reduction in anti-GPI antibodies was correlated with the therapeutic efficacy of imatinib, but not with that of nilotinib.	imatinib	83-91	glucose-6-phosphate isomerase 1	Mus musculus	20-23
21188449-10	2011	Imatinib dose-dependently inhibited tumor necrosis factor (TNF)-alpha, IL-6, interferon (IFN)-gamma, and IL-17 production by splenocytes in vitro, while nilotinib inhibited only IL-17 and IFN-gamma production in a dose-dependent fashion.	imatinib	0-8	tumor necrosis factor	Mus musculus	36-69
21188449-10	2011	Imatinib dose-dependently inhibited tumor necrosis factor (TNF)-alpha, IL-6, interferon (IFN)-gamma, and IL-17 production by splenocytes in vitro, while nilotinib inhibited only IL-17 and IFN-gamma production in a dose-dependent fashion.	imatinib	0-8	interleukin 6	Mus musculus	71-75
21188449-10	2011	Imatinib dose-dependently inhibited tumor necrosis factor (TNF)-alpha, IL-6, interferon (IFN)-gamma, and IL-17 production by splenocytes in vitro, while nilotinib inhibited only IL-17 and IFN-gamma production in a dose-dependent fashion.	imatinib	0-8	interferon gamma	Mus musculus	77-99
21188449-10	2011	Imatinib dose-dependently inhibited tumor necrosis factor (TNF)-alpha, IL-6, interferon (IFN)-gamma, and IL-17 production by splenocytes in vitro, while nilotinib inhibited only IL-17 and IFN-gamma production in a dose-dependent fashion.	imatinib	0-8	interleukin 17A	Mus musculus	105-110
21188449-10	2011	Imatinib dose-dependently inhibited tumor necrosis factor (TNF)-alpha, IL-6, interferon (IFN)-gamma, and IL-17 production by splenocytes in vitro, while nilotinib inhibited only IL-17 and IFN-gamma production in a dose-dependent fashion.	imatinib	0-8	interleukin 17A	Mus musculus	178-183
21188449-10	2011	Imatinib dose-dependently inhibited tumor necrosis factor (TNF)-alpha, IL-6, interferon (IFN)-gamma, and IL-17 production by splenocytes in vitro, while nilotinib inhibited only IL-17 and IFN-gamma production in a dose-dependent fashion.	imatinib	0-8	interferon gamma	Mus musculus	188-197
21624109-5	2011	CONCLUSION: This report demonstrates that platelet dysfunction and bleeding disorder in BCR-ABL+ chronic myeloid leukemia can successfully be treated with imatinib.	imatinib	155-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
21698178-3	2011	D816V-mutated KIT is constitutively active, and resistant to treatment with the anti-cancer drug Imatinib.	imatinib	97-105	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-17
21781496-0	2011	[Effects of HO-1 gene expression on proliferation of imatinib resistant CML cells].	imatinib	53-61	heme oxygenase 1	Homo sapiens	12-16
21781496-1	2011	OBJECTIVE: To investigate the effect of heme oxygenase-1 (HO-1) expression on cell growth and apoptosis in imatinib resistant chronic myeloid leukemia (CML) cells (K562/A02-IM), and explore the relationship between HO-1 gene and CML.	imatinib	107-115	heme oxygenase 1	Homo sapiens	40-56
21781496-1	2011	OBJECTIVE: To investigate the effect of heme oxygenase-1 (HO-1) expression on cell growth and apoptosis in imatinib resistant chronic myeloid leukemia (CML) cells (K562/A02-IM), and explore the relationship between HO-1 gene and CML.	imatinib	107-115	heme oxygenase 1	Homo sapiens	58-62
21600007-7	2011	Recently, it has been confirmed that the kinase genotype of KIT and platelet-derived growth factor receptor alpha can accurately predict a good response to imatinib mesylate therapy.	imatinib	156-164	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	60-63
24212821-0	2011	Activation of PDGFr-beta Signaling Pathway after Imatinib and Radioimmunotherapy Treatment in Experimental Pancreatic Cancer.	imatinib	49-57	platelet derived growth factor receptor beta	Homo sapiens	14-24
24212821-7	2011	Inhibition of the stromal PDGFr-beta with imatinib activates human PDGFr-beta/PDGF-B signaling loop, silent in untreated xenografts, via an apparent paracrine rescue pathway.	imatinib	42-50	platelet derived growth factor receptor beta	Homo sapiens	26-36
24212821-7	2011	Inhibition of the stromal PDGFr-beta with imatinib activates human PDGFr-beta/PDGF-B signaling loop, silent in untreated xenografts, via an apparent paracrine rescue pathway.	imatinib	42-50	platelet derived growth factor receptor beta	Homo sapiens	67-77
24212821-7	2011	Inhibition of the stromal PDGFr-beta with imatinib activates human PDGFr-beta/PDGF-B signaling loop, silent in untreated xenografts, via an apparent paracrine rescue pathway.	imatinib	42-50	platelet derived growth factor subunit B	Homo sapiens	78-84
24212821-9	2011	Soon after treatment, levels of human PDGFr-beta, compared to untreated tumors, are 3.4x, 12.4x, and 5.7x higher in imatinib-, radioimmunotherapy + imatinib-, and radioimmunotherapy-treated tumors, respectively.	imatinib	116-124	platelet derived growth factor receptor beta	Homo sapiens	38-48
24212821-9	2011	Soon after treatment, levels of human PDGFr-beta, compared to untreated tumors, are 3.4x, 12.4x, and 5.7x higher in imatinib-, radioimmunotherapy + imatinib-, and radioimmunotherapy-treated tumors, respectively.	imatinib	148-156	platelet derived growth factor receptor beta	Homo sapiens	38-48
24212821-10	2011	A continuous 14-day irradiation of imatinib-treated xenografts reduces levels of PDGFr-beta and phosphorylated PDGFr-beta by 5.3x and 4x, compared to earlier times.	imatinib	35-43	platelet derived growth factor receptor beta	Homo sapiens	81-91
24212821-10	2011	A continuous 14-day irradiation of imatinib-treated xenografts reduces levels of PDGFr-beta and phosphorylated PDGFr-beta by 5.3x and 4x, compared to earlier times.	imatinib	35-43	platelet derived growth factor receptor beta	Homo sapiens	111-121
21600007-7	2011	Recently, it has been confirmed that the kinase genotype of KIT and platelet-derived growth factor receptor alpha can accurately predict a good response to imatinib mesylate therapy.	imatinib	156-164	platelet derived growth factor receptor alpha	Homo sapiens	68-113
21474579-0	2011	HDAC inhibitors potentiate the activity of the BCR/ABL kinase inhibitor KW-2449 in imatinib-sensitive or -resistant BCR/ABL+ leukemia cells in vitro and in vivo.	imatinib	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
21454413-6	2011	Similarly, the treatment of primary MALT lymphoma cells with the ABL inhibitors imatinib and dasatinib prevented tumor cell growth.	imatinib	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-68
21454413-7	2011	Finally, we show that the treatment of tumor-bearing mice with imatinib induces MALT lymphoma regression in a preclinical model of the disease, implicating ABL1 in MALT lymphoma progression.	imatinib	63-71	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	156-160
21385851-1	2011	Dasatinib is a novel, potent, ATP-competitive inhibitor of Bcr-Abl, cKIT, and Src family kinases that exhibits efficacy in patients with imatinib-resistant chronic myelogenous leukemia.	imatinib	137-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
22829152-0	2011	The mTOR inhibitor, everolimus (RAD001), overcomes resistance to imatinib in quiescent Ph-positive acute lymphoblastic leukemia cells.	imatinib	65-73	mechanistic target of rapamycin kinase	Mus musculus	4-8
21310803-2	2011	Using a whole orbital tissue culture system, we tested the potential efficacy of imatinib mesylate (a tyrosine kinase inhibitor that blocks platelet-derived growth factor (PDGF)-receptor, c-Abl and c-Kit activity) and adalimumab (an anti-TNF-alpha antibody) for the treatment of Graves" ophthalmopathy (GO).	imatinib	81-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	188-193
21310803-2	2011	Using a whole orbital tissue culture system, we tested the potential efficacy of imatinib mesylate (a tyrosine kinase inhibitor that blocks platelet-derived growth factor (PDGF)-receptor, c-Abl and c-Kit activity) and adalimumab (an anti-TNF-alpha antibody) for the treatment of Graves" ophthalmopathy (GO).	imatinib	81-98	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	198-203
21310803-5	2011	RESULTS: Imatinib mesylate significantly (p=0.005) reduced IL-6 and hyaluronan production.	imatinib	9-17	interleukin 6	Homo sapiens	59-63
21350820-2	2011	Imatinib is a CYP3A4 inhibitor.	imatinib	0-8	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	14-20
21350820-11	2011	Despite a 42% decrease in CYP3A4 activity after 3 weeks of imatinib co-administration, docetaxel clearance was unchanged.	imatinib	59-67	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	26-32
21350820-13	2011	In conclusion, imatinib inhibited CYP3A4 but did not affect docetaxel clearance.	imatinib	15-23	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	34-40
21367918-12	2011	Imatinib suppressed the albumin-induced EMT and ER stress via inhibition of ROS and c-Src kinase.	imatinib	0-8	C-terminal Src kinase	Homo sapiens	84-96
21367918-13	2011	Imatinib also inhibited the albumin-induced mRNA expression of MCP-1, VCAM-1, transforming growth factor (TGF)-beta1, and collagen I (alpha1).	imatinib	0-8	C-C motif chemokine ligand 2	Homo sapiens	63-68
21367918-13	2011	Imatinib also inhibited the albumin-induced mRNA expression of MCP-1, VCAM-1, transforming growth factor (TGF)-beta1, and collagen I (alpha1).	imatinib	0-8	vascular cell adhesion molecule 1	Homo sapiens	70-76
21367918-13	2011	Imatinib also inhibited the albumin-induced mRNA expression of MCP-1, VCAM-1, transforming growth factor (TGF)-beta1, and collagen I (alpha1).	imatinib	0-8	transforming growth factor beta 1	Homo sapiens	78-116
21505103-2	2011	The BCR-ABL(T315I) mutant is highly resistant to imatinib, nilotinib, and dasatinib, and is frequently detected in relapsed patients.	imatinib	49-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
21520403-5	2011	In the K562-Lucena cell line, Pgp positive, imatinib caused an enhancing in Pgp expression at protein and mRNA levels, whereas in the Pgp negative cell line, this drug was capable of decreasing MDR1/Pgp mRNA levels.	imatinib	44-52	ATP binding cassette subfamily B member 1	Homo sapiens	30-33
21520403-5	2011	In the K562-Lucena cell line, Pgp positive, imatinib caused an enhancing in Pgp expression at protein and mRNA levels, whereas in the Pgp negative cell line, this drug was capable of decreasing MDR1/Pgp mRNA levels.	imatinib	44-52	ATP binding cassette subfamily B member 1	Homo sapiens	76-79
21520403-5	2011	In the K562-Lucena cell line, Pgp positive, imatinib caused an enhancing in Pgp expression at protein and mRNA levels, whereas in the Pgp negative cell line, this drug was capable of decreasing MDR1/Pgp mRNA levels.	imatinib	44-52	ATP binding cassette subfamily B member 1	Homo sapiens	76-79
21520403-5	2011	In the K562-Lucena cell line, Pgp positive, imatinib caused an enhancing in Pgp expression at protein and mRNA levels, whereas in the Pgp negative cell line, this drug was capable of decreasing MDR1/Pgp mRNA levels.	imatinib	44-52	ATP binding cassette subfamily B member 1	Homo sapiens	194-198
21520403-5	2011	In the K562-Lucena cell line, Pgp positive, imatinib caused an enhancing in Pgp expression at protein and mRNA levels, whereas in the Pgp negative cell line, this drug was capable of decreasing MDR1/Pgp mRNA levels.	imatinib	44-52	ATP binding cassette subfamily B member 1	Homo sapiens	76-79
22829152-4	2011	After ex vivo imatinib treatment, more residual cells were observed in the CD34(+)CD38(-) population than in the other populations.	imatinib	14-22	CD34 antigen	Mus musculus	75-79
22829152-4	2011	After ex vivo imatinib treatment, more residual cells were observed in the CD34(+)CD38(-) population than in the other populations.	imatinib	14-22	CD38 antigen	Mus musculus	82-86
22829152-6	2011	The leukemic non-obese diabetic/severe combined immunodeficiency (NOD/SCID) mouse system with the in vivo combination treatment with imatinib and everolimus showed a decrease of tumor burden including CD34(+) cells.	imatinib	133-141	protein kinase, DNA activated, catalytic polypeptide	Mus musculus	70-74
22829152-6	2011	The leukemic non-obese diabetic/severe combined immunodeficiency (NOD/SCID) mouse system with the in vivo combination treatment with imatinib and everolimus showed a decrease of tumor burden including CD34(+) cells.	imatinib	133-141	CD34 antigen	Mus musculus	201-205
21566429-7	2011	Activated mutant c-kit or platelet-derived growth factor receptor alpha (PDGFRA), which are potential therapeutic targets for imatinib, are constitutively expressed in most GIST.	imatinib	126-134	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	17-22
21336995-3	2011	The success in the treatment of chronic myelogenous leukemia by imatinib, inhibiting the bcr-abl-activated tyrosine kinase and thereby interrupting the signal transduction pathways that lead to leukemic transformation with impressive survival benefit, has paved the way for this new optimism.	imatinib	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
21566432-2	2011	Imatinib mesylate has shown significant safety and great effectiveness for patients with KIT-positive unresectable, advanced, or metastatic GIST.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	89-92
22977540-6	2011	These results indicate that STI-571 treatment may prove effective for MYCN-expressing or MYCN-amplified neuroblastoma.	imatinib	28-35	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	70-74
22977540-6	2011	These results indicate that STI-571 treatment may prove effective for MYCN-expressing or MYCN-amplified neuroblastoma.	imatinib	28-35	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	89-93
21566429-7	2011	Activated mutant c-kit or platelet-derived growth factor receptor alpha (PDGFRA), which are potential therapeutic targets for imatinib, are constitutively expressed in most GIST.	imatinib	126-134	platelet derived growth factor receptor alpha	Homo sapiens	26-71
21566433-3	2011	The cause of resistance to imatinib is the low sensitivity of gene mutations in the KIT gene or PDGFRalpha, or an acquisition of additional mutations, and a low plasma level of imatinib.	imatinib	27-35	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	84-87
21566433-3	2011	The cause of resistance to imatinib is the low sensitivity of gene mutations in the KIT gene or PDGFRalpha, or an acquisition of additional mutations, and a low plasma level of imatinib.	imatinib	27-35	platelet derived growth factor receptor alpha	Homo sapiens	96-106
21566429-7	2011	Activated mutant c-kit or platelet-derived growth factor receptor alpha (PDGFRA), which are potential therapeutic targets for imatinib, are constitutively expressed in most GIST.	imatinib	126-134	platelet derived growth factor receptor alpha	Homo sapiens	73-79
21460180-0	2011	MYC in chronic myeloid leukemia: induction of aberrant DNA synthesis and association with poor response to imatinib.	imatinib	107-115	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	0-3
21463117-7	2011	Imatinib has been used successfully to treat patients with chronic eosinophilic disorders with the FIP1L1-PDGFRA fusion kinase; limited clinical data indicate that dasatinib could be active in imatinib-resistant disease.	imatinib	0-8	factor interacting with PAPOLA and CPSF1	Homo sapiens	99-105
21463117-7	2011	Imatinib has been used successfully to treat patients with chronic eosinophilic disorders with the FIP1L1-PDGFRA fusion kinase; limited clinical data indicate that dasatinib could be active in imatinib-resistant disease.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	106-112
21364010-0	2011	hTERT promotes imatinib resistance in chronic myeloid leukemia cells: therapeutic implications.	imatinib	15-23	telomerase reverse transcriptase	Homo sapiens	0-5
21364010-5	2011	We showed that sensitivity to imatinib can be partly restored in imatinib-resistant cells by targeting telomerase expression, either by the introduction of a dominant-negative form of the catalytic protein subunit of the telomerase (hTERT) or by the treatment with all-trans-retinoic acid, a clinically used drug.	imatinib	30-38	telomerase reverse transcriptase	Homo sapiens	233-238
21364010-6	2011	Furthermore, we showed that hTERT overexpression favors the development of imatinib resistance through both its antiapoptotic and telomere maintenance functions.	imatinib	75-83	telomerase reverse transcriptase	Homo sapiens	28-33
21387285-2	2011	We examined whether inhibition of PDGF receptor (PDGF-R) tyrosine kinase signaling by imatinib affects tumor growth and metastasis in an orthotopic nude mouse model of human gastric carcinoma.	imatinib	86-94	platelet derived growth factor receptor, beta polypeptide	Mus musculus	34-47
21387285-2	2011	We examined whether inhibition of PDGF receptor (PDGF-R) tyrosine kinase signaling by imatinib affects tumor growth and metastasis in an orthotopic nude mouse model of human gastric carcinoma.	imatinib	86-94	platelet derived growth factor receptor, beta polypeptide	Mus musculus	49-55
21387287-2	2011	This review evaluates the clinical efficacy and safety of imatinib for adjuvant treatment of localized KIT (CD117)-positive resected GIST.	imatinib	58-66	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	103-106
21387287-2	2011	This review evaluates the clinical efficacy and safety of imatinib for adjuvant treatment of localized KIT (CD117)-positive resected GIST.	imatinib	58-66	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	108-113
21387287-11	2011	This study adds to the evidence (based on one RCT and a number of observational studies) that GIST patients treated with adjuvant imatinib therapy show an improvement in recurrence-free survival compared to placebo or no treatment after resection of KIT-positive localized GIST with tolerable toxicity.	imatinib	130-138	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	250-253
21239056-0	2011	BCR-ABL1 mutations in patients with imatinib-resistant Philadelphia chromosome-positive leukemia by use of the PCR-Invader assay.	imatinib	36-44	BCR activator of RhoGEF and GTPase	Homo sapiens	0-8
21239056-1	2011	BCR-ABL1 kinase domain mutations were evaluated in 60 imatinib-resistant patients with Philadelphia-positive (Ph(+)) leukemia using PCR-Invader assay and direct sequencing.	imatinib	54-62	BCR activator of RhoGEF and GTPase	Homo sapiens	0-8
21480391-5	2011	Blocking c-ABL kinase activity with the inhibitor imatinib further increased ERalpha downregulation induced by fulvestrant, decreased the number of proliferating cells entering the cell cycle, and increased cellular sensitivity to fulvestrant treatment.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-14
21460180-5	2011	In this report, we studied MYC activities in CML cell lines with conditional MYC expression with and without exposure to imatinib, the front-line drug in CML therapy.	imatinib	121-129	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	27-30
21480391-5	2011	Blocking c-ABL kinase activity with the inhibitor imatinib further increased ERalpha downregulation induced by fulvestrant, decreased the number of proliferating cells entering the cell cycle, and increased cellular sensitivity to fulvestrant treatment.	imatinib	50-58	estrogen receptor 1	Homo sapiens	77-84
21460180-7	2011	We studied MYC mRNA expression in 66 CML patients at different phases of the disease, and we found that MYC expression was higher in CML patients at diagnosis than control bone marrows or in patients responding to imatinib.	imatinib	214-222	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	104-107
21480391-7	2011	Consistent with the effects of imatinib, the silencing of endogenous c-ABL increased the sensitivity of breast cancer cells to fulvestrant treatment.	imatinib	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-74
21460180-8	2011	Further, high MYC levels at diagnosis correlated with a poor response to imatinib.	imatinib	73-81	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	14-17
21369701-1	2011	The persistence of Bcr-Abl-positive cells in patients on imatinib therapy indicates that inhibition of the Bcr-Abl kinase activity alone might not be sufficient to eradicate the leukemia cells.	imatinib	57-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
21369701-1	2011	The persistence of Bcr-Abl-positive cells in patients on imatinib therapy indicates that inhibition of the Bcr-Abl kinase activity alone might not be sufficient to eradicate the leukemia cells.	imatinib	57-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
21295132-3	2011	The imatinib targets, KIT and platelet derived growth factor receptor beta (PDGFRB), were shown here to be expressed in "germline stem" (GS) cell cultures that contain spermatogonia, including spermatogonial stem cells (SSCs).	imatinib	4-12	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	22-25
21330162-1	2011	Imatinib mesylate is a tyrosine kinase inhibitor which targets Bcr-Abl-protein, c-Kit, and platelet-derived growth factor receptor.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	80-85
21295132-3	2011	The imatinib targets, KIT and platelet derived growth factor receptor beta (PDGFRB), were shown here to be expressed in "germline stem" (GS) cell cultures that contain spermatogonia, including spermatogonial stem cells (SSCs).	imatinib	4-12	platelet derived growth factor receptor beta	Homo sapiens	30-74
21295132-3	2011	The imatinib targets, KIT and platelet derived growth factor receptor beta (PDGFRB), were shown here to be expressed in "germline stem" (GS) cell cultures that contain spermatogonia, including spermatogonial stem cells (SSCs).	imatinib	4-12	platelet derived growth factor receptor beta	Homo sapiens	76-82
21295132-6	2011	However, growth in imatinib led to decreased numbers of differentiated spermatogonia and reduced culture growth consistent with the known requirement for KIT in survival and proliferation of spermatogonia.	imatinib	19-27	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	154-157
20589679-1	2011	Platelet-derived growth factor receptor (PDGFR) signaling has been implicated in the pathogenesis of glioblastomas and represents a target for the tyrosine kinase inhibitor imatinib.	imatinib	173-181	platelet derived growth factor receptor beta	Homo sapiens	0-39
21501463-5	2011	RESULTS: To study the signal transduction pathways induced by NGF treatment in hematopoietic cells, we utilized the mastocytoma cell line HMC-1(V560G c-Kit) which expresses the NGF receptor, tropomyosin-receptor-kinase (Trk)A, as well as the constitutively activated SCF receptor, V560G c-Kit, which can be inhibited completely by treatment with the potent tyrosine kinase inhibitor imatinib mesylate (imatinib).	imatinib	383-400	nerve growth factor	Homo sapiens	62-65
21501463-5	2011	RESULTS: To study the signal transduction pathways induced by NGF treatment in hematopoietic cells, we utilized the mastocytoma cell line HMC-1(V560G c-Kit) which expresses the NGF receptor, tropomyosin-receptor-kinase (Trk)A, as well as the constitutively activated SCF receptor, V560G c-Kit, which can be inhibited completely by treatment with the potent tyrosine kinase inhibitor imatinib mesylate (imatinib).	imatinib	383-391	nerve growth factor	Homo sapiens	62-65
21501463-6	2011	NGF rescues HMC-1(V560G c-Kit) cells from imatinib mediated cell death and promotes proliferation.	imatinib	42-50	nerve growth factor	Homo sapiens	0-3
21501463-6	2011	NGF rescues HMC-1(V560G c-Kit) cells from imatinib mediated cell death and promotes proliferation.	imatinib	42-50	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	24-29
21501463-7	2011	To examine the NGF mediated proliferation and survival in these cells, we compared the NGF mediated upregulated genes (30 and 120 min after stimulation) to the downregulated genes by imatinib treatment (downregulation of c-Kit activity for 4 h) by transcriptome analysis.	imatinib	183-191	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	221-226
21501463-12	2011	Finally, the downregulation of KLF2 gene enhanced imatinib induced apoptosis.	imatinib	50-58	Kruppel like factor 2	Homo sapiens	31-35
21533122-0	2011	Imatinib treatment induces CD5+ B lymphocytes and IgM natural antibodies with anti-leukemic reactivity in patients with chronic myelogenous leukemia.	imatinib	0-8	CD5 molecule	Homo sapiens	27-30
21533122-9	2011	We propose that CD20(+)CD5(+)sIgM(+) lymphocytes producing anti-carbohydrate antibodies with anti-tumor activity, might contribute to the response to imatinib treatment.	imatinib	150-158	keratin 20	Homo sapiens	16-20
21533122-9	2011	We propose that CD20(+)CD5(+)sIgM(+) lymphocytes producing anti-carbohydrate antibodies with anti-tumor activity, might contribute to the response to imatinib treatment.	imatinib	150-158	CD5 molecule	Homo sapiens	23-26
20589679-1	2011	Platelet-derived growth factor receptor (PDGFR) signaling has been implicated in the pathogenesis of glioblastomas and represents a target for the tyrosine kinase inhibitor imatinib.	imatinib	173-181	platelet derived growth factor receptor beta	Homo sapiens	41-46
21417343-0	2011	Crystal structures of ABL-related gene (ABL2) in complex with imatinib, tozasertib (VX-680), and a type I inhibitor of the triazole carbothioamide class.	imatinib	62-70	ABL proto-oncogene 2, non-receptor tyrosine kinase	Homo sapiens	40-44
21417343-5	2011	To elucidate structural determinants for inhibitor interaction, we determined the cocrystal structure of ABL2 with the oncology drug imatinib.	imatinib	133-141	ABL proto-oncogene 2, non-receptor tyrosine kinase	Homo sapiens	105-109
20922524-5	2011	Imatinib mesylate was administered upon cytogenetic relapse or disease progression while on IFN-alpha.	imatinib	0-17	interferon alpha 1	Homo sapiens	92-101
21516268-0	2011	Imatinib plus Granulocyte Colony-Stimulating Factor in Chronic Myeloid Leukemia Patients Who Have Achieved Partial or Complete Cytogenetic Response while on Imatinib.	imatinib	157-165	colony stimulating factor 3	Homo sapiens	14-51
21516268-8	2011	CONCLUSIONS: We conclude that the addition of G-CSF should be considered for patients on imatinib who fail to obtain optimal response to imatinib alone and that this approach deserves further evaluation as frontline therapy for newly diagnosed CML.	imatinib	89-97	colony stimulating factor 3	Homo sapiens	46-51
21516268-8	2011	CONCLUSIONS: We conclude that the addition of G-CSF should be considered for patients on imatinib who fail to obtain optimal response to imatinib alone and that this approach deserves further evaluation as frontline therapy for newly diagnosed CML.	imatinib	137-145	colony stimulating factor 3	Homo sapiens	46-51
21239531-9	2011	The lungs of imatinib-treated pups had increased fibulin-5 content and an abnormal deposition of elastin.	imatinib	13-21	fibulin 5	Rattus norvegicus	49-58
21239531-9	2011	The lungs of imatinib-treated pups had increased fibulin-5 content and an abnormal deposition of elastin.	imatinib	13-21	elastin	Rattus norvegicus	97-104
21442641-10	2011	Imatinib has a therapeutic role in the presence of an imatinib-sensitive KIT mutation or in KITD816-unmutated patients.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
21442641-10	2011	Imatinib has a therapeutic role in the presence of an imatinib-sensitive KIT mutation or in KITD816-unmutated patients.	imatinib	54-62	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
20596710-1	2011	PURPOSE: Imatinib mesylate (Imatinib), clinically employed for chronic myeloid leukemia and gastrointestinal stromal tumors, is a selective inhibitor of the tyrosine kinases, c-abl, c-kit and PDGFRs.	imatinib	9-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-180
21275952-0	2011	Quantitative and functional analyses of CD4(+) CD25(+) FoxP3(+) regulatory T cells in chronic phase chronic myeloid leukaemia patients at diagnosis and on imatinib mesylate.	imatinib	155-172	CD4 molecule	Homo sapiens	40-43
21275952-0	2011	Quantitative and functional analyses of CD4(+) CD25(+) FoxP3(+) regulatory T cells in chronic phase chronic myeloid leukaemia patients at diagnosis and on imatinib mesylate.	imatinib	155-172	forkhead box P3	Homo sapiens	55-60
20596710-1	2011	PURPOSE: Imatinib mesylate (Imatinib), clinically employed for chronic myeloid leukemia and gastrointestinal stromal tumors, is a selective inhibitor of the tyrosine kinases, c-abl, c-kit and PDGFRs.	imatinib	9-26	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	182-187
20596710-1	2011	PURPOSE: Imatinib mesylate (Imatinib), clinically employed for chronic myeloid leukemia and gastrointestinal stromal tumors, is a selective inhibitor of the tyrosine kinases, c-abl, c-kit and PDGFRs.	imatinib	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-180
20596710-1	2011	PURPOSE: Imatinib mesylate (Imatinib), clinically employed for chronic myeloid leukemia and gastrointestinal stromal tumors, is a selective inhibitor of the tyrosine kinases, c-abl, c-kit and PDGFRs.	imatinib	9-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	182-187
20596710-9	2011	In promoter activation assays, Imatinib increased the promoter activity driven by both Wnt and MAPK/ERK-1/2.	imatinib	31-39	mitogen-activated protein kinase 3	Homo sapiens	100-107
21226671-2	2011	Several early- and late-phase clinical trials for chronic myelogeneous leukaemia (CML) have demonstrated the direct inhibition of BCR-ABL fusion protein and SFKs, which led to dasatinib approval by the Food and Drug Administration (FDA) and the European Union for the treatment of imatinib-resistant or -intolerant CML, and Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL).	imatinib	281-289	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
21327932-0	2011	Durable remission after treatment with very low doses of imatinib for FIP1L1-PDGFRalpha-positive chronic eosinophilic leukaemia.	imatinib	57-65	factor interacting with PAPOLA and CPSF1	Homo sapiens	70-76
21505592-4	2011	Research activities focusing on the mechanisms that underlie imatinib resistance have identified mutations in the BCR-ABL gene, clonal evolution, and amplification of the BCR-ABL gene as common causes.	imatinib	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
21505592-4	2011	Research activities focusing on the mechanisms that underlie imatinib resistance have identified mutations in the BCR-ABL gene, clonal evolution, and amplification of the BCR-ABL gene as common causes.	imatinib	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-178
20942869-0	2011	An investigation of reversal of imatinib resistance in the Bcr-Abl positive imatinib-resistant cell line K562r by dasatinib, nilotinib, rapamycin and bortezomib.	imatinib	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
20942869-0	2011	An investigation of reversal of imatinib resistance in the Bcr-Abl positive imatinib-resistant cell line K562r by dasatinib, nilotinib, rapamycin and bortezomib.	imatinib	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
20942869-8	2011	CONCLUSION: K562r due to duplication of autophosphorylation of wild-type Bcr-Abl induced by imatinib was still partially resistant to dasatinib and nilotinib, but this was overcome by incremental dosing.	imatinib	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
21249316-0	2011	Synergistic effects of imatinib and carboplatin on VEGF, PDGF and PDGF-Ralpha/ss expression in squamous cell carcinoma of the head and neck in vitro.	imatinib	23-31	vascular endothelial growth factor A	Homo sapiens	51-55
21249316-0	2011	Synergistic effects of imatinib and carboplatin on VEGF, PDGF and PDGF-Ralpha/ss expression in squamous cell carcinoma of the head and neck in vitro.	imatinib	23-31	platelet derived growth factor receptor alpha	Homo sapiens	66-77
21261505-8	2011	Nef is a candidate chemical that can increase STI571 chemosensitivity in STI571-resistant K562 cells by inhibition of P-gp expression and increasing intracellular STI571 accumulation.	imatinib	46-52	ATP binding cassette subfamily B member 1	Homo sapiens	118-122
21249316-8	2011	The purpose of this study was to investigate the potential synergism of imatinib and carboplatin on the expression of PDGF, PDGF-R alpha/ss and VEGF in different HNSCC cell lines.	imatinib	72-80	platelet derived growth factor receptor alpha	Homo sapiens	124-136
21249316-8	2011	The purpose of this study was to investigate the potential synergism of imatinib and carboplatin on the expression of PDGF, PDGF-R alpha/ss and VEGF in different HNSCC cell lines.	imatinib	72-80	vascular endothelial growth factor A	Homo sapiens	144-148
21249316-12	2011	We observed explicit significant reduction in VEGF levels with increasing concentrations of imatinib and with the combination of the two chemotherapeutic drugs (p<0.5).	imatinib	92-100	vascular endothelial growth factor A	Homo sapiens	46-50
21249316-13	2011	We report for the first time evidence of synergism of imatinib and carboplatin in suppressing VEGF, PDGF and PDGF-Ralpha/ss expression in HNSCC.	imatinib	54-62	vascular endothelial growth factor A	Homo sapiens	94-98
21249316-13	2011	We report for the first time evidence of synergism of imatinib and carboplatin in suppressing VEGF, PDGF and PDGF-Ralpha/ss expression in HNSCC.	imatinib	54-62	platelet derived growth factor receptor alpha	Homo sapiens	109-120
20857409-6	2011	On the contrary, an inhibitory antibody that neutralized the KIT ligand binding site, reduced growth of MCC-1 cells, as did high doses of the KIT kinase inhibitors imatinib and nilotinib.	imatinib	164-172	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	61-64
20857409-6	2011	On the contrary, an inhibitory antibody that neutralized the KIT ligand binding site, reduced growth of MCC-1 cells, as did high doses of the KIT kinase inhibitors imatinib and nilotinib.	imatinib	164-172	MCC regulator of WNT signaling pathway	Homo sapiens	104-109
20857409-6	2011	On the contrary, an inhibitory antibody that neutralized the KIT ligand binding site, reduced growth of MCC-1 cells, as did high doses of the KIT kinase inhibitors imatinib and nilotinib.	imatinib	164-172	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	142-145
20012337-1	2011	PURPOSE: This phase II study evaluated the activity of combined treatment with the mTOR inhibitor everolimus and the PDGFR inhibitor imatinib in patients with previously-treated, advanced renal carcinoma.	imatinib	133-141	platelet derived growth factor receptor beta	Homo sapiens	117-122
20684991-0	2011	Genomic characterization of Imatinib resistance in CD34+ cell populations from chronic myeloid leukaemia patients.	imatinib	28-36	CD34 molecule	Homo sapiens	51-55
21314483-0	2011	Role of hTERT and WT1 gene expression in disease progression and imatinib responsiveness of patients with BCR-ABL positive chronic myeloid leukemia.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
21314483-7	2011	Freshly diagnosed, imatinib-responsive, and -unresponsive patients among these revealed interesting changes in hTERT and WT1 gene expression profiles, especially in 25 patients with CML in whom sequential samples were analyzed.	imatinib	19-27	telomerase reverse transcriptase	Homo sapiens	111-116
21314483-7	2011	Freshly diagnosed, imatinib-responsive, and -unresponsive patients among these revealed interesting changes in hTERT and WT1 gene expression profiles, especially in 25 patients with CML in whom sequential samples were analyzed.	imatinib	19-27	WT1 transcription factor	Homo sapiens	121-124
21419931-2	2011	Recognition of the key role played by the receptor tyrosine kinases KIT and platelet-derived growth factor receptor alpha (PDGFRalpha) in the pathogenesis of GIST led to the development of imatinib, the first TKI for this indication and the current first-line standard of care for unresectable or metastatic GIST.	imatinib	189-197	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	68-71
21249321-0	2011	Down-regulation of MMP-2 expression due to inhibition of receptor tyrosine kinases by imatinib and carboplatin in HNSCC.	imatinib	86-94	matrix metallopeptidase 2	Homo sapiens	19-24
21249321-8	2011	But imatinib also has an inhibitory impact on the PTK receptor c-kit and on its PTK activity.	imatinib	4-12	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	63-68
21249321-13	2011	Especially the combination of 7.5 mumol carboplatin with 30 mumol imatinib resulted in a significant decrease in MMP-2 expression in all observed cell lines (p<0.05).	imatinib	66-74	matrix metallopeptidase 2	Homo sapiens	113-118
21249321-17	2011	Our results indicate that MMP-2 expression was suppressed in the presence of imatinib.	imatinib	77-85	matrix metallopeptidase 2	Homo sapiens	26-31
22034611-2	2011	The multikinase inhibitor imatinib that targets PDGF receptor (PDGFR), c-kit and Abl kinases, shows therapeutic efficacy against experimental pulmonary hypertension (PH); however, the role of PDGFR-b in experimental PH has not been examined by genetic approach.	imatinib	26-34	platelet derived growth factor receptor, beta polypeptide	Mus musculus	48-61
22034611-2	2011	The multikinase inhibitor imatinib that targets PDGF receptor (PDGFR), c-kit and Abl kinases, shows therapeutic efficacy against experimental pulmonary hypertension (PH); however, the role of PDGFR-b in experimental PH has not been examined by genetic approach.	imatinib	26-34	platelet derived growth factor receptor, beta polypeptide	Mus musculus	63-68
22034611-2	2011	The multikinase inhibitor imatinib that targets PDGF receptor (PDGFR), c-kit and Abl kinases, shows therapeutic efficacy against experimental pulmonary hypertension (PH); however, the role of PDGFR-b in experimental PH has not been examined by genetic approach.	imatinib	26-34	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	71-76
22034611-2	2011	The multikinase inhibitor imatinib that targets PDGF receptor (PDGFR), c-kit and Abl kinases, shows therapeutic efficacy against experimental pulmonary hypertension (PH); however, the role of PDGFR-b in experimental PH has not been examined by genetic approach.	imatinib	26-34	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	81-84
22034611-2	2011	The multikinase inhibitor imatinib that targets PDGF receptor (PDGFR), c-kit and Abl kinases, shows therapeutic efficacy against experimental pulmonary hypertension (PH); however, the role of PDGFR-b in experimental PH has not been examined by genetic approach.	imatinib	26-34	platelet derived growth factor receptor, beta polypeptide	Mus musculus	192-197
21159146-0	2011	V559A and N822I double KIT mutant melanoma with predictable response to imatinib?	imatinib	72-80	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	23-26
21419931-2	2011	Recognition of the key role played by the receptor tyrosine kinases KIT and platelet-derived growth factor receptor alpha (PDGFRalpha) in the pathogenesis of GIST led to the development of imatinib, the first TKI for this indication and the current first-line standard of care for unresectable or metastatic GIST.	imatinib	189-197	platelet derived growth factor receptor alpha	Homo sapiens	76-121
21419934-2	2011	The prototype TKI, imatinib, selectively inhibits BCR-ABL, as well as several other kinases, including stem cell factor receptor (KIT), discoidin domain receptor (DDR), platelet-derived growth factor receptor (PDGFR), and colony-stimulating factor receptor-1 (CSF-1R).	imatinib	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
21419934-2	2011	The prototype TKI, imatinib, selectively inhibits BCR-ABL, as well as several other kinases, including stem cell factor receptor (KIT), discoidin domain receptor (DDR), platelet-derived growth factor receptor (PDGFR), and colony-stimulating factor receptor-1 (CSF-1R).	imatinib	19-27	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	130-133
21419934-2	2011	The prototype TKI, imatinib, selectively inhibits BCR-ABL, as well as several other kinases, including stem cell factor receptor (KIT), discoidin domain receptor (DDR), platelet-derived growth factor receptor (PDGFR), and colony-stimulating factor receptor-1 (CSF-1R).	imatinib	19-27	platelet derived growth factor receptor beta	Homo sapiens	169-208
21419934-2	2011	The prototype TKI, imatinib, selectively inhibits BCR-ABL, as well as several other kinases, including stem cell factor receptor (KIT), discoidin domain receptor (DDR), platelet-derived growth factor receptor (PDGFR), and colony-stimulating factor receptor-1 (CSF-1R).	imatinib	19-27	platelet derived growth factor receptor beta	Homo sapiens	210-215
21419934-2	2011	The prototype TKI, imatinib, selectively inhibits BCR-ABL, as well as several other kinases, including stem cell factor receptor (KIT), discoidin domain receptor (DDR), platelet-derived growth factor receptor (PDGFR), and colony-stimulating factor receptor-1 (CSF-1R).	imatinib	19-27	colony stimulating factor 1 receptor	Homo sapiens	260-267
21419934-5	2011	Nilotinib, a second-generation oral TKI, was rationally designed based on the crystal structure of imatinib to be highly active against a wide range of imatinib-resistant BCR-ABL mutants and is approved for the treatment of newly diagnosed or imatinib-resistant or -intolerant CML, and has shown superiority over imatinib in first-line treatment for newly diagnosed CML.	imatinib	99-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-178
21419934-5	2011	Nilotinib, a second-generation oral TKI, was rationally designed based on the crystal structure of imatinib to be highly active against a wide range of imatinib-resistant BCR-ABL mutants and is approved for the treatment of newly diagnosed or imatinib-resistant or -intolerant CML, and has shown superiority over imatinib in first-line treatment for newly diagnosed CML.	imatinib	152-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-178
21419934-5	2011	Nilotinib, a second-generation oral TKI, was rationally designed based on the crystal structure of imatinib to be highly active against a wide range of imatinib-resistant BCR-ABL mutants and is approved for the treatment of newly diagnosed or imatinib-resistant or -intolerant CML, and has shown superiority over imatinib in first-line treatment for newly diagnosed CML.	imatinib	152-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-178
21419934-5	2011	Nilotinib, a second-generation oral TKI, was rationally designed based on the crystal structure of imatinib to be highly active against a wide range of imatinib-resistant BCR-ABL mutants and is approved for the treatment of newly diagnosed or imatinib-resistant or -intolerant CML, and has shown superiority over imatinib in first-line treatment for newly diagnosed CML.	imatinib	152-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-178
21311410-0	2011	Association of genetic polymorphisms in the influx transporter SLCO1B3 and the efflux transporter ABCB1 with imatinib pharmacokinetics in patients with chronic myeloid leukemia.	imatinib	109-117	solute carrier organic anion transporter family member 1B3	Homo sapiens	63-70
21421113-3	2011	Activating mutations in B-Raf and c-kit are associated with clinical response to the specific kinase inhibitors PLX4032 and imatinib, respectively.	imatinib	124-132	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	24-29
21311410-0	2011	Association of genetic polymorphisms in the influx transporter SLCO1B3 and the efflux transporter ABCB1 with imatinib pharmacokinetics in patients with chronic myeloid leukemia.	imatinib	109-117	ATP binding cassette subfamily B member 1	Homo sapiens	98-103
21311410-5	2011	Patients with the ABCB1 3435CC genotype had significantly higher imatinib clearance (12.7 +- 3.0 L/hr; n = 7) compared with patients with ABCB1 3435CT and TT genotypes (7.9 +- 2.7 L/hr; n = 27) (P = 0.035).	imatinib	65-73	ATP binding cassette subfamily B member 1	Homo sapiens	18-23
21311410-6	2011	In conclusion, the present study suggests that single nucleotide polymorphisms of the influx transporter SLCO1B3 and the efflux transporter ABCB1 were functionally associated with individual variability of imatinib pharmacokinetics in Japanese patients with chronic myeloid leukemia.	imatinib	206-214	solute carrier organic anion transporter family member 1B3	Homo sapiens	105-112
21421113-3	2011	Activating mutations in B-Raf and c-kit are associated with clinical response to the specific kinase inhibitors PLX4032 and imatinib, respectively.	imatinib	124-132	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	34-39
21311410-6	2011	In conclusion, the present study suggests that single nucleotide polymorphisms of the influx transporter SLCO1B3 and the efflux transporter ABCB1 were functionally associated with individual variability of imatinib pharmacokinetics in Japanese patients with chronic myeloid leukemia.	imatinib	206-214	ATP binding cassette subfamily B member 1	Homo sapiens	140-145
21277237-6	2011	Results indicate that c-Abl inhibition by STI571 significantly affects neutrophil adhesion via L-selectin, by decreasing the average rolling velocity and increasing the flux of rolling cells.	imatinib	42-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-27
21220747-0	2011	High STAT5 levels mediate imatinib resistance and indicate disease progression in chronic myeloid leukemia.	imatinib	26-34	signal transducer and activator of transcription 5A	Homo sapiens	5-10
21220747-2	2011	Here we show that the expression level of the transcription factor STAT5 is another parameter that determines the sensitivity of BCR-ABL1(+) cells against tyrosine kinase inhibitors (TKIs), such as imatinib, nilotinib, or dasatinib.	imatinib	198-206	signal transducer and activator of transcription 5A	Homo sapiens	67-72
21220747-2	2011	Here we show that the expression level of the transcription factor STAT5 is another parameter that determines the sensitivity of BCR-ABL1(+) cells against tyrosine kinase inhibitors (TKIs), such as imatinib, nilotinib, or dasatinib.	imatinib	198-206	BCR activator of RhoGEF and GTPase	Homo sapiens	129-137
21220747-5	2011	In support of this concept, under imatinib treatment and with disease progression, STAT5 mRNA and protein levels increased in patients with Ph(+) chronic myeloid leukemia.	imatinib	34-42	signal transducer and activator of transcription 5A	Homo sapiens	83-88
21220747-9	2011	It also suggests that STAT5 may serve as an attractive target to overcome imatinib resistance in BCR-ABL1(+) leukemia.	imatinib	74-82	signal transducer and activator of transcription 5A	Homo sapiens	22-27
21220747-9	2011	It also suggests that STAT5 may serve as an attractive target to overcome imatinib resistance in BCR-ABL1(+) leukemia.	imatinib	74-82	BCR activator of RhoGEF and GTPase	Homo sapiens	97-105
21233313-10	2011	Simultaneously inhibiting STAT5 with pimozide and the kinase inhibitors imatinib or nilotinib shows enhanced effects in inhibiting STAT5 phosphorylation and in inducing apoptosis.	imatinib	72-80	signal transducer and activator of transcription 5A	Homo sapiens	26-31
21233313-10	2011	Simultaneously inhibiting STAT5 with pimozide and the kinase inhibitors imatinib or nilotinib shows enhanced effects in inhibiting STAT5 phosphorylation and in inducing apoptosis.	imatinib	72-80	signal transducer and activator of transcription 5A	Homo sapiens	131-136
21248063-4	2011	Induction of apoptosis because of aggresomal compartmentalization of Bcr-Abl was observed in both imatinib-sensitive and -resistant cells.	imatinib	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
21277237-6	2011	Results indicate that c-Abl inhibition by STI571 significantly affects neutrophil adhesion via L-selectin, by decreasing the average rolling velocity and increasing the flux of rolling cells.	imatinib	42-48	selectin L	Homo sapiens	95-105
21224473-0	2011	Novel imatinib-sensitive PDGFRA-activating point mutations in hypereosinophilic syndrome induce growth factor independence and leukemia-like disease.	imatinib	6-14	platelet derived growth factor receptor alpha	Homo sapiens	25-31
21224473-5	2011	Imatinib antagonized Stat5 phosphorylation.	imatinib	0-8	signal transducer and activator of transcription 5A	Homo sapiens	21-26
21224473-9	2011	In conclusion, our data provide evidence that imatinib-sensitive PDGFRA point mutations play an important role in the pathogenesis of HES and we propose that more research should be performed to further define the frequency and treatment response of PDGFRA mutations in FIP1L1-PDGFRA-negative HES patients.	imatinib	46-54	platelet derived growth factor receptor alpha	Homo sapiens	65-71
21224473-9	2011	In conclusion, our data provide evidence that imatinib-sensitive PDGFRA point mutations play an important role in the pathogenesis of HES and we propose that more research should be performed to further define the frequency and treatment response of PDGFRA mutations in FIP1L1-PDGFRA-negative HES patients.	imatinib	46-54	platelet derived growth factor receptor alpha	Homo sapiens	250-256
21224473-9	2011	In conclusion, our data provide evidence that imatinib-sensitive PDGFRA point mutations play an important role in the pathogenesis of HES and we propose that more research should be performed to further define the frequency and treatment response of PDGFRA mutations in FIP1L1-PDGFRA-negative HES patients.	imatinib	46-54	factor interacting with PAPOLA and CPSF1	Homo sapiens	270-276
21224473-9	2011	In conclusion, our data provide evidence that imatinib-sensitive PDGFRA point mutations play an important role in the pathogenesis of HES and we propose that more research should be performed to further define the frequency and treatment response of PDGFRA mutations in FIP1L1-PDGFRA-negative HES patients.	imatinib	46-54	platelet derived growth factor receptor alpha	Homo sapiens	250-256
21198861-1	2011	BCR/ABL positive cells are known to be resistant to DNA damage induced by chemotherapy while they are sensitive to imatinib (IM), a tyrosine kinase inhibitor (TKI).	imatinib	115-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
20512393-1	2011	Point mutations in the kinase domain of BCR-ABL were described in 40-90% of patients with chronic myeloid leukemia (CML) resistant to Imatinib.	imatinib	134-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
21498698-4	2011	MATERIALS AND METHODS: The endogenous c-ABL kinase was silenced by RNA interference or inhibited by imatinib to test whether the co-treatment improves the responsiveness of the lapatinib-resistant breast cancer cell lines MDA-MB-468 and T47D, by measuring cell growth and cell-cycle progression.	imatinib	100-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-43
21498698-5	2011	CONCLUSION: The responsiveness to lapatinib can be improved by targeting the function of c-ABL, suggesting that combination treatment of lapatinib plus imatinib can lead to significant gains in therapeutic benefit.	imatinib	152-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-94
20945321-3	2011	The introduction of imatinib, a tyrosine kinase inhibitor (TKI) that is specific for BCR-ABL, was a major breakthrough in CML therapy.	imatinib	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
21143150-9	2011	Imatinib, a tyrosine kinase inhibitor, is now first line treatment for CML, but two large randomized studies show improved outcome when pegylated IFN-alpha is added to the treatment with imatinib.	imatinib	0-8	interferon alpha 1	Homo sapiens	146-155
21143150-9	2011	Imatinib, a tyrosine kinase inhibitor, is now first line treatment for CML, but two large randomized studies show improved outcome when pegylated IFN-alpha is added to the treatment with imatinib.	imatinib	187-195	interferon alpha 1	Homo sapiens	146-155
21143150-10	2011	One explanation for this might be that IFN-alpha, contrary to imatinib, stimulates the quiescent stem cells to proliferate and thereby potentially increases sensitivity to imatinib.	imatinib	172-180	interferon alpha 1	Homo sapiens	39-48
21418741-2	2011	This study investigated the effect of downregulation of X-chromosome-linked inhibitor of apoptosis (XIAP) and of simultaneous downregulation of XIAP and P-gp on sensitivity to imatinib.	imatinib	176-184	X-linked inhibitor of apoptosis	Homo sapiens	144-148
21134983-1	2011	BACKGROUND: Point mutations of the BCR-ABL tyrosine kinase domain are considered the predominant cause of imatinib resistance in chronic myeloid leukemia.	imatinib	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
21418741-2	2011	This study investigated the effect of downregulation of X-chromosome-linked inhibitor of apoptosis (XIAP) and of simultaneous downregulation of XIAP and P-gp on sensitivity to imatinib.	imatinib	176-184	phosphoglycolate phosphatase	Homo sapiens	153-157
21418740-0	2011	Imatinib induces autophagy through BECLIN-1 and ATG5 genes in chronic myeloid leukemia cells.	imatinib	0-8	beclin 1	Homo sapiens	35-43
21418740-0	2011	Imatinib induces autophagy through BECLIN-1 and ATG5 genes in chronic myeloid leukemia cells.	imatinib	0-8	autophagy related 5	Homo sapiens	48-52
21418741-4	2011	Targeting XIAP moderately enhanced sensitivity to imatinib in both cell lines.	imatinib	50-58	X-linked inhibitor of apoptosis	Homo sapiens	10-14
21418740-5	2011	Results suggested that imatinib induces autophagy in CML cells through inducing over-expression of BECLIN-1 and ATG5 genes with the statistical significance.	imatinib	23-31	beclin 1	Homo sapiens	99-107
21418740-5	2011	Results suggested that imatinib induces autophagy in CML cells through inducing over-expression of BECLIN-1 and ATG5 genes with the statistical significance.	imatinib	23-31	autophagy related 5	Homo sapiens	112-116
21418741-0	2011	Simultaneous targeting of P-gp and XIAP with siRNAs increases sensitivity of P-gp overexpressing CML cells to imatinib.	imatinib	110-118	phosphoglycolate phosphatase	Homo sapiens	26-30
21418741-5	2011	Simultaneous targeting of XIAP and P-gp further enhanced sensitivity to imatinib in the resistant K562Dox cells.	imatinib	72-80	X-linked inhibitor of apoptosis	Homo sapiens	26-30
21418741-5	2011	Simultaneous targeting of XIAP and P-gp further enhanced sensitivity to imatinib in the resistant K562Dox cells.	imatinib	72-80	phosphoglycolate phosphatase	Homo sapiens	35-39
21418741-6	2011	In conclusion, simultaneous targeting of P-gp and XIAP increases sensitivity of P-gp overexpressing chronic myeloid leukemia cells to imatinib.	imatinib	134-142	phosphoglycolate phosphatase	Homo sapiens	41-45
21418741-6	2011	In conclusion, simultaneous targeting of P-gp and XIAP increases sensitivity of P-gp overexpressing chronic myeloid leukemia cells to imatinib.	imatinib	134-142	X-linked inhibitor of apoptosis	Homo sapiens	50-54
21418741-6	2011	In conclusion, simultaneous targeting of P-gp and XIAP increases sensitivity of P-gp overexpressing chronic myeloid leukemia cells to imatinib.	imatinib	134-142	phosphoglycolate phosphatase	Homo sapiens	80-84
21418741-0	2011	Simultaneous targeting of P-gp and XIAP with siRNAs increases sensitivity of P-gp overexpressing CML cells to imatinib.	imatinib	110-118	X-linked inhibitor of apoptosis	Homo sapiens	35-39
20107936-3	2011	We administered WT1 peptide 22 times over 18 months in a CML patient who was being treated with imatinib.	imatinib	96-104	WT1 transcription factor	Homo sapiens	16-19
21418741-0	2011	Simultaneous targeting of P-gp and XIAP with siRNAs increases sensitivity of P-gp overexpressing CML cells to imatinib.	imatinib	110-118	phosphoglycolate phosphatase	Homo sapiens	77-81
21253680-2	2011	Survival of patients with chronic myeloid leukemia (CML) has dramatically improved with the introduction of the BCR-ABL-specific tyrosine kinase inhibitor imatinib.	imatinib	155-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
21253680-8	2011	The indications for allogenic stem cell transplantation and the administration of second generation BCR-ABL inhibitors will be discussed as therapeutic alternatives in cases of imatinib failure in a stage-specific manner.	imatinib	177-185	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
21093052-0	2011	Rapid reversal of quadraparesis in chronic eosinophilic leukaemia expressing the FIP1L1-PDGFRA transcript after therapy with imatinib.	imatinib	125-133	factor interacting with PAPOLA and CPSF1	Homo sapiens	81-87
21093052-0	2011	Rapid reversal of quadraparesis in chronic eosinophilic leukaemia expressing the FIP1L1-PDGFRA transcript after therapy with imatinib.	imatinib	125-133	platelet derived growth factor receptor alpha	Homo sapiens	88-94
20204543-4	2011	We investigated the MDR1 T1236C, G 2677T/A, and C3435T polymorphism in 52 patients with chronic myeloid leukemia treated with imatinib.	imatinib	126-134	ATP binding cassette subfamily B member 1	Homo sapiens	20-24
20204543-0	2011	Multidrug resistance gene (MDR1) polymorphisms correlate with imatinib response in chronic myeloid leukemia.	imatinib	62-70	ATP binding cassette subfamily B member 1	Homo sapiens	27-31
20204543-10	2011	In conclusion, determination of 1236T, C3435T, and G2677T MDR1 polymorphisms might be useful in response prediction to therapy with imatinib in patients with CML.	imatinib	132-140	ATP binding cassette subfamily B member 1	Homo sapiens	58-62
20204543-3	2011	Imatinib is a substrate of P-gp-mediated efflux.	imatinib	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	27-31
21072821-3	2011	Targeted therapy with imatinib induced a rapid hematologic response and reduction of TPM3-PDGFRB transcripts as monitored by reverse transcription real-time PCR (RT-qPCR).	imatinib	22-30	tropomyosin 3	Homo sapiens	85-89
21252289-4	2011	Results showed that imatinib, nilotinib, gefitinib, and erlotinib exerted selectively potent inhibitory effects, with unbound C(max,sys,p)/IC(50) values >=0.1, on MATE1, OCT3, MATE2-K, and OCT1, respectively.	imatinib	20-28	solute carrier family 47 member 1	Homo sapiens	166-171
21252289-4	2011	Results showed that imatinib, nilotinib, gefitinib, and erlotinib exerted selectively potent inhibitory effects, with unbound C(max,sys,p)/IC(50) values >=0.1, on MATE1, OCT3, MATE2-K, and OCT1, respectively.	imatinib	20-28	solute carrier family 22 member 3	Homo sapiens	173-177
21252289-4	2011	Results showed that imatinib, nilotinib, gefitinib, and erlotinib exerted selectively potent inhibitory effects, with unbound C(max,sys,p)/IC(50) values >=0.1, on MATE1, OCT3, MATE2-K, and OCT1, respectively.	imatinib	20-28	solute carrier family 47 member 2	Homo sapiens	179-186
21252289-4	2011	Results showed that imatinib, nilotinib, gefitinib, and erlotinib exerted selectively potent inhibitory effects, with unbound C(max,sys,p)/IC(50) values >=0.1, on MATE1, OCT3, MATE2-K, and OCT1, respectively.	imatinib	20-28	solute carrier family 22 member 1	Homo sapiens	192-196
21072821-3	2011	Targeted therapy with imatinib induced a rapid hematologic response and reduction of TPM3-PDGFRB transcripts as monitored by reverse transcription real-time PCR (RT-qPCR).	imatinib	22-30	platelet derived growth factor receptor beta	Homo sapiens	90-96
20972453-3	2011	The majority of patients with PDGFR-rearranged myeloproliferation respond to treatment with imatinib.	imatinib	92-100	platelet derived growth factor receptor beta	Homo sapiens	30-35
21181412-0	2011	Time-specific blockade of PDGFR with Imatinib (Glivec ) causes cataract and disruption of lens fiber cells in neonatal mice.	imatinib	37-45	platelet derived growth factor receptor, beta polypeptide	Mus musculus	26-31
21181412-0	2011	Time-specific blockade of PDGFR with Imatinib (Glivec ) causes cataract and disruption of lens fiber cells in neonatal mice.	imatinib	47-53	platelet derived growth factor receptor, beta polypeptide	Mus musculus	26-31
21181412-1	2011	This study aimed at investigating the response of lens epithelial cells in postnatal mice to Imatinib (Glivec , a potent inhibitor of platelet-derived growth factor receptor (PDGFR)) treatment.	imatinib	93-101	platelet derived growth factor receptor, beta polypeptide	Mus musculus	134-173
21181412-1	2011	This study aimed at investigating the response of lens epithelial cells in postnatal mice to Imatinib (Glivec , a potent inhibitor of platelet-derived growth factor receptor (PDGFR)) treatment.	imatinib	93-101	platelet derived growth factor receptor, beta polypeptide	Mus musculus	175-180
21181412-7	2011	Our results indicated that administration of Imatinib led to blockade of PDGFR signaling.	imatinib	45-53	platelet derived growth factor receptor, beta polypeptide	Mus musculus	73-78
21220745-5	2011	We show that treatment of CLL cells with Abl-specific siRNA or with imatinib, to inhibit c-Abl activity, results in the down-regulation of Mcl-1 protein and mRNA.	imatinib	68-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-94
21220745-5	2011	We show that treatment of CLL cells with Abl-specific siRNA or with imatinib, to inhibit c-Abl activity, results in the down-regulation of Mcl-1 protein and mRNA.	imatinib	68-76	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	139-144
20972453-10	2011	Our results suggest that the PDGFR kinase domain contains a limited number of residues where exchanges critically interfere with binding of and inhibition by available PDGFR kinase inhibitors at achievable concentrations, which might explain the low frequency of imatinib resistance in this patient population.	imatinib	263-271	platelet derived growth factor receptor beta	Homo sapiens	29-34
20972453-10	2011	Our results suggest that the PDGFR kinase domain contains a limited number of residues where exchanges critically interfere with binding of and inhibition by available PDGFR kinase inhibitors at achievable concentrations, which might explain the low frequency of imatinib resistance in this patient population.	imatinib	263-271	platelet derived growth factor receptor beta	Homo sapiens	168-173
20972453-11	2011	In addition, these findings would help to select the appropriate second-line drug in cases of imatinib-resistant disease and may be translated to other neoplasms driven by activated forms of PDGFR-A or -B.	imatinib	94-102	platelet derived growth factor receptor alpha	Homo sapiens	191-204
21479127-6	2011	KIT and PDGFRA-wild type tumors are expected to have lesser response to imatinib treatment.	imatinib	72-80	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
21479127-6	2011	KIT and PDGFRA-wild type tumors are expected to have lesser response to imatinib treatment.	imatinib	72-80	platelet derived growth factor receptor alpha	Homo sapiens	8-14
21195056-4	2011	In imatinib mesylate-resistant K562 cells that displayed decreased BCR-ABL expression, bortezomib/SKI treatment markedly increased apoptosis and inhibited colony-formation in association with the downregulation of Mcl-1.	imatinib	3-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
21347248-2	2011	The NLS function of BCR-ABL is re-activated by a kinase inhibitor, imatinib, and in a kinase-defective BCR-ABL mutant.	imatinib	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
21347248-4	2011	METHODOLOGY/PRINCIPAL FINDINGS: By examining the subcellular localization of mutant BCR-ABL proteins under conditions of imatinib and/or leptomycin B treatment to inhibit nuclear export, we have found that mutations of three specific tyrosines (Y232, Y253, Y257, according to ABL-1a numbering) in the kinase domain can inhibit the NLS function of kinase-proficient and kinase-defective BCR-ABL.	imatinib	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
21347248-4	2011	METHODOLOGY/PRINCIPAL FINDINGS: By examining the subcellular localization of mutant BCR-ABL proteins under conditions of imatinib and/or leptomycin B treatment to inhibit nuclear export, we have found that mutations of three specific tyrosines (Y232, Y253, Y257, according to ABL-1a numbering) in the kinase domain can inhibit the NLS function of kinase-proficient and kinase-defective BCR-ABL.	imatinib	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-91
21347248-4	2011	METHODOLOGY/PRINCIPAL FINDINGS: By examining the subcellular localization of mutant BCR-ABL proteins under conditions of imatinib and/or leptomycin B treatment to inhibit nuclear export, we have found that mutations of three specific tyrosines (Y232, Y253, Y257, according to ABL-1a numbering) in the kinase domain can inhibit the NLS function of kinase-proficient and kinase-defective BCR-ABL.	imatinib	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	386-393
21123820-3	2011	Moreover, we found that TWIST-1 was overexpressed in CML diagnostic samples of patients who later developed cytogenetic resistance to imatinib, even those without any detectable resistance mechanism.	imatinib	134-142	twist family bHLH transcription factor 1	Homo sapiens	24-31
21123820-4	2011	We confirmed the up-regulation of TWIST-1 at both RNA and protein levels in imatinib-resistant cell lines, irrespective of any other resistance mechanism.	imatinib	76-84	twist family bHLH transcription factor 1	Homo sapiens	34-41
20925044-0	2011	A phase 2 trial of imatinib mesylate in patients with recurrent nonresectable chondrosarcomas expressing platelet-derived growth factor receptor-alpha or -beta: An Italian Sarcoma Group study.	imatinib	19-36	platelet derived growth factor receptor alpha	Homo sapiens	105-159
20473908-0	2011	Imatinib response in two GIST patients carrying two hitherto functionally uncharacterized PDGFRA mutations: an imaging, biochemical and molecular modeling study.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	90-96
20473908-1	2011	Beside the well known "in vivo" and "in vitro" Imatinib resistant D842V mutation in PDGFRA receptor, very few are the information concerning the "in vivo" Imatinib activity with respect to the other PDGFRA mutations for which only "in vitro" data are available.	imatinib	47-55	platelet derived growth factor receptor alpha	Homo sapiens	84-90
20473908-2	2011	Two patients carrying PDGFRA mutations in exons 18 (involving residues DIMH842-845) and 12 (V561D), respectively, were treated with Imatinib at a dose of 400 mg/day.	imatinib	132-140	platelet derived growth factor receptor alpha	Homo sapiens	22-28
20473908-6	2011	Molecular modeling evidence was found to be consistent with sensitivity of mutated PDGFRA receptors to Imatinib.	imatinib	103-111	platelet derived growth factor receptor alpha	Homo sapiens	83-89
20473908-7	2011	Thus, the "in vivo" evidence that these two mutations of PDGFRA are sensitive to Imatinib was confirmed by a multidimensional approach comprising "in silico" experiments that, in association to molecular and biochemical analyses, constitutes a powerful tool to predict Imatinib sensitivity, clinically beneficial in the treatment of these tumors with molecularly targeted therapies.	imatinib	81-89	platelet derived growth factor receptor alpha	Homo sapiens	57-63
20473908-7	2011	Thus, the "in vivo" evidence that these two mutations of PDGFRA are sensitive to Imatinib was confirmed by a multidimensional approach comprising "in silico" experiments that, in association to molecular and biochemical analyses, constitutes a powerful tool to predict Imatinib sensitivity, clinically beneficial in the treatment of these tumors with molecularly targeted therapies.	imatinib	269-277	platelet derived growth factor receptor alpha	Homo sapiens	57-63
21299849-0	2011	BCR-ABL1-independent PI3Kinase activation causing imatinib-resistance.	imatinib	50-58	BCR activator of RhoGEF and GTPase	Homo sapiens	0-8
21299849-5	2011	We screened a panel of BCR-ABL1 positive ALL and CML cell lines to find models for imatinib-resistance.	imatinib	83-91	BCR activator of RhoGEF and GTPase	Homo sapiens	23-31
21299849-6	2011	RESULTS: Five of 19 BCR-ABL1 positive cell lines were resistant to imatinib-induced apoptosis (KCL-22, MHH-TALL1, NALM-1, SD-1, SUP-B15).	imatinib	67-75	BCR activator of RhoGEF and GTPase	Homo sapiens	20-28
21299849-6	2011	RESULTS: Five of 19 BCR-ABL1 positive cell lines were resistant to imatinib-induced apoptosis (KCL-22, MHH-TALL1, NALM-1, SD-1, SUP-B15).	imatinib	67-75	TNF superfamily member 13b	Homo sapiens	107-112
21299849-8	2011	STAT5, ERK1/2 and the ribosomal S6 protein (RPS6) are BCR-ABL1 downstream effectors, and all three proteins are dephosphorylated by imatinib in sensitive cell lines.	imatinib	132-140	signal transducer and activator of transcription 5A	Homo sapiens	0-5
21299849-8	2011	STAT5, ERK1/2 and the ribosomal S6 protein (RPS6) are BCR-ABL1 downstream effectors, and all three proteins are dephosphorylated by imatinib in sensitive cell lines.	imatinib	132-140	mitogen-activated protein kinase 3	Homo sapiens	7-13
21299849-8	2011	STAT5, ERK1/2 and the ribosomal S6 protein (RPS6) are BCR-ABL1 downstream effectors, and all three proteins are dephosphorylated by imatinib in sensitive cell lines.	imatinib	132-140	ribosomal protein S6	Homo sapiens	44-48
21299849-10	2011	PI3K pathway inhibitors effected dephosphorylation of RPS6 in imatinib-resistant cell lines suggesting that an oncogene other than BCR-ABL1 might be responsible for activation of the PI3K/AKT1/mTOR pathway, which would explain the TKI resistance of these cells.	imatinib	62-70	ribosomal protein S6	Homo sapiens	54-58
21299849-10	2011	PI3K pathway inhibitors effected dephosphorylation of RPS6 in imatinib-resistant cell lines suggesting that an oncogene other than BCR-ABL1 might be responsible for activation of the PI3K/AKT1/mTOR pathway, which would explain the TKI resistance of these cells.	imatinib	62-70	AKT serine/threonine kinase 1	Homo sapiens	188-192
21299849-10	2011	PI3K pathway inhibitors effected dephosphorylation of RPS6 in imatinib-resistant cell lines suggesting that an oncogene other than BCR-ABL1 might be responsible for activation of the PI3K/AKT1/mTOR pathway, which would explain the TKI resistance of these cells.	imatinib	62-70	mechanistic target of rapamycin kinase	Homo sapiens	193-197
21299849-15	2011	These cell lines are unique as they dephosphorylate ERK1/2 and STAT5 after treatment with imatinib, while PI3K/AKT1/mTOR activity remains unaffected.	imatinib	90-98	mitogen-activated protein kinase 3	Homo sapiens	52-58
21299849-15	2011	These cell lines are unique as they dephosphorylate ERK1/2 and STAT5 after treatment with imatinib, while PI3K/AKT1/mTOR activity remains unaffected.	imatinib	90-98	signal transducer and activator of transcription 5A	Homo sapiens	63-68
21299849-16	2011	Inhibition of AKT1 leads to apoptosis in the imatinib-resistant cell lines.	imatinib	45-53	AKT serine/threonine kinase 1	Homo sapiens	14-18
21299849-17	2011	In conclusion, Ph+ cell lines show a form of imatinib-resistance attributable to constitutive activation of the PI3K/AKT1 pathway.	imatinib	45-53	AKT serine/threonine kinase 1	Homo sapiens	117-121
21195056-4	2011	In imatinib mesylate-resistant K562 cells that displayed decreased BCR-ABL expression, bortezomib/SKI treatment markedly increased apoptosis and inhibited colony-formation in association with the downregulation of Mcl-1.	imatinib	3-20	SKI proto-oncogene	Homo sapiens	98-101
21195056-4	2011	In imatinib mesylate-resistant K562 cells that displayed decreased BCR-ABL expression, bortezomib/SKI treatment markedly increased apoptosis and inhibited colony-formation in association with the downregulation of Mcl-1.	imatinib	3-20	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	214-219
21163869-5	2011	To date, the role of both efflux transporters (ATP-binding cassette transporters, such as ABCB1 and ABCG2) and uptake transporters [solute carriers such as organic cation transporter 1 (OCT1) and organic anion transporting polypeptide 1A2 (OATP1A2)] in imatinib pharmacokinetics and pharmacodynamics has been studied.	imatinib	253-261	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	100-105
21355840-2	2011	The clinical success of the targeted agent Imatinib mesylate as an inhibitor of the tyrosine kinase associated with the breakpoint cluster region-Abelson oncogene locus (BCR-ABL) in the treatment of Philadelphia-positive chronic myelogenous leukemia (CML) has served as a paradigm.	imatinib	43-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-168
21355840-2	2011	The clinical success of the targeted agent Imatinib mesylate as an inhibitor of the tyrosine kinase associated with the breakpoint cluster region-Abelson oncogene locus (BCR-ABL) in the treatment of Philadelphia-positive chronic myelogenous leukemia (CML) has served as a paradigm.	imatinib	43-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-177
20589434-0	2011	Serum midkine correlates with tumor progression and imatinib response in gastrointestinal stromal tumors.	imatinib	52-60	midkine	Homo sapiens	6-13
20589434-9	2011	Patients receiving imatinib therapy had decreased median S-MK concentrations compared with those who were not treated with imatinib (331 vs 201; P < 0.001).	imatinib	19-27	midkine	Homo sapiens	59-61
20846303-13	2011	CONCLUSION: These data indicate that the SCF/c-KIT system plays an important role in scar pathogenesis, and underscore the role of imatinib as a key therapeutic agent in keloid scars.	imatinib	131-139	KIT ligand	Homo sapiens	41-44
20846303-13	2011	CONCLUSION: These data indicate that the SCF/c-KIT system plays an important role in scar pathogenesis, and underscore the role of imatinib as a key therapeutic agent in keloid scars.	imatinib	131-139	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	45-50
20886606-2	2011	Interferon alpha (IFN alpha) is efficacious in CML likely due to its immunomodulatory properties, and is synergistic in vitro with imatinib and granulocyte macrophage-colony stimulating factor (GM-CSF).	imatinib	131-139	interferon alpha 2	Homo sapiens	18-27
21163869-5	2011	To date, the role of both efflux transporters (ATP-binding cassette transporters, such as ABCB1 and ABCG2) and uptake transporters [solute carriers such as organic cation transporter 1 (OCT1) and organic anion transporting polypeptide 1A2 (OATP1A2)] in imatinib pharmacokinetics and pharmacodynamics has been studied.	imatinib	253-261	solute carrier family 22 member 1	Homo sapiens	156-184
21163869-5	2011	To date, the role of both efflux transporters (ATP-binding cassette transporters, such as ABCB1 and ABCG2) and uptake transporters [solute carriers such as organic cation transporter 1 (OCT1) and organic anion transporting polypeptide 1A2 (OATP1A2)] in imatinib pharmacokinetics and pharmacodynamics has been studied.	imatinib	253-261	solute carrier family 22 member 1	Homo sapiens	186-190
21158719-10	2011	Combined treatment with imatinib mesylate (IM) and ICG-001 significantly inhibited colony formation in sorted CD34(+) CML progenitors (survivin(+)/gamma-catenin(high)/beta-catenin(low)) isolated from one BC and one AP patient resistant to IM.	imatinib	24-41	CD34 molecule	Homo sapiens	110-114
21163869-5	2011	To date, the role of both efflux transporters (ATP-binding cassette transporters, such as ABCB1 and ABCG2) and uptake transporters [solute carriers such as organic cation transporter 1 (OCT1) and organic anion transporting polypeptide 1A2 (OATP1A2)] in imatinib pharmacokinetics and pharmacodynamics has been studied.	imatinib	253-261	solute carrier organic anion transporter family member 1A2	Homo sapiens	196-238
21158719-10	2011	Combined treatment with imatinib mesylate (IM) and ICG-001 significantly inhibited colony formation in sorted CD34(+) CML progenitors (survivin(+)/gamma-catenin(high)/beta-catenin(low)) isolated from one BC and one AP patient resistant to IM.	imatinib	24-41	catenin beta 1	Homo sapiens	167-179
21163869-6	2011	In vitro experiments show a significant role of ABCB1 and ABCG2 in cellular uptake and retention of imatinib, although pharmacokinetic and pharmacogenetic data are still scarce and contradictory.	imatinib	100-108	ATP binding cassette subfamily B member 1	Homo sapiens	48-53
21163869-6	2011	In vitro experiments show a significant role of ABCB1 and ABCG2 in cellular uptake and retention of imatinib, although pharmacokinetic and pharmacogenetic data are still scarce and contradictory.	imatinib	100-108	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	58-63
21264552-0	2011	A novel insertion mutation of K294RGG within BCR-ABL kinase domain confers imatinib resistance: sequential analysis of the clonal evolution in a patient with chronic myeloid leukemia in blast crisis.	imatinib	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
21091189-6	2011	Thus, our study provides support for STAT5 as a potential target downstream of BCR-ABL for CML treatment and helps establish the concept of targeting STAT5 by decoy ODN as a novel therapy approach for imatinib-resistant CML.	imatinib	201-209	signal transducer and activator of transcription 5A	Homo sapiens	37-42
21091189-6	2011	Thus, our study provides support for STAT5 as a potential target downstream of BCR-ABL for CML treatment and helps establish the concept of targeting STAT5 by decoy ODN as a novel therapy approach for imatinib-resistant CML.	imatinib	201-209	signal transducer and activator of transcription 5A	Homo sapiens	150-155
21086081-1	2011	Imatinib mesylate has become a therapy of interest for the treatment of systemic sclerosis because of its ability to inhibit c-Abl and platelet-derived growth factor receptor, tyrosine kinases involved in profibrotic pathways.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-130
21235428-2	2011	The great success of the BCR-ABL inhibitor imatinib in treating chronic myelogenous leukemia illustrates the high potential of kinase inhibitor (KI) therapeutics, but also unveils a major limitation: the development of drug resistance.	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
21152856-0	2011	Selective inhibition of PDGFR by imatinib elicits the sustained activation of ERK and downstream receptor signaling in malignant glioma cells.	imatinib	33-41	platelet derived growth factor receptor beta	Homo sapiens	24-29
21152856-0	2011	Selective inhibition of PDGFR by imatinib elicits the sustained activation of ERK and downstream receptor signaling in malignant glioma cells.	imatinib	33-41	mitogen-activated protein kinase 1	Homo sapiens	78-81
21152856-3	2011	In this study, we investigated the effects of imatinib on the platelet derived growth factor receptor (PDGFR) downstream signaling pathways as well as on other cellular functions in human glioblastoma cells.	imatinib	46-54	platelet derived growth factor receptor beta	Homo sapiens	62-101
21152856-3	2011	In this study, we investigated the effects of imatinib on the platelet derived growth factor receptor (PDGFR) downstream signaling pathways as well as on other cellular functions in human glioblastoma cells.	imatinib	46-54	platelet derived growth factor receptor beta	Homo sapiens	103-108
21152856-6	2011	Furthermore, the imatinib treatment induced the sustained activation of extracellular signal-regulated kinase (ERK 1/2) signaling as well as components of other downstream signaling pathways, such as PI3K/Akt, STAT3 and p38MAPK.	imatinib	17-25	mitogen-activated protein kinase 3	Homo sapiens	111-118
21152856-6	2011	Furthermore, the imatinib treatment induced the sustained activation of extracellular signal-regulated kinase (ERK 1/2) signaling as well as components of other downstream signaling pathways, such as PI3K/Akt, STAT3 and p38MAPK.	imatinib	17-25	AKT serine/threonine kinase 1	Homo sapiens	205-208
21152856-6	2011	Furthermore, the imatinib treatment induced the sustained activation of extracellular signal-regulated kinase (ERK 1/2) signaling as well as components of other downstream signaling pathways, such as PI3K/Akt, STAT3 and p38MAPK.	imatinib	17-25	signal transducer and activator of transcription 3	Homo sapiens	210-215
21152856-8	2011	Further analysis indicated that the activation of ERK induced by the imatinib treatment was related to the S-phase re-entry of the cell cycle in one of the three glioma cells.	imatinib	69-77	mitogen-activated protein kinase 1	Homo sapiens	50-53
21264552-1	2011	BCR-ABL kinase domain mutations were sequentially analyzed in a patient with chronic myeloid leukemia (CML) who exhibited repeated B-lymphoid blast crisis (CML-BC) during treatment with imatinib and dasatinib.	imatinib	186-194	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
21264552-2	2011	We first identified five mutant BCR-ABL clones: Y253H, G250E, F311L, F317L and K294RGG, which was generated by two-nucleotide mutations and six-nucleotide insertion, at the third BC during the imatinib treatment, and retrospectively found that three of them (Y253H, G250E, K294RGG) were already present at the second BC.	imatinib	193-201	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
21264552-3	2011	The in vitro analysis using K294RGG mutant BCR-ABL-expressing 32D cells revealed that K294RGG mutation was imatinib resistant but dasatinib sensitive.	imatinib	107-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
21279819-5	2011	In 2002, treatment with imatinib, a selective BCR-ABL tyrosine kinase inhibitor (TKI), was started but Ph-positive chromosomes remained at the levels of 42-65%, indicating imatinib failure.	imatinib	24-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
20717963-3	2011	Treatment of Bcr-Abl kinase inhibitor imatinib led to G1 growth arrest accompanied with reduced Skp2 expression.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
21279819-6	2011	In 2006, the point mutations of F359I and L387M were detected in BCR/ABL gene, which may be related to imatinib failure.	imatinib	103-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
21279819-8	2011	Administration of nilotinib offered an effective treatment in a CML patient with variant Ph chromosome translocations and BCR-ABL point mutations after imatinib failure.	imatinib	152-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
20717963-3	2011	Treatment of Bcr-Abl kinase inhibitor imatinib led to G1 growth arrest accompanied with reduced Skp2 expression.	imatinib	38-46	S-phase kinase associated protein 2	Homo sapiens	96-100
20717963-5	2011	The half-life of Skp2 protein was significantly attenuated in imatinib-treated cells.	imatinib	62-70	S-phase kinase associated protein 2	Homo sapiens	17-21
20717963-9	2011	Imatinib treatment or Bcr-Abl knockdown reduced Emi1, an endogenous inhibitor of the E3 ligase APC/Cdh1 which mediated Skp2 degradation.	imatinib	0-8	F-box protein 5	Homo sapiens	48-52
20717963-9	2011	Imatinib treatment or Bcr-Abl knockdown reduced Emi1, an endogenous inhibitor of the E3 ligase APC/Cdh1 which mediated Skp2 degradation.	imatinib	0-8	APC regulator of WNT signaling pathway	Homo sapiens	95-98
20717963-9	2011	Imatinib treatment or Bcr-Abl knockdown reduced Emi1, an endogenous inhibitor of the E3 ligase APC/Cdh1 which mediated Skp2 degradation.	imatinib	0-8	cadherin 1	Homo sapiens	99-103
20717963-9	2011	Imatinib treatment or Bcr-Abl knockdown reduced Emi1, an endogenous inhibitor of the E3 ligase APC/Cdh1 which mediated Skp2 degradation.	imatinib	0-8	S-phase kinase associated protein 2	Homo sapiens	119-123
20971815-2	2011	The OCT-1 activity in mononuclear cells reflects the efficiency of active influx of imatinib.	imatinib	84-92	solute carrier family 22 member 1	Homo sapiens	4-9
20717963-13	2011	Secondly, transfection of v-Src rescued the reduction of Emi1 by imatinib.	imatinib	65-73	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	28-31
20971815-3	2011	OCT-1 activity in mononuclear cells is highly variable between patients and significantly correlates with a patient"s molecular response to imatinib treatment and overall survival.	imatinib	140-148	solute carrier family 22 member 1	Homo sapiens	0-5
20717963-13	2011	Secondly, transfection of v-Src rescued the reduction of Emi1 by imatinib.	imatinib	65-73	F-box protein 5	Homo sapiens	57-61
20739063-3	2011	FB2 which orients Bcr-Abl and Src kinase activities, is shown to override imatinib-resistance CML involving Y253F mutation in the Abl kinase domain of the fusion protein except T315I in vivo and in vitro.	imatinib	74-82	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	130-133
21178640-0	2011	Potential role of platelet-derived growth factor receptor inhibition using imatinib in combination with docetaxel in the treatment of recurrent non-small cell lung cancer.	imatinib	75-83	platelet derived growth factor receptor beta	Homo sapiens	18-57
21178640-2	2011	Preclinical models demonstrated that imatinib (Im) regulates angiogenesis through PDGFR inhibition and enhances efficacy of chemotherapy.	imatinib	37-45	platelet derived growth factor receptor beta	Homo sapiens	82-87
21072049-0	2011	The first case of acute lymphoblastic leukemia with the e19a2 BCR-ABL1 transcript: imatinib therapy followed by unrelated donor transplantation induces a durable molecular response.	imatinib	83-91	BCR activator of RhoGEF and GTPase	Homo sapiens	62-70
21250825-1	2011	Imatinib mesylate (IM) has become standard therapy for patients with chronic myeloid leukemia (CML), but CML stem cells are intrinsically resistant to IM and to second/third-generation tyrosine kinase inhibitors (TKIs), allowing the persistence of a "reservoir" of BCR-ABL-expressing CML-initiating cells potentially responsible for disease progression.	imatinib	19-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	265-272
21113055-3	2011	The introduction of imatinib and rituximab has changed the mortality rates associated with chronic myeloid leukemia and CD20-positive lymphoma, respectively.	imatinib	20-28	keratin 20	Homo sapiens	120-124
20975605-9	2011	Imatinib presumably targets c-Kit, as the cells do not express platelet-derived growth factor receptor and as another c-Abl inhibitor was without effect.	imatinib	0-8	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	28-33
21281241-0	2011	Concomitant FIP1L1-PDGFRA fusion gene and T-cell clonality in a case of chronic eosinophilic leukemia with clonal evolution and an incomplete response to imatinib.	imatinib	154-162	factor interacting with PAPOLA and CPSF1	Homo sapiens	12-18
21281241-0	2011	Concomitant FIP1L1-PDGFRA fusion gene and T-cell clonality in a case of chronic eosinophilic leukemia with clonal evolution and an incomplete response to imatinib.	imatinib	154-162	platelet derived growth factor receptor alpha	Homo sapiens	19-25
21299455-3	2011	Imatinib, an inhibitor of BCR-ABL tyrosine kinase activity, has a dramatic effect on the natural history of the disease.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
21102429-7	2011	Sensitivity to the ABL kinase inhibitor imatinib was increased by RIN1 silencing, consistent with RIN1 stabilization of an activated BCR-ABL1 conformation having reduced drug affinity.	imatinib	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-22
21102429-7	2011	Sensitivity to the ABL kinase inhibitor imatinib was increased by RIN1 silencing, consistent with RIN1 stabilization of an activated BCR-ABL1 conformation having reduced drug affinity.	imatinib	40-48	Ras and Rab interactor 1	Homo sapiens	66-70
21102429-7	2011	Sensitivity to the ABL kinase inhibitor imatinib was increased by RIN1 silencing, consistent with RIN1 stabilization of an activated BCR-ABL1 conformation having reduced drug affinity.	imatinib	40-48	Ras and Rab interactor 1	Homo sapiens	98-102
21102429-7	2011	Sensitivity to the ABL kinase inhibitor imatinib was increased by RIN1 silencing, consistent with RIN1 stabilization of an activated BCR-ABL1 conformation having reduced drug affinity.	imatinib	40-48	BCR activator of RhoGEF and GTPase	Homo sapiens	133-141
21102429-9	2011	The findings suggest that RIN1 targeting could be efficacious for imatinib-resistant disease and might complement ABL kinase inhibitors in first-line therapy.	imatinib	66-74	Ras and Rab interactor 1	Homo sapiens	26-30
20975605-9	2011	Imatinib presumably targets c-Kit, as the cells do not express platelet-derived growth factor receptor and as another c-Abl inhibitor was without effect.	imatinib	0-8	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	118-123
20975605-12	2011	These data show that combination of two tyrosine kinase inhibitors, imatinib and vatalanib, increases the effects of paclitaxel on B16/PDGF-BB tumors, thus suggesting a novel strategy for the treatment of melanomas expressing c-Kit.	imatinib	68-76	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	226-231
21224352-8	2011	Cotreatment of K562 and BaF3/Bcr-AblT315I cells with amiloride and imatinib induced more loss of cell viability than either agent alone.	imatinib	67-75	BCR activator of RhoGEF and GTPase	Homo sapiens	29-32
21115411-6	2011	RESULTS: The IC(50) of single-agent ABT-737 at 72 h was 10 muM in imatinib-sensitive GIST-T1 and GIST882 cells, and 1 muM in imatinib-resistant GIST48IM cells.	imatinib	125-133	latexin	Homo sapiens	118-121
21115411-7	2011	ABT-737 and imatinib combined synergistically in a time- and dose-dependent manner to inhibit the proliferation and induce apoptosis of all GIST cells, as evidenced by cell viability and apoptosis assays, caspase activation, PARP cleavage, and morphologic changes.	imatinib	12-20	collagen type XI alpha 2 chain	Homo sapiens	225-229
21115411-10	2011	CONCLUSION: We provide the first preclinical evidence that Bcl-2/Bcl-x(L) inhibition with ABT-737 synergistically enhances imatinib-induced cytotoxicity via apoptosis, and that direct engagement of apoptotic cell death may be an effective approach to circumvent imatinib-resistance in GIST.	imatinib	123-131	BCL2 apoptosis regulator	Homo sapiens	59-64
21115411-10	2011	CONCLUSION: We provide the first preclinical evidence that Bcl-2/Bcl-x(L) inhibition with ABT-737 synergistically enhances imatinib-induced cytotoxicity via apoptosis, and that direct engagement of apoptotic cell death may be an effective approach to circumvent imatinib-resistance in GIST.	imatinib	123-131	BCL2 like 1	Homo sapiens	65-70
21115411-10	2011	CONCLUSION: We provide the first preclinical evidence that Bcl-2/Bcl-x(L) inhibition with ABT-737 synergistically enhances imatinib-induced cytotoxicity via apoptosis, and that direct engagement of apoptotic cell death may be an effective approach to circumvent imatinib-resistance in GIST.	imatinib	262-270	BCL2 apoptosis regulator	Homo sapiens	59-64
21115411-10	2011	CONCLUSION: We provide the first preclinical evidence that Bcl-2/Bcl-x(L) inhibition with ABT-737 synergistically enhances imatinib-induced cytotoxicity via apoptosis, and that direct engagement of apoptotic cell death may be an effective approach to circumvent imatinib-resistance in GIST.	imatinib	262-270	BCL2 like 1	Homo sapiens	65-70
21403427-6	2011	Because RT-PCR assay of bone marrow detected major-BCR-ABL mRNA (b3a2), treatment with imatinib (400 mg/day) was started.	imatinib	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
20845478-6	2011	RESULTS: For patients who received imatinib after failing on IFN-alpha, the 7-year EFS rate was 61%, whereas the CEFS rate was 69%.	imatinib	35-43	interferon alpha 1	Homo sapiens	61-70
21220945-1	2011	Therapies that target BCR-ABL in chronic myeloid leukemia, including imatinib, dasatinib and nilotinib, have dramatically improved patient outcome.	imatinib	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
21220945-3	2011	Clinical data indicate that developing BCR-ABL mutations during imatinib treatment is predictive for shorter progression-free survival, and that outcomes may depend on mutation type or location.	imatinib	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
21220945-4	2011	In vitro, dasatinib and nilotinib inhibit most imatinib-resistant BCR-ABL mutations, except for T315I.	imatinib	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
20851205-12	2011	Inhibition of EGF or PDGF receptor signaling using AG-1296, AG-1478 or imatinib prevented peroxynitrite-induced cell proliferation and ERK phosphorylation in PASMC.	imatinib	71-79	epidermal growth factor	Bos taurus	14-17
21058037-3	2011	As a result, CD117 has been identified as a target for therapy via the small molecule, tyrosine kinase inhibitor imatinib mesylate.	imatinib	113-130	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	13-18
21041018-0	2011	Carboxyamidotriazole inhibits cell growth of imatinib-resistant chronic myeloid leukaemia cells including T315I Bcr-Abl mutant by a redox-mediated mechanism.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
21041018-1	2011	Mutation of the Bcr-Abl oncoprotein is one of most frequent mechanisms by which chronic myelogenous leukemia (CML) cells become resistant to imatinib.	imatinib	141-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
21041018-4	2011	Clinically significant, CAI has also inhibitory effects on T315I Bcr-Abl mutant, a mutation that causes CML cells to become insensitive to imatinib and second generation abl kinase inhibitors.	imatinib	139-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
21098337-1	2011	Beginning with imatinib a decade ago, therapy based on targeted inhibition of the BCR-ABL kinase has greatly improved the prognosis for chronic myeloid leukemia (CML) patients.	imatinib	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
21368884-4	2011	Intriguingly, we found that several human tumors upregulated PON2 and such overexpression provided resistance to different chemotherapeutics (imatinib, doxorubicine, staurosporine, or actinomycin) in cell culture models.	imatinib	142-150	paraoxonase 2	Homo sapiens	61-65
20697894-0	2011	Characteristics of BCR-ABL kinase domain point mutations in Chinese imatinib-resistant chronic myeloid leukemia patients.	imatinib	68-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-26
21132731-8	2011	Inhibition of autophagy with ATG7 and Beclin1 siRNA significantly reduced the recovery of Imatinib-treated K562 cells, indicating the importance of autophagy for the recovery of treated cells.	imatinib	90-98	beclin 1	Homo sapiens	38-45
21606571-1	2011	Imatinib mesylate (IM) is a compound that inhibits both BCR-ABL tyrosine kinase and c-kit receptors.	imatinib	0-17	mast/stem cell growth factor receptor Kit	Oryctolagus cuniculus	84-89
20838376-10	2011	Finally, knocking down PRAME or EZH2, and consequently induction of TRAIL expression, enhances Imatinib sensibility.	imatinib	95-103	PRAME nuclear receptor transcriptional regulator	Homo sapiens	23-28
20838376-10	2011	Finally, knocking down PRAME or EZH2, and consequently induction of TRAIL expression, enhances Imatinib sensibility.	imatinib	95-103	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	32-36
20838376-10	2011	Finally, knocking down PRAME or EZH2, and consequently induction of TRAIL expression, enhances Imatinib sensibility.	imatinib	95-103	TNF superfamily member 10	Homo sapiens	68-73
21785586-7	2011	Research into the effect of a c-kit receptor inhibitor, imatinib mesylate, on bladder function implies that KIT-positive ICCs may be therapeutic target cells to reduce bladder overactivity and that the blockage of c-kit receptor may offer a new therapeutic strategy for OAB treatment, although further study will be needed.	imatinib	56-73	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	32-35
21785586-7	2011	Research into the effect of a c-kit receptor inhibitor, imatinib mesylate, on bladder function implies that KIT-positive ICCs may be therapeutic target cells to reduce bladder overactivity and that the blockage of c-kit receptor may offer a new therapeutic strategy for OAB treatment, although further study will be needed.	imatinib	56-73	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	108-111
21785586-7	2011	Research into the effect of a c-kit receptor inhibitor, imatinib mesylate, on bladder function implies that KIT-positive ICCs may be therapeutic target cells to reduce bladder overactivity and that the blockage of c-kit receptor may offer a new therapeutic strategy for OAB treatment, although further study will be needed.	imatinib	56-73	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	216-219
20807497-5	2011	This dual detection technique was used to evaluate the inhibition of c-Abl kinase by imatinib and dasatinib.	imatinib	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-74
21606571-1	2011	Imatinib mesylate (IM) is a compound that inhibits both BCR-ABL tyrosine kinase and c-kit receptors.	imatinib	19-21	mast/stem cell growth factor receptor Kit	Oryctolagus cuniculus	84-89
20697894-11	2011	ABL mutations are common in Chinese imatinib-resistant CML patients and are associated with clinical resistance.	imatinib	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
20974687-7	2011	Moreover, treatment with the BCR-ABL kinase inhibitor, Imatinib Mesylate, abolished CtIP accumulation.	imatinib	55-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
21212528-0	2011	Association of SLCO1B3 polymorphism with intracellular accumulation of imatinib in leukocytes in patients with chronic myeloid leukemia.	imatinib	71-79	solute carrier organic anion transporter family member 1B3	Homo sapiens	15-22
20473616-1	2011	Dasatinib is a highly potent Bcr-Abl inhibitor that is approved for the treatment of imatinib-resistant or -intolerant chronic myeloid leukemia (CML).	imatinib	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
21212528-7	2011	The intracellular imatinib concentration was significantly higher in patients with SLCO1B3 334TT than in those with 334TG/GG (p=0.0188).	imatinib	18-26	solute carrier organic anion transporter family member 1B3	Homo sapiens	83-90
21212528-9	2011	These results suggested that the SLCO1B3 334T>G polymorphism could have a significant impact on the intracellular concentration of imatinib in leukocytes as a promising biomarker for personalized treatment of CML patients.	imatinib	134-142	solute carrier organic anion transporter family member 1B3	Homo sapiens	33-40
20974687-7	2011	Moreover, treatment with the BCR-ABL kinase inhibitor, Imatinib Mesylate, abolished CtIP accumulation.	imatinib	55-72	RB binding protein 8, endonuclease	Homo sapiens	84-88
20952511-8	2011	Finally, CD34(+) cells from CML patients display a clear imatinib-dependent p57(Kip)2 upregulation, which was not observed in CD34(+) cells from control subjects.	imatinib	57-65	CD34 molecule	Homo sapiens	9-13
20952511-8	2011	Finally, CD34(+) cells from CML patients display a clear imatinib-dependent p57(Kip)2 upregulation, which was not observed in CD34(+) cells from control subjects.	imatinib	57-65	cyclin dependent kinase inhibitor 1C	Homo sapiens	76-85
20952511-2	2011	In this study, we show that BCR-ABL-positive CML cell lines treated with imatinib (STI571) undergo G1 cell cycle arrest associated with the accumulation of p57(Kip)2, a cyclin-dependent kinase inhibitor (CKI).	imatinib	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
20952511-2	2011	In this study, we show that BCR-ABL-positive CML cell lines treated with imatinib (STI571) undergo G1 cell cycle arrest associated with the accumulation of p57(Kip)2, a cyclin-dependent kinase inhibitor (CKI).	imatinib	73-81	cyclin dependent kinase inhibitor 1C	Homo sapiens	156-165
20978751-1	2011	Imatinib mesylate is a tyrosine kinase inhibitor used in the management of disorders in which activation of c-Abl, PDGFR, or c-Kit signaling plays a critical role.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-113
20952511-2	2011	In this study, we show that BCR-ABL-positive CML cell lines treated with imatinib (STI571) undergo G1 cell cycle arrest associated with the accumulation of p57(Kip)2, a cyclin-dependent kinase inhibitor (CKI).	imatinib	73-81	choline kinase alpha	Homo sapiens	204-207
20952511-2	2011	In this study, we show that BCR-ABL-positive CML cell lines treated with imatinib (STI571) undergo G1 cell cycle arrest associated with the accumulation of p57(Kip)2, a cyclin-dependent kinase inhibitor (CKI).	imatinib	83-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
20952511-2	2011	In this study, we show that BCR-ABL-positive CML cell lines treated with imatinib (STI571) undergo G1 cell cycle arrest associated with the accumulation of p57(Kip)2, a cyclin-dependent kinase inhibitor (CKI).	imatinib	83-89	cyclin dependent kinase inhibitor 1C	Homo sapiens	156-165
20952511-2	2011	In this study, we show that BCR-ABL-positive CML cell lines treated with imatinib (STI571) undergo G1 cell cycle arrest associated with the accumulation of p57(Kip)2, a cyclin-dependent kinase inhibitor (CKI).	imatinib	83-89	choline kinase alpha	Homo sapiens	204-207
20952511-3	2011	Interestingly, p57(Kip)2 increase precedes the reported STI571-dependent upregulation of p27(Kip)1.	imatinib	56-62	cyclin dependent kinase inhibitor 1C	Homo sapiens	15-24
20952511-3	2011	Interestingly, p57(Kip)2 increase precedes the reported STI571-dependent upregulation of p27(Kip)1.	imatinib	56-62	cyclin dependent kinase inhibitor 1B	Homo sapiens	89-98
20952511-6	2011	The imatinib-dependent p57(Kip)2 upregulation occurs only in STI571-responsive cells, while the CKI accumulation was not evidenced in an imatinib-resistant clone.	imatinib	4-12	cyclin dependent kinase inhibitor 1C	Homo sapiens	23-32
20952511-8	2011	Finally, CD34(+) cells from CML patients display a clear imatinib-dependent p57(Kip)2 upregulation, which was not observed in CD34(+) cells from control subjects.	imatinib	57-65	CD34 molecule	Homo sapiens	126-130
20978751-1	2011	Imatinib mesylate is a tyrosine kinase inhibitor used in the management of disorders in which activation of c-Abl, PDGFR, or c-Kit signaling plays a critical role.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	115-120
20978751-1	2011	Imatinib mesylate is a tyrosine kinase inhibitor used in the management of disorders in which activation of c-Abl, PDGFR, or c-Kit signaling plays a critical role.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	125-130
21631962-0	2011	In vitro effects of imatinib on glucose-6-phosphate dehydrogenase and glutathione reductase.	imatinib	20-28	glucose-6-phosphate dehydrogenase	Bos taurus	32-65
21140148-2	2011	Imatinib has exceptional activity in controlling gastrointestinal stromal tumor (GIST) due to inhibition of the constitutively active conformation of KIT and PDGFRA which is found in the majority of patients with GIST.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	150-153
21140148-2	2011	Imatinib has exceptional activity in controlling gastrointestinal stromal tumor (GIST) due to inhibition of the constitutively active conformation of KIT and PDGFRA which is found in the majority of patients with GIST.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	158-164
21181476-2	2011	Imatinib mesylate potently abrogates the effects of KIT signaling by directly binding into the ATP-binding pocket of the kinase.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	52-55
21181476-4	2011	Within KIT, patients whose tumor has an exon 9 mutation are treated by many clinicians with higher doses of imatinib than those patients with mutations within exon 11.	imatinib	108-116	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	7-10
21181476-6	2011	Secondary KIT mutations generally occur at a codon where imatinib binds resulting in KIT reactivation and resistance.	imatinib	57-65	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	10-13
21181476-6	2011	Secondary KIT mutations generally occur at a codon where imatinib binds resulting in KIT reactivation and resistance.	imatinib	57-65	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	85-88
21181476-7	2011	Sunitinib malate, a second-generation KIT inhibitor is active in imatinib-resistant disease and is FDA-approved for use in this setting.	imatinib	65-73	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	38-41
21792346-1	2011	The treatment of chronic myelogenous leukemia (CML) was revolutionized by the development of imatinib mesylate, a small molecule inhibitor of several protein tyrosine kinases, including the ABL1 protein tyrosine kinase.	imatinib	93-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	190-194
20304669-7	2011	Since c-kit can be readily inhibited by several small molecule inhibitors including imatinib, sunitinib and dasatinib, targeting immune suppressing cells can be readily accomplished in the clinic.	imatinib	84-92	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	6-11
21631962-5	2011	Imatinib inhibits glucose- 6-phosphate dehydrogenase with an IC50 value of 0.7 mM.	imatinib	0-8	glucose-6-phosphate dehydrogenase	Bos taurus	18-52
22606444-1	2011	Imatinib mesylate is a tyrosine kinase inhibitor of c-KIT and PDGFRA.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	52-57
22606444-1	2011	Imatinib mesylate is a tyrosine kinase inhibitor of c-KIT and PDGFRA.	imatinib	0-17	platelet derived growth factor receptor alpha	Homo sapiens	62-68
22606444-5	2011	PET imaging indicated a positive response, and so we continued imatinib treatment in an NAC setting for 4 months.	imatinib	63-71	synuclein alpha	Homo sapiens	88-91
22174597-5	2011	Imatinib is now also approved in adult patients following resection of KIT-positive GIST.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	71-74
22262331-2	2011	The recognition that KIT mutations were present in the majority of patients with GIST led to clinical trials of imatinib in this disease.	imatinib	112-120	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	21-24
22262331-3	2011	Indeed, imatinib inhibits KIT kinase activity and represents the best drug for the treatment of unresectable and advanced GIST, achieving a partial response or stable disease in 85-90% of patients with metastatic disease.	imatinib	8-16	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	26-29
22262331-6	2011	The presence and the type of KIT or PDGFRA mutation status are predictive of response to imatinib therapy in patients with advanced or metastatic GIST, as well as prognostic for relapse-free survival (RFS) after surgical resection of primary GIST.	imatinib	89-97	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	29-32
22262331-6	2011	The presence and the type of KIT or PDGFRA mutation status are predictive of response to imatinib therapy in patients with advanced or metastatic GIST, as well as prognostic for relapse-free survival (RFS) after surgical resection of primary GIST.	imatinib	89-97	platelet derived growth factor receptor alpha	Homo sapiens	36-42
22262331-9	2011	Based on the results of ACOSOG Z9001 trial, in December 2008, the FDA approved imatinib for postoperative treatment of patients with resected KIT-positive GIST; optimum duration of adjuvant treatment was not stated.	imatinib	79-87	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	142-145
22087818-1	2011	In chronic myeloid leukemia (CML), BCR-ABL-mediated oncogenic signaling can be successfully targeted with the BCRABL- inhibitors imatinib, nilotinib, and dasatinib leading to complete cytogenetic (Philadelphia chromosome not detectable upon cytogenetic testing of bone marrow) and even complete molecular (BCR-ABL not detectable by PCR in peripheral blood) responses.	imatinib	129-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
22087818-1	2011	In chronic myeloid leukemia (CML), BCR-ABL-mediated oncogenic signaling can be successfully targeted with the BCRABL- inhibitors imatinib, nilotinib, and dasatinib leading to complete cytogenetic (Philadelphia chromosome not detectable upon cytogenetic testing of bone marrow) and even complete molecular (BCR-ABL not detectable by PCR in peripheral blood) responses.	imatinib	129-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	306-313
21631962-0	2011	In vitro effects of imatinib on glucose-6-phosphate dehydrogenase and glutathione reductase.	imatinib	20-28	glutathione-disulfide reductase	Bos taurus	70-91
21631962-3	2011	The purpose of the present work is to evaluate the in vitro effects of imatinib on sheep brain cortex glucose-6-phosphate dehydrogenase, and on bovine kidney cortex, bovine liver and yeast glutathione reductase.	imatinib	71-79	glucose-6-phosphate 1-dehydrogenase	Ovis aries	102-135
21841248-0	2011	gamma-Secretase-mediated regulation of neprilysin: influence of cell density and aging and modulation by imatinib.	imatinib	105-113	membrane metalloendopeptidase	Homo sapiens	39-49
22135725-9	2011	Imatinib mesylate decreased the rates of cell growth of osteosarcoma cells in low doses and invasion in high doses C-kit-positive tumors had worse response to chemotherapy and imatinib mesylate can play a role in blocking or decreasing the rate of growth of osteosarcoma cells, but not the invasive capacity of these neoplastic cells.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	115-120
22135725-9	2011	Imatinib mesylate decreased the rates of cell growth of osteosarcoma cells in low doses and invasion in high doses C-kit-positive tumors had worse response to chemotherapy and imatinib mesylate can play a role in blocking or decreasing the rate of growth of osteosarcoma cells, but not the invasive capacity of these neoplastic cells.	imatinib	176-193	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	115-120
21841248-8	2011	We show here an Imatinib-dependent effect on NEP expression and activity in murine fibroblasts and establish that Imatinib-induced modulation of NEP was abolished by the depletion of AbetaPP or its homologues APLP1 and APLP2, thereby confirming that Imatinib-mediated control of NEP could indeed be accounted for its effect on AICD.	imatinib	114-122	amyloid beta (A4) precursor-like protein 2	Mus musculus	219-224
22160005-4	2011	This article provides a brief overview of the role of angiogenesis in leukemias, discusses recent insights into the role of placenta growth factor (PlGF), a VEGF family member, as a novel disease candidate in chronic myeloid leukemia (CML), and highlights the therapeutic potential of PlGF blockade for imatinib-resistant CML.	imatinib	303-311	placental growth factor	Homo sapiens	124-146
22160005-4	2011	This article provides a brief overview of the role of angiogenesis in leukemias, discusses recent insights into the role of placenta growth factor (PlGF), a VEGF family member, as a novel disease candidate in chronic myeloid leukemia (CML), and highlights the therapeutic potential of PlGF blockade for imatinib-resistant CML.	imatinib	303-311	placental growth factor	Homo sapiens	148-152
22160025-1	2011	Patients with chronic myeloid leukemia (CML) who have achieved a complete molecular response (CMR) defined by no detectable BCR-ABL mRNA on imatinib (IM) treatment often ask whether it is necessary for treatment to continue.	imatinib	140-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
22160058-2	2011	The development of first-generation (imatinib) and second-generation (dasatinib and nilotinib) tyrosine kinase inhibitors (TKIs) that target the BCR-ABL1 fusion protein produced by the Ph chromosome revolutionized the treatment of chronic myelogenous leukemia (CML).	imatinib	37-45	BCR activator of RhoGEF and GTPase	Homo sapiens	145-153
21293142-2	2011	The tyrosine kinase inhibitor imatinib mesylate was developed to inhibit BCR-ABL kinase activity; however, it also has potent inhibitory activity against the c-Kit and platelet-derived growth factor receptors.	imatinib	30-47	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	158-163
21293142-9	2011	Imatinib treatment significantly reduced the levels of interleukin-4, -5 and -13.	imatinib	0-8	interleukin 4	Mus musculus	55-80
21293142-10	2011	In addition, TGF-beta1 and SCF were significantly reduced in the imatinib-treated animals.	imatinib	65-73	transforming growth factor, beta 1	Mus musculus	13-22
21293142-10	2011	In addition, TGF-beta1 and SCF were significantly reduced in the imatinib-treated animals.	imatinib	65-73	kit ligand	Mus musculus	27-30
22135755-11	2011	Bcr-abl fusion was negative, and FIP1L1-PDGFRA gene was detected after and imatinib mesylate was given.	imatinib	75-92	platelet derived growth factor receptor alpha	Homo sapiens	40-46
21841248-8	2011	We show here an Imatinib-dependent effect on NEP expression and activity in murine fibroblasts and establish that Imatinib-induced modulation of NEP was abolished by the depletion of AbetaPP or its homologues APLP1 and APLP2, thereby confirming that Imatinib-mediated control of NEP could indeed be accounted for its effect on AICD.	imatinib	114-122	membrane metallo endopeptidase	Mus musculus	145-148
21841248-6	2011	Furthermore, Imatinib (Gleevec), a known tyrosine kinase inhibitor was recently shown to elevate AICD in H4 human neuroglioma cells, and this was accompanied by concomitant increases of NEP protein, mRNA levels, and activity.	imatinib	13-21	membrane metalloendopeptidase	Homo sapiens	186-189
21841248-8	2011	We show here an Imatinib-dependent effect on NEP expression and activity in murine fibroblasts and establish that Imatinib-induced modulation of NEP was abolished by the depletion of AbetaPP or its homologues APLP1 and APLP2, thereby confirming that Imatinib-mediated control of NEP could indeed be accounted for its effect on AICD.	imatinib	16-24	membrane metallo endopeptidase	Mus musculus	45-48
21841248-8	2011	We show here an Imatinib-dependent effect on NEP expression and activity in murine fibroblasts and establish that Imatinib-induced modulation of NEP was abolished by the depletion of AbetaPP or its homologues APLP1 and APLP2, thereby confirming that Imatinib-mediated control of NEP could indeed be accounted for its effect on AICD.	imatinib	16-24	membrane metallo endopeptidase	Mus musculus	145-148
21841248-8	2011	We show here an Imatinib-dependent effect on NEP expression and activity in murine fibroblasts and establish that Imatinib-induced modulation of NEP was abolished by the depletion of AbetaPP or its homologues APLP1 and APLP2, thereby confirming that Imatinib-mediated control of NEP could indeed be accounted for its effect on AICD.	imatinib	16-24	amyloid beta (A4) precursor-like protein 1	Mus musculus	209-214
21841248-8	2011	We show here an Imatinib-dependent effect on NEP expression and activity in murine fibroblasts and establish that Imatinib-induced modulation of NEP was abolished by the depletion of AbetaPP or its homologues APLP1 and APLP2, thereby confirming that Imatinib-mediated control of NEP could indeed be accounted for its effect on AICD.	imatinib	16-24	amyloid beta (A4) precursor-like protein 2	Mus musculus	219-224
21841248-8	2011	We show here an Imatinib-dependent effect on NEP expression and activity in murine fibroblasts and establish that Imatinib-induced modulation of NEP was abolished by the depletion of AbetaPP or its homologues APLP1 and APLP2, thereby confirming that Imatinib-mediated control of NEP could indeed be accounted for its effect on AICD.	imatinib	16-24	membrane metallo endopeptidase	Mus musculus	145-148
21841248-8	2011	We show here an Imatinib-dependent effect on NEP expression and activity in murine fibroblasts and establish that Imatinib-induced modulation of NEP was abolished by the depletion of AbetaPP or its homologues APLP1 and APLP2, thereby confirming that Imatinib-mediated control of NEP could indeed be accounted for its effect on AICD.	imatinib	114-122	membrane metallo endopeptidase	Mus musculus	45-48
21841248-8	2011	We show here an Imatinib-dependent effect on NEP expression and activity in murine fibroblasts and establish that Imatinib-induced modulation of NEP was abolished by the depletion of AbetaPP or its homologues APLP1 and APLP2, thereby confirming that Imatinib-mediated control of NEP could indeed be accounted for its effect on AICD.	imatinib	114-122	membrane metallo endopeptidase	Mus musculus	145-148
21841248-8	2011	We show here an Imatinib-dependent effect on NEP expression and activity in murine fibroblasts and establish that Imatinib-induced modulation of NEP was abolished by the depletion of AbetaPP or its homologues APLP1 and APLP2, thereby confirming that Imatinib-mediated control of NEP could indeed be accounted for its effect on AICD.	imatinib	114-122	amyloid beta (A4) precursor-like protein 1	Mus musculus	209-214
21841248-8	2011	We show here an Imatinib-dependent effect on NEP expression and activity in murine fibroblasts and establish that Imatinib-induced modulation of NEP was abolished by the depletion of AbetaPP or its homologues APLP1 and APLP2, thereby confirming that Imatinib-mediated control of NEP could indeed be accounted for its effect on AICD.	imatinib	114-122	amyloid beta (A4) precursor-like protein 2	Mus musculus	219-224
21841248-8	2011	We show here an Imatinib-dependent effect on NEP expression and activity in murine fibroblasts and establish that Imatinib-induced modulation of NEP was abolished by the depletion of AbetaPP or its homologues APLP1 and APLP2, thereby confirming that Imatinib-mediated control of NEP could indeed be accounted for its effect on AICD.	imatinib	114-122	membrane metallo endopeptidase	Mus musculus	145-148
21841248-8	2011	We show here an Imatinib-dependent effect on NEP expression and activity in murine fibroblasts and establish that Imatinib-induced modulation of NEP was abolished by the depletion of AbetaPP or its homologues APLP1 and APLP2, thereby confirming that Imatinib-mediated control of NEP could indeed be accounted for its effect on AICD.	imatinib	114-122	membrane metallo endopeptidase	Mus musculus	45-48
21841248-8	2011	We show here an Imatinib-dependent effect on NEP expression and activity in murine fibroblasts and establish that Imatinib-induced modulation of NEP was abolished by the depletion of AbetaPP or its homologues APLP1 and APLP2, thereby confirming that Imatinib-mediated control of NEP could indeed be accounted for its effect on AICD.	imatinib	114-122	membrane metallo endopeptidase	Mus musculus	145-148
21841248-8	2011	We show here an Imatinib-dependent effect on NEP expression and activity in murine fibroblasts and establish that Imatinib-induced modulation of NEP was abolished by the depletion of AbetaPP or its homologues APLP1 and APLP2, thereby confirming that Imatinib-mediated control of NEP could indeed be accounted for its effect on AICD.	imatinib	114-122	amyloid beta (A4) precursor-like protein 1	Mus musculus	209-214
21157039-1	2011	Imatinib therapy, which targets the oncogene product BCR-ABL, has transformed chronic myeloid leukemia (CML) from a life-threatening disease into a chronic condition.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
22210962-8	2011	The calculated binding free energy is also in agreement with the experimentally determined binding affinity for c-Abl tyrosine kinase complex with Imatinib.Electronic supplementary material The online version of this article (doi:10.1007/s10867-010-9199-z) contains supplementary material, which is available to authorized users.	imatinib	147-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-117
20876428-0	2011	Good clinical response to imatinib mesylate in atypical thymic carcinoid With KIT overexpression.	imatinib	26-43	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	78-81
21157039-5	2011	Imatinib inhibited BCR-ABL activity to the same degree in all stem (CD34+CD38-, CD133+) and progenitor (CD34+CD38+) cells and in quiescent and cycling progenitors from newly diagnosed CML patients.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
21125679-5	2011	Indeed, imatinib mesylate inhibits KIT kinase activity and represents the front-line drug for the treatment of unresectable and advanced GISTs, achieving a partial response or stable disease in about 80% of patients with metastatic GIST.	imatinib	8-25	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	35-38
21672337-2	2011	Treatment with molecular-targeted therapy is usually initiated with imatinib, an inhibitor of BCR-ABL tyrosine kinase.	imatinib	68-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
20512610-6	2011	The half maximal inhibitory concentration (IC(50)) concentration of imatinib was between 15.7 and 18.7 muM, which did not affect invasion activity of the cell lines.	imatinib	68-76	latexin	Homo sapiens	103-106
20512610-8	2011	The combination of imatinib at 13.5 muM and docetaxel at 14.9 nM, however, synergistically inhibited cell growth and invasion activity and could not be reversed by drug removal.	imatinib	19-27	latexin	Homo sapiens	36-39
20605207-0	2011	Pegylated IFN-alpha2a combined to imatinib mesylate 600mg daily can induce complete cytogenetic and molecular responses in a subset of chronic phase CML patients refractory to IFN alone or to imatinib 600mg daily alone.	imatinib	34-51	interferon alpha 2	Homo sapiens	10-20
20944676-0	2011	Pre-transplant imatinib-based therapy improves the outcome of allogeneic hematopoietic stem cell transplantation for BCR-ABL-positive acute lymphoblastic leukemia.	imatinib	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
19714578-3	2011	The central role of Bcr-Abl in the pathogenesis of CML culminated in the discovery of imatinib (an ATP-competitive inhibitor), which is currently the frontline therapy for CML.	imatinib	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
19714578-5	2011	To overcome imatinib resistance, several second-generation ATP-competitive inhibitors endowed with increased potency against imatinib-resistant mutants have been developed: the dual Src/Abl inhibitor dasatinib and the Abl inhibitor nilotinib have been recently approved by US-FDA for the treatment of imatinib-resistant CML, and many other compounds are currently in clinical trial.	imatinib	125-133	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	182-185
19714578-5	2011	To overcome imatinib resistance, several second-generation ATP-competitive inhibitors endowed with increased potency against imatinib-resistant mutants have been developed: the dual Src/Abl inhibitor dasatinib and the Abl inhibitor nilotinib have been recently approved by US-FDA for the treatment of imatinib-resistant CML, and many other compounds are currently in clinical trial.	imatinib	125-133	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	182-185
19714578-5	2011	To overcome imatinib resistance, several second-generation ATP-competitive inhibitors endowed with increased potency against imatinib-resistant mutants have been developed: the dual Src/Abl inhibitor dasatinib and the Abl inhibitor nilotinib have been recently approved by US-FDA for the treatment of imatinib-resistant CML, and many other compounds are currently in clinical trial.	imatinib	125-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-189
19714578-5	2011	To overcome imatinib resistance, several second-generation ATP-competitive inhibitors endowed with increased potency against imatinib-resistant mutants have been developed: the dual Src/Abl inhibitor dasatinib and the Abl inhibitor nilotinib have been recently approved by US-FDA for the treatment of imatinib-resistant CML, and many other compounds are currently in clinical trial.	imatinib	125-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-189
22870150-6	2011	In the suboptimal responders, an increased BCR promoter DNA methylation at six months compared with the baseline was related to a rapid reduction in the BCR-ABL/ABL transcript level following dose escalation (p=0.001) and a longer time to treatment failure (TTFx) of the dose-escalated imatinib (p=0.008).	imatinib	286-294	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
20962097-3	2011	Furthermore, release of CEV from the cell requires Abl but not Src family tyrosine kinases and is blocked by imatinib mesylate (STI-571; Gleevec), an Abl family kinase inhibitor used to treat chronic myelogenous leukemia in humans.	imatinib	109-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-153
20962097-3	2011	Furthermore, release of CEV from the cell requires Abl but not Src family tyrosine kinases and is blocked by imatinib mesylate (STI-571; Gleevec), an Abl family kinase inhibitor used to treat chronic myelogenous leukemia in humans.	imatinib	128-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-153
21632458-0	2011	Choosing the best second-line tyrosine kinase inhibitor in imatinib-resistant chronic myeloid leukemia patients harboring Bcr-Abl kinase domain mutations: how reliable is the IC50?	imatinib	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
21632458-1	2011	Development of drug resistance to imatinib mesylate in chronic myeloid leukemia (CML) patients is often accompanied by selection of point mutations in the kinase domain (KD) of the Bcr-Abl oncoprotein, where imatinib binds.	imatinib	34-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	181-188
21632458-1	2011	Development of drug resistance to imatinib mesylate in chronic myeloid leukemia (CML) patients is often accompanied by selection of point mutations in the kinase domain (KD) of the Bcr-Abl oncoprotein, where imatinib binds.	imatinib	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	181-188
22870150-6	2011	In the suboptimal responders, an increased BCR promoter DNA methylation at six months compared with the baseline was related to a rapid reduction in the BCR-ABL/ABL transcript level following dose escalation (p=0.001) and a longer time to treatment failure (TTFx) of the dose-escalated imatinib (p=0.008).	imatinib	286-294	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-160
22870150-7	2011	When multivariate analysis was performed with regard to the baseline BCR-ABL transcript level, baseline BCR promoter DNA methylation, and a change in the BCR promoter DNA methylation following dose escalation, the increase in the BCR promoter DNA methylation following dose escalation was an independent predictive factor for TTFx of dose-escalated imatinib (hazard ratio, 0.294; p=0.015).	imatinib	349-357	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
22096574-7	2011	Furthermore, the inhibition of CSF-1/CSF-1R signaling, by CSF-1R siRNA or imatinib treatment, impaired CSF-1 induced ERK1/2 activation and cell proliferation.	imatinib	74-82	colony stimulating factor 1	Homo sapiens	31-36
21474977-3	2011	Imatinib pharmacokinetics are influenced by body weight, comedication and pharmacogenetic factors, and the drug is excreted into the bile by the breast cancer resistance protein (ABCG2 gene).	imatinib	0-8	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	145-177
21474977-3	2011	Imatinib pharmacokinetics are influenced by body weight, comedication and pharmacogenetic factors, and the drug is excreted into the bile by the breast cancer resistance protein (ABCG2 gene).	imatinib	0-8	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	179-184
21474977-5	2011	Knowledge of the ABCG2 421 genotype could be useful when making dosing decisions aimed at achieving the optimal imatinib exposure.	imatinib	112-120	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	17-22
22096574-7	2011	Furthermore, the inhibition of CSF-1/CSF-1R signaling, by CSF-1R siRNA or imatinib treatment, impaired CSF-1 induced ERK1/2 activation and cell proliferation.	imatinib	74-82	colony stimulating factor 1 receptor	Homo sapiens	37-43
22096574-7	2011	Furthermore, the inhibition of CSF-1/CSF-1R signaling, by CSF-1R siRNA or imatinib treatment, impaired CSF-1 induced ERK1/2 activation and cell proliferation.	imatinib	74-82	colony stimulating factor 1	Homo sapiens	37-42
22096574-7	2011	Furthermore, the inhibition of CSF-1/CSF-1R signaling, by CSF-1R siRNA or imatinib treatment, impaired CSF-1 induced ERK1/2 activation and cell proliferation.	imatinib	74-82	mitogen-activated protein kinase 3	Homo sapiens	117-123
21949869-2	2011	To investigate the mechanisms behind this oncogenic stress response we used Bcr-Abl over-expressing cells cultivated in presence of imatinib.	imatinib	132-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
22140458-1	2011	Chronic myeloid leukemia (CML) is the first human malignancy to be successfully treated with a small molecule inhibitor, imatinib, targeting a mutant oncoprotein (BCR-ABL).	imatinib	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
21935477-3	2011	The aim of this study was to investigate control of NF-kappaB post-translational modifications exerted by Imatinib and whether any such effects are associated with altered islet gene expression and chemokine production in vitro.	imatinib	106-114	nuclear factor kappa B subunit 1	Homo sapiens	52-61
21935477-8	2011	FINDINGS: Human islet IkappaB-alpha and Ser276-p65 phosphorylation were increased by a 20 minute Imatinib exposure.	imatinib	97-105	NFKB inhibitor alpha	Homo sapiens	22-35
21949869-3	2011	Imatinib deprivation led to rapid induction of Bcr-Abl activity and over-stimulation of PI3K/Akt-, Ras/MAPK-, and JAK/STAT pathways.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
21935477-8	2011	FINDINGS: Human islet IkappaB-alpha and Ser276-p65 phosphorylation were increased by a 20 minute Imatinib exposure.	imatinib	97-105	RELA proto-oncogene, NF-kB subunit	Homo sapiens	47-50
21935477-9	2011	Methylation of p65 at position Lys221 was increased after 60 min of Imatinib exposure and persisted for 3 hours.	imatinib	68-76	RELA proto-oncogene, NF-kB subunit	Homo sapiens	15-18
21949869-3	2011	Imatinib deprivation led to rapid induction of Bcr-Abl activity and over-stimulation of PI3K/Akt-, Ras/MAPK-, and JAK/STAT pathways.	imatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	93-96
21935477-10	2011	Microarray analysis of islets exposed to Imatinib for 4 hours revealed increased expression of the inflammatory genes IL-4R, TCF5, DR5, I-TRAF, I-CAM, HSP27 and IL-8.	imatinib	41-49	interleukin 4 receptor	Homo sapiens	118-123
21949869-7	2011	Therefore, these data provide first evidence that metabolic changes induced by Bcr-Abl hyper-activation are important mediators of oncogenic stress-induced cell death.During the first 30 hours after imatinib deprivation, Bcr-Abl hyper-activation did not affect proliferation but resulted in cellular swelling, vacuolization, and induction of eIF2alpha phosphorylation, CHOP expression, as well as alternative splicing of XPB, indicating endoplasmic reticulum stress response.	imatinib	199-207	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
21949869-7	2011	Therefore, these data provide first evidence that metabolic changes induced by Bcr-Abl hyper-activation are important mediators of oncogenic stress-induced cell death.During the first 30 hours after imatinib deprivation, Bcr-Abl hyper-activation did not affect proliferation but resulted in cellular swelling, vacuolization, and induction of eIF2alpha phosphorylation, CHOP expression, as well as alternative splicing of XPB, indicating endoplasmic reticulum stress response.	imatinib	199-207	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	221-228
21935477-10	2011	Microarray analysis of islets exposed to Imatinib for 4 hours revealed increased expression of the inflammatory genes IL-4R, TCF5, DR5, I-TRAF, I-CAM, HSP27 and IL-8.	imatinib	41-49	CCAAT enhancer binding protein beta	Homo sapiens	125-129
21949869-10	2011	As corticosteroids are used together with imatinib for treatment of Bcr-Abl positive acute lymphoblastic leukemia these data could have important implications for the design of combination therapy protocols.In conclusion, excessive induction of Warburg type metabolic alterations can cause cell death.	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
21935477-10	2011	Microarray analysis of islets exposed to Imatinib for 4 hours revealed increased expression of the inflammatory genes IL-4R, TCF5, DR5, I-TRAF, I-CAM, HSP27 and IL-8.	imatinib	41-49	TNF receptor superfamily member 10b	Homo sapiens	131-134
21935477-10	2011	Microarray analysis of islets exposed to Imatinib for 4 hours revealed increased expression of the inflammatory genes IL-4R, TCF5, DR5, I-TRAF, I-CAM, HSP27 and IL-8.	imatinib	41-49	TRAF family member associated NFKB activator	Homo sapiens	136-142
21935477-10	2011	Microarray analysis of islets exposed to Imatinib for 4 hours revealed increased expression of the inflammatory genes IL-4R, TCF5, DR5, I-TRAF, I-CAM, HSP27 and IL-8.	imatinib	41-49	heat shock protein family B (small) member 1	Homo sapiens	151-156
21935477-10	2011	Microarray analysis of islets exposed to Imatinib for 4 hours revealed increased expression of the inflammatory genes IL-4R, TCF5, DR5, I-TRAF, I-CAM, HSP27 and IL-8.	imatinib	41-49	C-X-C motif chemokine ligand 8	Homo sapiens	161-165
21760961-10	2011	Abnormal methylation of a Src suppressor gene PDLIM4 was associated with shortened survival independently of CML stage and imatinib responsiveness.	imatinib	123-131	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	26-29
21935477-11	2011	The islet release of IL-8 was augmented in islets cultured over night in the presence of Imatinib.	imatinib	89-97	C-X-C motif chemokine ligand 8	Homo sapiens	21-25
21935477-12	2011	Following 30 hours of Imatinib exposure, the cytokine-induced IkappaB-alpha and STAT1 phosphorylation was abolished and diminished, respectively.	imatinib	22-30	NFKB inhibitor alpha	Homo sapiens	62-75
21935477-12	2011	Following 30 hours of Imatinib exposure, the cytokine-induced IkappaB-alpha and STAT1 phosphorylation was abolished and diminished, respectively.	imatinib	22-30	signal transducer and activator of transcription 1	Homo sapiens	80-85
21935477-13	2011	The cytokine-induced release of the chemokines MIG and IP10 was lower in islets exposed to Imatinib for 30 hours.	imatinib	91-99	C-X-C motif chemokine ligand 9	Homo sapiens	47-50
21935477-13	2011	The cytokine-induced release of the chemokines MIG and IP10 was lower in islets exposed to Imatinib for 30 hours.	imatinib	91-99	C-X-C motif chemokine ligand 10	Homo sapiens	55-59
21935477-14	2011	CONCLUSION: Imatinib by itself promotes a modest activation of NF-kappaB.	imatinib	12-20	nuclear factor kappa B subunit 1	Homo sapiens	63-72
21935477-16	2011	It is possible that Imatinib induces NF-kappaB preconditioning of islet cells leading to lowered cytokine sensitivity and a mitigated islet inflammation.	imatinib	20-28	nuclear factor kappa B subunit 1	Homo sapiens	37-46
21789194-5	2011	Consistently, expression of key glycolytic enzymes, at least partly mediated by HIF-1alpha, was modified in imatinib-resistant cells suggesting that imatinib-resistant cells uncouple glycolytic flux from pyruvate oxidation.	imatinib	108-116	hypoxia inducible factor 1 subunit alpha	Homo sapiens	80-90
21789194-5	2011	Consistently, expression of key glycolytic enzymes, at least partly mediated by HIF-1alpha, was modified in imatinib-resistant cells suggesting that imatinib-resistant cells uncouple glycolytic flux from pyruvate oxidation.	imatinib	149-157	hypoxia inducible factor 1 subunit alpha	Homo sapiens	80-90
21789226-7	2011	We also found that the ABL1 kinase inhibitor imatinib was very effective in suppressing PU.1 expression in BCR-ABL1-positive K562 cells but not in HEL cells.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-27
21789226-7	2011	We also found that the ABL1 kinase inhibitor imatinib was very effective in suppressing PU.1 expression in BCR-ABL1-positive K562 cells but not in HEL cells.	imatinib	45-53	Spi-1 proto-oncogene	Homo sapiens	88-92
21789226-7	2011	We also found that the ABL1 kinase inhibitor imatinib was very effective in suppressing PU.1 expression in BCR-ABL1-positive K562 cells but not in HEL cells.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-115
21760961-10	2011	Abnormal methylation of a Src suppressor gene PDLIM4 was associated with shortened survival independently of CML stage and imatinib responsiveness.	imatinib	123-131	PDZ and LIM domain 4	Homo sapiens	46-52
23049298-0	2011	Monitoring of BCR-ABL levels in chronic myeloid leukemia patients treated with imatinib in the chronic phase - the importance of a major molecular response.	imatinib	79-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
21659722-2	2011	However, imatinib also has potent inhibitory activity against the platelet-derived growth factor receptor (PDGFR).	imatinib	9-17	platelet derived growth factor receptor, beta polypeptide	Mus musculus	66-105
21659722-2	2011	However, imatinib also has potent inhibitory activity against the platelet-derived growth factor receptor (PDGFR).	imatinib	9-17	platelet derived growth factor receptor, beta polypeptide	Mus musculus	107-112
21659722-4	2011	Like imatinib, nilotinib selectively inhibits the tyrosine kinase activity of PDGFR.	imatinib	5-13	platelet derived growth factor receptor, beta polypeptide	Mus musculus	78-83
21659722-10	2011	The numbers of inflammatory cells and levels of IL-6, IL-1beta and tumor necrosis factor-alpha were decreased in the imatinib and nilotinib groups on days 3 and 7.	imatinib	117-125	interleukin 6	Mus musculus	48-52
21853672-0	2011	[H-oCT1 gene expression as a predictor of major and complete molecular response to imatinib of chronic myeloid leukemia.	imatinib	83-91	solute carrier family 22 member 1	Homo sapiens	3-7
21853672-5	2011	Imatinib is a substrate of human organic cation transporter-1 (hOCT1), which actively delivers the drug into the cells, and efflux transporters.	imatinib	0-8	solute carrier family 22 member 1	Homo sapiens	33-61
21853672-5	2011	Imatinib is a substrate of human organic cation transporter-1 (hOCT1), which actively delivers the drug into the cells, and efflux transporters.	imatinib	0-8	solute carrier family 22 member 1	Homo sapiens	63-68
21853672-7	2011	Patients with low pretreatment hOCT1 expression had inferior major and complete molecular response (MMR and CMR) rates (p = 0.0001, p = 0.0001) achieved any time or at 18 months of imatinib treatment (p = 0.023, p = 0.022).	imatinib	181-189	solute carrier family 22 member 1	Homo sapiens	31-36
21853672-8	2011	The expression of hOCT1 is important in determining the clinical response to imatinib.	imatinib	77-85	solute carrier family 22 member 1	Homo sapiens	18-23
21659722-10	2011	The numbers of inflammatory cells and levels of IL-6, IL-1beta and tumor necrosis factor-alpha were decreased in the imatinib and nilotinib groups on days 3 and 7.	imatinib	117-125	interleukin 1 beta	Mus musculus	54-94
23049298-2	2011	The aim of this study was to evaluate BCR-ABL levels of chronic myeloid leukemia patients treated with imatinib in the chronic phase and correlate the response to therapy and event-free survival.	imatinib	103-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
21659722-11	2011	Imatinib and nilotinib therapy significantly reduced the levels of hydroxyproline on days 14 and 21, which was accompanied by decreased expression levels of transforming growth factor (TGF)-beta1 and PDGFR-beta.	imatinib	0-8	transforming growth factor, beta 1	Mus musculus	157-195
23049298-3	2011	METHODS: BCR-ABL levels were measured in peripheral blood cell samples using Real time PCR at diagnosis and then every 3 months after starting therapy with imatinib.	imatinib	156-164	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
21659722-11	2011	Imatinib and nilotinib therapy significantly reduced the levels of hydroxyproline on days 14 and 21, which was accompanied by decreased expression levels of transforming growth factor (TGF)-beta1 and PDGFR-beta.	imatinib	0-8	platelet derived growth factor receptor, beta polypeptide	Mus musculus	200-210
21659722-12	2011	Imatinib and nilotinib also significantly reduced the expression levels of the genes for TGF-beta1 and platelet-derived growth factor (PDGF).	imatinib	0-8	transforming growth factor, beta 1	Mus musculus	89-98
23284246-1	2011	Imatinib mesylate was the first BCR-ABL-target agent approved for the treatment of chronic myeloid leukemia.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
23049365-1	2011	The development of point mutations in the BCR-ABL kinase domain is the main reason for imatinib resistance in chronic myeloid leukemia.	imatinib	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-49
21192792-3	2010	Imatinib and nilotinib directly inhibit the kinase activity of KIT, while RAD001 (everolimus) inhibits mTOR.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	63-66
21892537-4	2011	The objective of this paper is to present the monitoring of imatinib therapy in two children with CML by the BCR-ABL fusion gene expression assessment from peripheral blood with quantitative real-time polymerase chain reaction (PCR) method.	imatinib	60-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
21429397-0	2011	[Clinical significance of CRKL protein phosphorylation level in the treatment of chronic myeloid leukemia with imatinib].	imatinib	111-119	CRK like proto-oncogene, adaptor protein	Homo sapiens	26-30
21429397-1	2011	OBJECTIVE: To investigate the adaptor protein CRKL phosphorylation level (p-CRKL) and its significance in chronic myeloid leukemia (CML) treated with imatinib.	imatinib	150-158	CRK like proto-oncogene, adaptor protein	Homo sapiens	46-50
21429397-1	2011	OBJECTIVE: To investigate the adaptor protein CRKL phosphorylation level (p-CRKL) and its significance in chronic myeloid leukemia (CML) treated with imatinib.	imatinib	150-158	CRK like proto-oncogene, adaptor protein	Homo sapiens	76-80
21429397-5	2011	The BCR-ABL mRNA level in newly diagnosed CML was higher than that in imatinib-responded patients (P = 0.01); and so did in imatinib-resistant patients than in imatinib-effective patients (P = 0.03).	imatinib	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
21429397-5	2011	The BCR-ABL mRNA level in newly diagnosed CML was higher than that in imatinib-responded patients (P = 0.01); and so did in imatinib-resistant patients than in imatinib-effective patients (P = 0.03).	imatinib	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
21429397-7	2011	p-CRKL%, MFI showed a high degree of phosphorylation in newly diagnosed CML and imatinib-resistant patients (P = 5.130; P = 3.178).	imatinib	80-88	CRK like proto-oncogene, adaptor protein	Homo sapiens	2-7
21429397-8	2011	The level of p-CRKL % and MFI in newly diagnosed group was higher than that in imatinib responded group (P = 0.000; P = 0.01) and also higher in imatinib-effective group than in imatinib-resistant group (P = 0.000; P = 0.02).	imatinib	79-87	CRK like proto-oncogene, adaptor protein	Homo sapiens	15-19
21429397-8	2011	The level of p-CRKL % and MFI in newly diagnosed group was higher than that in imatinib responded group (P = 0.000; P = 0.01) and also higher in imatinib-effective group than in imatinib-resistant group (P = 0.000; P = 0.02).	imatinib	145-153	CRK like proto-oncogene, adaptor protein	Homo sapiens	15-19
21429397-8	2011	The level of p-CRKL % and MFI in newly diagnosed group was higher than that in imatinib responded group (P = 0.000; P = 0.01) and also higher in imatinib-effective group than in imatinib-resistant group (P = 0.000; P = 0.02).	imatinib	145-153	CRK like proto-oncogene, adaptor protein	Homo sapiens	15-19
21429397-10	2011	CONCLUSION: It seems that p-CRKL detection might be helpful in predicting imatinib treatment outcomes.	imatinib	74-82	CRK like proto-oncogene, adaptor protein	Homo sapiens	28-32
21183698-0	2010	Polymorphisms in the multidrug resistance gene MDR1 (ABCB1) predict for molecular resistance in patients with newly diagnosed chronic myeloid leukemia receiving high-dose imatinib.	imatinib	171-179	ATP binding cassette subfamily B member 1	Homo sapiens	47-51
20855863-0	2010	EVI-1 oncogene expression predicts survival in chronic-phase CML patients resistant to imatinib treated with second-generation tyrosine kinase inhibitors.	imatinib	87-95	MDS1 and EVI1 complex locus	Homo sapiens	0-5
20855863-5	2010	In a multivariate analysis, EVI-1 expression status and the best cytogenetic response obtained on imatinib were the only independent predictors for overall survival, progression-free survival, and event-free survival.	imatinib	98-106	MDS1 and EVI1 complex locus	Homo sapiens	28-33
20855863-6	2010	Our data suggest that screening for EVI-1 expression at the time of imatinib failure may predict for response to second-line TKI therapy and consequently aid clinical management.	imatinib	68-76	MDS1 and EVI1 complex locus	Homo sapiens	36-41
21183698-0	2010	Polymorphisms in the multidrug resistance gene MDR1 (ABCB1) predict for molecular resistance in patients with newly diagnosed chronic myeloid leukemia receiving high-dose imatinib.	imatinib	171-179	ATP binding cassette subfamily B member 1	Homo sapiens	53-58
21138592-0	2010	Patan hospital experience in treating philadelphia chromosome/BCR-ABL1 positive chronic myeloid leukemia patients with gleevec (imatinib mesylate); the first generation specific tyrosine kinase inhibitor.	imatinib	119-126	BCR activator of RhoGEF and GTPase	Homo sapiens	62-70
20869412-1	2010	Chronic Myeloid Leukemia (CML) stem/progenitor cells, which over-express Bcr-Abl, respond to imatinib by a reversible block in proliferation without significant apoptosis.	imatinib	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
20869412-3	2010	Previously, we have reported that intracellular levels of imatinib in primary primitive CML cells (CD34+38(lo/-)), are significantly lower than in CML progenitor cells (total CD34+) and leukemic cell lines.	imatinib	58-66	CD34 molecule	Homo sapiens	99-103
20869412-3	2010	Previously, we have reported that intracellular levels of imatinib in primary primitive CML cells (CD34+38(lo/-)), are significantly lower than in CML progenitor cells (total CD34+) and leukemic cell lines.	imatinib	58-66	CD34 molecule	Homo sapiens	175-179
20830748-2	2010	We explored the effects of imatinib mesylate, an inhibitor of Bcr-Abl protein used in front-line CML therapy, on the adhesivity of JURL-MK1 cells to fibronectin and searched for underlying changes in the cell proteome.	imatinib	27-44	fibronectin 1	Homo sapiens	149-160
20830748-4	2010	Imatinib treatment caused a transient increase in JURL-MK1 cell adhesivity to fibronectin, possibly due to the switch off of Bcr-Abl activity.	imatinib	0-8	fibronectin 1	Homo sapiens	78-89
20830748-4	2010	Imatinib treatment caused a transient increase in JURL-MK1 cell adhesivity to fibronectin, possibly due to the switch off of Bcr-Abl activity.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
21138592-0	2010	Patan hospital experience in treating philadelphia chromosome/BCR-ABL1 positive chronic myeloid leukemia patients with gleevec (imatinib mesylate); the first generation specific tyrosine kinase inhibitor.	imatinib	128-145	BCR activator of RhoGEF and GTPase	Homo sapiens	62-70
21138592-12	2010	Furthermore, we demonstrate that imatinib is very effective and induced long lasting responses in a high proportion of patients with Ph chromosome/BCR-ABL1 positive CML.	imatinib	33-41	BCR activator of RhoGEF and GTPase	Homo sapiens	147-155
20729917-8	2010	By contrast, knockdown of Abl family kinases or their inhibition with imatinib enhanced anchorage-independent growth and tumorigenesis induced by Crk.	imatinib	70-78	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	26-29
21188137-7	2010	Testing for mutations in BCR-ABL1 may predict lack of response to imatinib or may inform the choice between alternative TKIs.	imatinib	66-74	BCR activator of RhoGEF and GTPase	Homo sapiens	25-33
20729917-8	2010	By contrast, knockdown of Abl family kinases or their inhibition with imatinib enhanced anchorage-independent growth and tumorigenesis induced by Crk.	imatinib	70-78	v-crk avian sarcoma virus CT10 oncogene homolog	Mus musculus	146-149
20632368-0	2010	Co-encapsulation of anti-BCR-ABL siRNA and imatinib mesylate in transferrin receptor-targeted sterically stabilized liposomes for chronic myeloid leukemia treatment.	imatinib	43-51	transferrin receptor	Homo sapiens	64-84
20804740-1	2010	Induction of the breast cancer resistance protein (BCRP/ABCG2) expression has been found in various tissues and cell-types after exposure to chemicals including 17beta-estradiol, rosiglitazone, imatinib, as well as aryl hydrocarbon receptor (AhR) activators such as 2,3,7,8-tetrachlorodibenzodioxin, 3-methylcholanthrene (3MC), and omeprazole.	imatinib	194-202	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	17-49
20804740-1	2010	Induction of the breast cancer resistance protein (BCRP/ABCG2) expression has been found in various tissues and cell-types after exposure to chemicals including 17beta-estradiol, rosiglitazone, imatinib, as well as aryl hydrocarbon receptor (AhR) activators such as 2,3,7,8-tetrachlorodibenzodioxin, 3-methylcholanthrene (3MC), and omeprazole.	imatinib	194-202	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	51-55
20804740-1	2010	Induction of the breast cancer resistance protein (BCRP/ABCG2) expression has been found in various tissues and cell-types after exposure to chemicals including 17beta-estradiol, rosiglitazone, imatinib, as well as aryl hydrocarbon receptor (AhR) activators such as 2,3,7,8-tetrachlorodibenzodioxin, 3-methylcholanthrene (3MC), and omeprazole.	imatinib	194-202	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	56-61
20632368-4	2010	The present work aimed at the development and application of transferrin receptor (TrfR) targeted liposomes co-encapsulating anti-BCR-ABL siRNA and imatinib at different molar ratios.	imatinib	148-156	transferrin receptor	Homo sapiens	61-81
20632368-4	2010	The present work aimed at the development and application of transferrin receptor (TrfR) targeted liposomes co-encapsulating anti-BCR-ABL siRNA and imatinib at different molar ratios.	imatinib	148-156	transferrin receptor	Homo sapiens	83-87
21098700-0	2010	Persistent activation of the Fyn/ERK kinase signaling axis mediates imatinib resistance in chronic myelogenous leukemia cells through upregulation of intracellular SPARC.	imatinib	68-76	FYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	29-32
20955401-7	2010	One patient had a PDGFRA/FIP1L1 fusion and achieved hematologic and molecular remission after imatinib therapy.	imatinib	94-102	platelet derived growth factor receptor alpha	Homo sapiens	18-24
20955401-7	2010	One patient had a PDGFRA/FIP1L1 fusion and achieved hematologic and molecular remission after imatinib therapy.	imatinib	94-102	factor interacting with PAPOLA and CPSF1	Homo sapiens	25-31
21156236-0	2010	GSTT1 copy number gain is a poor predictive marker for escalated-dose imatinib treatment in chronic myeloid leukemia: genetic predictive marker found using array comparative genomic hybridization.	imatinib	70-78	glutathione S-transferase theta 1	Homo sapiens	0-5
21098700-0	2010	Persistent activation of the Fyn/ERK kinase signaling axis mediates imatinib resistance in chronic myelogenous leukemia cells through upregulation of intracellular SPARC.	imatinib	68-76	mitogen-activated protein kinase 1	Homo sapiens	33-36
21098700-0	2010	Persistent activation of the Fyn/ERK kinase signaling axis mediates imatinib resistance in chronic myelogenous leukemia cells through upregulation of intracellular SPARC.	imatinib	68-76	secreted protein acidic and cysteine rich	Homo sapiens	164-169
21098700-2	2010	Chronic myelogenous leukemia (CML) cells resistant to the BCR-ABL inhibitor imatinib (IM-R cells) were found to overexpress SPARC mRNA.	imatinib	76-84	secreted protein acidic and cysteine rich	Homo sapiens	124-129
21098700-3	2010	In this study, we show that imatinib triggers SPARC accumulation in a variety of tyrosine kinase inhibitor (TKI)-resistant CML cell lines.	imatinib	28-36	secreted protein acidic and cysteine rich	Homo sapiens	46-51
21098700-4	2010	SPARC silencing in IM-R cells restored imatinib sensitivity, whereas enforced SPARC expression in imatinib-sensitive cells promoted viability as well as protection against imatinib-mediated apoptosis.	imatinib	39-47	secreted protein acidic and cysteine rich	Homo sapiens	0-5
21098700-4	2010	SPARC silencing in IM-R cells restored imatinib sensitivity, whereas enforced SPARC expression in imatinib-sensitive cells promoted viability as well as protection against imatinib-mediated apoptosis.	imatinib	98-106	secreted protein acidic and cysteine rich	Homo sapiens	78-83
21098700-4	2010	SPARC silencing in IM-R cells restored imatinib sensitivity, whereas enforced SPARC expression in imatinib-sensitive cells promoted viability as well as protection against imatinib-mediated apoptosis.	imatinib	98-106	secreted protein acidic and cysteine rich	Homo sapiens	78-83
21098700-8	2010	Pharmacologic inhibition of this pathway or siRNA-mediated knockdown of Fyn kinase resensitized IM-R cells to imatinib.	imatinib	110-118	FYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	72-75
21098700-9	2010	In support of our findings, increased levels of SPARC mRNA were documented in blood cells from CML patients after 1 year of imatinib therapy compared with initial diagnosis.	imatinib	124-132	secreted protein acidic and cysteine rich	Homo sapiens	48-53
21098700-10	2010	Taken together, our results highlight an important role for the Fyn/ERK signaling pathway in imatinib-resistant cells that is driven by accumulation of intracellular SPARC.	imatinib	93-101	FYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	64-67
21098700-10	2010	Taken together, our results highlight an important role for the Fyn/ERK signaling pathway in imatinib-resistant cells that is driven by accumulation of intracellular SPARC.	imatinib	93-101	mitogen-activated protein kinase 1	Homo sapiens	68-71
21098700-10	2010	Taken together, our results highlight an important role for the Fyn/ERK signaling pathway in imatinib-resistant cells that is driven by accumulation of intracellular SPARC.	imatinib	93-101	secreted protein acidic and cysteine rich	Homo sapiens	166-171
21258186-7	2010	Among 4 patients who continued high-dose imatinib for late suboptimal response, 2 patients subsequently achieved MMR, and BCR-ABL mRNA transcript levels were decreasing in 2 patients.	imatinib	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
21073351-6	2010	WHAT THE READER WILL GAIN: Mutations in the BCR-ABL kinase domain are responsible for the majority of resistance to imatinib.	imatinib	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
20409582-8	2010	We further show that a lower frequency of PRAME-positive samples during imatinib treatment was not caused by gene-specific downregulation.	imatinib	72-80	PRAME nuclear receptor transcriptional regulator	Homo sapiens	42-47
20409582-11	2010	PRAME-specific immunotherapy might represent a promising approach for the eradication of residual therapy-resistant leukemic cells due to its frequent expression and stability under imatinib treatment.	imatinib	182-190	PRAME nuclear receptor transcriptional regulator	Homo sapiens	0-5
20427086-0	2010	A Phase 1 study of imatinib mesylate in combination with cytarabine and daunorubicin for c-kit positive relapsed acute myeloid leukemia.	imatinib	19-36	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	89-94
20427086-2	2010	We conducted a Phase 1 study of the c-kit inhibitor, imatinib mesylate (IM), in combination with cytarabine and daunorubicin (7+3) in c-kit+ relapsed AML.	imatinib	53-70	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	36-41
20427086-2	2010	We conducted a Phase 1 study of the c-kit inhibitor, imatinib mesylate (IM), in combination with cytarabine and daunorubicin (7+3) in c-kit+ relapsed AML.	imatinib	53-70	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	134-139
21154127-3	2010	Besides Abl, bafetinib targets the Src family kinase Lyn, which has been associated with resistance to imatinib in CML.	imatinib	103-111	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	53-56
21154127-5	2010	Bafetinib inhibits 12 of the 13 most frequent imatinib-resistant Bcr-Abl point mutations, but not a Thr315Ile mutation.	imatinib	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
20553674-7	2010	RESULT(S): Imatinib treatment at 10 muM had no effect on ESC attachment.	imatinib	11-19	latexin	Homo sapiens	36-39
20553674-9	2010	The 0.1 muM dose of imatinib had no effect on proliferation.	imatinib	20-28	latexin	Homo sapiens	8-11
20553674-10	2010	Treatment with 5 muM and 10 muM of imatinib reduced ESC invasion by 30% and 73%, respectively.	imatinib	35-43	latexin	Homo sapiens	28-31
21108851-1	2010	Imatinib, a tyrosine kinase inhibitor (TKI) of BCR-ABL, was the standard first-line therapy for chronic myeloid leukemia (CML) for almost 10 years.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
21108851-2	2010	Dasatinib and nilotinib, two newer drugs with higher potency than imatinib against BCR-ABL and activity against most imatinib-resistant BCR-ABL mutations, have each shown superior efficacy compared with imatinib for first-line treatment of chronic-phase CML in randomized phase 3 trials.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
21124949-5	2010	We apply this procedure to the target profile of the second-generation BCR-ABL inhibitor bafetinib which is in development for the treatment of imatinib-resistant chronic myeloid leukemia.	imatinib	144-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
20866107-5	2010	We used SILAC to measure how cellular treatment with the Bcr-Abl inhibitor imatinib affects protein binding to a generic kinase inhibitor resin and further quantified site-specific phosphorylations on resin-retained proteins.	imatinib	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
21087500-12	2010	Changing of imatinib on the basis of BCR-ABL/BCR% sustained increase and mutational studies is a prudent approach for preserving other therapeutic options in imatinib-resistant patients.	imatinib	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
21087500-12	2010	Changing of imatinib on the basis of BCR-ABL/BCR% sustained increase and mutational studies is a prudent approach for preserving other therapeutic options in imatinib-resistant patients.	imatinib	12-20	BCR activator of RhoGEF and GTPase	Homo sapiens	37-40
20499235-0	2010	Standard-dose imatinib plus low-dose homoharringtonine and granulocyte colony-stimulating factor is an effective induction therapy for patients with chronic myeloid leukemia in myeloid blast crisis who have failed prior single-agent therapy with imatinib.	imatinib	246-254	colony stimulating factor 3	Homo sapiens	59-96
21368869-1	2010	One proposed strategy to suppress the proliferation of imatinib-resistant cells in chronic myeloid leukemia (CML) is to inhibit key proteins downstream of Bcr-Abl.	imatinib	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-162
20835477-4	2010	We validated the MS method by determining the IC(50) value of imatinib, an Abl inhibitor for clinical treatment of chronic myelogenous leukaemia (CML).	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-78
20675402-4	2010	Interestingly, Bag1 (Bcl-2-associated athanogene-1), a nucleotide exchange factor for Hsc70, directly bound BCR-ABL with a high affinity, which was enhanced by CHIP and Hsp90 inhibitors, inhibited by imatinib and competed with Hsc70.	imatinib	200-208	BCL2-associated athanogene 1	Mus musculus	15-19
20675402-4	2010	Interestingly, Bag1 (Bcl-2-associated athanogene-1), a nucleotide exchange factor for Hsc70, directly bound BCR-ABL with a high affinity, which was enhanced by CHIP and Hsp90 inhibitors, inhibited by imatinib and competed with Hsc70.	imatinib	200-208	BCL2-associated athanogene 1	Mus musculus	21-50
20675402-4	2010	Interestingly, Bag1 (Bcl-2-associated athanogene-1), a nucleotide exchange factor for Hsc70, directly bound BCR-ABL with a high affinity, which was enhanced by CHIP and Hsp90 inhibitors, inhibited by imatinib and competed with Hsc70.	imatinib	200-208	heat shock protein 8	Mus musculus	86-91
20675402-4	2010	Interestingly, Bag1 (Bcl-2-associated athanogene-1), a nucleotide exchange factor for Hsc70, directly bound BCR-ABL with a high affinity, which was enhanced by CHIP and Hsp90 inhibitors, inhibited by imatinib and competed with Hsc70.	imatinib	200-208	heat shock protein, 3	Mus musculus	169-174
20581169-3	2010	OBJECTIVES: To assess safety, tolerability, and efficacy of the PDGFR inhibitor imatinib in patients with PAH.	imatinib	80-88	platelet derived growth factor receptor beta	Homo sapiens	64-69
20581169-5	2010	Patients received imatinib (an inhibitor of PDGFR activity) 200 mg orally once daily (or placebo), which was increased to 400 mg if the initial dose was well tolerated.	imatinib	18-26	platelet derived growth factor receptor beta	Homo sapiens	44-49
20499235-1	2010	We investigated the efficacy of the induction therapy involving granulocyte colony-stimulating factor (G-CSF) and low-dose homoharringtonine as well as standard-dose imatinib, which we called the G-CSF + homoharringtonine + imatinib (GHI) regimen, in patients with chronic myelogenous leukemia (CML) in blast crisis who have failed prior single-agent therapy with imatinib.	imatinib	166-174	colony stimulating factor 3	Homo sapiens	196-201
20629032-5	2010	Blockage of c-Abl using the tyrosine kinase inhibitor imatinib resulted in reduced cellular growth in both cell lines.	imatinib	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-17
20977456-10	2010	The CYP3A inhibitors ketoconazole and troleandomycin, and the CYP2C8 inhibitors quercetin and paclitaxel decreased imatinib oxidation.	imatinib	115-123	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	62-68
20977456-11	2010	From molecular modelling, the imatinib structure could be superimposed on a pharmacophore for CYP2C8 substrates.	imatinib	30-38	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	94-100
20977456-12	2010	CONCLUSIONS AND IMPLICATIONS: CYP2C8 and CYPs 3A contribute to imatinib N-demethylation in human liver.	imatinib	63-71	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	30-36
20977456-13	2010	The involvement of CYP2C8 may account in part for the wide inter-patient variation in imatinib pharmacokinetics observed in clinical practice.	imatinib	86-94	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	19-25
20977456-0	2010	Participation of CYP2C8 and CYP3A4 in the N-demethylation of imatinib in human hepatic microsomes.	imatinib	61-69	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	17-23
20977456-0	2010	Participation of CYP2C8 and CYP3A4 in the N-demethylation of imatinib in human hepatic microsomes.	imatinib	61-69	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	28-34
20977456-3	2010	Hepatic cytochrome P450 (CYP) 3A4 has been implicated in imatinib N-demethylation, but the clearance of imatinib decreases during prolonged therapy.	imatinib	57-65	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	8-33
20977456-4	2010	CYP3A phenotype correlates with imatinib clearance at the commencement of therapy, but not at steady state.	imatinib	32-40	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-5
21037371-0	2010	Imatinib inhibits bone marrow-derived c-kit+ cell mobilisation in hypoxic pulmonary hypertension.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	38-43
20809224-4	2010	Trials of the ABL kinase inhibitor, imatinib, have revolutionized the treatment of CML, and there are ongoing studies with other kinase inhibitors in MPN and AML.	imatinib	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-17
20959405-0	2010	The IFNG (IFN-gamma) genotype predicts cytogenetic and molecular response to imatinib therapy in chronic myeloid leukemia.	imatinib	77-85	interferon gamma	Homo sapiens	4-8
20959405-0	2010	The IFNG (IFN-gamma) genotype predicts cytogenetic and molecular response to imatinib therapy in chronic myeloid leukemia.	imatinib	77-85	interferon gamma	Homo sapiens	10-19
20959405-1	2010	PURPOSE: The present study analyzed treatment outcomes of imatinib therapy by interindividual genetic variants in candidate biological pathways of chronic myeloid leukemia (CML) such as apoptosis, angiogenesis, IFN-gamma signaling pathways, or drug transport/metabolism of imatinib.	imatinib	58-66	interferon gamma	Homo sapiens	211-220
20959405-5	2010	CONCLUSIONS: The IFNG genotype was predictive for response to imatinib therapy, suggesting potential involvement of the IFN-gamma signaling pathway in the mechanism of action of imatinib in CML.	imatinib	62-70	interferon gamma	Homo sapiens	17-21
20959405-5	2010	CONCLUSIONS: The IFNG genotype was predictive for response to imatinib therapy, suggesting potential involvement of the IFN-gamma signaling pathway in the mechanism of action of imatinib in CML.	imatinib	62-70	interferon gamma	Homo sapiens	120-129
20959405-5	2010	CONCLUSIONS: The IFNG genotype was predictive for response to imatinib therapy, suggesting potential involvement of the IFN-gamma signaling pathway in the mechanism of action of imatinib in CML.	imatinib	178-186	interferon gamma	Homo sapiens	17-21
20959405-5	2010	CONCLUSIONS: The IFNG genotype was predictive for response to imatinib therapy, suggesting potential involvement of the IFN-gamma signaling pathway in the mechanism of action of imatinib in CML.	imatinib	178-186	interferon gamma	Homo sapiens	120-129
20585028-7	2010	Specific inhibition of c-Abl by imatinib, siRNA, or c-Abl kinase dead drastically reduces high NaCl-induced TonEBP/OREBP activity by reducing its nuclear location and transactivating activity.	imatinib	32-40	nuclear factor of activated T-cells 5	Rattus norvegicus	108-114
20965785-3	2010	METHODS: In our prospective, multicentre, non-randomised Stop Imatinib (STIM) study, imatinib treatment (of >2 years duration) was discontinued in patients with CML who were aged 18 years and older and in CMR (>5-log reduction in BCR-ABL and ABL levels and undetectable transcripts on quantitative RT-PCR).	imatinib	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	236-243
20143399-0	2010	The BCR/ABL-inhibitors imatinib, nilotinib and dasatinib differentially affect NK cell reactivity.	imatinib	23-31	BCR activator of RhoGEF and GTPase	Homo sapiens	4-7
20143399-0	2010	The BCR/ABL-inhibitors imatinib, nilotinib and dasatinib differentially affect NK cell reactivity.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-11
20143399-1	2010	In chronic myeloid leukemia (CML), BCR/ABL-mediated oncogenic signaling can be targeted with the BCR/ABL-inhibitors Imatinib, Nilotinib and Dasatinib.	imatinib	116-124	BCR activator of RhoGEF and GTPase	Homo sapiens	35-38
20143399-1	2010	In chronic myeloid leukemia (CML), BCR/ABL-mediated oncogenic signaling can be targeted with the BCR/ABL-inhibitors Imatinib, Nilotinib and Dasatinib.	imatinib	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-42
20143399-1	2010	In chronic myeloid leukemia (CML), BCR/ABL-mediated oncogenic signaling can be targeted with the BCR/ABL-inhibitors Imatinib, Nilotinib and Dasatinib.	imatinib	116-124	BCR activator of RhoGEF and GTPase	Homo sapiens	97-100
20143399-1	2010	In chronic myeloid leukemia (CML), BCR/ABL-mediated oncogenic signaling can be targeted with the BCR/ABL-inhibitors Imatinib, Nilotinib and Dasatinib.	imatinib	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-104
20143399-4	2010	Exposure of CML cells (K562, Meg-01) to pharmacological concentrations of Imatinib, Nilotinib and Dasatinib diminished expression of ligands for the activating immunoreceptor NKG2D to a similar extent.	imatinib	74-82	killer cell lectin like receptor K1	Homo sapiens	175-180
20699436-9	2010	Furthermore, both CA-4 and CA-432 induced significantly more apoptosis compared with imatinib mesylate in ex vivo samples from patients with CML, including those positive for the T315I mutation displaying resistance to imatinib mesylate and dasatinib.	imatinib	219-236	carbonic anhydrase 4	Homo sapiens	18-22
20720558-0	2010	Influence of CYP3A5 and drug transporter polymorphisms on imatinib trough concentration and clinical response among patients with chronic phase chronic myeloid leukemia.	imatinib	58-66	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	13-19
20811406-0	2010	OCT-1 activity measurement provides a superior imatinib response predictor than screening for single-nucleotide polymorphisms of OCT-1.	imatinib	47-55	solute carrier family 22 member 1	Homo sapiens	0-5
20965785-3	2010	METHODS: In our prospective, multicentre, non-randomised Stop Imatinib (STIM) study, imatinib treatment (of >2 years duration) was discontinued in patients with CML who were aged 18 years and older and in CMR (>5-log reduction in BCR-ABL and ABL levels and undetectable transcripts on quantitative RT-PCR).	imatinib	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	240-243
20965785-13	2010	All patients who relapsed responded to reintroduction of imatinib: 16 of the 42 patients who relapsed showed decreases in their BCR-ABL levels, and 26 achieved CMR that was sustained after imatinib rechallenge.	imatinib	57-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
20832303-0	2010	Identification of the first non-peptidic small molecule inhibitor of the c-Abl/14-3-3 protein-protein interactions able to drive sensitive and Imatinib-resistant leukemia cells to apoptosis.	imatinib	143-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-78
20860375-5	2010	To validate the assay, the activity of two small-molecule kinase inhibitors, imatinib and dasatinib, which target the oncogenic mutant tyrosine kinase Bcr-Abl to treat chronic myeloid leukemia (CML), was tested.	imatinib	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-158
20693279-3	2010	Profiling micro-RNA (miRNA) expression in a model of Lyn-mediated imatinib-resistant CML (MYL-R) identified approximately 30 miRNAs whose expression differed >2-fold compared with drug-sensitive MYL cells.	imatinib	66-74	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	53-56
20693279-6	2010	A similar Lyn-dependent regulation of miR181b and miR181d was observed in imatinib-resistant K562 CML cells.	imatinib	74-82	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	10-13
20693279-6	2010	A similar Lyn-dependent regulation of miR181b and miR181d was observed in imatinib-resistant K562 CML cells.	imatinib	74-82	microRNA 181d	Homo sapiens	50-57
20519627-0	2010	BCR-ABL SH3-SH2 domain mutations in chronic myeloid leukemia patients on imatinib.	imatinib	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
20519627-1	2010	Point mutations in the kinase domain of BCR-ABL are the most common mechanism of drug resistance in chronic myeloid leukemia (CML) patients treated with ABL kinase inhibitors, including imatinib.	imatinib	186-194	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
20519627-1	2010	Point mutations in the kinase domain of BCR-ABL are the most common mechanism of drug resistance in chronic myeloid leukemia (CML) patients treated with ABL kinase inhibitors, including imatinib.	imatinib	186-194	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-47
20883053-1	2010	Imatinib is a protein-tyrosine kinase inhibitor with antitumour effects in patients with gastrointestinal stromal tumour (GIST) that is indicated for the treatment of unresectable and/or metastatic GIST and as adjuvant therapy in patients with KIT-positive GIST.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	244-247
20883053-2	2010	Imatinib binds to and inhibits KIT and platelet-derived growth factor receptor (PDGFR)-alpha tyrosine kinases, interfering with their downstream tumourogenic processes.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	31-34
20883053-2	2010	Imatinib binds to and inhibits KIT and platelet-derived growth factor receptor (PDGFR)-alpha tyrosine kinases, interfering with their downstream tumourogenic processes.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	80-85
20883053-3	2010	Cell lines with KIT mutations that are common in patients with GIST were sensitive to imatinib at low in vitro concentrations.	imatinib	86-94	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	16-19
20828158-1	2010	Inhibition of Bcr-Abl kinase activity by imatinib for the treatment of chronic myeloid leukemia (CML) currently serves as the paradigm for targeting dominant oncogenes with small molecules.	imatinib	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
20634379-0	2010	The poor response to imatinib observed in CML patients with low OCT-1 activity is not attributable to lower uptake of imatinib into their CD34+ cells.	imatinib	21-29	solute carrier family 22 member 1	Homo sapiens	64-69
20634379-1	2010	The functional activity of the organic cation transporter 1 (OCT-1) protein in chronic myeloid leukemia (CML) mononuclear cells (MNCs) is highly predictive of molecular response in imatinib treated patients.	imatinib	181-189	solute carrier family 22 member 1	Homo sapiens	31-59
20927104-5	2010	In addition, ETV1 is universally highly expressed in GISTs and is required for growth of imatinib-sensitive and resistant GIST cell lines.	imatinib	89-97	ETS variant transcription factor 1	Homo sapiens	13-17
20634379-1	2010	The functional activity of the organic cation transporter 1 (OCT-1) protein in chronic myeloid leukemia (CML) mononuclear cells (MNCs) is highly predictive of molecular response in imatinib treated patients.	imatinib	181-189	solute carrier family 22 member 1	Homo sapiens	61-66
20608939-0	2010	Trough plasma concentration of imatinib reflects BCR-ABL kinase inhibitory activity and clinical response in chronic-phase chronic myeloid leukemia: a report from the BINGO study.	imatinib	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
20019577-1	2010	BACKGROUND: Imatinib mesylate (Gleevec) was evaluated as a treatment for Merkel cell carcinoma (MCC, neuroendocrine carcinoma of the skin) based on the identification of strong c-KIT staining of these neoplasms.	imatinib	12-29	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	177-182
20019577-1	2010	BACKGROUND: Imatinib mesylate (Gleevec) was evaluated as a treatment for Merkel cell carcinoma (MCC, neuroendocrine carcinoma of the skin) based on the identification of strong c-KIT staining of these neoplasms.	imatinib	31-38	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	177-182
20453818-0	2010	A case of imatinib-naive ileal fibrous stromal tumor with unusual morphology and double PDGFRA mutation.	imatinib	10-18	platelet derived growth factor receptor alpha	Homo sapiens	88-94
20684544-12	2010	The SP could be targeted by addition of imatinib mesylate, a tyrosine kinase inhibitor which inhibits the ATPase activity of ABCG2, and prevents efflux of substrates.	imatinib	40-57	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	125-130
20701289-0	2010	A new intestinal cell culture model to discriminate the relative contribution of P-gp and BCRP on transport of substrates such as imatinib.	imatinib	130-138	phosphoglycolate phosphatase	Homo sapiens	81-85
20701289-0	2010	A new intestinal cell culture model to discriminate the relative contribution of P-gp and BCRP on transport of substrates such as imatinib.	imatinib	130-138	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	90-94
20701289-2	2010	Transport of some drugs, for example the tyrosine kinase inhibitor imatinib, is influenced by both P-gp and BCRP.	imatinib	67-75	phosphoglycolate phosphatase	Homo sapiens	99-103
20701289-2	2010	Transport of some drugs, for example the tyrosine kinase inhibitor imatinib, is influenced by both P-gp and BCRP.	imatinib	67-75	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	108-112
20701289-11	2010	Bidirectional transport studies with (14)C-imatinib revealed an abrogation of asymmetric transport when P-gp was knocked down, either in single or double knock-down clones compared to wild-type cells.	imatinib	43-51	phosphoglycolate phosphatase	Homo sapiens	104-108
20701289-14	2010	For imatinib transport, the contribution of P-gp seems to be more important compared to BCRP in this Caco-2 cell system.	imatinib	4-12	phosphoglycolate phosphatase	Homo sapiens	44-48
20943625-5	2010	Shortly after the detection of gain-of-function mutations in the type III receptor tyrosine kinases KIT and PDGFRalpha a targeted treatment with the tyrosine kinase inhibitor imatinib was introduced and became the gold standard in advanced GIST disease.	imatinib	175-183	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	100-103
20943625-5	2010	Shortly after the detection of gain-of-function mutations in the type III receptor tyrosine kinases KIT and PDGFRalpha a targeted treatment with the tyrosine kinase inhibitor imatinib was introduced and became the gold standard in advanced GIST disease.	imatinib	175-183	platelet derived growth factor receptor alpha	Homo sapiens	108-118
20417730-0	2010	Gaining insights into the Bcr-Abl activity-independent mechanisms of resistance to imatinib mesylate in KCL22 cells: a comparative proteomic approach.	imatinib	83-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
20417730-1	2010	Imatinib mesylate is a potent inhibitor of Bcr-Abl tyrosine kinase, an oncoprotein that plays a key role in the development of chronic myeloid leukemia.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
20417730-4	2010	Here we used the imatinib-resistant KCL22R and imatinib-sensitive KCL22S cells in which none of the known resistance mechanisms has been detected and hence novel Bcr-Abl activity-independent mechanisms could be envisaged.	imatinib	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-169
20690803-3	2010	Imatinib is more effective in patients with KIT exon 11 mutations compared with KIT exon 9 mutations and wild-type genotype, while sunitinib confers greater in vitro efficacy in patients with KIT exon 9 mutants and wild-type genotype than in KIT exon 11 mutants.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	44-47
20608939-4	2010	We further examined whether the C(min) level of imatinib actually reflects inhibitory activity against BCR-ABL kinase using the plasma inhibitory activity (PIA) assay.	imatinib	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
20608939-8	2010	There was a weak correlation between PIA against phospho (P)-BCR-ABL and the C(min) level of imatinib (r(2) = 0.2501, P = 0.0007), and patient plasma containing >974 ng/mL imatinib sufficiently inhibited P-BCR-ABL.	imatinib	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
20947481-4	2010	The introduction of the kinase inhibitor imatinib mesylate, and sunitinib in second line, against KIT and PDGFRA has provided the first evidence of directed therapy in GIST.	imatinib	41-58	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	98-101
20947481-4	2010	The introduction of the kinase inhibitor imatinib mesylate, and sunitinib in second line, against KIT and PDGFRA has provided the first evidence of directed therapy in GIST.	imatinib	41-58	platelet derived growth factor receptor alpha	Homo sapiens	106-112
20518073-1	2010	In previous in vitro studies, we showed that imatinib abrogated platelet-derived growth factor receptor alpha (PDGFRalpha) signaling, disrupting both breast cancer and smooth muscle cells (SMC).	imatinib	45-53	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	64-109
20597967-3	2010	The BCR/ABL1 kinase blocker imatinib shows major antileukaemic effects in most patients and is considered standard frontline therapy.	imatinib	28-36	BCR activator of RhoGEF and GTPase	Homo sapiens	4-7
20597967-3	2010	The BCR/ABL1 kinase blocker imatinib shows major antileukaemic effects in most patients and is considered standard frontline therapy.	imatinib	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-12
20607847-1	2010	In patients with chronic myeloid leukemia (CML), resistance against imatinib is associated with mutations in the kinase domain (KD) of the BCR-ABL1 fusion gene and/or with additional chromosomal abnormalities (ACAs) secondary to the Philadelphia chromosome.	imatinib	68-76	BCR activator of RhoGEF and GTPase	Homo sapiens	139-147
20425130-13	2010	The finding of a mutation in one of two acral melanomas suggests that KIT inhibitors, for example imatinib, which are already used in clinics for treatment of GIST, can also be used for melanoma.	imatinib	98-106	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	70-73
20633041-0	2010	WT1 peptide vaccine induces reduction in minimal residual disease in an Imatinib-treated CML patient.	imatinib	72-80	WT1 transcription factor	Homo sapiens	0-3
20633041-1	2010	How to treat CML patients who are resistant to inhibitors of BCR-ABL tyrosine kinase such as Imatinib is a very important and urgent issue in clinical hematology.	imatinib	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
20633041-2	2010	Here, we report a case of Imatinib-treated CML in which intradermally administered WT1 peptide vaccine elicited WT1-specific immune responses and the resultant reduction in the persistent residual disease in co-administration of Imatinib.	imatinib	26-34	WT1 transcription factor	Homo sapiens	83-86
20633041-2	2010	Here, we report a case of Imatinib-treated CML in which intradermally administered WT1 peptide vaccine elicited WT1-specific immune responses and the resultant reduction in the persistent residual disease in co-administration of Imatinib.	imatinib	26-34	WT1 transcription factor	Homo sapiens	112-115
20633041-2	2010	Here, we report a case of Imatinib-treated CML in which intradermally administered WT1 peptide vaccine elicited WT1-specific immune responses and the resultant reduction in the persistent residual disease in co-administration of Imatinib.	imatinib	229-237	WT1 transcription factor	Homo sapiens	83-86
20633041-6	2010	The case presented here indicates that WT1 peptide vaccine may become a safe and cure-oriented therapy for CML patients who have residual disease regardless of the treatment with Imatinib.	imatinib	179-187	WT1 transcription factor	Homo sapiens	39-42
20562316-9	2010	We also demonstrated that platelet-derived growth factor activated the PI3-k/Akt signaling pathway, while addition of imatinib mesylate reduced p-Akt expression.	imatinib	118-135	thymoma viral proto-oncogene 1	Mus musculus	146-149
21047493-0	2010	Imatinib as adjuvant treatment following resection of KIT-positive gastrointestinal stromal tumours.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	54-57
21047493-1	2010	This is a summary of the evidence review group (ERG) report on the clinical effectiveness and cost-effectiveness of adjuvant imatinib post resection of KIT-positive gastrointestinal stromal tumours (GISTs) compared with resection only in patients at significant risk of relapse.	imatinib	125-133	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	152-155
20811709-6	2010	Western blotting showed that imatinib treatment inhibited phosphorylation of PDGFRbeta, Akt, and Erk1/2 in the fibroblasts.	imatinib	29-37	platelet derived growth factor receptor beta	Homo sapiens	77-86
20811709-6	2010	Western blotting showed that imatinib treatment inhibited phosphorylation of PDGFRbeta, Akt, and Erk1/2 in the fibroblasts.	imatinib	29-37	AKT serine/threonine kinase 1	Homo sapiens	88-91
20811709-6	2010	Western blotting showed that imatinib treatment inhibited phosphorylation of PDGFRbeta, Akt, and Erk1/2 in the fibroblasts.	imatinib	29-37	mitogen-activated protein kinase 3	Homo sapiens	97-103
20659895-6	2010	C/EBPalpha activation induced changes in the expression of more cell cycle- and apoptosis-related genes than the other proteins and enhanced Imatinib-induced apoptosis of K562 cells.	imatinib	141-149	CCAAT enhancer binding protein alpha	Homo sapiens	0-10
20518073-1	2010	In previous in vitro studies, we showed that imatinib abrogated platelet-derived growth factor receptor alpha (PDGFRalpha) signaling, disrupting both breast cancer and smooth muscle cells (SMC).	imatinib	45-53	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	111-121
20518073-10	2010	Imatinib further inhibited PDGFRalpha expression and activity, as confirmed by the down-regulation of downstream Erk signaling pathway.	imatinib	0-8	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	27-37
20537386-3	2010	The treatment of CML was revolutionized by the introduction of imatinib mesylate (IM, Gleevec), a BCR-ABL tyrosine kinase inhibitor (TKI).	imatinib	63-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
20811403-6	2010	BCR-ABL1 DNA levels increased in all of the 10 patients who lost CMR soon after imatinib cessation, whereas serial testing of patients in sustained CMR showed a stable level of BCR-ABL1 DNA.	imatinib	80-88	BCR activator of RhoGEF and GTPase	Homo sapiens	0-8
20811403-7	2010	This more sensitive assay for BCR-ABL1 provides evidence that even patients who maintain a CMR after stopping imatinib may harbor residual leukemia.	imatinib	110-118	BCR activator of RhoGEF and GTPase	Homo sapiens	30-38
20811403-4	2010	We used a highly sensitive patient-specific nested quantitative PCR to look for evidence of genomic BCR-ABL1 DNA in patients who sustained CMR after stopping imatinib therapy.	imatinib	158-166	BCR activator of RhoGEF and GTPase	Homo sapiens	100-108
20537386-6	2010	The second-generation BCR-ABL TKIs nilotinib (Tasigna) and dasatinib (Sprycel), showed significant activity in clinical trials in patients intolerant or resistant to imatinib therapy, except in those patients with the T315I BCR-ABL mutation.	imatinib	166-174	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
20519366-10	2010	STI571 (a pharmacological inhibitor of c-Abl) or PFT co-injection prevented etoposide-induced up-regulation of phospho-p73 and pro-apoptotic TAp73 isoform levels.	imatinib	0-6	tumor protein p73	Rattus norvegicus	119-122
20849385-0	2010	Suppression of STAT5A increases chemotherapeutic sensitivity in imatinib-resistant and imatinib-sensitive K562 cells.	imatinib	64-72	signal transducer and activator of transcription 5A	Homo sapiens	15-21
20849385-0	2010	Suppression of STAT5A increases chemotherapeutic sensitivity in imatinib-resistant and imatinib-sensitive K562 cells.	imatinib	87-95	signal transducer and activator of transcription 5A	Homo sapiens	15-21
20849385-3	2010	The XTT cell proliferation assay showed that both sensitive and resistant K562 cells were sensitized to imatinib upon transfection with STAT5A siRNA.	imatinib	104-112	signal transducer and activator of transcription 5A	Homo sapiens	136-142
20589620-0	2010	Myeloid neoplasm with prominent eosinophilia and PDGFRA rearrangement treated with imatinib mesylate.	imatinib	83-100	platelet derived growth factor receptor alpha	Homo sapiens	49-55
20574046-0	2010	Properties of CD34+ CML stem/progenitor cells that correlate with different clinical responses to imatinib mesylate.	imatinib	98-115	CD34 molecule	Homo sapiens	14-18
20875551-2	2010	The introduction of imatinib, a tyrosine kinase inhibitor (TKI) specific for BCR-ABL, was a major breakthrough in CML therapy.	imatinib	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
20823226-4	2010	STI-571, a c-Abl-family kinase inhibitor, prevents the phosphorylation of parkin, maintaining parkin in a catalytically active and protective state.	imatinib	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-16
20548094-0	2010	Activity of the multitargeted kinase inhibitor, AT9283, in imatinib-resistant BCR-ABL-positive leukemic cells.	imatinib	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
20930519-3	2010	The success of targeted therapy with kinase inhibitors has been well documented with BCR-ABL, where imatinib specifically inhibits kinase activity with impressive pharmacological responses in chronic myelogenous leukemia (CML).	imatinib	100-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
20583816-1	2010	The Bcr-Abl and Lyn protein tyrosine kinases have been separately linked to the emergence of imatinib resistance in patients with chronic myelogenous leukemia.	imatinib	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
20583816-1	2010	The Bcr-Abl and Lyn protein tyrosine kinases have been separately linked to the emergence of imatinib resistance in patients with chronic myelogenous leukemia.	imatinib	93-101	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	16-19
20583816-3	2010	Multicolor monitoring revealed that an imatinib-resistant cell line (MYL-R) displays a remarkable 13-fold enhancement in Lyn kinase activity relative to its imatinib-sensitive counterpart (MYL).	imatinib	39-47	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	121-124
20583816-7	2010	Finally, studies with an activating SH2 ligand revealed that Lyn from imatinib-resistant MYL-R cells is primed and active, whereas Lyn from imatinib-sensitive cells is dependent upon phosphorylated SH2 ligands for activity.	imatinib	70-78	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	61-64
20583816-7	2010	Finally, studies with an activating SH2 ligand revealed that Lyn from imatinib-resistant MYL-R cells is primed and active, whereas Lyn from imatinib-sensitive cells is dependent upon phosphorylated SH2 ligands for activity.	imatinib	140-148	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	131-134
20807813-4	2010	Furthermore, a synthetic phosphotyrosyl peptide that binds to the CRKL SH2 domain with high affinity blocks association of endogenous CRKL with the p210(BCR-ABL) complex and reduces c-MYC levels in K562 human leukemic cells as well as in mouse hematopoietic cells transformed by p210(BCR-ABL) or the imatinib-resistant mutant T315I.	imatinib	300-308	v-crk avian sarcoma virus CT10 oncogene homolog-like	Mus musculus	66-70
20807813-4	2010	Furthermore, a synthetic phosphotyrosyl peptide that binds to the CRKL SH2 domain with high affinity blocks association of endogenous CRKL with the p210(BCR-ABL) complex and reduces c-MYC levels in K562 human leukemic cells as well as in mouse hematopoietic cells transformed by p210(BCR-ABL) or the imatinib-resistant mutant T315I.	imatinib	300-308	CRK like proto-oncogene, adaptor protein	Homo sapiens	134-138
20807813-4	2010	Furthermore, a synthetic phosphotyrosyl peptide that binds to the CRKL SH2 domain with high affinity blocks association of endogenous CRKL with the p210(BCR-ABL) complex and reduces c-MYC levels in K562 human leukemic cells as well as in mouse hematopoietic cells transformed by p210(BCR-ABL) or the imatinib-resistant mutant T315I.	imatinib	300-308	envoplakin	Mus musculus	148-152
20807813-4	2010	Furthermore, a synthetic phosphotyrosyl peptide that binds to the CRKL SH2 domain with high affinity blocks association of endogenous CRKL with the p210(BCR-ABL) complex and reduces c-MYC levels in K562 human leukemic cells as well as in mouse hematopoietic cells transformed by p210(BCR-ABL) or the imatinib-resistant mutant T315I.	imatinib	300-308	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
20807813-4	2010	Furthermore, a synthetic phosphotyrosyl peptide that binds to the CRKL SH2 domain with high affinity blocks association of endogenous CRKL with the p210(BCR-ABL) complex and reduces c-MYC levels in K562 human leukemic cells as well as in mouse hematopoietic cells transformed by p210(BCR-ABL) or the imatinib-resistant mutant T315I.	imatinib	300-308	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	182-187
20807813-4	2010	Furthermore, a synthetic phosphotyrosyl peptide that binds to the CRKL SH2 domain with high affinity blocks association of endogenous CRKL with the p210(BCR-ABL) complex and reduces c-MYC levels in K562 human leukemic cells as well as in mouse hematopoietic cells transformed by p210(BCR-ABL) or the imatinib-resistant mutant T315I.	imatinib	300-308	envoplakin	Mus musculus	279-283
20807813-4	2010	Furthermore, a synthetic phosphotyrosyl peptide that binds to the CRKL SH2 domain with high affinity blocks association of endogenous CRKL with the p210(BCR-ABL) complex and reduces c-MYC levels in K562 human leukemic cells as well as in mouse hematopoietic cells transformed by p210(BCR-ABL) or the imatinib-resistant mutant T315I.	imatinib	300-308	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	284-291
20806443-9	2010	CONCLUSION: Most patients with different genotypes of GIST and KIT exon 11-mutant will benefit from the individualized treatment of imatinib.	imatinib	132-140	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	63-66
20682400-0	2010	Chronic myeloid leukemia with a novel four-way t(6;13;9;22)(p21;q32;q34;q11.2) successfully treated with imatinib mesylate.	imatinib	105-122	H3 histone pseudogene 16	Homo sapiens	60-63
20674368-6	2010	Two molecules were identified with Kis about three orders of magnitude lower than reported for Imatinib.	imatinib	95-103	U2AF homology motif kinase 1	Homo sapiens	35-38
20811458-11	2010	We demonstrate that imatinib, an anticancer drug previously found to inhibit amyloid-beta formation without affecting Notch cleavage, achieves its amyloid-beta-lowering effect by preventing GSAP interaction with the gamma-secretase substrate, APP-CTF.	imatinib	20-28	gamma-secretase activating protein	Mus musculus	190-194
20553795-0	2010	In vitro and in vivo growth-inhibitory effects of cladribine on neoplastic mast cells exhibiting the imatinib-resistant KIT mutation D816V.	imatinib	101-109	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	120-123
20557306-1	2010	Treatment of CML with the tyrosine kinase inhibitor (TKI) imatinib mesylate results in the emergence of point mutations within the kinase domain (KD) of the BCR-ABL1 fusion transcript.	imatinib	58-66	BCR activator of RhoGEF and GTPase	Homo sapiens	157-165
20640942-1	2010	The introduction of imatinib mesylate, a Bcr-Abl1 tyrosine kinase inhibitor (TKI), has revolutionized the treatment of chronic myeloid leukemia (CML).	imatinib	20-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
20640942-2	2010	By directly targeting the Bcr-Abl kinase, imatinib leads to durable cytogenetic remissions and in turn improved survival.	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
20610572-9	2010	In high-fat-fed apolipoprotein E(-/-) mice, inhibition of PDGFRbeta activity by imatinib reduced aortic total lipid staining area by 35% (P < 0.05).	imatinib	80-88	platelet derived growth factor receptor, beta polypeptide	Mus musculus	58-67
20471447-1	2010	OBJECTIVE: The BCR-ABL mutation, T315I, is a common mutation and is resistant to both imatinib and second-generation Abl kinase inhibitors.	imatinib	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
20553795-1	2010	OBJECTIVE: In most patients with systemic mastocytosis (SM), including aggressive SM (ASM) and mast cell (MC) leukemia (MCL), neoplastic cells express the oncogenic KIT mutation D816V, which confers resistance to imatinib.	imatinib	213-221	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	165-168
20807977-0	2010	Successful treatment with low-dose imatinib mesylate of therapy-related myeloid neoplasm harboring TEL-PDGFRB in a patient with acute promyelocytic leukemia.	imatinib	35-52	ETS variant transcription factor 6	Homo sapiens	99-102
20922699-12	2010	Inhibitors of the BCR-Abl tyrosine kinase domain on the Philadelphia chromosome (imatinib, nilotinib and dasatinib) may cause acute renal failure.	imatinib	81-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
20621681-2	2010	Kit/Pdgfra inhibitors such as imatinib mesylate have increased progression-free survival in metastatic GIST but are not curative.	imatinib	30-47	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	0-3
20621681-2	2010	Kit/Pdgfra inhibitors such as imatinib mesylate have increased progression-free survival in metastatic GIST but are not curative.	imatinib	30-47	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	4-10
20621681-9	2010	The Kit(low)Cd44(+)Cd34(+) cells were resistant to in vitro Kit blockade, including by imatinib, and occurred in normal numbers in mice with reduced Kit signaling.	imatinib	87-95	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	4-7
20807977-0	2010	Successful treatment with low-dose imatinib mesylate of therapy-related myeloid neoplasm harboring TEL-PDGFRB in a patient with acute promyelocytic leukemia.	imatinib	35-52	platelet derived growth factor receptor beta	Homo sapiens	103-109
20206383-0	2010	Bcr-Abl-independent mechanism of resistance to imatinib in K562 cells: Induction of cyclooxygenase-2 (COX-2) by histone deacetylases (HDACs).	imatinib	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
20596030-6	2010	The forced expression of PTEN negatively regulated these signal pathways and sensitized EOL-1R cells to imatinib.	imatinib	104-112	phosphatase and tensin homolog	Homo sapiens	25-29
20596030-7	2010	Notably, hypermethylation of the promoter region of the PTEN gene in association with the downregulation of this gene"s transcripts was identified in imatinib-resistant leukemia cells isolated from individuals with CEL, CML and Philadelphia-positive acute lymphoblastic leukemia.	imatinib	150-158	phosphatase and tensin homolog	Homo sapiens	56-60
20596030-8	2010	In addition, anti-epigenetic agents restored PTEN expression, resulting in the sensitization of EOL-1R cells to imatinib.	imatinib	112-120	phosphatase and tensin homolog	Homo sapiens	45-49
20596030-9	2010	Taken together, epigenetic silence of PTEN is one of the mechanisms that cause drug resistance in individuals with leukemia after exposure to imatinib.	imatinib	142-150	phosphatase and tensin homolog	Homo sapiens	38-42
20726677-1	2010	BACKGROUND: Imatinib mesylate, an orally administered kinase inhibitor that targets the Kit (CD117) protein, currently has 10 approved indications including treatment of chronic myelogenous leukemia and metastatic gastrointestinal stromal tumors (GIST).	imatinib	12-29	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	93-98
20953927-0	2010	Multicenter phase II trial assessing effectiveness of imatinib mesylate on relapsed or refractory KIT-positive or PDGFR-positive sarcoma.	imatinib	54-71	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	98-101
20953927-3	2010	We conducted a multicenter Phase II trial of imatinib in patients with relapsed or refractory KIT-positive (excluding GISTs) or PDGFR-positive sarcomas.	imatinib	45-53	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	94-97
20953927-3	2010	We conducted a multicenter Phase II trial of imatinib in patients with relapsed or refractory KIT-positive (excluding GISTs) or PDGFR-positive sarcomas.	imatinib	45-53	platelet derived growth factor receptor beta	Homo sapiens	128-133
20206383-0	2010	Bcr-Abl-independent mechanism of resistance to imatinib in K562 cells: Induction of cyclooxygenase-2 (COX-2) by histone deacetylases (HDACs).	imatinib	47-55	prostaglandin-endoperoxide synthase 2	Homo sapiens	84-100
20206383-0	2010	Bcr-Abl-independent mechanism of resistance to imatinib in K562 cells: Induction of cyclooxygenase-2 (COX-2) by histone deacetylases (HDACs).	imatinib	47-55	prostaglandin-endoperoxide synthase 2	Homo sapiens	102-107
20206383-1	2010	Our previous studies have shown that overexpression of MDR1 and cyclooygenase-2 (COX-2) resulted in resistance development to imatinib in chronic myelogenous leukemia (CML) K562 (IR-K562) cells.	imatinib	126-134	ATP binding cassette subfamily B member 1	Homo sapiens	55-59
19653139-6	2010	hnRNPK expression levels in K562 cell line and imatinib-resistant leukemic cell line K562R, following the treatments with the inhibitors of Ras-MAPK (PD98059), PI3K/AKT (LY294002), JAK/STAT (AG490) signaling pathways, and BCR-ABL [imatinib mesylate (IM)], were also determined.	imatinib	47-55	heterogeneous nuclear ribonucleoprotein K	Homo sapiens	0-6
19653139-6	2010	hnRNPK expression levels in K562 cell line and imatinib-resistant leukemic cell line K562R, following the treatments with the inhibitors of Ras-MAPK (PD98059), PI3K/AKT (LY294002), JAK/STAT (AG490) signaling pathways, and BCR-ABL [imatinib mesylate (IM)], were also determined.	imatinib	231-248	heterogeneous nuclear ribonucleoprotein K	Homo sapiens	0-6
20206383-1	2010	Our previous studies have shown that overexpression of MDR1 and cyclooygenase-2 (COX-2) resulted in resistance development to imatinib in chronic myelogenous leukemia (CML) K562 (IR-K562) cells.	imatinib	126-134	prostaglandin-endoperoxide synthase 2	Homo sapiens	81-86
20718683-4	2010	Imatinib inhibits tyrosine kinase activity of Bcr-ABL and PDGF.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
20736294-2	2010	Imatinib inhibits Kit and is front-line therapy for GIST.	imatinib	0-8	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	18-21
20736294-6	2010	The SFKs Src and Lyn were active in GIST, and surprisingly, imatinib treatment stimulated their phosphorylation/activation.	imatinib	60-68	Rous sarcoma oncogene	Mus musculus	9-12
20736294-6	2010	The SFKs Src and Lyn were active in GIST, and surprisingly, imatinib treatment stimulated their phosphorylation/activation.	imatinib	60-68	LYN proto-oncogene, Src family tyrosine kinase	Mus musculus	17-20
20658618-9	2010	Up-regulation of CD117 in NB cells correlated with increased sensitivity for the kinase inhibitor imatinib mesylate.	imatinib	98-115	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	17-22
20419513-2	2010	The tyrosine kinase inhibitor (TKI) imatinib, which blocks the pro-fibrotic c-Abl kinase and PDGF receptor, is currently evaluated in clinical proof-of-concept trials for the treatment of patients with SSc.	imatinib	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-81
20809971-2	2010	The duplication of the Ph chromosome is a recurring abnormality acquired during disease progression, whereas intrachromosomal amplification of BCR/ABL1 is a rare phenomenon and has been associated with imatinib therapy resistance.	imatinib	202-210	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-151
20718683-5	2010	We hypothesize that patients with ATC that over-expresses PDGF receptors or cABL will respond to imatinib.	imatinib	97-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-80
20564078-6	2010	METHODS: The effect of combined imatinib mesylate (Gleevec) and TRAIL on EWS cell growth and apoptosis was tested in vitro.	imatinib	32-49	EWS RNA binding protein 1	Homo sapiens	73-76
20013807-9	2010	However, imatinib and sunitinib did induce secretion of anti-inflammatory IL-10 in macrophage cultures, indicating that treatment with these inhibitors might contribute to an immune suppressive microenvironment in GIST.	imatinib	9-17	interleukin 10	Homo sapiens	74-79
20564078-0	2010	Platelet-derived growth factor receptor beta inhibition increases tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) sensitivity: imatinib and TRAIL dual therapy.	imatinib	143-151	TNF superfamily member 10	Homo sapiens	66-121
20629201-1	2010	Imatinib, a selective inhibitor of c-KIT and Bcr-Abl tyrosine kinases, approved for the treatment of chronic myelogenous leukemia and gastrointestinal stromal tumors, shows further therapeutic potential for gliomas, glioblastoma, renal cell carcinoma, autoimmune nephritis and other neoplasms.	imatinib	0-8	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	35-40
20564078-0	2010	Platelet-derived growth factor receptor beta inhibition increases tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) sensitivity: imatinib and TRAIL dual therapy.	imatinib	143-151	TNF superfamily member 10	Homo sapiens	123-128
20564078-10	2010	RESULTS: Imatinib mesylate induced a significant TRAIL proapoptotic effect in EWS cells in vitro.	imatinib	9-26	TNF superfamily member 10	Homo sapiens	49-54
20564078-10	2010	RESULTS: Imatinib mesylate induced a significant TRAIL proapoptotic effect in EWS cells in vitro.	imatinib	9-26	EWS RNA binding protein 1	Homo sapiens	78-81
20564078-12	2010	The combination of imatinib mesylate and TRAIL significantly inhibited the growth of primary tumors and decreased the incidence of spontaneous EWS pulmonary metastasis compared with either drug alone.	imatinib	19-36	EWS RNA binding protein 1	Homo sapiens	143-146
20691121-3	2010	Imatinib mesylate is a selective inhibitor of bcr-abl, PRGFR alpha, beta and c-kit.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	77-82
20691121-11	2010	CONCLUSIONS: Imatinib treatment combined with radiotherapy leads in breast cancer cell lines to a significant benefit which might be influenced through inhibition of PDGFR phosphorylation.	imatinib	13-21	platelet derived growth factor receptor beta	Homo sapiens	166-171
20660757-1	2010	Although gastrointestinal stromal tumors (GISTs) harboring activating KIT or platelet-derived growth factor receptor A (PDGFRA) mutations respond to treatment with targeted KIT/PDGFRA inhibitors such as imatinib mesylate, these treatments are rarely curative.	imatinib	203-220	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	70-73
20660757-1	2010	Although gastrointestinal stromal tumors (GISTs) harboring activating KIT or platelet-derived growth factor receptor A (PDGFRA) mutations respond to treatment with targeted KIT/PDGFRA inhibitors such as imatinib mesylate, these treatments are rarely curative.	imatinib	203-220	platelet derived growth factor receptor alpha	Homo sapiens	77-118
20660757-1	2010	Although gastrointestinal stromal tumors (GISTs) harboring activating KIT or platelet-derived growth factor receptor A (PDGFRA) mutations respond to treatment with targeted KIT/PDGFRA inhibitors such as imatinib mesylate, these treatments are rarely curative.	imatinib	203-220	platelet derived growth factor receptor alpha	Homo sapiens	120-126
20660757-1	2010	Although gastrointestinal stromal tumors (GISTs) harboring activating KIT or platelet-derived growth factor receptor A (PDGFRA) mutations respond to treatment with targeted KIT/PDGFRA inhibitors such as imatinib mesylate, these treatments are rarely curative.	imatinib	203-220	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	173-176
20660757-1	2010	Although gastrointestinal stromal tumors (GISTs) harboring activating KIT or platelet-derived growth factor receptor A (PDGFRA) mutations respond to treatment with targeted KIT/PDGFRA inhibitors such as imatinib mesylate, these treatments are rarely curative.	imatinib	203-220	platelet derived growth factor receptor alpha	Homo sapiens	177-183
20615173-4	2010	Dasatinib is an oral kinase inhibitor of BCR-ABL that has been developed for treating CML patients across all phases of disease who are resistant or intolerant to imatinib.	imatinib	163-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
20702476-1	2010	The development of imatinib is a milestone in the treatment of chronic myeloid leukaemia (CML), and its therapeutic effect has been extensively investigated in patients with CML who carry M-bcr and m-bcr BCR-ABL fusion transcripts.	imatinib	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	204-211
20150913-5	2010	Cells expressing Gal3 and treated with the c-Abl/Arg inhibitor STI571, Gal3-depleted cells, and Gal3-depleted cells expressing Gal3 phosphorylation mutants all display an increased sensitivity to apoptosis-inducing agents.	imatinib	63-69	galectin 3	Homo sapiens	17-21
20150913-5	2010	Cells expressing Gal3 and treated with the c-Abl/Arg inhibitor STI571, Gal3-depleted cells, and Gal3-depleted cells expressing Gal3 phosphorylation mutants all display an increased sensitivity to apoptosis-inducing agents.	imatinib	63-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-48
20564079-1	2010	BACKGROUND: In KIT-expressing Ewing sarcoma cell lines, the addition of doxorubicin to imatinib increases apoptosis, compared with imatinib or doxorubicin alone.	imatinib	87-95	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	15-18
20423956-3	2010	We compared the interactions of the TKIs imatinib, nilotinib, and dasatinib with ABCB1 and ABCG2 in ex vivo and in vitro systems.	imatinib	41-49	ATP binding cassette subfamily B member 1	Homo sapiens	81-86
20423956-3	2010	We compared the interactions of the TKIs imatinib, nilotinib, and dasatinib with ABCB1 and ABCG2 in ex vivo and in vitro systems.	imatinib	41-49	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	91-96
20423956-10	2010	Taken together, the results suggest that therapeutic doses of imatinib and nilotinib may diminish the potential of ABCB1 and ABCG2 to limit oral absorption or confer resistance.	imatinib	62-70	ATP binding cassette subfamily B member 1	Homo sapiens	115-120
20423956-10	2010	Taken together, the results suggest that therapeutic doses of imatinib and nilotinib may diminish the potential of ABCB1 and ABCG2 to limit oral absorption or confer resistance.	imatinib	62-70	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	125-130
20670950-4	2010	RESULTS: After optimization, we obtained a biosensor that possesses higher sensitivity than that of established techniques with respect to measuring BCR-ABL activity and its suppression by imatinib.	imatinib	189-197	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
20565230-5	2010	The tyrosine kinase inhibitor, imatinib, is first-line treatment for FIP1L1-PDGFRA-positive patients).	imatinib	31-39	factor interacting with PAPOLA and CPSF1	Homo sapiens	69-75
20565230-5	2010	The tyrosine kinase inhibitor, imatinib, is first-line treatment for FIP1L1-PDGFRA-positive patients).	imatinib	31-39	platelet derived growth factor receptor alpha	Homo sapiens	76-82
20305142-6	2010	Moreover, in full-term cord blood erythroid cultures, kit ligand induced a marked increase of HbF (up to 80%) specifically abrogated by addition of the kit inhibitor imatinib, thus reversing the Hb switch.	imatinib	166-174	KIT ligand	Homo sapiens	54-64
20466781-0	2010	Plasma adiponectin levels are markedly elevated in imatinib-treated chronic myeloid leukemia (CML) patients: a mechanism for improved insulin sensitivity in type 2 diabetic CML patients?	imatinib	51-59	adiponectin, C1Q and collagen domain containing	Homo sapiens	7-18
20466781-0	2010	Plasma adiponectin levels are markedly elevated in imatinib-treated chronic myeloid leukemia (CML) patients: a mechanism for improved insulin sensitivity in type 2 diabetic CML patients?	imatinib	51-59	insulin	Homo sapiens	134-141
20466781-4	2010	We therefore hypothesized that imatinib therapy would be associated with an increase in peripheral and intramedullary adiposity and elevated plasma adiponectin levels.	imatinib	31-39	adiponectin, C1Q and collagen domain containing	Homo sapiens	148-159
20466781-5	2010	RESEARCH DESIGN AND METHODS: Adiponectin levels in CML patient plasma, at diagnosis and then during imatinib mesylate therapy, was measured using an ELISA.	imatinib	100-108	adiponectin, C1Q and collagen domain containing	Homo sapiens	29-40
20466781-9	2010	CONCLUSIONS: Elevated adiponectin levels in imatinib-treated CML patients provide a possible mechanism for improved glucose and lipid metabolism reported for some imatinib-treated patients.	imatinib	44-52	adiponectin, C1Q and collagen domain containing	Homo sapiens	22-33
20466781-9	2010	CONCLUSIONS: Elevated adiponectin levels in imatinib-treated CML patients provide a possible mechanism for improved glucose and lipid metabolism reported for some imatinib-treated patients.	imatinib	163-171	adiponectin, C1Q and collagen domain containing	Homo sapiens	22-33
19703239-1	2010	BACKGROUND: Imatinib mesylate (Gleevec) is a selective Bcr-Abl protein tyrosine-kinase inhibitor, and it also inhibits the receptor tyrosine kinases for stem cell factor (c-kit) and platelet-derived growth factor (PDGFR).	imatinib	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
19703239-1	2010	BACKGROUND: Imatinib mesylate (Gleevec) is a selective Bcr-Abl protein tyrosine-kinase inhibitor, and it also inhibits the receptor tyrosine kinases for stem cell factor (c-kit) and platelet-derived growth factor (PDGFR).	imatinib	12-29	KIT ligand	Homo sapiens	153-169
19703239-1	2010	BACKGROUND: Imatinib mesylate (Gleevec) is a selective Bcr-Abl protein tyrosine-kinase inhibitor, and it also inhibits the receptor tyrosine kinases for stem cell factor (c-kit) and platelet-derived growth factor (PDGFR).	imatinib	12-29	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	171-176
19703239-1	2010	BACKGROUND: Imatinib mesylate (Gleevec) is a selective Bcr-Abl protein tyrosine-kinase inhibitor, and it also inhibits the receptor tyrosine kinases for stem cell factor (c-kit) and platelet-derived growth factor (PDGFR).	imatinib	12-29	platelet derived growth factor receptor beta	Homo sapiens	182-212
19703239-1	2010	BACKGROUND: Imatinib mesylate (Gleevec) is a selective Bcr-Abl protein tyrosine-kinase inhibitor, and it also inhibits the receptor tyrosine kinases for stem cell factor (c-kit) and platelet-derived growth factor (PDGFR).	imatinib	12-29	platelet derived growth factor receptor beta	Homo sapiens	214-219
20658954-1	2010	The introduction of BCR-ABL tyrosine kinase inhibitors such as imatinib has changed the treatment of chronic myelogenous leukemia (CML).	imatinib	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
20031210-4	2010	The induction of FLT3 in CML cells attenuated imatinib-induced apoptosis.	imatinib	46-54	fms related receptor tyrosine kinase 3	Homo sapiens	17-21
20658954-6	2010	Patients who stopped imatinib for at least 3 weeks prior to HPC collection had significantly higher CD34+ cell yields (median: 6.52 x 10(6)/kg body weight) when compared with patients who continued imatinib through the collection (median: 3.74 x 10(6)/kg body weight).	imatinib	21-29	CD34 molecule	Homo sapiens	100-104
20031210-6	2010	An increased level of cleaved PARP and decreased level of pro-caspase 3 were noted when K562/FLT3-siRNA cells were treated with imatinib.	imatinib	128-136	poly(ADP-ribose) polymerase 1	Homo sapiens	30-34
20031210-6	2010	An increased level of cleaved PARP and decreased level of pro-caspase 3 were noted when K562/FLT3-siRNA cells were treated with imatinib.	imatinib	128-136	caspase 3	Homo sapiens	58-71
20031210-6	2010	An increased level of cleaved PARP and decreased level of pro-caspase 3 were noted when K562/FLT3-siRNA cells were treated with imatinib.	imatinib	128-136	fms related receptor tyrosine kinase 3	Homo sapiens	93-97
20658954-9	2010	In conclusion, a significant number of CD34+ cells can be safely collected in patients with CML who are on imatinib therapy, but CD34+ cell yields improve when imatinib is temporarily withheld.	imatinib	107-115	CD34 molecule	Homo sapiens	39-43
20658954-9	2010	In conclusion, a significant number of CD34+ cells can be safely collected in patients with CML who are on imatinib therapy, but CD34+ cell yields improve when imatinib is temporarily withheld.	imatinib	160-168	CD34 molecule	Homo sapiens	129-133
20599448-4	2010	Imatinib, an inhibitor of the tyrosine kinase ABL, the prototype of these targeting drugs, is yielding complete remissions in most CML patients.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-49
20164240-1	2010	We have previously demonstrated that chordomas express activated platelet-derived growth factor receptor (PDGFRB) and that treatment with imatinib, which is capable of switching off the activation of various receptor tyrosine kinases (RTKs) including PDGFRB, benefits a number of patients.	imatinib	138-146	platelet derived growth factor receptor beta	Homo sapiens	106-112
20813688-1	2010	OBJECTIVE: To investigate the changes in the expression of beta-catenin in patients with chronic myeloid leukemia (CML) in different phases, and explore the relationship between beta-catenin and the cytogenetic response to imatinib mesylate.	imatinib	223-240	catenin beta 1	Homo sapiens	178-190
20164240-1	2010	We have previously demonstrated that chordomas express activated platelet-derived growth factor receptor (PDGFRB) and that treatment with imatinib, which is capable of switching off the activation of various receptor tyrosine kinases (RTKs) including PDGFRB, benefits a number of patients.	imatinib	138-146	platelet derived growth factor receptor beta	Homo sapiens	251-257
20813688-6	2010	CONCLUSION: Beta-catenin overexpression in the progression of CML, consistent high level of beta-catenin or a positive transformation may indicate a poor response to imatinib, and early measures should be taken to increase the remission rate.	imatinib	166-174	catenin beta 1	Homo sapiens	92-104
20575039-0	2010	XPC genetic polymorphisms correlate with the response to imatinib treatment in patients with chronic phase chronic myeloid leukemia.	imatinib	57-65	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	0-3
20723293-0	2010	[Effects of STI571 combined with As2O3 on proliferation, apoptosis and caspase 3, Bcl-xL expression of K562 cells].	imatinib	12-18	caspase 3	Homo sapiens	71-80
20723293-0	2010	[Effects of STI571 combined with As2O3 on proliferation, apoptosis and caspase 3, Bcl-xL expression of K562 cells].	imatinib	12-18	BCL2 like 1	Homo sapiens	82-88
20723293-1	2010	This study was aimed to explore the effects of STI571 alone or with As2O3 on proliferation, apoptosis and caspase 3, bcl-xL mRNA expression of K562 cells, and the molecular mechanism of As2O3 enhancing the anti-leukemia effect of STI571 so as to provide the scientific basis for clinical treatment of chronic myeloid leukemia.	imatinib	47-53	caspase 3	Homo sapiens	106-115
20723293-8	2010	The STI571 combined with As2O3 can enhance these two effects, increase the expression of caspase-3 mRNA and decrease the expression of bcl-xL mRNA.	imatinib	4-10	caspase 3	Homo sapiens	89-98
20723293-8	2010	The STI571 combined with As2O3 can enhance these two effects, increase the expression of caspase-3 mRNA and decrease the expression of bcl-xL mRNA.	imatinib	4-10	BCL2 like 1	Homo sapiens	135-141
20723293-9	2010	Therefore, the effect of STI571 combined with As2O3 on expression of caspase 3 and bcl-xL mRNA may be one of molecular mechanisms underlying their synergic antileukemia efficacy.	imatinib	25-31	caspase 3	Homo sapiens	69-78
20723293-9	2010	Therefore, the effect of STI571 combined with As2O3 on expression of caspase 3 and bcl-xL mRNA may be one of molecular mechanisms underlying their synergic antileukemia efficacy.	imatinib	25-31	BCL2 like 1	Homo sapiens	83-89
20668669-7	2010	PR1-CTL were functionally anergic in one patient 6 months prior to cytogenetic relapse at 26 months after IFN withdrawal, and in three relapsed patients PR1-CTL were undetectable but re-emerged 3-6 months after starting imatinib.	imatinib	220-228	transmembrane protein 37	Homo sapiens	0-3
20486169-1	2010	Imatinib is an inhibitor of the BCR-ABL fusion gene product that characterizes chronic myeloid leukemia (CML), and of the related tyrosine kinases c-KIT and platelet-derived growth factor (PDGF) receptor.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
20486169-1	2010	Imatinib is an inhibitor of the BCR-ABL fusion gene product that characterizes chronic myeloid leukemia (CML), and of the related tyrosine kinases c-KIT and platelet-derived growth factor (PDGF) receptor.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	147-152
20452982-1	2010	The Bcr-Abl kinase inhibitor imatinib is remarkably effective in chronic myelogenous leukemia (CML), although drug resistance is an emerging problem.	imatinib	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
20452982-2	2010	Myeloid Src family kinases such as Hck and Lyn are often overexpressed in imatinib-resistant CML cells that lack Bcr-Abl mutations.	imatinib	74-82	HCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	35-38
20452982-2	2010	Myeloid Src family kinases such as Hck and Lyn are often overexpressed in imatinib-resistant CML cells that lack Bcr-Abl mutations.	imatinib	74-82	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	43-46
20452982-2	2010	Myeloid Src family kinases such as Hck and Lyn are often overexpressed in imatinib-resistant CML cells that lack Bcr-Abl mutations.	imatinib	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
20452982-3	2010	Here we tested whether Hck overexpression is sufficient to induce imatinib resistance using both wild-type Hck and a mutant (Hck-T338A) that is uniquely sensitive to the pyrazolo-pyrimidine inhibitor, NaPP1.	imatinib	66-74	HCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	23-26
20452982-5	2010	Treatment with NaPP1 restored sensitivity to imatinib in cells expressing T338A but not wild-type Hck, demonstrating that resistance requires Hck kinase activity.	imatinib	45-53	itchy E3 ubiquitin protein ligase	Homo sapiens	15-20
20452982-6	2010	NaPP1 also reduced Hck-mediated phosphorylation of Bcr-Abl at sites that may affect imatinib sensitivity exclusively in cells expressing Hck-T338A.	imatinib	84-92	itchy E3 ubiquitin protein ligase	Homo sapiens	0-5
20452982-6	2010	NaPP1 also reduced Hck-mediated phosphorylation of Bcr-Abl at sites that may affect imatinib sensitivity exclusively in cells expressing Hck-T338A.	imatinib	84-92	HCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	19-22
20452982-6	2010	NaPP1 also reduced Hck-mediated phosphorylation of Bcr-Abl at sites that may affect imatinib sensitivity exclusively in cells expressing Hck-T338A.	imatinib	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
20452982-7	2010	These data show that elevated Src family kinase activity is sufficient to induce imatinib resistance through a mechanism that may involve phosphorylation of Bcr-Abl.	imatinib	81-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-164
21086937-12	2010	Biological therapy with imatinib mesylate is recommended for patients with newly diagnosed, locally advanced, inoperable, or metastasizing gastrointestinal GISTs that express the c-KIT protein.	imatinib	24-41	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	179-184
20582941-2	2010	DFSP is characterized by a specific fusion of the platelet-derived growth factor beta (PDGFbeta) with the collagen type 1alpha1 (COL1alpha1) gene which renders these tumors responsive to targeted therapy with tyrosine kinase inhibitors, such as imatinib mesylate, as is reported in adults.	imatinib	245-262	platelet derived growth factor subunit B	Homo sapiens	87-95
20633291-3	2010	Single- and double-mutant isoforms of Kit were evaluated for their sensitivity to motesanib or imatinib in autophosphorylation assays and in Ba/F3 cell proliferation assays.	imatinib	95-103	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	38-41
20598160-3	2010	Furthermore, in advanced GIST disease with proven KIT exon 9 mutation the doubled daily dose of 800 mg imatinib increases the progression free survival and is now recommended both in the European and the American Guidelines.	imatinib	103-111	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	50-53
20575039-5	2010	ERCC5 and XPC SNPs correlated with the response to imatinib.	imatinib	51-59	ERCC excision repair 5, endonuclease	Homo sapiens	0-5
20575039-5	2010	ERCC5 and XPC SNPs correlated with the response to imatinib.	imatinib	51-59	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	10-13
20575039-6	2010	Haplotype analysis of XPC showed that the wild-type haplotype (499C-939A) was associated with a better response to imatinib.	imatinib	115-123	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	22-25
20307198-0	2010	Combination of fludarabine and imatinib induces apoptosis synergistically through loss of mitochondrial membrane potential and increases in caspase-3 enzyme activity in human K562 chronic myleloid leukemia cells.	imatinib	31-39	caspase 3	Homo sapiens	140-149
19862526-5	2010	Annexin V/propidium iodide staining revealed a significant enhancement of nilotinib-induced apoptosis in imatinib-resistant Ba/F3T315I and LAMA84-R cells upon combination with daunorubicin and mitoxantrone, respectively.	imatinib	105-113	annexin A5	Mus musculus	0-9
20489620-1	2010	PURPOSE OF REVIEW: Imatinib has exceptional activity in controlling gastrointestinal stromal tumor (GIST) due to inhibition of the constitutively active conformation of KIT and platelet-derived growth factor-alpha (PDGFRA), which is commonly seen in this tumor.	imatinib	19-27	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	169-172
20551067-3	2010	In this study, we show that myeloid cells expressing activated c-KIT mutants that are imatinib sensitive (V560G) or imatinib resistant (D816V) can inhibit the tumor suppressor activity of protein phosphatase 2A (PP2A).	imatinib	86-94	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	63-68
20551067-3	2010	In this study, we show that myeloid cells expressing activated c-KIT mutants that are imatinib sensitive (V560G) or imatinib resistant (D816V) can inhibit the tumor suppressor activity of protein phosphatase 2A (PP2A).	imatinib	86-94	protein phosphatase 2 phosphatase activator	Homo sapiens	212-216
20551067-3	2010	In this study, we show that myeloid cells expressing activated c-KIT mutants that are imatinib sensitive (V560G) or imatinib resistant (D816V) can inhibit the tumor suppressor activity of protein phosphatase 2A (PP2A).	imatinib	116-124	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	63-68
20551067-3	2010	In this study, we show that myeloid cells expressing activated c-KIT mutants that are imatinib sensitive (V560G) or imatinib resistant (D816V) can inhibit the tumor suppressor activity of protein phosphatase 2A (PP2A).	imatinib	116-124	protein phosphatase 2 phosphatase activator	Homo sapiens	212-216
20630823-0	2010	Phase II trial of imatinib maintenance therapy after irinotecan and cisplatin in patients with c-Kit-positive, extensive-stage small-cell lung cancer.	imatinib	18-26	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	95-100
20630823-2	2010	This trial was designed to evaluate irinotecan/cisplatin plus maintenance imatinib in patients with c-Kit-positive disease (the transmembrane receptor c-Kit is the product of the c-KIT protooncogene).	imatinib	74-82	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	100-105
20489620-1	2010	PURPOSE OF REVIEW: Imatinib has exceptional activity in controlling gastrointestinal stromal tumor (GIST) due to inhibition of the constitutively active conformation of KIT and platelet-derived growth factor-alpha (PDGFRA), which is commonly seen in this tumor.	imatinib	19-27	platelet derived growth factor receptor alpha	Homo sapiens	215-221
20571063-8	2010	In addition, hGal9 showed the additive growth-inhibitory effect with imatinib on CML cell lines.	imatinib	69-77	galectin 9	Homo sapiens	13-18
20509775-2	2010	The efforts in this area have been greatly enhanced by the approval of tyrosine kinase inhibitors with PDGFR inhibitory activity such as imatinib, sunitinib and sorafenib.	imatinib	137-145	platelet derived growth factor receptor beta	Homo sapiens	103-108
20179085-0	2010	Bone marrow mesenchymal stromal cells non-selectively protect chronic myeloid leukemia cells from imatinib-induced apoptosis via the CXCR4/CXCL12 axis.	imatinib	98-106	C-X-C motif chemokine receptor 4	Homo sapiens	133-138
20179085-0	2010	Bone marrow mesenchymal stromal cells non-selectively protect chronic myeloid leukemia cells from imatinib-induced apoptosis via the CXCR4/CXCL12 axis.	imatinib	98-106	C-X-C motif chemokine ligand 12	Homo sapiens	139-145
20179085-8	2010	Furthermore, chronic myeloid leukemia cells exposed to imatinib in the presence of mesenchymal stromal cells retained the ability to engraft into NOD/SCID mice.	imatinib	55-63	atrophin 1	Homo sapiens	146-149
20179085-10	2010	Finally, the CXCR4 antagonist, AMD3100 restored apoptosis by imatinib and the susceptibility of the SCID leukemia repopulating cells to the tyrosine kinase inhibitor.	imatinib	61-69	C-X-C motif chemokine receptor 4	Homo sapiens	13-18
20179085-12	2010	Disruption of the CXCL12/CXCR4 axis restores, at least in part, the leukemic cells" sensitivity to imatinib.	imatinib	99-107	C-X-C motif chemokine ligand 12	Homo sapiens	18-24
20179085-12	2010	Disruption of the CXCL12/CXCR4 axis restores, at least in part, the leukemic cells" sensitivity to imatinib.	imatinib	99-107	C-X-C motif chemokine receptor 4	Homo sapiens	25-30
20043176-1	2010	AIMS AND BACKGROUND: Most gastrointestinal stromal tumor (GIST) patients respond to KIT inhibition therapy of imatinib, but eventually become resistant with a median time to progression of 2 years.	imatinib	110-118	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	84-87
20043176-8	2010	Secondary KIT mutations were identified in 11/14 (78.6%) imatinib-acquired-resistance patients, with nine patients in KIT gene exon17, and the other two in exon 13.	imatinib	57-65	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	10-13
20043176-8	2010	Secondary KIT mutations were identified in 11/14 (78.6%) imatinib-acquired-resistance patients, with nine patients in KIT gene exon17, and the other two in exon 13.	imatinib	57-65	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	118-121
20043176-9	2010	The expressions of p-KIT, p-AKT, PCNA and BCL-2 were higher in the samples of imatinib-resistant GISTs than those of imatinib-responsive ones.	imatinib	78-86	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	21-24
20043176-9	2010	The expressions of p-KIT, p-AKT, PCNA and BCL-2 were higher in the samples of imatinib-resistant GISTs than those of imatinib-responsive ones.	imatinib	78-86	AKT serine/threonine kinase 1	Homo sapiens	28-31
20043176-9	2010	The expressions of p-KIT, p-AKT, PCNA and BCL-2 were higher in the samples of imatinib-resistant GISTs than those of imatinib-responsive ones.	imatinib	78-86	proliferating cell nuclear antigen	Homo sapiens	33-37
20043176-9	2010	The expressions of p-KIT, p-AKT, PCNA and BCL-2 were higher in the samples of imatinib-resistant GISTs than those of imatinib-responsive ones.	imatinib	78-86	BCL2 apoptosis regulator	Homo sapiens	42-47
20043176-10	2010	P-KIT, p-AKT expressions were higher in imatinib acquired-resistance GISTs with secondary KIT mutations than imatinib-responsive ones with primary mutation.	imatinib	40-48	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	2-5
20043176-10	2010	P-KIT, p-AKT expressions were higher in imatinib acquired-resistance GISTs with secondary KIT mutations than imatinib-responsive ones with primary mutation.	imatinib	40-48	AKT serine/threonine kinase 1	Homo sapiens	9-12
20043176-10	2010	P-KIT, p-AKT expressions were higher in imatinib acquired-resistance GISTs with secondary KIT mutations than imatinib-responsive ones with primary mutation.	imatinib	40-48	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	90-93
20043176-12	2010	CONCLUSIONS: Novel additional mutations of KIT gene exon 13 or exon 17 indicate the likely mechanism of secondary resistance to imatinib.	imatinib	128-136	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	43-46
20043176-13	2010	The PI3-K/AKT pathway might be more relevant than MEK/MAPK for therapeutic targeting in imatinib-resistant GIST patients with secondary mutation.	imatinib	88-96	AKT serine/threonine kinase 1	Homo sapiens	10-13
20043176-13	2010	The PI3-K/AKT pathway might be more relevant than MEK/MAPK for therapeutic targeting in imatinib-resistant GIST patients with secondary mutation.	imatinib	88-96	mitogen-activated protein kinase kinase 7	Homo sapiens	50-53
20508612-0	2010	Beneficial effects of combining a type II ATP competitive inhibitor with an allosteric competitive inhibitor of BCR-ABL for the treatment of imatinib-sensitive and imatinib-resistant CML.	imatinib	141-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
20508612-0	2010	Beneficial effects of combining a type II ATP competitive inhibitor with an allosteric competitive inhibitor of BCR-ABL for the treatment of imatinib-sensitive and imatinib-resistant CML.	imatinib	164-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
20139893-1	2010	Abl tyrosine kinase inhibitors (TKIs) such as imatinib and dasatinib are ineffective against Bcr-Abl(+) leukemic stem cells.	imatinib	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
20520639-1	2010	Nilotinib is a highly selective Bcr-Abl inhibitor approved for imatinib-resistant chronic myeloid leukemia (CML).	imatinib	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
20147328-1	2010	Previous studies have shown that during imatinib therapy, the decline of chronic myeloid leukaemia BCR-ABL transcript numbers involves a fast phase followed by a slow phase in averaged datasets.	imatinib	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
20440266-9	2010	This correlated with an increased protection from imatinib-induced apoptosis in Abl transformants.	imatinib	50-58	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	80-83
20658364-0	2010	[Expression of MDR1 and KIT in imatinib-resistant gastrointestinal stromal tumor cells].	imatinib	31-39	ATP binding cassette subfamily B member 1	Homo sapiens	15-19
20658364-0	2010	[Expression of MDR1 and KIT in imatinib-resistant gastrointestinal stromal tumor cells].	imatinib	31-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	24-27
20658364-1	2010	OBJECTIVE: To explore the relationship between imatinib resistance and genes MDR1 and KIT in gastrointestinal stromal tumor (GIST) cells.	imatinib	47-55	ATP binding cassette subfamily B member 1	Homo sapiens	77-81
20658364-1	2010	OBJECTIVE: To explore the relationship between imatinib resistance and genes MDR1 and KIT in gastrointestinal stromal tumor (GIST) cells.	imatinib	47-55	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	86-89
20658364-8	2010	CONCLUSIONS: Over-expression of gene MDR1 may be associated with imatinib resistance in GIST.	imatinib	65-73	ATP binding cassette subfamily B member 1	Homo sapiens	37-41
19875757-0	2010	Clinical relevance of vascular endothelial growth factor (VEGFA) and VEGF receptor (VEGFR2) gene polymorphism on the treatment outcome following imatinib therapy.	imatinib	145-153	vascular endothelial growth factor A	Homo sapiens	22-56
20533592-4	2010	Imatinib and sunitinib, both tyrosine kinase inhibitors directed to KIT, were approved for first- and second-line treatment of metastatic and unresectable GISTs.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	68-71
20305692-1	2010	The use of c-abl-specific inhibitors such as Imatinib (IM) or Dasatinib has revolutionized the treatment of chronic myeloid leukemia (CML).	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-16
20525481-4	2010	By inhibiting KIT, imatinib has a cytostatic and cytotoxic effect on melanomas with KIT mutations, and probably has the same effect on another subgroup of melanomas with other as yet imperfectly understood KIT mutations.	imatinib	19-27	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-17
20525481-4	2010	By inhibiting KIT, imatinib has a cytostatic and cytotoxic effect on melanomas with KIT mutations, and probably has the same effect on another subgroup of melanomas with other as yet imperfectly understood KIT mutations.	imatinib	19-27	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	84-87
20525481-4	2010	By inhibiting KIT, imatinib has a cytostatic and cytotoxic effect on melanomas with KIT mutations, and probably has the same effect on another subgroup of melanomas with other as yet imperfectly understood KIT mutations.	imatinib	19-27	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	84-87
19875757-6	2010	Haplotype analyses showed good correlations between VEGFR2 haplotype and CCyR and treatment failure to imatinib.	imatinib	103-111	kinase insert domain receptor	Homo sapiens	52-58
20585556-7	2010	HIV-1 Env-dependent cell-cell fusion, virus-cell fusion and infection were also inhibited by Abl kinase inhibitors, imatinib, nilotinib, and dasatinib.	imatinib	116-124	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	6-9
19875757-8	2010	CONCLUSION: The VEGFR2 gene polymorphism correlates with cytogenetic response, treatment failure following imatinib therapy for CML, while VEGFA genotype correlates with progression to advanced disease.	imatinib	107-115	kinase insert domain receptor	Homo sapiens	16-22
19875757-0	2010	Clinical relevance of vascular endothelial growth factor (VEGFA) and VEGF receptor (VEGFR2) gene polymorphism on the treatment outcome following imatinib therapy.	imatinib	145-153	kinase insert domain receptor	Homo sapiens	84-90
19875757-1	2010	BACKGROUND: Imatinib could reverse marrow angiogenesis and decrease the plasma level of vascular endothelial growth factor (VEGF) in chronic myeloid leukemia (CML) patients.	imatinib	12-20	vascular endothelial growth factor A	Homo sapiens	88-122
19875757-1	2010	BACKGROUND: Imatinib could reverse marrow angiogenesis and decrease the plasma level of vascular endothelial growth factor (VEGF) in chronic myeloid leukemia (CML) patients.	imatinib	12-20	vascular endothelial growth factor A	Homo sapiens	124-128
20497911-5	2010	Imatinib is used in the treatment of DFSP, characterized by a translocation of the gene PDGF, or in pigmented villonodular synovitis (PVNS), a tumor of soft part also locally aggressive, caused by an abnormality of the gene coding for the M-CSF.	imatinib	0-8	colony stimulating factor 1	Homo sapiens	239-244
20201077-13	2010	Inhibition of PDGF-B and TGFbeta pathways by treatment with imatinib restored the levels of miR-29a in vitro and in the bleomycin model in vivo.	imatinib	60-68	platelet derived growth factor subunit B	Homo sapiens	14-20
20201077-13	2010	Inhibition of PDGF-B and TGFbeta pathways by treatment with imatinib restored the levels of miR-29a in vitro and in the bleomycin model in vivo.	imatinib	60-68	transforming growth factor beta 1	Homo sapiens	25-32
20201077-13	2010	Inhibition of PDGF-B and TGFbeta pathways by treatment with imatinib restored the levels of miR-29a in vitro and in the bleomycin model in vivo.	imatinib	60-68	microRNA 29a	Homo sapiens	92-99
20451394-0	2010	Dual Src and Abl inhibitors target wild type Abl and the AblT315I Imatinib-resistant mutant with different mechanisms.	imatinib	66-74	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	5-8
20451394-0	2010	Dual Src and Abl inhibitors target wild type Abl and the AblT315I Imatinib-resistant mutant with different mechanisms.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
20451394-1	2010	The tyrosine kinase Src and its close homolog Abl, both play important roles in chronic myelogenous leukemia (CML) progression and Imatinib resistance.	imatinib	131-139	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	20-23
20451394-1	2010	The tyrosine kinase Src and its close homolog Abl, both play important roles in chronic myelogenous leukemia (CML) progression and Imatinib resistance.	imatinib	131-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-49
20222756-3	2010	Imatinib and dasatinib both target the tyrosine kinase activity of the BCR/ABL oncogenic fusion protein.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
20042273-0	2010	p21(Cip1) confers resistance to imatinib in human chronic myeloid leukemia cells.	imatinib	32-40	H3 histone pseudogene 16	Homo sapiens	0-3
20042273-0	2010	p21(Cip1) confers resistance to imatinib in human chronic myeloid leukemia cells.	imatinib	32-40	cyclin dependent kinase inhibitor 1A	Homo sapiens	4-8
20042273-1	2010	Imatinib is a Bcr-Abl inhibitor used as first-line therapy of chronic myeloid leukemia (CML).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
20042273-3	2010	We describe that imatinib down-regulates p21(Cip1) expression in CML cells.	imatinib	17-25	H3 histone pseudogene 16	Homo sapiens	41-44
20042273-3	2010	We describe that imatinib down-regulates p21(Cip1) expression in CML cells.	imatinib	17-25	cyclin dependent kinase inhibitor 1A	Homo sapiens	45-49
20042273-4	2010	Using K562 cells with inducible p21 expression and transient transfections we found that p21 confers partial resistance to imatinib-induced apoptosis.	imatinib	123-131	H3 histone pseudogene 16	Homo sapiens	32-35
20042273-4	2010	Using K562 cells with inducible p21 expression and transient transfections we found that p21 confers partial resistance to imatinib-induced apoptosis.	imatinib	123-131	H3 histone pseudogene 16	Homo sapiens	89-92
20042273-5	2010	This protection is not related to the G2-arrest provoked by p21, a decrease in the imatinib activity against Bcr-Abl or a cytoplasmic localization of p21.	imatinib	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
20042273-6	2010	The results suggest an involvement of p21(Cip1) in the response to imatinib in CML.	imatinib	67-75	H3 histone pseudogene 16	Homo sapiens	38-41
20042273-6	2010	The results suggest an involvement of p21(Cip1) in the response to imatinib in CML.	imatinib	67-75	cyclin dependent kinase inhibitor 1A	Homo sapiens	42-46
19754668-7	2010	In high fat fed ApoE(-/-) mice, imatinib reduced total lipid staining area by approximately 31% (P < 0.05).	imatinib	32-40	apolipoprotein E	Mus musculus	16-20
20529808-3	2010	The introduction of imatinib, a TK inhibitor (TKI) specific for BCR-ABL, was a major breakthrough in CML therapy.	imatinib	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
19728396-1	2010	A small subgroup of patients with hypereosinophilic syndrome (HES) demonstrates imatinib-sensitive fusion transcript-the FIP1L1-PDGFRA (F/P+).	imatinib	80-88	factor interacting with PAPOLA and CPSF1	Homo sapiens	121-127
19728396-1	2010	A small subgroup of patients with hypereosinophilic syndrome (HES) demonstrates imatinib-sensitive fusion transcript-the FIP1L1-PDGFRA (F/P+).	imatinib	80-88	platelet derived growth factor receptor alpha	Homo sapiens	128-134
20507731-12	2010	CONCLUSIONS: The MDR of K562/A02 cells may be partially reversed by imatinib or BrTet, and the mechanism may be related to the downregulation of mdr1 mRNA and P-gp expression and the upregulation of the rate of apoptosis in K562/A02 cells.	imatinib	68-76	ATP binding cassette subfamily B member 1	Homo sapiens	145-149
20507731-12	2010	CONCLUSIONS: The MDR of K562/A02 cells may be partially reversed by imatinib or BrTet, and the mechanism may be related to the downregulation of mdr1 mRNA and P-gp expression and the upregulation of the rate of apoptosis in K562/A02 cells.	imatinib	68-76	ATP binding cassette subfamily B member 1	Homo sapiens	159-163
19768693-1	2010	We analysed the dynamic change of imatinib-resistant mutations in BCR-ABL kinase domain focusing on T315I mutation during dasatinib or nilotinib therapy.	imatinib	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-73
19508387-0	2010	Inhibition of IGF-IR tyrosine kinase induces apoptosis and cell cycle arrest in imatinib-resistant chronic myeloid leukaemia cells.	imatinib	80-88	insulin like growth factor 1 receptor	Homo sapiens	14-20
19508387-8	2010	Importantly, inhibition of IGF-IR decreased the viability of cells resistant to imatinib mesylate including BaF3 cells transfected with p210 BCR-ABL mutants, CML cell lines and primary neoplastic cells from patients.	imatinib	80-97	insulin like growth factor 1 receptor	Homo sapiens	27-33
19508387-10	2010	Our findings suggest that IGF-IR could represent a potential molecular target particularly for advanced stage or imatinib-resistant cases.	imatinib	113-121	insulin like growth factor 1 receptor	Homo sapiens	26-32
20445575-0	2010	Synergistic activity of the Src/Abl inhibitor bosutinib in combination with imatinib.	imatinib	76-84	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	28-31
20367437-9	2010	The BCR-ABL fusion gene was over-expressed in five patients (5/18); the mean BCR-ABL/ABL ratio was 75.38 vs. 28.72 for imatinib responders, p < 0.001.	imatinib	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
20421539-0	2010	Functional activity of the OCT-1 protein is predictive of long-term outcome in patients with chronic-phase chronic myeloid leukemia treated with imatinib.	imatinib	145-153	solute carrier family 22 member 1	Homo sapiens	27-32
20421539-1	2010	PURPOSE: Organic cation transporter-1 (OCT-1) activity (OA), a measure of the OCT-1-mediated influx of imatinib into CML mononuclear cells (MNCs), is predictive of major molecular response (MMR) at 12 and 24 months in patients with untreated CML.	imatinib	103-111	solute carrier family 22 member 1	Homo sapiens	9-37
20421539-1	2010	PURPOSE: Organic cation transporter-1 (OCT-1) activity (OA), a measure of the OCT-1-mediated influx of imatinib into CML mononuclear cells (MNCs), is predictive of major molecular response (MMR) at 12 and 24 months in patients with untreated CML.	imatinib	103-111	solute carrier family 22 member 1	Homo sapiens	39-44
20421539-1	2010	PURPOSE: Organic cation transporter-1 (OCT-1) activity (OA), a measure of the OCT-1-mediated influx of imatinib into CML mononuclear cells (MNCs), is predictive of major molecular response (MMR) at 12 and 24 months in patients with untreated CML.	imatinib	103-111	solute carrier family 22 member 1	Homo sapiens	78-83
20006997-0	2010	OSU-03012 sensitizes TIB-196 myeloma cells to imatinib mesylate via AMP-activated protein kinase and STAT3 pathways.	imatinib	46-63	signal transducer and activator of transcription 3	Homo sapiens	101-106
20367437-9	2010	The BCR-ABL fusion gene was over-expressed in five patients (5/18); the mean BCR-ABL/ABL ratio was 75.38 vs. 28.72 for imatinib responders, p < 0.001.	imatinib	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-11
20445576-0	2010	hOCT1 transcript levels and single nucleotide polymorphisms as predictive factors for response to imatinib in chronic myeloid leukemia.	imatinib	98-106	solute carrier family 22 member 1	Homo sapiens	0-5
20500152-3	2010	Although previously refractory to any course of action but surgery, GIST heralded a triumph in targeted cancer therapy when administration of a specific first-generation tyrosine-kinase inhibitor Imatinib mesylate (STI571) was shown to inhibit c-Kit and demonstrated a significant increase in patient survival.	imatinib	196-213	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	244-249
20500152-7	2010	However, extensive research regarding both primary and secondary c-KIT mutations has illuminated the mechanisms of Imatinib resistance and has the potential to ameliorate this therapeutic setback.	imatinib	115-123	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	65-70
20233975-5	2010	Interestingly, although the parental cell line was strictly dependent on continuous signaling of the BCR-ABL oncogene, also termed oncogene addiction, reprogrammed cells lost this dependency and became resistant to the BCR-ABL inhibitor imatinib.	imatinib	237-245	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	219-226
19697154-5	2010	Cells incubated with STI571, a highly specific inhibitor of BCR/ABL, displayed resistance to these agents associated with an accelerated kinetics of DSBs repair, as measured by the neutral comet assay and pulsed field gel electrophoresis.	imatinib	21-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
19697154-6	2010	However, in a functional NHEJ assay, cells preincubated with STI571 repaired DSBs induced by a restriction enzyme with a lower efficacy than without the preincubation and addition of wortmannin, a specific inhibitor of DNA-PK(CS), did not change efficacy of the NHEJ reaction.	imatinib	61-67	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	219-229
20228846-0	2010	Imatinib resistance associated with BCR-ABL upregulation is dependent on HIF-1alpha-induced metabolic reprograming.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
20228846-0	2010	Imatinib resistance associated with BCR-ABL upregulation is dependent on HIF-1alpha-induced metabolic reprograming.	imatinib	0-8	hypoxia inducible factor 1 subunit alpha	Homo sapiens	73-83
20407778-8	2010	In pediatric populations, GISTs of the small intestine were expected to show a better response to imatinib treatment than gastric GISTs because of the alterations in the c-kit gene.	imatinib	98-106	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	170-175
20407438-1	2010	BACKGROUND: Imatinib is a direct and potent inhibitor of the constitutively active tyrosine kinase, breakpoint cluster region-Abelson (Bcr-Abl), which is central to the pathogenesis of chronic myeloid leukaemia (CML) patients.	imatinib	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-133
20482842-0	2010	Pristimerin induces apoptosis in imatinib-resistant chronic myelogenous leukemia cells harboring T315I mutation by blocking NF-kappaB signaling and depleting Bcr-Abl.	imatinib	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-165
20482842-2	2010	Bcr-Abl-T315I is the notorious point mutation that causes resistance to imatinib and the second generation tyrosine kinase inhibitors, leading to poor prognosis.	imatinib	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
20482842-5	2010	Additionally, pristimerin inhibited the growth of imatinib-resistant Bcr-Abl-T315I xenografts in nude mice.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
20482842-9	2010	The mRNA and protein levels of Bcr-Abl in imatinib-sensitive (KBM5) or imatinib-resistant (KBM5-T315I) CML cells were reduced after pristimerin treatment.	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
20482842-9	2010	The mRNA and protein levels of Bcr-Abl in imatinib-sensitive (KBM5) or imatinib-resistant (KBM5-T315I) CML cells were reduced after pristimerin treatment.	imatinib	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
20482842-10	2010	Further, inactivation of Bcr-Abl by imatinib pretreatment did not abrogate the TNFalpha-induced NF-kappaB activation while silencing p65 by siRNA did not affect the levels of Bcr-Abl, both results together indicating that NF-kappaB inactivation and Bcr-Abl inhibition may be parallel independent pathways.	imatinib	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
20228846-3	2010	In this study, we show that when BCR-ABL-transformed cell lines were selected for imatinib resistance in vitro, the cells that grew out displayed a higher BCR-ABL expression comparable to the increase seen in accelerated forms of the disease.	imatinib	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
20228846-3	2010	In this study, we show that when BCR-ABL-transformed cell lines were selected for imatinib resistance in vitro, the cells that grew out displayed a higher BCR-ABL expression comparable to the increase seen in accelerated forms of the disease.	imatinib	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-162
20228846-7	2010	The reduction in oxidative PPP-mediated ribose synthesis was compensated by the HIF-1alpha-dependent activation of the nonoxidative PPP enzyme, transketolase, in imatinib-resistant CML cells.	imatinib	162-170	hypoxia inducible factor 1 subunit alpha	Homo sapiens	80-90
20228846-7	2010	The reduction in oxidative PPP-mediated ribose synthesis was compensated by the HIF-1alpha-dependent activation of the nonoxidative PPP enzyme, transketolase, in imatinib-resistant CML cells.	imatinib	162-170	transketolase	Homo sapiens	144-157
20470368-7	2010	Secondary KIT mutations were additionally found in two of four samples obtained after imatinib treatment.	imatinib	86-94	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	10-13
20407438-1	2010	BACKGROUND: Imatinib is a direct and potent inhibitor of the constitutively active tyrosine kinase, breakpoint cluster region-Abelson (Bcr-Abl), which is central to the pathogenesis of chronic myeloid leukaemia (CML) patients.	imatinib	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
20337484-0	2010	Analysis of imatinib and sorafenib binding to p38alpha compared with c-Abl and b-Raf provides structural insights for understanding the selectivity of inhibitors targeting the DFG-out form of protein kinases.	imatinib	12-20	mitogen-activated protein kinase 14	Homo sapiens	46-54
20231287-0	2010	Role for the proapoptotic factor BIM in mediating imatinib-induced apoptosis in a c-KIT-dependent gastrointestinal stromal tumor cell line.	imatinib	50-58	BCL2 like 11	Homo sapiens	33-36
20231287-0	2010	Role for the proapoptotic factor BIM in mediating imatinib-induced apoptosis in a c-KIT-dependent gastrointestinal stromal tumor cell line.	imatinib	50-58	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	82-87
20231287-2	2010	The identification of selective inhibitors of c-KIT, such as imatinib, has provided a novel therapeutic approach in the treatment of this chemotherapy refractory tumor.	imatinib	61-69	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	46-51
20231287-4	2010	Here, we show that inhibition of c-KIT with imatinib in gastrointestinal stromal tumors (GISTs) triggered the up-regulation of the proapoptotic protein BIM via both transcriptional and post-translational mechanisms.	imatinib	44-52	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	33-38
20231287-4	2010	Here, we show that inhibition of c-KIT with imatinib in gastrointestinal stromal tumors (GISTs) triggered the up-regulation of the proapoptotic protein BIM via both transcriptional and post-translational mechanisms.	imatinib	44-52	BCL2 like 11	Homo sapiens	152-155
20231287-5	2010	The inhibition of c-KIT by imatinib increased levels of the dephosphorylated and deubiquitinated form of BIM as well as triggered the accumulation of the transcription factor FOXO3a on the BIM promoter to activate transcription of BIM mRNA.	imatinib	27-35	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	18-23
20231287-5	2010	The inhibition of c-KIT by imatinib increased levels of the dephosphorylated and deubiquitinated form of BIM as well as triggered the accumulation of the transcription factor FOXO3a on the BIM promoter to activate transcription of BIM mRNA.	imatinib	27-35	BCL2 like 11	Homo sapiens	105-108
20231287-5	2010	The inhibition of c-KIT by imatinib increased levels of the dephosphorylated and deubiquitinated form of BIM as well as triggered the accumulation of the transcription factor FOXO3a on the BIM promoter to activate transcription of BIM mRNA.	imatinib	27-35	forkhead box O3	Homo sapiens	175-181
20231287-5	2010	The inhibition of c-KIT by imatinib increased levels of the dephosphorylated and deubiquitinated form of BIM as well as triggered the accumulation of the transcription factor FOXO3a on the BIM promoter to activate transcription of BIM mRNA.	imatinib	27-35	BCL2 like 11	Homo sapiens	189-192
20231287-5	2010	The inhibition of c-KIT by imatinib increased levels of the dephosphorylated and deubiquitinated form of BIM as well as triggered the accumulation of the transcription factor FOXO3a on the BIM promoter to activate transcription of BIM mRNA.	imatinib	27-35	BCL2 like 11	Homo sapiens	189-192
20231287-6	2010	Furthermore, using RNA interference directed against BIM, we demonstrated that BIM knockdown attenuated the effects of imatinib, suggesting that BIM functionally contributes to imatinib-induced apoptosis in GIST.	imatinib	119-127	BCL2 like 11	Homo sapiens	79-82
20231287-6	2010	Furthermore, using RNA interference directed against BIM, we demonstrated that BIM knockdown attenuated the effects of imatinib, suggesting that BIM functionally contributes to imatinib-induced apoptosis in GIST.	imatinib	119-127	BCL2 like 11	Homo sapiens	79-82
20231287-6	2010	Furthermore, using RNA interference directed against BIM, we demonstrated that BIM knockdown attenuated the effects of imatinib, suggesting that BIM functionally contributes to imatinib-induced apoptosis in GIST.	imatinib	177-185	BCL2 like 11	Homo sapiens	79-82
20231287-6	2010	Furthermore, using RNA interference directed against BIM, we demonstrated that BIM knockdown attenuated the effects of imatinib, suggesting that BIM functionally contributes to imatinib-induced apoptosis in GIST.	imatinib	177-185	BCL2 like 11	Homo sapiens	79-82
20337484-5	2010	To improve our understanding of these determinants, we determined cocrystal structures of Imatinib and Sorafenib with p38alpha.	imatinib	90-98	mitogen-activated protein kinase 14	Homo sapiens	118-126
20337484-6	2010	We also conducted a detailed analysis of Imatinib and Sorafenib binding to p38alpha in comparison with BIRB-796, including binding kinetics, binding interactions, the solvent accessible surface area (SASA) of the ligands, and stabilization of key structural elements of the protein upon ligand binding.	imatinib	41-49	mitogen-activated protein kinase 14	Homo sapiens	75-83
20337484-2	2010	c-Abl and b-Raf are major targets of marketed oncology drugs Imatinib (Gleevec) and Sorafenib (Nexavar), respectively, and BIRB-796 is a p38alpha inhibitor that reached Phase II clinical trials.	imatinib	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
20337484-2	2010	c-Abl and b-Raf are major targets of marketed oncology drugs Imatinib (Gleevec) and Sorafenib (Nexavar), respectively, and BIRB-796 is a p38alpha inhibitor that reached Phase II clinical trials.	imatinib	61-69	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	10-15
20094798-0	2010	Enhancement of imatinib-induced apoptosis of BCR/ABL-expressing cells by nutlin-3 through synergistic activation of the mitochondrial apoptotic pathway.	imatinib	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
20094798-1	2010	The BCR/ABL tyrosine kinase inhibitor imatinib is highly effective for treatment of chronic myeloid leukemia (CML) and Philadelphia-chromosome positive (Ph+) acute lymphoblastic leukemia (ALL).	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
20094798-2	2010	However, relapses with emerging imatinib-resistance mutations in the BCR/ABL kinase domain pose a significant problem.	imatinib	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
20094798-4	2010	Moreover, nutlin-3 drastically enhanced imatinib-induced apoptosis in a p53-dependent manner in various BCR/ABL-expressing cells, which included primary leukemic cells from patients with CML blast crisis or Ph+ ALL and cells expressing the imatinib-resistant E255K BCR/ABL mutant.	imatinib	40-48	tumor protein p53	Homo sapiens	72-75
20094798-5	2010	Nutlin-3 and imatinib synergistically induced Bax activation, mitochondrial membrane depolarization, and caspase-3 cleavage leading to caspase-dependent apoptosis, which was inhibited by overexpression of Bcl-XL.	imatinib	13-21	BCL2 associated X, apoptosis regulator	Homo sapiens	46-49
20094798-5	2010	Nutlin-3 and imatinib synergistically induced Bax activation, mitochondrial membrane depolarization, and caspase-3 cleavage leading to caspase-dependent apoptosis, which was inhibited by overexpression of Bcl-XL.	imatinib	13-21	caspase 3	Homo sapiens	105-114
20094798-5	2010	Nutlin-3 and imatinib synergistically induced Bax activation, mitochondrial membrane depolarization, and caspase-3 cleavage leading to caspase-dependent apoptosis, which was inhibited by overexpression of Bcl-XL.	imatinib	13-21	BCL2 like 1	Homo sapiens	205-211
20094798-6	2010	Imatinib did not significantly affect the nutlin-3-induced expression of p53 but abrogated that of p21.	imatinib	0-8	H3 histone pseudogene 16	Homo sapiens	99-102
20094798-7	2010	Furthermore, activation of Bax as well as caspase-3 induced by combined treatment with imatinib and nutlin-3 was observed preferentially in cells expressing p21 at reduced levels.	imatinib	87-95	BCL2 associated X, apoptosis regulator	Homo sapiens	27-30
20094798-7	2010	Furthermore, activation of Bax as well as caspase-3 induced by combined treatment with imatinib and nutlin-3 was observed preferentially in cells expressing p21 at reduced levels.	imatinib	87-95	caspase 3	Homo sapiens	42-51
20094798-7	2010	Furthermore, activation of Bax as well as caspase-3 induced by combined treatment with imatinib and nutlin-3 was observed preferentially in cells expressing p21 at reduced levels.	imatinib	87-95	H3 histone pseudogene 16	Homo sapiens	157-160
20094798-8	2010	The present study indicates that combined treatment with nutlin-3 and imatinib activates p53 without inducing p21 and synergistically activates Bax-mediated intrinsic mitochondrial pathway to induce apoptosis in BCR/ABL-expressing cells.	imatinib	70-78	tumor protein p53	Homo sapiens	89-92
20094798-8	2010	The present study indicates that combined treatment with nutlin-3 and imatinib activates p53 without inducing p21 and synergistically activates Bax-mediated intrinsic mitochondrial pathway to induce apoptosis in BCR/ABL-expressing cells.	imatinib	70-78	H3 histone pseudogene 16	Homo sapiens	110-113
20094798-8	2010	The present study indicates that combined treatment with nutlin-3 and imatinib activates p53 without inducing p21 and synergistically activates Bax-mediated intrinsic mitochondrial pathway to induce apoptosis in BCR/ABL-expressing cells.	imatinib	70-78	BCL2 associated X, apoptosis regulator	Homo sapiens	144-147
20094798-8	2010	The present study indicates that combined treatment with nutlin-3 and imatinib activates p53 without inducing p21 and synergistically activates Bax-mediated intrinsic mitochondrial pathway to induce apoptosis in BCR/ABL-expressing cells.	imatinib	70-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	212-219
19643477-0	2010	mTOR inhibitor RAD001 (Everolimus) enhances the effects of imatinib in chronic myeloid leukemia by raising the nuclear expression of c-ABL protein.	imatinib	59-67	mechanistic target of rapamycin kinase	Homo sapiens	0-4
19701750-0	2010	LLL-3, a STAT3 inhibitor, represses BCR-ABL-positive cell proliferation, activates apoptosis and improves the effects of Imatinib mesylate.	imatinib	121-138	signal transducer and activator of transcription 3	Homo sapiens	9-14
19701750-2	2010	Here, we evaluated the effect of LLL-3, an inhibitor of STAT3 activity, on cell viability and its addictive effects with Imatinib mesylate (IM) treatment in BCR-ABL-positive cells.	imatinib	121-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-164
20079431-4	2010	The binding of GADS to Bcr-Abl requires Bcr-Abl tyrosine kinase activity and is sensitive to the Bcr-Abl inhibitor imatinib, while the GADS/Slp-76 and Slp-76/Nck interactions are tyrosine phosphorylation independent.	imatinib	115-123	GRB2 related adaptor protein 2	Homo sapiens	15-19
20079431-4	2010	The binding of GADS to Bcr-Abl requires Bcr-Abl tyrosine kinase activity and is sensitive to the Bcr-Abl inhibitor imatinib, while the GADS/Slp-76 and Slp-76/Nck interactions are tyrosine phosphorylation independent.	imatinib	115-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
20079431-4	2010	The binding of GADS to Bcr-Abl requires Bcr-Abl tyrosine kinase activity and is sensitive to the Bcr-Abl inhibitor imatinib, while the GADS/Slp-76 and Slp-76/Nck interactions are tyrosine phosphorylation independent.	imatinib	115-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
20079431-4	2010	The binding of GADS to Bcr-Abl requires Bcr-Abl tyrosine kinase activity and is sensitive to the Bcr-Abl inhibitor imatinib, while the GADS/Slp-76 and Slp-76/Nck interactions are tyrosine phosphorylation independent.	imatinib	115-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
20079431-4	2010	The binding of GADS to Bcr-Abl requires Bcr-Abl tyrosine kinase activity and is sensitive to the Bcr-Abl inhibitor imatinib, while the GADS/Slp-76 and Slp-76/Nck interactions are tyrosine phosphorylation independent.	imatinib	115-123	lymphocyte cytosolic protein 2	Homo sapiens	151-157
20079431-4	2010	The binding of GADS to Bcr-Abl requires Bcr-Abl tyrosine kinase activity and is sensitive to the Bcr-Abl inhibitor imatinib, while the GADS/Slp-76 and Slp-76/Nck interactions are tyrosine phosphorylation independent.	imatinib	115-123	NCK adaptor protein 1	Homo sapiens	158-161
20107158-5	2010	Furthermore, significant overexpression of PDGFRB was found in a patient with an eosinophilia-associated myeloproliferative neoplasm with uninformative cytogenetics and an excellent response to imatinib.	imatinib	194-202	platelet derived growth factor receptor beta	Homo sapiens	43-49
20020482-1	2010	Imatinib is an important anticancer drug, which binds specifically to the Abl kinase and blocks its signalling activity.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-77
20020482-8	2010	To apply the force field to imatinib:Abl simulations, it is also necessary to determine the most likely imatinib protonation state when it binds to Abl.	imatinib	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-40
20020482-8	2010	To apply the force field to imatinib:Abl simulations, it is also necessary to determine the most likely imatinib protonation state when it binds to Abl.	imatinib	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	148-151
20020482-8	2010	To apply the force field to imatinib:Abl simulations, it is also necessary to determine the most likely imatinib protonation state when it binds to Abl.	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	148-151
20020482-9	2010	This was done using molecular dynamics free energy simulations, where imatinib is reversibly protonated during a series of MD simulations, both in solution and in complex with Abl.	imatinib	70-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	176-179
20020482-10	2010	The simulations indicate that imatinib binds to Abl in its protonated, positively-charged form.	imatinib	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-51
20020482-11	2010	To help test the force field and the protonation prediction, we did MD free energy simulations that compare the Abl binding affinities of two imatinib analogs, obtaining good agreement with experiment.	imatinib	142-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-115
20020482-12	2010	Finally, two new imatinib variants were considered, one of which is predicted to have improved Abl binding.	imatinib	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-98
20164854-0	2010	KANK1, a candidate tumor suppressor gene, is fused to PDGFRB in an imatinib-responsive myeloid neoplasm with severe thrombocythemia.	imatinib	67-75	KN motif and ankyrin repeat domains 1	Homo sapiens	0-5
20164854-0	2010	KANK1, a candidate tumor suppressor gene, is fused to PDGFRB in an imatinib-responsive myeloid neoplasm with severe thrombocythemia.	imatinib	67-75	platelet derived growth factor receptor beta	Homo sapiens	54-60
20180814-12	2010	A KIT-independent mechanism, such as activation of other RTKs, might participate in the proliferation of late-stage GISTs and might be a cause of secondary imatinib resistance.	imatinib	156-164	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	2-5
20546334-10	2010	CONCLUSIONS: Overexpression of HSP90 is predictive of adverse behaviour in GISTs and may provide a therapeutic solution to the challenge of imatinib-resistant GISTs and other mesenchymal sarcomas.	imatinib	140-148	heat shock protein 90 alpha family class A member 1	Homo sapiens	31-36
19643477-0	2010	mTOR inhibitor RAD001 (Everolimus) enhances the effects of imatinib in chronic myeloid leukemia by raising the nuclear expression of c-ABL protein.	imatinib	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-138
19643477-2	2010	Accordingly, its inhibition by imatinib mesylate (IM) lets p145 c-ABL translocate into the nuclear compartment, which drives cell growth arrest and apoptotic death.	imatinib	31-48	POM121 transmembrane nucleoporin	Homo sapiens	59-63
19643477-2	2010	Accordingly, its inhibition by imatinib mesylate (IM) lets p145 c-ABL translocate into the nuclear compartment, which drives cell growth arrest and apoptotic death.	imatinib	31-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-69
20499309-4	2010	RESULTS: Three cases who showed response to imatinib carried primary mutations in KIT gene, with 2 cases possessing mutation in exon 11, 1 case in exon 13.	imatinib	44-52	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	82-85
27392989-3	2010	However, the absence of response among patients and the metabolic profile of imatinib (involving the CYP3A4) suggested the existence of a great interindividual variability.	imatinib	77-85	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	101-107
20442311-0	2010	Preclinical evaluation of nilotinib efficacy in an imatinib-resistant KIT-driven tumor model.	imatinib	51-59	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	70-73
20442311-4	2010	Nilotinib inhibited the proliferation of imatinib-responsive V560G-KIT FDC-P1 and imatinib-resistant D816V-KIT FDC-P1 cells with a GI(50) of 4.9 and 630 nmol/L, respectively, whereas apoptosis studies revealed that nilotinib and imatinib were equipotent against the V560G cell line.	imatinib	41-49	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	67-70
20442314-4	2010	Herein, we show that Bcr-Abl strongly downregulates the BRCA1 protein level, which is partially reversed on treatment with imatinib, an inhibitor of Bcr-Abl tyrosine kinase.	imatinib	123-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
20442314-4	2010	Herein, we show that Bcr-Abl strongly downregulates the BRCA1 protein level, which is partially reversed on treatment with imatinib, an inhibitor of Bcr-Abl tyrosine kinase.	imatinib	123-131	BRCA1 DNA repair associated	Homo sapiens	56-61
20442314-4	2010	Herein, we show that Bcr-Abl strongly downregulates the BRCA1 protein level, which is partially reversed on treatment with imatinib, an inhibitor of Bcr-Abl tyrosine kinase.	imatinib	123-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
20442314-8	2010	Additionally, Bcr-Abl-expressing cells showed resistance to death activated by spindle defects, reversed by imatinib.	imatinib	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
20699073-3	2010	However, the absence of response among patients and the metabolic profile of imatinib (involving the CYP3A4) suggested the existence of a great interindividual variability.	imatinib	77-85	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	101-107
20200154-2	2010	The cancer drug imatinib binds tightly to several homologous kinases, including Abl, but weakly to others, including Src.	imatinib	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
20200154-2	2010	The cancer drug imatinib binds tightly to several homologous kinases, including Abl, but weakly to others, including Src.	imatinib	16-24	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	117-120
20200154-3	2010	Imatinib specifically targets the inactive, so-called "DFG-out" conformation of Abl, which differs from the preferred, "DFG-in" conformation of Src in the orientation of a conserved Asp-Phe-Gly (DFG) activation loop.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
20200154-4	2010	However, recent x-ray structures showed that Src can also adopt the DFG-out conformation and uses it to bind imatinib.	imatinib	109-117	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	45-48
20200154-11	2010	Thus, conformational selection, easy in Abl, difficult in Src, underpins imatinib specificity.	imatinib	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-43
20499309-5	2010	One case with imatinib-resistance developed KIT secondary mutation, but all the cases had no PDGFRa mutation.	imatinib	14-22	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	44-47
20200154-11	2010	Thus, conformational selection, easy in Abl, difficult in Src, underpins imatinib specificity.	imatinib	73-81	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	58-61
20499309-6	2010	p-KIT and p-AKT expressions were higher in the samples of imatinib-resistant GIST than those of imatinib-responsive GIST.	imatinib	58-66	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	2-5
20200154-13	2010	Additional calculations show that conformational selection also governs the relative binding of imatinib to the kinases c-Kit and Lck.	imatinib	96-104	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	120-125
20200154-13	2010	Additional calculations show that conformational selection also governs the relative binding of imatinib to the kinases c-Kit and Lck.	imatinib	96-104	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	130-133
20499309-6	2010	p-KIT and p-AKT expressions were higher in the samples of imatinib-resistant GIST than those of imatinib-responsive GIST.	imatinib	58-66	AKT serine/threonine kinase 1	Homo sapiens	12-15
20499309-6	2010	p-KIT and p-AKT expressions were higher in the samples of imatinib-resistant GIST than those of imatinib-responsive GIST.	imatinib	96-104	AKT serine/threonine kinase 1	Homo sapiens	12-15
20499309-10	2010	The KIT secondary mutation and PI3-K/AKT/MTOR pathway are particularly relevant for therapeutic targeting in imatinib-resistant GIST.	imatinib	109-117	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	4-7
20499309-10	2010	The KIT secondary mutation and PI3-K/AKT/MTOR pathway are particularly relevant for therapeutic targeting in imatinib-resistant GIST.	imatinib	109-117	AKT serine/threonine kinase 1	Homo sapiens	37-40
20499309-10	2010	The KIT secondary mutation and PI3-K/AKT/MTOR pathway are particularly relevant for therapeutic targeting in imatinib-resistant GIST.	imatinib	109-117	mechanistic target of rapamycin kinase	Homo sapiens	41-45
20428337-8	2010	The present study showed that WT1 peptide vaccination in combination with TKI is feasible and effective in the therapy for imatinib-resistant CML.	imatinib	123-131	WT1 transcription factor	Homo sapiens	30-33
20053753-6	2010	Reversion of BCR-ABL, or treatment with imatinib, eradicates mature cells, whereas leukemic stem cells persist, giving rise to relapsed chronic myeloid leukemia on reinduction of BCR-ABL, or imatinib withdrawal.	imatinib	191-199	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
20372153-0	2010	Clinical responses observed with imatinib or sorafenib in melanoma patients expressing mutations in KIT.	imatinib	33-41	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	100-103
20164181-8	2010	In an in vitro kinase assay, DeltaTM-TPbeta was more active than TPbeta and less sensitive to imatinib, a PDGFR inhibitor.	imatinib	94-102	hydroxyacyl-CoA dehydrogenase trifunctional multienzyme complex subunit beta	Homo sapiens	37-43
20164181-8	2010	In an in vitro kinase assay, DeltaTM-TPbeta was more active than TPbeta and less sensitive to imatinib, a PDGFR inhibitor.	imatinib	94-102	platelet derived growth factor receptor beta	Homo sapiens	106-111
20194843-0	2010	Comparative In vitro cellular data alone are insufficient to predict clinical responses and guide the choice of BCR-ABL inhibitor for treating imatinib-resistant chronic myeloid leukemia.	imatinib	143-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
20425399-1	2010	The treatment of chronic myeloid leukemia (CML) drastically changed with the introduction of imatinib mesylate, a Bcr-Abl1 tyrosine kinase inhibitor (TKI), in 1998.	imatinib	93-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
20377918-4	2010	OBJECTIVE: To investigate the dynamic change of clonal proliferation of T cell receptor (TCR) Valpha and Vbeta subfamilies in one CML patient who developed Ph-negative acute lymphoblastic leukemia (ALL) after interferon and imatinib therapy.	imatinib	224-232	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	72-87
20377918-4	2010	OBJECTIVE: To investigate the dynamic change of clonal proliferation of T cell receptor (TCR) Valpha and Vbeta subfamilies in one CML patient who developed Ph-negative acute lymphoblastic leukemia (ALL) after interferon and imatinib therapy.	imatinib	224-232	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	89-92
20124512-7	2010	STI-571 (imatinib), a targeted therapy for BCR-ABL1(+) leukemias and inhibitor of c-Abl, platelet-derived growth factor receptor, and c-Kit, decreased endothelial apoptosis.	imatinib	0-7	BCR activator of RhoGEF and GTPase	Homo sapiens	43-51
20124512-7	2010	STI-571 (imatinib), a targeted therapy for BCR-ABL1(+) leukemias and inhibitor of c-Abl, platelet-derived growth factor receptor, and c-Kit, decreased endothelial apoptosis.	imatinib	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-87
20124512-7	2010	STI-571 (imatinib), a targeted therapy for BCR-ABL1(+) leukemias and inhibitor of c-Abl, platelet-derived growth factor receptor, and c-Kit, decreased endothelial apoptosis.	imatinib	0-7	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	134-139
20124512-7	2010	STI-571 (imatinib), a targeted therapy for BCR-ABL1(+) leukemias and inhibitor of c-Abl, platelet-derived growth factor receptor, and c-Kit, decreased endothelial apoptosis.	imatinib	9-17	BCR activator of RhoGEF and GTPase	Homo sapiens	43-51
20124512-7	2010	STI-571 (imatinib), a targeted therapy for BCR-ABL1(+) leukemias and inhibitor of c-Abl, platelet-derived growth factor receptor, and c-Kit, decreased endothelial apoptosis.	imatinib	9-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	134-139
20425400-3	2010	The known molecular basis of CML has enabled the development of Abl-specific tyrosine kinase inhibitors, such as imatinib mesylate.	imatinib	113-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-67
20054526-0	2010	CYP3A activity influences imatinib response in patients with chronic myeloid leukemia: a pilot study on in vivo CYP3A activity.	imatinib	26-34	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-5
20446917-2	2010	By using RNA interference-mediated knockdown of MDR1, we have investigated and compared the specific functional consequence of Pgp on the cellular disposition of the major clinically in use TKIs imatinib, dasatinib, nilotinib, sunitinib and sorafenib.	imatinib	195-203	ATP binding cassette subfamily B member 1	Homo sapiens	127-130
20446917-4	2010	In these conditions, abrogating specifically Pgp-mediated efflux in vitro revealed the remarkable and statistically significant cellular accumulation of imatinib (difference in cellular levels between Pgp-expressing and silenced cells, at high and low incubation concentration, respectively: 6.1 and 6.6), dasatinib (4.9 and 5.6), sunitinib (3.7 and 7.3) and sorafenib (1.2 and 1.4), confirming that these TKIs are all substrates of Pgp.	imatinib	153-161	ATP binding cassette subfamily B member 1	Homo sapiens	45-48
20446917-4	2010	In these conditions, abrogating specifically Pgp-mediated efflux in vitro revealed the remarkable and statistically significant cellular accumulation of imatinib (difference in cellular levels between Pgp-expressing and silenced cells, at high and low incubation concentration, respectively: 6.1 and 6.6), dasatinib (4.9 and 5.6), sunitinib (3.7 and 7.3) and sorafenib (1.2 and 1.4), confirming that these TKIs are all substrates of Pgp.	imatinib	153-161	ATP binding cassette subfamily B member 1	Homo sapiens	201-204
20446917-4	2010	In these conditions, abrogating specifically Pgp-mediated efflux in vitro revealed the remarkable and statistically significant cellular accumulation of imatinib (difference in cellular levels between Pgp-expressing and silenced cells, at high and low incubation concentration, respectively: 6.1 and 6.6), dasatinib (4.9 and 5.6), sunitinib (3.7 and 7.3) and sorafenib (1.2 and 1.4), confirming that these TKIs are all substrates of Pgp.	imatinib	153-161	ATP binding cassette subfamily B member 1	Homo sapiens	201-204
20054526-4	2010	We designed this study to investigate the role of the CYP3A activity in the response to imatinib therapy.	imatinib	88-96	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	54-59
20054526-9	2010	CONCLUSIONS: These results indicate a clinical significance of the CYP3A activity and its metabolic products in CML patients treated with imatinib.	imatinib	138-146	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	67-72
20147973-0	2010	Lck is a key target of imatinib and dasatinib in T-cell activation.	imatinib	23-31	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	0-3
20717479-4	2010	Interestingly, this compound also directly inhibits the kinase activity of both wild-type and imatinib-resistant (T315I) forms of the BCR-ABL kinase.	imatinib	94-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
19768386-1	2010	Imatinib, an orally administered tyrosine kinase inhibitor of PDGF receptor, c-abl and c-kit, is currently in clinical trials to assess its efficacy in malignant gliomas.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-82
19768386-1	2010	Imatinib, an orally administered tyrosine kinase inhibitor of PDGF receptor, c-abl and c-kit, is currently in clinical trials to assess its efficacy in malignant gliomas.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	87-92
20146241-10	2010	On the other hand, the Abl/Kit inhibitor imatinib did not affect cell growth or apoptosis in the four types of spheroids.	imatinib	41-49	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	27-30
20147974-9	2010	These results indicate that low imatinib accumulation in primitive CML cells, mediated through reduced OCT-1 Activity may be a critical determinant of long-term disease persistence.	imatinib	32-40	solute carrier family 22 member 1	Homo sapiens	103-108
19833389-0	2010	A thrombocytosis occurring in Philadelphia positive CML in molecular response to imatinib can reveal an underlying JAK2(V617F) myeloproliferative neoplasm.	imatinib	81-89	Janus kinase 2	Homo sapiens	115-119
20147974-0	2010	Chronic myeloid leukemia CD34+ cells have reduced uptake of imatinib due to low OCT-1 activity.	imatinib	60-68	CD34 molecule	Homo sapiens	25-29
20147974-0	2010	Chronic myeloid leukemia CD34+ cells have reduced uptake of imatinib due to low OCT-1 activity.	imatinib	60-68	solute carrier family 22 member 1	Homo sapiens	80-85
20147974-1	2010	Active influx of imatinib in chronic myeloid leukemia (CML) cells is mediated by the organic cation transporter 1 (OCT-1).	imatinib	17-25	solute carrier family 22 member 1	Homo sapiens	85-113
20147974-1	2010	Active influx of imatinib in chronic myeloid leukemia (CML) cells is mediated by the organic cation transporter 1 (OCT-1).	imatinib	17-25	solute carrier family 22 member 1	Homo sapiens	115-120
20147974-2	2010	Functional activity of OCT-1 (OCT-1 Activity) in mononuclear cells is an excellent predictor of molecular response over the first 24 months of imatinib therapy for chronic phase patients.	imatinib	143-151	solute carrier family 22 member 1	Homo sapiens	23-28
20147974-2	2010	Functional activity of OCT-1 (OCT-1 Activity) in mononuclear cells is an excellent predictor of molecular response over the first 24 months of imatinib therapy for chronic phase patients.	imatinib	143-151	solute carrier family 22 member 1	Homo sapiens	30-35
20147974-4	2010	We investigated whether alterations in the expression and function of OCT-1 have a role in imatinib resistance in progenitors.	imatinib	91-99	solute carrier family 22 member 1	Homo sapiens	70-75
20213318-3	2010	Inhibition of v-Abl by addition of the small molecule inhibitor STI-571 causes these cells to arrest in the G1 phase of the cell cycle prior to undergoing apoptosis.	imatinib	64-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
20167399-0	2010	[Efficiency of imatinib in polyserositis revealing a FIP1L1-PDGFRA-negative hypereosinophilic syndrome].	imatinib	15-23	factor interacting with PAPOLA and CPSF1	Homo sapiens	53-59
20371728-7	2010	STI571 inhibits IR-induced RelB nuclear translocation, leading to increased radiosensitivity in aggressive androgen-independent PC-3 and DU-145 cells.	imatinib	0-6	RELB proto-oncogene, NF-kB subunit	Homo sapiens	27-31
20371728-10	2010	STI571 inhibits the phosphoinositide 3-kinase-AKT-IkappaB kinase-alpha pathway in PC-3 cells by decreasing the phosphorylation levels of phosphoinositide 3-kinase (Tyr458) and AKT (Ser473), whereas STI571 increases NF-kappaB inducible kinase (Thr559) phosphorylation, leading to activation of IkappaB kinase-alpha in LNCaP cells.	imatinib	0-6	AKT serine/threonine kinase 1	Homo sapiens	46-49
20371728-10	2010	STI571 inhibits the phosphoinositide 3-kinase-AKT-IkappaB kinase-alpha pathway in PC-3 cells by decreasing the phosphorylation levels of phosphoinositide 3-kinase (Tyr458) and AKT (Ser473), whereas STI571 increases NF-kappaB inducible kinase (Thr559) phosphorylation, leading to activation of IkappaB kinase-alpha in LNCaP cells.	imatinib	0-6	component of inhibitor of nuclear factor kappa B kinase complex	Homo sapiens	50-70
20371728-10	2010	STI571 inhibits the phosphoinositide 3-kinase-AKT-IkappaB kinase-alpha pathway in PC-3 cells by decreasing the phosphorylation levels of phosphoinositide 3-kinase (Tyr458) and AKT (Ser473), whereas STI571 increases NF-kappaB inducible kinase (Thr559) phosphorylation, leading to activation of IkappaB kinase-alpha in LNCaP cells.	imatinib	0-6	AKT serine/threonine kinase 1	Homo sapiens	176-179
20371728-10	2010	STI571 inhibits the phosphoinositide 3-kinase-AKT-IkappaB kinase-alpha pathway in PC-3 cells by decreasing the phosphorylation levels of phosphoinositide 3-kinase (Tyr458) and AKT (Ser473), whereas STI571 increases NF-kappaB inducible kinase (Thr559) phosphorylation, leading to activation of IkappaB kinase-alpha in LNCaP cells.	imatinib	0-6	component of inhibitor of nuclear factor kappa B kinase complex	Homo sapiens	293-313
20371728-11	2010	These results reveal that STI571 exhibits differential effects on the upstream kinases leading to different downstream effects on the NF-kappaB alternative pathway in prostate cancer cells and suggest that STI571 is effective for the treatment of androgen-independent prostate cancer in the context of high constitutive levels of RelB.	imatinib	26-32	RELB proto-oncogene, NF-kB subunit	Homo sapiens	330-334
20167399-3	2010	A response to imatinib has also been reported in FIP1L1-PDGFRA-negative hypereosinophilic syndromes.	imatinib	14-22	platelet derived growth factor receptor alpha	Homo sapiens	56-62
20394535-0	2010	Imatinib-loaded polyelectrolyte microcapsules for sustained targeting of BCR-ABL+ leukemia stem cells.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
20095048-2	2010	Biophysical, biochemical, and structural studies have provided insight into the molecular basis of resistance to the KIT inhibitors, imatinib and sunitinib.	imatinib	133-141	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	117-120
20167399-8	2010	CONCLUSION: This report evidences the association of polyserositis with hypereosinophilic syndromes and the potential efficacy of imatinib mesylate even in FIP1L1-PDGFRA-negative patients.	imatinib	130-138	factor interacting with PAPOLA and CPSF1	Homo sapiens	156-162
20167399-0	2010	[Efficiency of imatinib in polyserositis revealing a FIP1L1-PDGFRA-negative hypereosinophilic syndrome].	imatinib	15-23	platelet derived growth factor receptor alpha	Homo sapiens	60-66
20167399-8	2010	CONCLUSION: This report evidences the association of polyserositis with hypereosinophilic syndromes and the potential efficacy of imatinib mesylate even in FIP1L1-PDGFRA-negative patients.	imatinib	130-138	platelet derived growth factor receptor alpha	Homo sapiens	163-169
20167399-2	2010	Imatinib mesylate is the reference treatment for myeloid variants of FIP1L1-PDGFRA-positive hypereosinophilic syndromes.	imatinib	0-17	factor interacting with PAPOLA and CPSF1	Homo sapiens	69-75
20167399-2	2010	Imatinib mesylate is the reference treatment for myeloid variants of FIP1L1-PDGFRA-positive hypereosinophilic syndromes.	imatinib	0-17	platelet derived growth factor receptor alpha	Homo sapiens	76-82
20303627-8	2010	Some FIPL1-PDGFRA negative patients respond to imatinib, suggesting the role of other tyrosine kinases (or other partners than FIP1L1 in a fusion gene implicating PDGFRA).	imatinib	47-55	platelet derived growth factor receptor alpha	Homo sapiens	11-17
20303627-8	2010	Some FIPL1-PDGFRA negative patients respond to imatinib, suggesting the role of other tyrosine kinases (or other partners than FIP1L1 in a fusion gene implicating PDGFRA).	imatinib	47-55	platelet derived growth factor receptor alpha	Homo sapiens	163-169
20167399-3	2010	A response to imatinib has also been reported in FIP1L1-PDGFRA-negative hypereosinophilic syndromes.	imatinib	14-22	factor interacting with PAPOLA and CPSF1	Homo sapiens	49-55
20360932-6	2010	In keratinocyte-melanoma cocultures stained for the Ki67 proliferation marker, incubation with KGF induced enhanced growth not only of the keratinocytes but also of the melanoma cells, which could be blocked by the c-KIT inhibitor imatinib, demonstrating the establishment of a KGF-induced paracrine signaling network owing to the coexpression of biologically active SCF released from keratinocytes and functional c-KIT on melanoma cells.	imatinib	231-239	fibroblast growth factor 7	Homo sapiens	95-98
20064605-5	2010	The molecularly targeted cancer therapeutics, sunitinib and imatinib, exhibited profound effects on Ca(i)(2+), combining effects of cytotoxic chemotherapeutics, TdP inducers and potent hERG channel blockers.	imatinib	60-68	ETS transcription factor ERG	Homo sapiens	185-189
20360932-6	2010	In keratinocyte-melanoma cocultures stained for the Ki67 proliferation marker, incubation with KGF induced enhanced growth not only of the keratinocytes but also of the melanoma cells, which could be blocked by the c-KIT inhibitor imatinib, demonstrating the establishment of a KGF-induced paracrine signaling network owing to the coexpression of biologically active SCF released from keratinocytes and functional c-KIT on melanoma cells.	imatinib	231-239	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	215-220
20153728-0	2010	Spred2 is involved in imatinib-induced cytotoxicity in chronic myeloid leukemia cells.	imatinib	22-30	sprouty related EVH1 domain containing 2	Homo sapiens	0-6
20153728-6	2010	In K562 cells and primary CML cells, imatinib induces endogenous Spred2 expression.	imatinib	37-45	sprouty related EVH1 domain containing 2	Homo sapiens	65-71
20153728-7	2010	Spred2 silencing by stable RNA interference partly protects K562 cells against imatinib-induced apoptosis.	imatinib	79-87	sprouty related EVH1 domain containing 2	Homo sapiens	0-6
20153728-8	2010	Together, these data implicate Spred2 in imatinib-induced cytotoxicity in CML cells, possibly by inhibiting the Ras-ERK cascade and the pro-survival signaling molecules SPHK1 and Mcl-1.	imatinib	41-49	sprouty related EVH1 domain containing 2	Homo sapiens	31-37
20153728-8	2010	Together, these data implicate Spred2 in imatinib-induced cytotoxicity in CML cells, possibly by inhibiting the Ras-ERK cascade and the pro-survival signaling molecules SPHK1 and Mcl-1.	imatinib	41-49	mitogen-activated protein kinase 1	Homo sapiens	116-119
20153728-8	2010	Together, these data implicate Spred2 in imatinib-induced cytotoxicity in CML cells, possibly by inhibiting the Ras-ERK cascade and the pro-survival signaling molecules SPHK1 and Mcl-1.	imatinib	41-49	sphingosine kinase 1	Homo sapiens	169-174
20153728-8	2010	Together, these data implicate Spred2 in imatinib-induced cytotoxicity in CML cells, possibly by inhibiting the Ras-ERK cascade and the pro-survival signaling molecules SPHK1 and Mcl-1.	imatinib	41-49	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	179-184
20120030-2	2010	Imatinib, a potent BCR-ABL inhibitor, is the standard of care for the first-line treatment of patients with chronic-phase CML because of its high long-term response rates and favorable tolerability profile compared with previous standard therapies.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
20043988-4	2010	Stimulation was abrogated by the addition of catalase, the extracellular Ca(2+) chelator BAPTA, the T-type Ca(2+) channel inhibitor mibefradil, the PKCdelta inhibitor rottlerin, or the c-Abl nonreceptor tyrosine kinase inhibitor imatinib mesylate or by overexpression of a dominant-negative form of c-Abl.	imatinib	229-246	catalase	Homo sapiens	45-53
20043988-5	2010	H(2)O(2) induced phosphorylation of tyrosine 311 on PKCdelta and this activating phosphorylation was blocked by treatment with rottlerin, imatinib mesylate, or BAPTA.	imatinib	138-155	protein kinase C delta	Homo sapiens	52-60
21171248-4	2010	These recent discoveries have legitimized the use of tyrosine kinase inhibitors such as imatinib, which, by inhibiting PDGFRA, have transformed the prognosis of chronic eosinophilic leukemia, and also the use of monoclonal anti-IL-5 antibodies, which are promising treatment for steroid-dependent HES.	imatinib	88-96	platelet derived growth factor receptor alpha	Homo sapiens	119-125
20197479-2	2010	BCR-ABL inhibition with imatinib results in high levels of efficacy in patients with newly diagnosed CML in chronic phase (CP), but an estimated 35% of patients could benefit from more effective treatment.	imatinib	24-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
19965667-9	2010	We conclude that allo SCT could become the preferred second-line option after imatinib failure for suitable patients with a donor.	imatinib	78-86	secretin	Homo sapiens	22-25
20188579-1	2010	Novel (E)-alpha-benzylthio chalcones are reported with preliminary in vitro activity data indicating that several of them are potent inhibitors (comparable to imatinib, the reference compound) of BCR-ABL phosphorylation in leukemic K562 cells, known to express high levels of BCR-ABL.	imatinib	159-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	196-203
20142590-4	2010	PATIENTS AND METHODS: Imatinib therapy was stopped in 20 patients who had concomitantly been pretreated with imatinib and IFN for a median of 2.4 years (range, 0.2 to 4.8 years) and 2.5 years (range, 0.2 to 4.9 years), respectively.	imatinib	22-30	interferon alpha 1	Homo sapiens	122-125
20142590-11	2010	CONCLUSION: Treatment with IFN enables discontinuation of imatinib in most patients after prior imatinib/IFN combination therapy and may result in improved molecular response.	imatinib	58-66	interferon alpha 1	Homo sapiens	27-30
20142590-11	2010	CONCLUSION: Treatment with IFN enables discontinuation of imatinib in most patients after prior imatinib/IFN combination therapy and may result in improved molecular response.	imatinib	96-104	interferon alpha 1	Homo sapiens	27-30
19714331-0	2010	Response to Imatinib mesylate in chronic myeloid leukemia patients with variant BCR-ABL fusion transcripts.	imatinib	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
19714331-1	2010	Chronic myeloid leukemia patients with different BCR-ABL transcripts might respond differently to Imatinib mesylate.	imatinib	98-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
19714331-2	2010	This prompted us to study BCR-ABL transcripts in chronic myeloid leukemia (CML) patients and their correlation with response to Imatinib.	imatinib	128-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
19714331-11	2010	Our preliminary findings suggest that CML patients with b2a2 BCR-ABL transcript might have higher CGRs to Imatinib mesylate (Gleevec).	imatinib	106-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
20149665-0	2010	Design, synthesis, and biological evaluation of novel water-soluble triptolide derivatives: Antineoplastic activity against imatinib-resistant CML cells bearing T315I mutant Bcr-Abl.	imatinib	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-181
20149665-2	2010	However, resistance to imatinib due to point mutations in Bcr-Abl kinase domain is an emerging problem.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
20149665-12	2010	Our results suggest that this series of derivatives may be promising agents to overcome imatinib-resistance caused by the Bcr-Abl-T315I mutation.	imatinib	88-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
21171248-4	2010	These recent discoveries have legitimized the use of tyrosine kinase inhibitors such as imatinib, which, by inhibiting PDGFRA, have transformed the prognosis of chronic eosinophilic leukemia, and also the use of monoclonal anti-IL-5 antibodies, which are promising treatment for steroid-dependent HES.	imatinib	88-96	interleukin 5	Homo sapiens	228-232
20201032-7	2010	However, Stat5- but not Stat3-deletion induces G(0)/G(1) cell cycle arrest and apoptosis of imatinib-sensitive and imatinib-resistant stable leukaemic cells in vitro.	imatinib	92-100	signal transducer and activator of transcription 5A	Homo sapiens	9-14
20040619-1	2010	BACKGROUND: Imatinib effectively inhibits the tyrosine kinase activity conferred by the BCR-ABL gene [fusion gene of BCR (breakpoint cluster region) and ABL1 (c-abl oncogene 1, receptor tyrosine kinase)] and thereby appreciably improves outcomes for chronic myelogenous leukemia (CML).	imatinib	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
20040619-1	2010	BACKGROUND: Imatinib effectively inhibits the tyrosine kinase activity conferred by the BCR-ABL gene [fusion gene of BCR (breakpoint cluster region) and ABL1 (c-abl oncogene 1, receptor tyrosine kinase)] and thereby appreciably improves outcomes for chronic myelogenous leukemia (CML).	imatinib	12-20	BCR activator of RhoGEF and GTPase	Homo sapiens	88-91
20040619-1	2010	BACKGROUND: Imatinib effectively inhibits the tyrosine kinase activity conferred by the BCR-ABL gene [fusion gene of BCR (breakpoint cluster region) and ABL1 (c-abl oncogene 1, receptor tyrosine kinase)] and thereby appreciably improves outcomes for chronic myelogenous leukemia (CML).	imatinib	12-20	BCR activator of RhoGEF and GTPase	Homo sapiens	122-147
20040619-1	2010	BACKGROUND: Imatinib effectively inhibits the tyrosine kinase activity conferred by the BCR-ABL gene [fusion gene of BCR (breakpoint cluster region) and ABL1 (c-abl oncogene 1, receptor tyrosine kinase)] and thereby appreciably improves outcomes for chronic myelogenous leukemia (CML).	imatinib	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-157
20040619-1	2010	BACKGROUND: Imatinib effectively inhibits the tyrosine kinase activity conferred by the BCR-ABL gene [fusion gene of BCR (breakpoint cluster region) and ABL1 (c-abl oncogene 1, receptor tyrosine kinase)] and thereby appreciably improves outcomes for chronic myelogenous leukemia (CML).	imatinib	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-201
20201032-7	2010	However, Stat5- but not Stat3-deletion induces G(0)/G(1) cell cycle arrest and apoptosis of imatinib-sensitive and imatinib-resistant stable leukaemic cells in vitro.	imatinib	115-123	signal transducer and activator of transcription 5A	Homo sapiens	9-14
20184741-8	2010	Furthermore hypermethylation of an autophagy related gene ATG16L2 was associated with poorer prognosis in terms of molecular response to Imatinib treatment.	imatinib	137-145	autophagy related 16 like 2	Homo sapiens	58-65
20002159-0	2010	BCR-ABL-independent and RAS / MAPK pathway-dependent form of imatinib resistance in Ph-positive acute lymphoblastic leukemia cell line with activation of EphB4.	imatinib	61-69	EPH receptor B4	Homo sapiens	154-159
23484445-7	2010	BCR-ABL1 kinase domain mutation screening has added another level of complexity that informs the management of some patients with imatinib resistance.	imatinib	130-138	BCR activator of RhoGEF and GTPase	Homo sapiens	0-8
20124181-10	2010	CONCLUSION: This analysis confirms a small PFS advantage of high-dose imatinib, essentially among patients with KIT exon 9 mutations, but no OS advantage.	imatinib	70-78	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	112-115
20038231-1	2010	The BCR-ABL inhibitor imatinib revolutionized the treatment of chronic myeloid leukemia (CML).	imatinib	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
20038231-4	2010	Two second-line BCR-ABL inhibitors are now approved for treatment of patients with resistance or intolerance to imatinib.	imatinib	112-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
20207846-5	2010	RESULTS: Co-administration of BCR-ABL small interfering RNA with imatinib or nilotinib dramatically reduced BCR-ABL expression in wild-type and mutated BCR-ABL cells and increased the lethal capacity.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
20207846-5	2010	RESULTS: Co-administration of BCR-ABL small interfering RNA with imatinib or nilotinib dramatically reduced BCR-ABL expression in wild-type and mutated BCR-ABL cells and increased the lethal capacity.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
20207846-5	2010	RESULTS: Co-administration of BCR-ABL small interfering RNA with imatinib or nilotinib dramatically reduced BCR-ABL expression in wild-type and mutated BCR-ABL cells and increased the lethal capacity.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
20207846-7	2010	Co-treatment with BCR-ABL small interfering RNA and imatinib or nilotinib resulted in increased inhibition of proliferation and induction of apoptosis in T315I cells as compared to imatinib or nilotinib alone (P<0.0001).	imatinib	181-189	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
20207846-8	2010	Furthermore, the combination of BCR-ABL small interfering RNA with imatinib or nilotinib significantly (P<0.01) reversed multidrug resistance-1 gene-dependent resistance of mutated cells.	imatinib	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
20207846-8	2010	Furthermore, the combination of BCR-ABL small interfering RNA with imatinib or nilotinib significantly (P<0.01) reversed multidrug resistance-1 gene-dependent resistance of mutated cells.	imatinib	67-75	ATP binding cassette subfamily B member 1	Homo sapiens	124-146
20207846-10	2010	CONCLUSIONS: Our data suggest that silencing by BCR-ABL small interfering RNA combined with imatinib or nilotinib may be associated with an additive antileukemic activity against tyrosine kinase inhibitor-sensitive and resistant BCR-ABL cells, and might be an alternative approach to overcome BCR-ABL mutations.	imatinib	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	229-236
20207846-10	2010	CONCLUSIONS: Our data suggest that silencing by BCR-ABL small interfering RNA combined with imatinib or nilotinib may be associated with an additive antileukemic activity against tyrosine kinase inhibitor-sensitive and resistant BCR-ABL cells, and might be an alternative approach to overcome BCR-ABL mutations.	imatinib	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	229-236
20033343-0	2010	Emergence of imatinib resistance associated with downregulation of c-kit expression in recurrent gastrointestinal stromal tumor (GIST): optimal timing of resection.	imatinib	13-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	67-72
19949796-1	2010	The discovery of activating oncogenic C-KIT and PDGFRA mutations in gastrointestinal stromal tumors (GIST) represented the key for the development of innovative targeted molecular therapy using the tyrosine kinase inhibitors (TKI) Imatinib (Glivec(R)), Sunitinib and other substances.	imatinib	231-239	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	38-43
19949796-1	2010	The discovery of activating oncogenic C-KIT and PDGFRA mutations in gastrointestinal stromal tumors (GIST) represented the key for the development of innovative targeted molecular therapy using the tyrosine kinase inhibitors (TKI) Imatinib (Glivec(R)), Sunitinib and other substances.	imatinib	231-239	platelet derived growth factor receptor alpha	Homo sapiens	48-54
20007806-0	2010	Emergence of BCR-ABL-specific cytotoxic T cells in the bone marrow of patients with Ph+ acute lymphoblastic leukemia during long-term imatinib mesylate treatment.	imatinib	134-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
20007806-2	2010	A total of 10 Philadelphia chromosome-positive acute lymphoblastic leukemia patients receiving high-dose imatinib mesylate maintenance underwent long-term immunological monitoring (range, 2-65 months) of (p190)BCR-ABL-specific T cells in the bone marrow and peripheral blood.	imatinib	105-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	210-217
20007699-1	2010	Acquired resistance through genetic mutations is a common phenomenon in several cancer therapies using molecularly targeted drugs, best exemplified by the BCR-ABL inhibitor imatinib in treating chronic myelogenous leukemia (CML).	imatinib	173-181	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-162
20145140-0	2010	Polo-like kinase 1 (Plk1) as a novel drug target in chronic myeloid leukemia: overriding imatinib resistance with the Plk1 inhibitor BI 2536.	imatinib	89-97	polo like kinase 1	Homo sapiens	0-18
20145140-0	2010	Polo-like kinase 1 (Plk1) as a novel drug target in chronic myeloid leukemia: overriding imatinib resistance with the Plk1 inhibitor BI 2536.	imatinib	89-97	polo like kinase 1	Homo sapiens	20-24
20145140-1	2010	In most patients with chronic myeloid leukemia (CML), the disease can be kept under control using the BCR/ABL kinase inhibitor imatinib.	imatinib	127-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
20145140-7	2010	Inhibition of BCR/ABL by imatinib or nilotinib (AMN107) led to decreased expression of the Plk1 protein in CML cells, suggesting that BCR/ABL promotes Plk1 generation.	imatinib	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
20145140-7	2010	Inhibition of BCR/ABL by imatinib or nilotinib (AMN107) led to decreased expression of the Plk1 protein in CML cells, suggesting that BCR/ABL promotes Plk1 generation.	imatinib	25-33	polo like kinase 1	Homo sapiens	91-95
20145140-7	2010	Inhibition of BCR/ABL by imatinib or nilotinib (AMN107) led to decreased expression of the Plk1 protein in CML cells, suggesting that BCR/ABL promotes Plk1 generation.	imatinib	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
20145140-7	2010	Inhibition of BCR/ABL by imatinib or nilotinib (AMN107) led to decreased expression of the Plk1 protein in CML cells, suggesting that BCR/ABL promotes Plk1 generation.	imatinib	25-33	polo like kinase 1	Homo sapiens	151-155
20145140-9	2010	Furthermore, the Plk1-targeting drug BI 2536 was found to inhibit proliferation of imatinib-sensitive and imatinib-resistant CML cells, including leukemic cells, carrying the T315 mutation of BCR/ABL with reasonable IC(50) values (1-50 nmol/L).	imatinib	83-91	polo like kinase 1	Homo sapiens	17-21
20145140-9	2010	Furthermore, the Plk1-targeting drug BI 2536 was found to inhibit proliferation of imatinib-sensitive and imatinib-resistant CML cells, including leukemic cells, carrying the T315 mutation of BCR/ABL with reasonable IC(50) values (1-50 nmol/L).	imatinib	106-114	polo like kinase 1	Homo sapiens	17-21
20145140-12	2010	In conclusion, Plk1 is expressed in CML cells and may represent a novel, interesting target in imatinib-sensitive and imatinib-resistant CML.	imatinib	95-103	polo like kinase 1	Homo sapiens	15-19
20145140-12	2010	In conclusion, Plk1 is expressed in CML cells and may represent a novel, interesting target in imatinib-sensitive and imatinib-resistant CML.	imatinib	118-126	polo like kinase 1	Homo sapiens	15-19
19965620-3	2010	Notably, platelet-derived growth factor receptor alpha and its phosphorylated form were confirmed at the protein level, and in vitro the MEC04 NKTCL cell line was sensitive to imatinib.	imatinib	176-184	platelet derived growth factor receptor alpha	Homo sapiens	9-54
20007699-4	2010	We demonstrate that the emergence of BCR-ABL mutations do not require pre-existing BCR-ABL mutations derived from the original patient as the subclones of KCL-22 cells can form various BCR-ABL mutations upon imatinib treatment.	imatinib	208-216	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
20007699-6	2010	Strikingly, development of BCR-ABL mutations depends on its gene expression because BCR-ABL knockdown completely blocks KCL-22 cell relapse on imatinib and acquisition of mutations.	imatinib	143-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
20007699-6	2010	Strikingly, development of BCR-ABL mutations depends on its gene expression because BCR-ABL knockdown completely blocks KCL-22 cell relapse on imatinib and acquisition of mutations.	imatinib	143-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
20184539-2	2010	The BCR-ABL kinase inhibitor imatinib is a standard treatment for Ph+ leukemia, and has been shown to induce a complete hematologic and cytogenetic response in most chronic phrase CML patients.	imatinib	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
19881535-5	2010	Short-term imatinib treatment of Bcr-Abl-positive cells caused dephosphorylation of p70S6-K and S6-protein without inactivation of Akt.	imatinib	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
19881535-5	2010	Short-term imatinib treatment of Bcr-Abl-positive cells caused dephosphorylation of p70S6-K and S6-protein without inactivation of Akt.	imatinib	11-19	ribosomal protein S6 kinase B1	Homo sapiens	84-91
19881535-8	2010	In Bcr-Abl-expressing cells, we detected strong PLC-gamma1 activation, which was suppressed by imatinib.	imatinib	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	3-10
19881535-8	2010	In Bcr-Abl-expressing cells, we detected strong PLC-gamma1 activation, which was suppressed by imatinib.	imatinib	95-103	phospholipase C gamma 1	Homo sapiens	48-58
19818327-2	2010	Disruption of Abl kinase signaling through the Philadelphia chromosome (causing the Bcr-Abl mutation) in chronic myeloid leukemia (CML) has provided a paradigm for development of kinase inhibitor drugs such as the specific inhibitor imatinib (also known as STI571 or Gleevec).	imatinib	233-241	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
19818327-2	2010	Disruption of Abl kinase signaling through the Philadelphia chromosome (causing the Bcr-Abl mutation) in chronic myeloid leukemia (CML) has provided a paradigm for development of kinase inhibitor drugs such as the specific inhibitor imatinib (also known as STI571 or Gleevec).	imatinib	257-263	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
20016370-0	2010	Interleukin-2 treatment effect on imatinib pharmacokinetic, P-gp and BCRP expression in mice.	imatinib	34-42	interleukin 2	Mus musculus	0-13
20016370-1	2010	The aim of this study was to investigate the effect that recombinant interleukin-2 (rIL-2) (0.16 MUI/injection) had on the pharmacokinetics of imatinib (IM) in plasma.	imatinib	143-151	interleukin 2	Mus musculus	69-82
20016370-1	2010	The aim of this study was to investigate the effect that recombinant interleukin-2 (rIL-2) (0.16 MUI/injection) had on the pharmacokinetics of imatinib (IM) in plasma.	imatinib	143-151	interleukin 2	Rattus norvegicus	84-89
20124232-5	2010	One of these TGF-beta pathways results in the activation of the nonreceptor tyrosine kinase cellular Abelson (c-Abl), and c-Abl inhibitors, including imatinib mesylate, diminishing the fibrogenic effects of TGF-beta.	imatinib	150-167	transforming growth factor beta 1	Homo sapiens	13-21
20124232-5	2010	One of these TGF-beta pathways results in the activation of the nonreceptor tyrosine kinase cellular Abelson (c-Abl), and c-Abl inhibitors, including imatinib mesylate, diminishing the fibrogenic effects of TGF-beta.	imatinib	150-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-127
20124232-5	2010	One of these TGF-beta pathways results in the activation of the nonreceptor tyrosine kinase cellular Abelson (c-Abl), and c-Abl inhibitors, including imatinib mesylate, diminishing the fibrogenic effects of TGF-beta.	imatinib	150-167	transforming growth factor beta 1	Homo sapiens	207-215
20042679-7	2010	Treatment of the hPDGF-B- and mVEGF-164-expressing tumors with imatinib mesylate to block PDGF-B signaling reverses this effect.	imatinib	63-80	platelet derived growth factor subunit B	Homo sapiens	17-24
20042679-7	2010	Treatment of the hPDGF-B- and mVEGF-164-expressing tumors with imatinib mesylate to block PDGF-B signaling reverses this effect.	imatinib	63-80	platelet derived growth factor subunit B	Homo sapiens	18-24
20332468-0	2010	Phase II clinical trial of imatinib mesylate in therapy of KIT and/or PDGFRalpha-expressing Ewing sarcoma family of tumors and desmoplastic small round cell tumors.	imatinib	27-44	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	59-62
20332468-0	2010	Phase II clinical trial of imatinib mesylate in therapy of KIT and/or PDGFRalpha-expressing Ewing sarcoma family of tumors and desmoplastic small round cell tumors.	imatinib	27-44	platelet derived growth factor receptor alpha	Homo sapiens	70-80
20332468-1	2010	BACKGROUND: We have previously shown that the receptor tyrosine kinases, KIT and PDGFRalpha, are expressed on ESFT cell lines, and that imatinib induces dose-dependent apoptosis (1).	imatinib	136-144	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
20332468-1	2010	BACKGROUND: We have previously shown that the receptor tyrosine kinases, KIT and PDGFRalpha, are expressed on ESFT cell lines, and that imatinib induces dose-dependent apoptosis (1).	imatinib	136-144	platelet derived growth factor receptor alpha	Homo sapiens	81-91
20332468-2	2010	We conducted a Phase II trial to evaluate the effectiveness of imatinib for patients with recurrent ESFT or DSRCT expressing KIT and/or PDGFRalpha.	imatinib	63-71	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	125-128
20332468-2	2010	We conducted a Phase II trial to evaluate the effectiveness of imatinib for patients with recurrent ESFT or DSRCT expressing KIT and/or PDGFRalpha.	imatinib	63-71	platelet derived growth factor receptor alpha	Homo sapiens	136-146
20139391-0	2010	Potent, transient inhibition of BCR-ABL with dasatinib 100 mg daily achieves rapid and durable cytogenetic responses and high transformation-free survival rates in chronic phase chronic myeloid leukemia patients with resistance, suboptimal response or intolerance to imatinib.	imatinib	267-275	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
20109338-7	2010	Pearson product moment correlation and t test were used to analyze the correlation betweeen C-KIT overexpression, C-KIT gene mutation, and the inhibitory effect of Imatinib.	imatinib	164-172	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	92-97
20132660-0	2010	Nilotinib significantly induces apoptosis in imatinib-resistant K562 cells with wild-type BCR-ABL, as effectively as in parental sensitive counterparts.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
20132660-3	2010	Imatinib and nilotinib are chemotherapeutic drugs which specifically bind to the BCR-ABL and inhibit cancer cells.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
20132660-5	2010	We have shown that nilotinib induces apoptosis in imatinib-resistant K562 CML cells which have the wild-type BCR-ABL fusion gene almost to the same extent as it does in the parental sensitive cells by the increase in caspase-3 enzyme activity and the decrease in mitochondrial membrane potential.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
20132660-5	2010	We have shown that nilotinib induces apoptosis in imatinib-resistant K562 CML cells which have the wild-type BCR-ABL fusion gene almost to the same extent as it does in the parental sensitive cells by the increase in caspase-3 enzyme activity and the decrease in mitochondrial membrane potential.	imatinib	50-58	caspase 3	Homo sapiens	217-226
20038234-0	2010	Kinase domain mutations of BCR-ABL identified at diagnosis before imatinib-based therapy are associated with progression in patients with high Sokal risk chronic phase chronic myeloid leukemia.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
20038234-1	2010	Acquired resistance to imatinib in the advanced phase of chronic myeloid leukemia (CML) has been associated with mutations in the kinase domain (KD) of BCR-ABL.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-159
21203982-5	2010	Currently, inhibition of BCR-ABL kinase activity by its kinase inhibitor such as imatinib mesylate (Gleevec) is a major therapeutic strategy for CML.	imatinib	81-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
21203982-5	2010	Currently, inhibition of BCR-ABL kinase activity by its kinase inhibitor such as imatinib mesylate (Gleevec) is a major therapeutic strategy for CML.	imatinib	100-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
20137125-6	2010	When K562/A02 cells were treated with Imatinib or Nilotinib alone for 48 hours, the expressions of mdr-1 mRNA, der/abl mRNA, P-gp and P210 protein were all down-regulated, furthermore the effect of Nilotinib was stronger than that of Imatinib.	imatinib	38-46	ATP binding cassette subfamily B member 1	Homo sapiens	99-104
20001232-5	2010	Early studies demonstrate that the use of the BCR-ABL tyrosine kinase inhibitor (TKI), imatinib, before alloSCT results in improved response rates and DFS when combined with standard chemotherapy regimens.	imatinib	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
20001232-9	2010	The dual BCR-ABL/SRC family kinase inhibitor, dasatinib, has shown promising activity in the treatment of Ph+ ALL after imatinib failure and has recently been approved in this indication.	imatinib	120-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
20165865-6	2010	Although, KIT (CD117) immunohistochemistry is a reliable diagnostic tool in the diagnosis of GIST, KIT-negative GISTs, GISTs showing unusual morphology as well as GISTs which progress during or after treatment with imatinib/sunitinib can be a challenge for pathologists and clinicians.	imatinib	215-223	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	10-13
20165865-6	2010	Although, KIT (CD117) immunohistochemistry is a reliable diagnostic tool in the diagnosis of GIST, KIT-negative GISTs, GISTs showing unusual morphology as well as GISTs which progress during or after treatment with imatinib/sunitinib can be a challenge for pathologists and clinicians.	imatinib	215-223	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	15-20
20137125-6	2010	When K562/A02 cells were treated with Imatinib or Nilotinib alone for 48 hours, the expressions of mdr-1 mRNA, der/abl mRNA, P-gp and P210 protein were all down-regulated, furthermore the effect of Nilotinib was stronger than that of Imatinib.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-118
20137125-6	2010	When K562/A02 cells were treated with Imatinib or Nilotinib alone for 48 hours, the expressions of mdr-1 mRNA, der/abl mRNA, P-gp and P210 protein were all down-regulated, furthermore the effect of Nilotinib was stronger than that of Imatinib.	imatinib	38-46	ATP binding cassette subfamily B member 1	Homo sapiens	125-129
20137358-23	2010	Targeted therapy such as imatinib, a KIT tyrosine kinase inhibitor, may play an important role in the treatment of GIST.	imatinib	25-33	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	37-40
20109225-12	2010	Seventeen patients with locally advanced and/or metastatic disease expressing platelet-derived growth factor receptor (PDGFR) beta were treated with imatinib mesylate.	imatinib	149-166	platelet derived growth factor receptor beta	Homo sapiens	119-130
20026060-0	2010	Blockade of the ERK or PI3K-Akt signaling pathway enhances the cytotoxicity of histone deacetylase inhibitors in tumor cells resistant to gefitinib or imatinib.	imatinib	151-159	mitogen-activated protein kinase 1	Homo sapiens	16-19
20026060-0	2010	Blockade of the ERK or PI3K-Akt signaling pathway enhances the cytotoxicity of histone deacetylase inhibitors in tumor cells resistant to gefitinib or imatinib.	imatinib	151-159	histone deacetylase 9	Homo sapiens	79-98
19890095-6	2010	In particular, it examines recent studies suggesting that imatinib has direct effects on bone-resorbing osteoclasts and bone-forming osteoblasts through inhibition of c-fms, c-kit, carbonic anhydrase II, and the platelet-derived growth factor receptor.	imatinib	58-66	colony stimulating factor 1 receptor	Homo sapiens	167-172
19890095-6	2010	In particular, it examines recent studies suggesting that imatinib has direct effects on bone-resorbing osteoclasts and bone-forming osteoblasts through inhibition of c-fms, c-kit, carbonic anhydrase II, and the platelet-derived growth factor receptor.	imatinib	58-66	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	174-179
19890095-6	2010	In particular, it examines recent studies suggesting that imatinib has direct effects on bone-resorbing osteoclasts and bone-forming osteoblasts through inhibition of c-fms, c-kit, carbonic anhydrase II, and the platelet-derived growth factor receptor.	imatinib	58-66	carbonic anhydrase 2	Homo sapiens	181-202
19837975-0	2010	A gene expression signature of CD34+ cells to predict major cytogenetic response in chronic-phase chronic myeloid leukemia patients treated with imatinib.	imatinib	145-153	CD34 molecule	Homo sapiens	31-35
19837975-6	2010	Bioinformatics analysis and comparison with published studies revealed overlap of classifier genes with CML progression signatures and implicated beta-catenin in their regulation, suggesting that chronic-phase CML patients destined to fail imatinib have more advanced disease than evident by morphologic criteria.	imatinib	240-248	catenin beta 1	Homo sapiens	146-158
20460883-3	2010	This report presents the case of a patient with a post-transplant persistent positive BCR/ABL value, who was treated with imatinib and dasatinib before a second allo-HSCT.	imatinib	122-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
20005615-1	2010	The introduction of imatinib, a tyrosine kinase inhibitor (TKI) that targets the BCR-ABL protein, has revolutionised the treatment of chronic myeloid leukaemia (CML), producing high rates of response that have been durable in many patients.	imatinib	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
21188243-5	2010	Protein kinase inhibitors, including imatinib mesylate and gefitinib, are suggested to potentially enhance the efficacy of photodynamic therapy by blocking ABCG2-mediated porphyrin efflux from cancer cells.	imatinib	37-54	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	156-161
19846571-5	2010	Treatment with c-Abl or mTOR inhibitors, imatinib mesylate and rapamycin, respectively, each blocks noncanonical (non-smad) TGF-beta pathways in the kidney in vivo and diminishes the number of interstitial fibroblasts and myofibroblasts as well as the interstitial accumulation of extracellular matrix proteins.	imatinib	41-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-20
19846571-5	2010	Treatment with c-Abl or mTOR inhibitors, imatinib mesylate and rapamycin, respectively, each blocks noncanonical (non-smad) TGF-beta pathways in the kidney in vivo and diminishes the number of interstitial fibroblasts and myofibroblasts as well as the interstitial accumulation of extracellular matrix proteins.	imatinib	41-58	mechanistic target of rapamycin kinase	Homo sapiens	24-28
20146711-7	2010	Others have shown that dendritic cell treatment with inhibitors of c-kit activation, such as imatinib mesylate (Gleevec), favored breaking of T-cell tolerance, skewing of responses toward production of Th1 cytokines, and activation of natural killer cells.	imatinib	93-110	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	67-72
20146711-7	2010	Others have shown that dendritic cell treatment with inhibitors of c-kit activation, such as imatinib mesylate (Gleevec), favored breaking of T-cell tolerance, skewing of responses toward production of Th1 cytokines, and activation of natural killer cells.	imatinib	93-110	negative elongation factor complex member C/D	Homo sapiens	202-205
20380722-7	2010	The effect of 2GF on TNFalpha-induced gene expression was transcriptionally mediated; blocked by imatinib mesylate; and occurred even if 2GF was added as much as four hours prior to TNFalpha.	imatinib	97-105	tumor necrosis factor	Homo sapiens	21-29
19900123-2	2010	The receptor tyrosine kinase (RTK) inhibitor imatinib mesylate has been approved as the first-line choice of therapy for this group of patients, while the RTK inhibitor, sunitinib malate, has been approved for the treatment of GIST after disease progression or intolerance to imatinib.	imatinib	45-62	ret proto-oncogene	Homo sapiens	4-28
19900123-2	2010	The receptor tyrosine kinase (RTK) inhibitor imatinib mesylate has been approved as the first-line choice of therapy for this group of patients, while the RTK inhibitor, sunitinib malate, has been approved for the treatment of GIST after disease progression or intolerance to imatinib.	imatinib	45-62	ret proto-oncogene	Homo sapiens	30-33
19900123-2	2010	The receptor tyrosine kinase (RTK) inhibitor imatinib mesylate has been approved as the first-line choice of therapy for this group of patients, while the RTK inhibitor, sunitinib malate, has been approved for the treatment of GIST after disease progression or intolerance to imatinib.	imatinib	45-53	ret proto-oncogene	Homo sapiens	4-28
19900123-2	2010	The receptor tyrosine kinase (RTK) inhibitor imatinib mesylate has been approved as the first-line choice of therapy for this group of patients, while the RTK inhibitor, sunitinib malate, has been approved for the treatment of GIST after disease progression or intolerance to imatinib.	imatinib	45-53	ret proto-oncogene	Homo sapiens	30-33
20023271-1	2010	Mutational analysis of c-KIT or PDGFRA has become an important laboratory assay for patients with gastrointestinal stromal tumors (GISTs) because the results are useful in predicting the responsiveness to imatinib.	imatinib	205-213	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	23-28
20023271-1	2010	Mutational analysis of c-KIT or PDGFRA has become an important laboratory assay for patients with gastrointestinal stromal tumors (GISTs) because the results are useful in predicting the responsiveness to imatinib.	imatinib	205-213	platelet derived growth factor receptor alpha	Homo sapiens	32-38
19995744-3	2010	The small molecule tyrosine kinase inhibitor imatinib and related drugs such as dasatinib and nilotinib target simultaneously two of the major profibrotic pathways, TGFbeta- and PDGF- signaling.	imatinib	45-53	transforming growth factor beta 1	Homo sapiens	165-172
20181277-2	2010	We previously demonstrated that imatinib mesylate--a Food and Drug Administration (FDA)-approved, antineoplastic drug that potently inhibits the tyrosine kinases Abl, c-Kit, platelet-derived growth factor receptor (PDGFR), and c-Fms--ameliorates murine autoimmune arthritis.	imatinib	32-49	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	162-165
20181277-2	2010	We previously demonstrated that imatinib mesylate--a Food and Drug Administration (FDA)-approved, antineoplastic drug that potently inhibits the tyrosine kinases Abl, c-Kit, platelet-derived growth factor receptor (PDGFR), and c-Fms--ameliorates murine autoimmune arthritis.	imatinib	32-49	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	167-172
20181277-2	2010	We previously demonstrated that imatinib mesylate--a Food and Drug Administration (FDA)-approved, antineoplastic drug that potently inhibits the tyrosine kinases Abl, c-Kit, platelet-derived growth factor receptor (PDGFR), and c-Fms--ameliorates murine autoimmune arthritis.	imatinib	32-49	platelet derived growth factor receptor, beta polypeptide	Mus musculus	174-213
20181277-2	2010	We previously demonstrated that imatinib mesylate--a Food and Drug Administration (FDA)-approved, antineoplastic drug that potently inhibits the tyrosine kinases Abl, c-Kit, platelet-derived growth factor receptor (PDGFR), and c-Fms--ameliorates murine autoimmune arthritis.	imatinib	32-49	platelet derived growth factor receptor, beta polypeptide	Mus musculus	215-220
20181277-2	2010	We previously demonstrated that imatinib mesylate--a Food and Drug Administration (FDA)-approved, antineoplastic drug that potently inhibits the tyrosine kinases Abl, c-Kit, platelet-derived growth factor receptor (PDGFR), and c-Fms--ameliorates murine autoimmune arthritis.	imatinib	32-49	colony stimulating factor 1 receptor	Mus musculus	227-232
20181277-5	2010	METHODS: We tested the therapeutic efficacy of orally administered imatinib or GW2580, a small molecule that specifically inhibits c-Fms, in three mouse models of RA: collagen-induced arthritis (CIA), anti-collagen antibody-induced arthritis (CAIA), and K/BxN serum transfer-induced arthritis (K/BxN).	imatinib	67-75	colony stimulating factor 1 receptor	Mus musculus	131-136
20181277-8	2010	Further, we determined the effects of imatinib and GW2580 on the ability of macrophage colony-stimulating factor (M-CSF; the ligand for c-Fms) to prime bone marrow-derived macrophages to produce tumor necrosis factor (TNF) upon subsequent Fc receptor ligation.	imatinib	38-46	colony stimulating factor 1 (macrophage)	Mus musculus	76-112
20181277-8	2010	Further, we determined the effects of imatinib and GW2580 on the ability of macrophage colony-stimulating factor (M-CSF; the ligand for c-Fms) to prime bone marrow-derived macrophages to produce tumor necrosis factor (TNF) upon subsequent Fc receptor ligation.	imatinib	38-46	colony stimulating factor 1 (macrophage)	Mus musculus	114-119
19950162-0	2010	Novel imatinib derivatives with altered specificity between Bcr-Abl and FMS, KIT, and PDGF receptors.	imatinib	6-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
19804453-0	2010	Mutations in the fifth immunoglobulin-like domain of kit are common and potentially sensitive to imatinib mesylate in feline mast cell tumours.	imatinib	97-114	KIT proto-oncogene, receptor tyrosine kinase	Felis catus	53-56
19804453-6	2010	The tyrosine kinase inhibitor imatinib mesylate suppressed the phosphorylation of these mutant kit proteins in transfectant cells.	imatinib	30-47	KIT proto-oncogene, receptor tyrosine kinase	Felis catus	95-98
19804453-7	2010	In a clinical study of 10 cats with MCTs, beneficial response to imatinib mesylate was observed in 7/8 cats that had a mutation in the fifth IgD of kit in tumour cells.	imatinib	65-82	KIT proto-oncogene, receptor tyrosine kinase	Felis catus	148-151
19804453-8	2010	Mutations in the fifth IgD of kit thus appear to be common and potentially sensitive to imatinib mesylate in feline MCTs.	imatinib	88-105	KIT proto-oncogene, receptor tyrosine kinase	Felis catus	30-33
20028860-3	2010	Upregulation of soluble, non-chromatin-bound histone H2AX has an important role in imatinib-induced apoptosis of GIST cells.	imatinib	83-91	H2A.X variant histone	Homo sapiens	45-57
20028869-7	2010	Proliferation of CSCs was inhibited by SCF-neutralizing antibodies or by imatinib (Gleevec), an inhibitor of c-kit.	imatinib	73-81	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	109-114
20028869-7	2010	Proliferation of CSCs was inhibited by SCF-neutralizing antibodies or by imatinib (Gleevec), an inhibitor of c-kit.	imatinib	83-90	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	109-114
20085582-0	2010	Fusion of PDGFRB to two distinct loci at 3p21 and a third at 12q13 in imatinib-responsive myeloproliferative neoplasms.	imatinib	70-78	platelet derived growth factor receptor beta	Homo sapiens	10-16
20085582-4	2010	Imatinib, a known inhibitor of PDGFRbeta, selectively blocked the growth of t(3;5) myeloid colonies and produced clinically significant responses in all patients.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	31-40
19843070-0	2010	Contribution of BCR-ABL-independent activation of ERK1/2 to acquired imatinib resistance in K562 chronic myeloid leukemia cells.	imatinib	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
19843070-0	2010	Contribution of BCR-ABL-independent activation of ERK1/2 to acquired imatinib resistance in K562 chronic myeloid leukemia cells.	imatinib	69-77	mitogen-activated protein kinase 3	Homo sapiens	50-56
19843070-2	2010	BCR-ABL is inhibited by imatinib; however, several mechanisms of imatinib resistance have been proposed that account for loss of imatinib efficacy in patients with CML.	imatinib	24-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
19843070-7	2010	In both cell lines, imatinib effectively reduced the phosphorylation of all the above, except ERK1/2, whose phosphorylation was, interestingly, only inhibited in the wild-type cells.	imatinib	20-28	mitogen-activated protein kinase 3	Homo sapiens	94-100
19843070-9	2010	However, using an ERK1/2 inhibitor, U0126, we found that we could reduce phospho-ERK1/2 levels in K562/R cells and restore their sensitivity to imatinib.	imatinib	144-152	mitogen-activated protein kinase 3	Homo sapiens	18-24
19843070-9	2010	However, using an ERK1/2 inhibitor, U0126, we found that we could reduce phospho-ERK1/2 levels in K562/R cells and restore their sensitivity to imatinib.	imatinib	144-152	mitogen-activated protein kinase 3	Homo sapiens	81-87
19843070-10	2010	Taken together, we conclude that the BCR-ABL-independent activation of ERK1/2 contributes to imatinib resistance in K562/R cells, and that ERK1/2 could be a target for the treatment of CML patients whose imatinib resistance is due to this mechanism.	imatinib	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
19843070-10	2010	Taken together, we conclude that the BCR-ABL-independent activation of ERK1/2 contributes to imatinib resistance in K562/R cells, and that ERK1/2 could be a target for the treatment of CML patients whose imatinib resistance is due to this mechanism.	imatinib	93-101	mitogen-activated protein kinase 3	Homo sapiens	71-77
19843070-10	2010	Taken together, we conclude that the BCR-ABL-independent activation of ERK1/2 contributes to imatinib resistance in K562/R cells, and that ERK1/2 could be a target for the treatment of CML patients whose imatinib resistance is due to this mechanism.	imatinib	204-212	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
19843070-10	2010	Taken together, we conclude that the BCR-ABL-independent activation of ERK1/2 contributes to imatinib resistance in K562/R cells, and that ERK1/2 could be a target for the treatment of CML patients whose imatinib resistance is due to this mechanism.	imatinib	204-212	mitogen-activated protein kinase 3	Homo sapiens	71-77
19843070-10	2010	Taken together, we conclude that the BCR-ABL-independent activation of ERK1/2 contributes to imatinib resistance in K562/R cells, and that ERK1/2 could be a target for the treatment of CML patients whose imatinib resistance is due to this mechanism.	imatinib	204-212	mitogen-activated protein kinase 3	Homo sapiens	139-145
19950162-0	2010	Novel imatinib derivatives with altered specificity between Bcr-Abl and FMS, KIT, and PDGF receptors.	imatinib	6-14	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	77-80
19950162-1	2010	Imatinib is a clinically important ATP analogue inhibitor that targets the tyrosine kinase domain of the intracellular Abl kinase and the PDGF receptor family.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-122
19950162-2	2010	Imatinib has revolutionised the treatment of chronic myeloid leukaemia, which is caused by the oncogene Bcr-Abl and certain solid tumours that harbor oncogenic mutations of the PDGF receptor family.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
19950162-4	2010	Herein we report a new series of imatinib derivatives that in general have greater activity against the family of PDGF receptors and poorer activity against Abl, as a result of modifications of the phenyl and N-methylpiperazine rings.	imatinib	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-160
20048335-0	2010	K562/GM-CSF immunotherapy reduces tumor burden in chronic myeloid leukemia patients with residual disease on imatinib mesylate.	imatinib	109-126	colony stimulating factor 2	Homo sapiens	5-11
20523072-3	2010	FIP1L1/PDGFR alpha-positive disorders are characterized by clonal hypereosinophilia, multiple organ dysfunctions due to eosinophil infiltration, systemic mastocytosis (SM) and a dramatic response to treatment with imatinib mesylate.	imatinib	214-231	FIP1 like 1 (S. cerevisiae)	Mus musculus	0-6
20048335-3	2010	A pilot study was developed to determine if K562/GM-CSF immunotherapy could improve clinical responses to imatinib mesylate (IM) in patients with chronic myeloid leukemia.	imatinib	106-123	colony stimulating factor 2	Homo sapiens	49-55
20048335-11	2010	CONCLUSIONS: K562/GM-CSF vaccine appears to improve molecular responses in patients on imatinib mesylate, including achieving complete molecular remissions, despite long durations of previous imatinib mesylate therapy.	imatinib	87-104	colony stimulating factor 2	Homo sapiens	18-24
20048335-11	2010	CONCLUSIONS: K562/GM-CSF vaccine appears to improve molecular responses in patients on imatinib mesylate, including achieving complete molecular remissions, despite long durations of previous imatinib mesylate therapy.	imatinib	192-209	colony stimulating factor 2	Homo sapiens	18-24
21319518-8	2010	The fact that PDGFRA and PDGFRB are overexpressed in these tumors opens new treatment options with imatinib.	imatinib	99-107	platelet derived growth factor receptor alpha	Homo sapiens	14-20
21319518-8	2010	The fact that PDGFRA and PDGFRB are overexpressed in these tumors opens new treatment options with imatinib.	imatinib	99-107	platelet derived growth factor receptor beta	Homo sapiens	25-31
19996579-2	2010	Imatinib has become the standard of care in other cancers with KIT mutations such as gastrointestinal stromal tumors.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	63-66
19996579-3	2010	Recently 12 cases of metastatic melanoma and KIT-activating mutations have been published to be successfully treated with c-KIT blockers such as imatinib, sunitinib, dasatinib or sorafenib.	imatinib	145-153	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	45-48
19996579-3	2010	Recently 12 cases of metastatic melanoma and KIT-activating mutations have been published to be successfully treated with c-KIT blockers such as imatinib, sunitinib, dasatinib or sorafenib.	imatinib	145-153	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	122-127
19996579-4	2010	We report here on one of our patients with KIT-activating mutation in metastatic anal mucosal melanoma, who showed a response to imatinib therapy and summarize the available literature regarding this new therapeutic option.	imatinib	129-137	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	43-46
19837125-0	2010	Constant BCR-ABL transcript level >or=0.1% (IS) in patients with CML responding to imatinib with complete cytogenetic remission may indicate mutation analysis.	imatinib	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
19837125-1	2010	OBJECTIVE: Of 140 chronic myeloid leukemia patients responding to imatinib with complete cytogenetic remission, 32 exhibited a plateau of BCR-ABL values at >or=0.1% level in a minimum of three subsequent samples (minimal duration, 6 - 9 months).	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
19837125-9	2010	CONCLUSION: We show here that the BCR-ABL constant levels >or=0.1% (BCR-ABL plateau) in imatinib-responding patients may indicate mutation analysis.	imatinib	91-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
19837125-9	2010	CONCLUSION: We show here that the BCR-ABL constant levels >or=0.1% (BCR-ABL plateau) in imatinib-responding patients may indicate mutation analysis.	imatinib	91-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
19837126-1	2010	OBJECTIVE: Imatinib mesylate (IM) is a tyrosine kinase inhibitor selective for BCR-ABL and indicated for the treatment of chronic myeloid leukemia.	imatinib	11-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
20089016-1	2010	BACKGROUND: Imatinib mesylate [tyrosine kinase (TK) inhibitor] is a novel medication in the treatment of chronic myelogenous leukaemia (CML).	imatinib	12-29	TXK tyrosine kinase	Homo sapiens	31-46
20523072-3	2010	FIP1L1/PDGFR alpha-positive disorders are characterized by clonal hypereosinophilia, multiple organ dysfunctions due to eosinophil infiltration, systemic mastocytosis (SM) and a dramatic response to treatment with imatinib mesylate.	imatinib	214-231	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	7-18
20089016-1	2010	BACKGROUND: Imatinib mesylate [tyrosine kinase (TK) inhibitor] is a novel medication in the treatment of chronic myelogenous leukaemia (CML).	imatinib	12-29	TXK tyrosine kinase	Homo sapiens	48-50
19968734-6	2010	The molecular characterization (genotyping) of GISTs has become an essential part of the routine management of the disease as KIT and PDGFRA mutation status predicts the likelihood of achieving response to imatinib.	imatinib	206-214	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	126-129
20558942-0	2010	Pure red cell aplasia associated with imatinib-treated FIP1L1-PDGFRA positive chronic eosinophilic leukemia.	imatinib	38-46	factor interacting with PAPOLA and CPSF1	Homo sapiens	55-61
20558942-0	2010	Pure red cell aplasia associated with imatinib-treated FIP1L1-PDGFRA positive chronic eosinophilic leukemia.	imatinib	38-46	platelet derived growth factor receptor alpha	Homo sapiens	62-68
20047097-4	2010	However, JAK2 V617F alleles diminished when BCR-ABL mRNA burden increased and reappeared once the patient was commenced on imatinib.	imatinib	123-131	Janus kinase 2	Homo sapiens	9-13
20047097-5	2010	The dynamic interaction between JAK2 V617F and BCR-ABL implies that two independent clones exist with the JAK2 V617F clone only achieving clonal dominance when BCR-ABL positive clones are suppressed by imatinib.	imatinib	202-210	Janus kinase 2	Homo sapiens	32-36
20047097-5	2010	The dynamic interaction between JAK2 V617F and BCR-ABL implies that two independent clones exist with the JAK2 V617F clone only achieving clonal dominance when BCR-ABL positive clones are suppressed by imatinib.	imatinib	202-210	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
20047097-5	2010	The dynamic interaction between JAK2 V617F and BCR-ABL implies that two independent clones exist with the JAK2 V617F clone only achieving clonal dominance when BCR-ABL positive clones are suppressed by imatinib.	imatinib	202-210	Janus kinase 2	Homo sapiens	106-110
20047097-5	2010	The dynamic interaction between JAK2 V617F and BCR-ABL implies that two independent clones exist with the JAK2 V617F clone only achieving clonal dominance when BCR-ABL positive clones are suppressed by imatinib.	imatinib	202-210	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-167
19968734-6	2010	The molecular characterization (genotyping) of GISTs has become an essential part of the routine management of the disease as KIT and PDGFRA mutation status predicts the likelihood of achieving response to imatinib.	imatinib	206-214	platelet derived growth factor receptor alpha	Homo sapiens	134-140
19968734-9	2010	Multiple novel tyrosine kinase inhibitors may be potentially useful for the treatment of imatinib-resistant GISTs as they interfere with KIT and PDGFRA receptors or with the downstream-signalling proteins.	imatinib	89-97	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	137-140
19968734-9	2010	Multiple novel tyrosine kinase inhibitors may be potentially useful for the treatment of imatinib-resistant GISTs as they interfere with KIT and PDGFRA receptors or with the downstream-signalling proteins.	imatinib	89-97	platelet derived growth factor receptor alpha	Homo sapiens	145-151
19798095-7	2010	Here, we propose a treatment algorithm for imatinib-resistant patients based on BCR-ABL mutation status and patient history.	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
20175840-9	2010	Imatinib mesylate may be a novel new therapy for fibrosis and vasculopathy in SSc because it reverses the expression levels of Fli1, which is a transcription factor downregulated in SSc through an epigenetic mechanism and is likely to be involved in the development of fibrosis and vasculopathy in this disease.	imatinib	0-17	Fli-1 proto-oncogene, ETS transcription factor	Homo sapiens	127-131
20224640-1	2010	We report a case of a successful mobilization and harvest of the peripheral blood stem cells (PBSCs) in imatinib-pretreated and nilotinib treated 52-year-old woman diagnosed with Philadelphia chromosome-positive and BCR-ABL (b2a2) positive chronic phase CML in 2/2002.	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	216-223
19748671-0	2010	Response to imatinib in a patient with chronic myeloid leukemia simultaneously expressing p190(BCR-ABL) oncoprotein and JAK2V617F mutation.	imatinib	12-20	contactin associated protein 1	Homo sapiens	90-94
19924144-0	2010	Cathepsin B release after imatinib-mediated lysosomal membrane permeabilization triggers BCR-ABL cleavage and elimination of chronic myelogenous leukemia cells.	imatinib	26-34	cathepsin B	Homo sapiens	0-11
19748671-0	2010	Response to imatinib in a patient with chronic myeloid leukemia simultaneously expressing p190(BCR-ABL) oncoprotein and JAK2V617F mutation.	imatinib	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
19890374-1	2010	Resistance to the BCR-ABL tyrosine kinase inhibitor imatinib poses a pressing challenge in treating chronic myeloid leukemia (CML).	imatinib	52-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
19924144-7	2010	Hence, we describe an original pathway by which Imatinib participates to the elimination of CML cells through LMP and CB-mediated specific degradation of BCR-ABL.	imatinib	48-56	cathepsin B	Homo sapiens	118-120
19924144-0	2010	Cathepsin B release after imatinib-mediated lysosomal membrane permeabilization triggers BCR-ABL cleavage and elimination of chronic myelogenous leukemia cells.	imatinib	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
19924144-7	2010	Hence, we describe an original pathway by which Imatinib participates to the elimination of CML cells through LMP and CB-mediated specific degradation of BCR-ABL.	imatinib	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-161
19924144-2	2010	Through inhibition of BCR-ABL, Imatinib blocks several downstream pathways and induces apoptosis of BCR-ABL positive cells.	imatinib	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
19924144-2	2010	Through inhibition of BCR-ABL, Imatinib blocks several downstream pathways and induces apoptosis of BCR-ABL positive cells.	imatinib	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
19924144-5	2010	Pharmacological inhibition of CB by CA-074Me or small interfering RNA-mediated knock-down of CB partly protects K562 cells from Imatinib-induced cell death and CB overexpression sensitizes these cells to Imatinib killing.	imatinib	128-136	cathepsin B	Homo sapiens	30-32
19924144-5	2010	Pharmacological inhibition of CB by CA-074Me or small interfering RNA-mediated knock-down of CB partly protects K562 cells from Imatinib-induced cell death and CB overexpression sensitizes these cells to Imatinib killing.	imatinib	128-136	cathepsin B	Homo sapiens	93-95
19924144-5	2010	Pharmacological inhibition of CB by CA-074Me or small interfering RNA-mediated knock-down of CB partly protects K562 cells from Imatinib-induced cell death and CB overexpression sensitizes these cells to Imatinib killing.	imatinib	128-136	cathepsin B	Homo sapiens	93-95
19924144-5	2010	Pharmacological inhibition of CB by CA-074Me or small interfering RNA-mediated knock-down of CB partly protects K562 cells from Imatinib-induced cell death and CB overexpression sensitizes these cells to Imatinib killing.	imatinib	204-212	cathepsin B	Homo sapiens	30-32
19924144-5	2010	Pharmacological inhibition of CB by CA-074Me or small interfering RNA-mediated knock-down of CB partly protects K562 cells from Imatinib-induced cell death and CB overexpression sensitizes these cells to Imatinib killing.	imatinib	204-212	cathepsin B	Homo sapiens	93-95
19924144-5	2010	Pharmacological inhibition of CB by CA-074Me or small interfering RNA-mediated knock-down of CB partly protects K562 cells from Imatinib-induced cell death and CB overexpression sensitizes these cells to Imatinib killing.	imatinib	204-212	cathepsin B	Homo sapiens	93-95
19924144-6	2010	Strikingly, Imatinib-triggered LMP, CB activation and BCR-ABL cleavage in CD34+ cells from CML patients and inhibition of CB confers protection against cell death in clonogenic assays of CD34+ primary cells from CML patients.	imatinib	12-20	cathepsin B	Homo sapiens	36-38
19924144-6	2010	Strikingly, Imatinib-triggered LMP, CB activation and BCR-ABL cleavage in CD34+ cells from CML patients and inhibition of CB confers protection against cell death in clonogenic assays of CD34+ primary cells from CML patients.	imatinib	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
19924144-6	2010	Strikingly, Imatinib-triggered LMP, CB activation and BCR-ABL cleavage in CD34+ cells from CML patients and inhibition of CB confers protection against cell death in clonogenic assays of CD34+ primary cells from CML patients.	imatinib	12-20	CD34 molecule	Homo sapiens	74-78
19924144-6	2010	Strikingly, Imatinib-triggered LMP, CB activation and BCR-ABL cleavage in CD34+ cells from CML patients and inhibition of CB confers protection against cell death in clonogenic assays of CD34+ primary cells from CML patients.	imatinib	12-20	CD34 molecule	Homo sapiens	187-191
20339212-0	2010	[An elderly case of chronic myeloid leukemia in which BCR/ABL decreased or disappeared, following imatinib therapy after each episode of blast crisis].	imatinib	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
20053766-2	2010	The various juxtamembrane type of KIT mutations, including V560G, are found in 60% to 70% of patients with gastrointestinal stromal tumors; loop mutant D816V, which exists in approximately 80% of SM patients, is completely resistant to imatinib.	imatinib	236-244	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	34-37
20053766-4	2010	Imatinib-sensitive HMC-1.1 cells harboring the mutation V560G in the juxtamembrane domain of KIT, imatinib-resistant HMC-1.2 cells harboring both V560G and D816V mutations, and murine P815 cells were treated with HHT and analyzed in terms of growth, apoptosis, and signal transduction.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	93-96
20053766-4	2010	Imatinib-sensitive HMC-1.1 cells harboring the mutation V560G in the juxtamembrane domain of KIT, imatinib-resistant HMC-1.2 cells harboring both V560G and D816V mutations, and murine P815 cells were treated with HHT and analyzed in terms of growth, apoptosis, and signal transduction.	imatinib	98-106	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	93-96
20053766-9	2010	Collectively, we show that HHT circumvents D816V KIT-elicited imatinib resistance.	imatinib	62-70	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	49-52
19956885-0	2010	Imatinib mesylate (STI571) enhances amrubicin-induced cytotoxic activity through inhibition of the phosphatidylinositol 3-kinase/Akt pathway in small cell lung cancer cells.	imatinib	0-17	AKT serine/threonine kinase 1	Homo sapiens	129-132
19956885-0	2010	Imatinib mesylate (STI571) enhances amrubicin-induced cytotoxic activity through inhibition of the phosphatidylinositol 3-kinase/Akt pathway in small cell lung cancer cells.	imatinib	19-25	AKT serine/threonine kinase 1	Homo sapiens	129-132
19956885-3	2010	Imatinib mesylate (STI571) can inhibit c-kit tyrosine kinase activity, but clinical trials have resulted in failure.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	39-44
19956885-3	2010	Imatinib mesylate (STI571) can inhibit c-kit tyrosine kinase activity, but clinical trials have resulted in failure.	imatinib	19-25	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	39-44
19956885-7	2010	Treatment with SCF activated Akt and Erk and the activations were inhibited by STI571 in H209 but not in H69 cells.	imatinib	79-85	KIT ligand	Homo sapiens	15-18
19956885-13	2010	STI571 restored the AMR-sensitivity of SCF-treated H209 cells to the basal level.	imatinib	0-6	KIT ligand	Homo sapiens	39-42
20067864-1	2010	Imatinib inhibits Bcr-Abl, c-KIT and PDGFR kinases.	imatinib	0-8	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	27-32
20067864-1	2010	Imatinib inhibits Bcr-Abl, c-KIT and PDGFR kinases.	imatinib	0-8	platelet derived growth factor receptor, beta polypeptide	Mus musculus	37-42
20072835-4	2010	Interestingly, distinctly lower concentrations of the dual src/abl inhibitor are required to ablate Bcr-Abl phosphorylation when compared to first-generation tyrosine kinase inhibitor imatinib (IM).	imatinib	184-192	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	59-62
20072827-3	2010	Imatinib is a rationally designed oral signal transduction inhibitor that specifically targets several protein tyrosine kinases, Abl, Arg (Abl-related gene), the stem-cell factor receptor (c-KIT), platelet-derived growth factor receptor (PDGF-R), and their oncogenic forms, most notably Bcr-Abl.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-132
20072827-3	2010	Imatinib is a rationally designed oral signal transduction inhibitor that specifically targets several protein tyrosine kinases, Abl, Arg (Abl-related gene), the stem-cell factor receptor (c-KIT), platelet-derived growth factor receptor (PDGF-R), and their oncogenic forms, most notably Bcr-Abl.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-142
21344772-3	2010	Its employment in neuroblastoma treatment is potentially possible because of expression of c-kit and PDGFR, which are cellular targets of imatinib.	imatinib	138-146	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	91-96
21344772-3	2010	Its employment in neuroblastoma treatment is potentially possible because of expression of c-kit and PDGFR, which are cellular targets of imatinib.	imatinib	138-146	platelet derived growth factor receptor beta	Homo sapiens	101-106
20072827-3	2010	Imatinib is a rationally designed oral signal transduction inhibitor that specifically targets several protein tyrosine kinases, Abl, Arg (Abl-related gene), the stem-cell factor receptor (c-KIT), platelet-derived growth factor receptor (PDGF-R), and their oncogenic forms, most notably Bcr-Abl.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	189-194
20072840-8	2010	However, this particular mutation is predicted to play an even more important clinical role in the future, since in addition to Imatinib, it also confers resistance to second-generation Bcr-Abl inhibitors such as Nilotinib, Dasatinib, and Bosutinib.	imatinib	128-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-193
20072827-3	2010	Imatinib is a rationally designed oral signal transduction inhibitor that specifically targets several protein tyrosine kinases, Abl, Arg (Abl-related gene), the stem-cell factor receptor (c-KIT), platelet-derived growth factor receptor (PDGF-R), and their oncogenic forms, most notably Bcr-Abl.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	197-236
20072827-3	2010	Imatinib is a rationally designed oral signal transduction inhibitor that specifically targets several protein tyrosine kinases, Abl, Arg (Abl-related gene), the stem-cell factor receptor (c-KIT), platelet-derived growth factor receptor (PDGF-R), and their oncogenic forms, most notably Bcr-Abl.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	238-244
20072827-3	2010	Imatinib is a rationally designed oral signal transduction inhibitor that specifically targets several protein tyrosine kinases, Abl, Arg (Abl-related gene), the stem-cell factor receptor (c-KIT), platelet-derived growth factor receptor (PDGF-R), and their oncogenic forms, most notably Bcr-Abl.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	287-294
20113282-2	2010	It has a 325 times stronger in vitro activity against to native BCR-ABL when comparing with imatinib.	imatinib	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
20072827-6	2010	Clonal evolution, amplification, or overexpression of Bcr-Abl as well as mutations in the catalytic domain, P-loop, and other mutations have been demonstrated to play a role in primary and secondary resistance to imatinib, respectively.	imatinib	213-221	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
20024108-6	2009	Subsequent biochemical screenings revealed a set of moderately potent inhibitors, a few of which have comparable potency to Imatinib (an FDA-approved drug for treatment of chronic myeloid leukemia) against Abl.	imatinib	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	206-209
23960476-8	2010	CONCLUSIONS: These results suggested that c-kit could be used as a prognostic marker for ACC and specific c-kit tyrosine kinase inhibitors such as imatinib, might be used in future therapeutic approaches against subgroups of ACC.	imatinib	147-155	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	106-111
20041122-0	2009	Steered molecular dynamics simulations reveal the likelier dissociation pathway of imatinib from its targeting kinases c-Kit and Abl.	imatinib	83-91	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	119-124
20041122-0	2009	Steered molecular dynamics simulations reveal the likelier dissociation pathway of imatinib from its targeting kinases c-Kit and Abl.	imatinib	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-132
20041122-4	2009	In this investigation, steered molecular dynamics simulations have been carried out to explore the possible dissociation pathways of typical type II inhibitor imatinib from its targeting protein kinases c-Kit and Abl.	imatinib	159-167	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	203-208
20041122-4	2009	In this investigation, steered molecular dynamics simulations have been carried out to explore the possible dissociation pathways of typical type II inhibitor imatinib from its targeting protein kinases c-Kit and Abl.	imatinib	159-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	213-216
20339585-0	2010	A V530I Mutation in c-KIT Exon 10 Is Associated to Imatinib Response in Extraabdominal Aggressive Fibromatosis.	imatinib	51-59	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	20-25
20339585-5	2010	Here, we describe for the first time a V530I KIT exon 10 mutant that was associated to a dramatic imatinib response in an extraabdominal aggressive fibromatosis.	imatinib	98-106	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	45-48
19934315-0	2009	Imatinib mesylate induces cisplatin hypersensitivity in Bcr-Abl+ cells by differential modulation of p53 transcriptional and proapoptotic activity.	imatinib	0-17	tumor protein p53	Homo sapiens	101-104
19934315-4	2009	Inhibition of Bcr-Abl by imatinib induced a hypersensitive phenotype both in Bcr-Abl(+) cell lines and in CD34(+) cells from CML patients.	imatinib	25-33	CD34 molecule	Homo sapiens	106-110
19934315-7	2009	Imatinib abrogated ATM activation on cisplatin selectively in Bcr-Abl(+) cells.	imatinib	0-8	ATM serine/threonine kinase	Homo sapiens	19-22
19934315-9	2009	Furthermore, p53 accumulated predominantly in the cytoplasm in Bcr-Abl(+) cells treated with imatinib and cisplatin.	imatinib	93-101	tumor protein p53	Homo sapiens	13-16
19934315-10	2009	Silencing of p53 significantly reduced sensitivity to cisplatin in imatinib-treated Bcr-Abl(+) cells, indicating that p53 retains its proapoptotic activity.	imatinib	67-75	tumor protein p53	Homo sapiens	13-16
19934315-10	2009	Silencing of p53 significantly reduced sensitivity to cisplatin in imatinib-treated Bcr-Abl(+) cells, indicating that p53 retains its proapoptotic activity.	imatinib	67-75	tumor protein p53	Homo sapiens	118-121
19934315-12	2009	We conclude that imatinib sensitizes Bcr-Abl(+) cells to cisplatin by simultaneous inhibition of p53 transactivation, induction of p53 accumulation predominantly in the cytoplasm, and reduction of Bcl-x(L).	imatinib	17-25	tumor protein p53	Homo sapiens	97-100
19934315-12	2009	We conclude that imatinib sensitizes Bcr-Abl(+) cells to cisplatin by simultaneous inhibition of p53 transactivation, induction of p53 accumulation predominantly in the cytoplasm, and reduction of Bcl-x(L).	imatinib	17-25	tumor protein p53	Homo sapiens	131-134
19934315-12	2009	We conclude that imatinib sensitizes Bcr-Abl(+) cells to cisplatin by simultaneous inhibition of p53 transactivation, induction of p53 accumulation predominantly in the cytoplasm, and reduction of Bcl-x(L).	imatinib	17-25	BCL2 like 1	Homo sapiens	197-205
19779040-1	2009	Dasatinib is a BCR-ABL inhibitor with 325-fold higher potency than imatinib against unmutated BCR-ABL in vitro.	imatinib	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
19779040-2	2009	Imatinib failure is commonly caused by BCR-ABL mutations.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
20044640-1	2009	BACKGROUND: The tyrosine kinase inhibitors (TKI) sunitinib and imatinib were shown to induce macrocytosis in patients with renal cell cancer (RCC) and gastrointestinal stromal tumors (GIST), presumably through inhibition of the c-KIT dependent signaling pathway of erythroid progenitor cells of the bone marrow.	imatinib	63-71	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	228-233
19801450-6	2009	Inhibition of PDGF-Rbeta signaling with imatinib, however, was sufficient to reverse the PAH observed in the Tie2 PPARgamma(-/-) mice.	imatinib	40-48	platelet derived growth factor receptor, beta polypeptide	Mus musculus	14-24
19735261-5	2009	Low-dose, short-course imatinib may represent a rational choice for identifying responsive cases, both within and outside the pre-defined FIP1L1 rearrangement subset.	imatinib	23-31	factor interacting with PAPOLA and CPSF1	Homo sapiens	138-144
19903850-7	2009	Pursuing these findings, we have determined that imatinib-induced DNA damage is responsible for the increased activity of p53, identifying a novel off-target activity for this drug.	imatinib	49-57	tumor protein p53	Homo sapiens	122-125
19855080-0	2009	Molecular and functional analysis of the stem cell compartment of chronic myelogenous leukemia reveals the presence of a CD34- cell population with intrinsic resistance to imatinib.	imatinib	172-180	CD34 molecule	Homo sapiens	121-125
19910029-8	2009	Imatinib (used in 68 patients) was more effective in patients with the FIP1L1-PDGFRA mutation (88%) than in those without (23%; P < .001).	imatinib	0-8	factor interacting with PAPOLA and CPSF1	Homo sapiens	71-77
19708828-5	2009	Furthermore, we also review evidence suggesting that tyrosine kinase inhibitors, including imatinib and gefitinib, are both direct and downstream inactivators of ABCG2 and, therefore, serve as candidates to reverse cancer stem cell chemoresistance and potentially target cancer stem cells.	imatinib	91-99	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	162-167
19955950-1	2009	Imatinib mesylate inhibits platelet-derived growth factor receptor (PDGFR), and there are evidences that the PDGFR participates in development and progression of cervical cancer.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	27-66
19955950-1	2009	Imatinib mesylate inhibits platelet-derived growth factor receptor (PDGFR), and there are evidences that the PDGFR participates in development and progression of cervical cancer.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	68-73
19910029-8	2009	Imatinib (used in 68 patients) was more effective in patients with the FIP1L1-PDGFRA mutation (88%) than in those without (23%; P < .001).	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	78-84
19735720-1	2009	The effect of cyclosporin A (CsA) on imatinib treated Bcr-Abl positive K562 cells was studied.	imatinib	37-45	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	29-32
19484755-4	2009	The Src/Abl kinase inhibitor dasatinib has recently been approved for use in Ph+ leukemias after failure with imatinib.	imatinib	110-118	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	4-7
20010464-0	2009	Frequency of BCR-ABL gene mutations in Polish patients with chronic myeloid leukemia treated with imatinib: a final report of the MAPTEST study.	imatinib	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
20010464-2	2009	OBJECTIVES: The aim of the study was to evaluate the frequency of BCR-ABL gene mutations in patients with CML (the MAPTEST study) treated with imatinib (IM).	imatinib	143-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
20010473-0	2009	A diagnostically difficult case of chronic myeloid neoplasm with eosinophilia and abnormalities of PDGFRA effectively treated with imatinib in accelerated phase: case report.	imatinib	131-139	platelet derived growth factor receptor alpha	Homo sapiens	99-105
20010473-8	2009	We present the case of a 52-year-old patient with chronic myeloid neoplasm with eosinophilia and abnormalities of PDGFRA, in whom acceleration occurred after a year of cytostatic therapy with hydroxyurea and was successfully treated with imatinib.	imatinib	238-246	platelet derived growth factor receptor alpha	Homo sapiens	114-120
19735720-10	2009	Therefore we excluded the possibility that CsA increased sensitivity of cells to imatinib by the inhibition of P-gp-mediated drug efflux or by another mechanism involving modulation of intracellular drug concentration.	imatinib	81-89	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	43-46
19672773-1	2009	Dasatinib, a dual Src/Abl tyrosine kinase inhibitor, has significant antileukemic effects against various imatinib mesylate-resistant BCR/ABL mutants.	imatinib	106-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
19672773-3	2009	We provide evidence that p38 Map kinase (MAPK) pathway is activated leading to increased upregulation of mixed lineage kinase 3, MKK3/6, MSK1, and Mapkapk2, upon treatment of BCR/ABL expressing cells with dasatinib, including cells expressing various imatinib-resistant mutants, except for T315I.	imatinib	251-259	mitogen-activated protein kinase 14	Homo sapiens	25-39
19672773-3	2009	We provide evidence that p38 Map kinase (MAPK) pathway is activated leading to increased upregulation of mixed lineage kinase 3, MKK3/6, MSK1, and Mapkapk2, upon treatment of BCR/ABL expressing cells with dasatinib, including cells expressing various imatinib-resistant mutants, except for T315I.	imatinib	251-259	mitogen-activated protein kinase kinase kinase 11	Homo sapiens	105-127
19672773-3	2009	We provide evidence that p38 Map kinase (MAPK) pathway is activated leading to increased upregulation of mixed lineage kinase 3, MKK3/6, MSK1, and Mapkapk2, upon treatment of BCR/ABL expressing cells with dasatinib, including cells expressing various imatinib-resistant mutants, except for T315I.	imatinib	251-259	mitogen-activated protein kinase kinase 3	Homo sapiens	129-133
19672773-3	2009	We provide evidence that p38 Map kinase (MAPK) pathway is activated leading to increased upregulation of mixed lineage kinase 3, MKK3/6, MSK1, and Mapkapk2, upon treatment of BCR/ABL expressing cells with dasatinib, including cells expressing various imatinib-resistant mutants, except for T315I.	imatinib	251-259	MAPK activated protein kinase 2	Homo sapiens	147-155
19672773-3	2009	We provide evidence that p38 Map kinase (MAPK) pathway is activated leading to increased upregulation of mixed lineage kinase 3, MKK3/6, MSK1, and Mapkapk2, upon treatment of BCR/ABL expressing cells with dasatinib, including cells expressing various imatinib-resistant mutants, except for T315I.	imatinib	251-259	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-182
19934277-6	2009	Imatinib, gefitinib, bortezomib, and Bim protein itself are spotlighted as current and future Bim-targeting therapeutic agents.	imatinib	0-8	BCL2 like 11	Homo sapiens	94-97
19293394-2	2009	The North American Brain Tumor Consortium conducted a phase II study to evaluate the therapeutic potential of imatinib mesylate (Gleevec), a PDGFR inhibitor, in patients with recurrent meningiomas.	imatinib	110-127	platelet derived growth factor receptor beta	Homo sapiens	141-146
19735720-4	2009	We found that CsA significantly potentiated cytotoxic effects of imatinib.	imatinib	65-73	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	14-17
19735720-7	2009	We further observed that CsA might sensitise cells to apoptosis due to a changed cellular redox status as combined treatment of cells with imatinib and CsA resulted in a dramatic decrease of the ratio between reduced (GSH) and oxidised (GSSG) glutathione GSH/GSSG and in a significant suppression of thioredoxin reductase enzymatic activity.	imatinib	139-147	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	25-28
19861442-10	2009	In contrast, in vitro resistance to imatinib produces a broader spectrum of secondary mutations including mutations in both KIT kinase domains.	imatinib	36-44	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	124-127
19748901-0	2009	Successful PDGFR-{alpha}/{beta} targeting with imatinib in uterine sarcoma.	imatinib	47-55	platelet derived growth factor receptor alpha	Homo sapiens	11-23
19878872-1	2009	Inhibition of BCR-ABL by imatinib induces durable responses in many patients with chronic myeloid leukemia (CML), but resistance attributable to kinase domain mutations can lead to relapse and a switch to second-line therapy with nilotinib or dasatinib.	imatinib	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
19838099-2	2009	It binds to both active and inactive conformations of the ABL gene and is 325 times more potent than imatinib in inhibiting the growth of BCR/ABL cells in vitro (Morelock and Sahn, Chest 1999;116:212-21; Huggins and Sahn, Clin Chest Med 2004;25:141-53).	imatinib	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-145
19903356-0	2009	Insulin-like growth factor binding protein-3 has dual effects on gastrointestinal stromal tumor cell viability and sensitivity to the anti-tumor effects of imatinib mesylate in vitro.	imatinib	156-173	insulin like growth factor binding protein 3	Homo sapiens	0-44
19903356-3	2009	Previously, we found up-regulation of insulin-like growth factor binding protein-3 (IGFBP3) expression in imatinib-responsive GIST cells and tumor samples.	imatinib	106-114	insulin like growth factor binding protein 3	Homo sapiens	38-82
19903356-3	2009	Previously, we found up-regulation of insulin-like growth factor binding protein-3 (IGFBP3) expression in imatinib-responsive GIST cells and tumor samples.	imatinib	106-114	insulin like growth factor binding protein 3	Homo sapiens	84-90
19903356-4	2009	Because IGFBP3 regulates cell proliferation and survival and mediates the anti-tumor effects of a number of anti-cancer agents through both IGF-dependent and IGF-independent mechanisms, we hypothesized that IGFBP3 mediates GIST cell response to imatinib.	imatinib	245-253	insulin like growth factor binding protein 3	Homo sapiens	207-213
19903356-6	2009	RESULTS: In the GIST882 cell line, imatinib treatment induced endogenous IGFBP3 expression, and IGFBP3 down-modulation by neutralization or RNA interference resulted in partial resistance to imatinib.	imatinib	35-43	insulin like growth factor binding protein 3	Homo sapiens	73-79
19903356-9	2009	CONCLUSION: This data demonstrates that IGFBP3 has dual, opposing roles in modulating GIST cell viability and response to imatinib in vitro.	imatinib	122-130	insulin like growth factor binding protein 3	Homo sapiens	40-46
20032406-1	2009	Imatinib mesylate (STI571), an inhibitor of alpha- and beta-platelet-derived growth factor receptors (PDGFR) and other tyrosine kinases, is a well established treatment for chronic myeloid leukaemia and gastrointestinal stromal tumours.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	55-100
20032453-16	2009	Imatinib was effective against GIST that were positive for KIT protein, but future study is needed to clarify the risk factors for recurrence and indications for adjuvant therapy in cases of GIST.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	59-62
19917964-2	2009	Imatinib mesylate is an inhibitor of c-kit and is indicated in the treatment of chronic myeloid leukemia and GISTs.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	37-42
20032406-1	2009	Imatinib mesylate (STI571), an inhibitor of alpha- and beta-platelet-derived growth factor receptors (PDGFR) and other tyrosine kinases, is a well established treatment for chronic myeloid leukaemia and gastrointestinal stromal tumours.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	102-107
20032406-1	2009	Imatinib mesylate (STI571), an inhibitor of alpha- and beta-platelet-derived growth factor receptors (PDGFR) and other tyrosine kinases, is a well established treatment for chronic myeloid leukaemia and gastrointestinal stromal tumours.	imatinib	19-25	platelet derived growth factor receptor beta	Homo sapiens	55-100
20032406-1	2009	Imatinib mesylate (STI571), an inhibitor of alpha- and beta-platelet-derived growth factor receptors (PDGFR) and other tyrosine kinases, is a well established treatment for chronic myeloid leukaemia and gastrointestinal stromal tumours.	imatinib	19-25	platelet derived growth factor receptor beta	Homo sapiens	102-107
19755855-5	2009	Treatment of NCI-H1703 cells with PDGFRA-specific shRNAs or with the PDGFRalpha/KIT small molecule inhibitors imatinib or sunitinib leads to cell growth inhibition.	imatinib	110-118	platelet derived growth factor receptor alpha	Homo sapiens	69-79
19540211-4	2009	Imatinib markedly reduced cisplatin-induced cytotoxicity and platinum accumulation in OCT2-expressing HEK293 cells, but almost no change was found in the cells expressing human MATE1, MATE2-K and rat MATE1.	imatinib	0-8	solute carrier family 22 member 2	Homo sapiens	86-90
19540211-4	2009	Imatinib markedly reduced cisplatin-induced cytotoxicity and platinum accumulation in OCT2-expressing HEK293 cells, but almost no change was found in the cells expressing human MATE1, MATE2-K and rat MATE1.	imatinib	0-8	solute carrier family 47 member 1	Rattus norvegicus	200-205
19540211-8	2009	In conclusion, the concomitant administration of imatinib with cisplatin prevents cisplatin-induced nephrotoxicity inhibiting the OCT2-mediated renal accumulation of cisplatin.	imatinib	49-57	solute carrier family 22 member 2	Homo sapiens	130-134
19671059-2	2009	HES usually shows good response to the tyrosine kinase inhibitor imatinib, but mutations in FIP1L1-PDGFRalpha (e.g. T674I) can confer acquired resistance to imatinib.	imatinib	157-165	factor interacting with PAPOLA and CPSF1	Homo sapiens	92-98
19671059-2	2009	HES usually shows good response to the tyrosine kinase inhibitor imatinib, but mutations in FIP1L1-PDGFRalpha (e.g. T674I) can confer acquired resistance to imatinib.	imatinib	157-165	platelet derived growth factor receptor alpha	Homo sapiens	99-109
19755855-5	2009	Treatment of NCI-H1703 cells with PDGFRA-specific shRNAs or with the PDGFRalpha/KIT small molecule inhibitors imatinib or sunitinib leads to cell growth inhibition.	imatinib	110-118	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	80-83
19652585-1	2009	KIT alterations have been identified in melanoma and treatment with imatinib has met with some success.	imatinib	68-76	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
19801102-4	2009	RESULTS: Dramatic phosphorylated (p)-c-Kit and p-PDGFRbeta attenuation, a modest dose- and time-dependent growth inhibition, and significant radiosensitization were observed after STI-571 treatment in view of apoptosis, although the levels of growth inhibition and increased radiosensitization were different according to cell lines.	imatinib	180-187	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	37-42
19801102-4	2009	RESULTS: Dramatic phosphorylated (p)-c-Kit and p-PDGFRbeta attenuation, a modest dose- and time-dependent growth inhibition, and significant radiosensitization were observed after STI-571 treatment in view of apoptosis, although the levels of growth inhibition and increased radiosensitization were different according to cell lines.	imatinib	180-187	platelet derived growth factor receptor beta	Homo sapiens	49-58
19394692-0	2009	ZD6474 inhibits Src kinase leading to apoptosis of imatinib-resistant K562 cells.	imatinib	51-59	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	16-19
19394692-2	2009	This study explores the effect of ZD6474 on imatinib-resistant K562 cell lines, which show markedly increased SRC family kinases (SFKs) activity.	imatinib	44-52	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	110-113
19446878-1	2009	Imatinib-induced macrocytic anemia was known to result from c-kit inhibition in chronic myeloid leukemia (CML).	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	60-65
19841739-0	2009	Imatinib and nilotinib reverse multidrug resistance in cancer cells by inhibiting the efflux activity of the MRP7 (ABCC10).	imatinib	0-8	ATP binding cassette subfamily C member 10	Homo sapiens	109-113
19841739-0	2009	Imatinib and nilotinib reverse multidrug resistance in cancer cells by inhibiting the efflux activity of the MRP7 (ABCC10).	imatinib	0-8	ATP binding cassette subfamily C member 10	Homo sapiens	115-121
19841739-4	2009	In this study, we examined the effects of BCR-Abl tyrosine kinase inhibitors imatinib, nilotinib and dasatinib on the activity and expression of MRP7 in HEK293 cells transfected with MRP7, designated HEK-MRP7-2.	imatinib	77-85	ATP binding cassette subfamily C member 10	Homo sapiens	145-149
19841739-5	2009	METHODOLOGY AND/OR PRINCIPAL FINDINGS: We report for the first time that imatinib and nilotinib reversed MRP7-mediated multidrug resistance.	imatinib	73-81	ATP binding cassette subfamily C member 10	Homo sapiens	105-109
19841739-7	2009	In addition, imatinib and nilotinib (1-5 microM) produced a significant concentration-dependent reversal of MRP7-mediated multidrug resistance by enhancing the sensitivity of HEK-MRP7-2 cells to paclitaxel and vincristine.	imatinib	13-21	ATP binding cassette subfamily C member 10	Homo sapiens	108-112
19841739-7	2009	In addition, imatinib and nilotinib (1-5 microM) produced a significant concentration-dependent reversal of MRP7-mediated multidrug resistance by enhancing the sensitivity of HEK-MRP7-2 cells to paclitaxel and vincristine.	imatinib	13-21	ATP binding cassette subfamily C member 10	Homo sapiens	179-183
19841739-8	2009	Imatinib and nilotinib, at 5 microM, significantly increased the accumulation of [(3)H]-paclitaxel in HEK-MRP7-2 cells.	imatinib	0-8	ATP binding cassette subfamily C member 10	Homo sapiens	106-110
19841739-9	2009	The incubation of the HEK-MRP7-2 cells with imatinib or nilotinib (5 microM) also significantly inhibited the efflux of paclitaxel.	imatinib	44-52	ATP binding cassette subfamily C member 10	Homo sapiens	26-30
19841739-10	2009	CONCLUSIONS: Imatinib and nilotinib reverse MRP7-mediated paclitaxel resistance, most likely due to their inhibition of the efflux of paclitaxel via MRP7.	imatinib	13-21	ATP binding cassette subfamily C member 10	Homo sapiens	44-48
19841739-10	2009	CONCLUSIONS: Imatinib and nilotinib reverse MRP7-mediated paclitaxel resistance, most likely due to their inhibition of the efflux of paclitaxel via MRP7.	imatinib	13-21	ATP binding cassette subfamily C member 10	Homo sapiens	149-153
19811659-8	2009	From all conventional RCC, CD 117 was detected (overexpression) in membrane of cells ChRCC.Overexpression of CD117 on cellular membranes of ChRCC could be a potential target for kinase inhibitors like: imatinib, dasatinib, nilotinib.	imatinib	202-210	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	109-114
19933079-2	2009	In this phase II trial, we added imatinib, a PDGFR inhibitor, to docetaxel in the first-line treatment of women with metastatic breast cancer (MBC).	imatinib	33-41	platelet derived growth factor receptor beta	Homo sapiens	45-50
19766113-6	2009	Inhibition of c-Abl by STI571 or suppression of c-Abl expression by shRNA blocked ING2 induction and p73alpha acetylation induced by this alkylator.	imatinib	23-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
19880777-6	2009	Functionally, ABCA3 levels are critical for the susceptibility of chronic myeloid leukemia blast cell lines to specific BCR-ABL inhibition by imatinib.	imatinib	142-150	ATP binding cassette subfamily A member 3	Homo sapiens	14-19
19880777-6	2009	Functionally, ABCA3 levels are critical for the susceptibility of chronic myeloid leukemia blast cell lines to specific BCR-ABL inhibition by imatinib.	imatinib	142-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
19880777-8	2009	The lysosomal storage capacity increases with ABCA3 expression, thus regulating imatinib sequestration.	imatinib	80-88	ATP binding cassette subfamily A member 3	Homo sapiens	46-51
19767223-1	2009	Inhibition of tyrosine kinases (such as the epidermal growth factor receptor, EGFR, and/or Abelson leukemia virus protein kinase, ABL) represents a major advancement in the treatment of solid tumors, supported by the clinical administration of gefitinib, erlotinib, imatinib, and dasatinib.	imatinib	266-274	epidermal growth factor receptor	Homo sapiens	44-76
19767223-6	2009	Our results indicate that imatinib is a weak binder to the active state of ABL but a strong binder to EGFR.	imatinib	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-78
19767223-6	2009	Our results indicate that imatinib is a weak binder to the active state of ABL but a strong binder to EGFR.	imatinib	26-34	epidermal growth factor receptor	Homo sapiens	102-106
19193436-2	2009	Twenty patients with SM were enrolled during 2003-2005 in phase II clinical trial with imatinib mesylate (400mg daily), a KIT inhibitor.	imatinib	87-104	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	122-125
19329185-2	2009	Treatment of Imatinib or LY294002 reduced Skp2 mRNA in BCR-ABL-positive K562 cells.	imatinib	13-21	S-phase kinase associated protein 2	Homo sapiens	42-46
19329185-2	2009	Treatment of Imatinib or LY294002 reduced Skp2 mRNA in BCR-ABL-positive K562 cells.	imatinib	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
19329185-4	2009	We found that BCR-ABL up-regulated Skp2 via Sp1 because (1) the Sp1 site located at the -386/-380 promoter region was important for BCR-ABL-induced Skp2 promoter activity, (2) chromatin immunoprecipitation assay demonstrated that Imatinib inhibited the recruitment of p300 to the Sp1 site of Skp2 promoter and (3) knockdown of Sp1 reduced Skp2 expression in K562 cells.	imatinib	230-238	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
19329185-4	2009	We found that BCR-ABL up-regulated Skp2 via Sp1 because (1) the Sp1 site located at the -386/-380 promoter region was important for BCR-ABL-induced Skp2 promoter activity, (2) chromatin immunoprecipitation assay demonstrated that Imatinib inhibited the recruitment of p300 to the Sp1 site of Skp2 promoter and (3) knockdown of Sp1 reduced Skp2 expression in K562 cells.	imatinib	230-238	S-phase kinase associated protein 2	Homo sapiens	35-39
19329185-4	2009	We found that BCR-ABL up-regulated Skp2 via Sp1 because (1) the Sp1 site located at the -386/-380 promoter region was important for BCR-ABL-induced Skp2 promoter activity, (2) chromatin immunoprecipitation assay demonstrated that Imatinib inhibited the recruitment of p300 to the Sp1 site of Skp2 promoter and (3) knockdown of Sp1 reduced Skp2 expression in K562 cells.	imatinib	230-238	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
19706883-1	2009	Pioneering work with the Bcr-Abl inhibitor, imatinib, demonstrated a requirement for constant Bcr-Abl inhibition to achieve maximal therapeutic benefit in treating chronic myeloid leukemia (CML), establishing a paradigm that has guided further drug development for this disease.	imatinib	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
19706883-1	2009	Pioneering work with the Bcr-Abl inhibitor, imatinib, demonstrated a requirement for constant Bcr-Abl inhibition to achieve maximal therapeutic benefit in treating chronic myeloid leukemia (CML), establishing a paradigm that has guided further drug development for this disease.	imatinib	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
19785662-2	2009	It has been documented that ABCB1 and ABCG2 interact with several first-generation, small-molecule, tyrosine kinase inhibitors (TKIs), including the Bcr-Abl fusion kinase inhibitor imatinib, used for the treatment of chronic myeloid leukaemia.	imatinib	181-189	ATP binding cassette subfamily B member 1	Homo sapiens	28-33
19538165-3	2009	Imatinib was designed on the basis of the structure of the ATP binding site of the Abl protein kinase with the aim to stabilizes the inactive form of Bcr-Abl, an oncoprotein involved in malignant transformation in chronic myelogenous leukemia (CML).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-86
19538165-3	2009	Imatinib was designed on the basis of the structure of the ATP binding site of the Abl protein kinase with the aim to stabilizes the inactive form of Bcr-Abl, an oncoprotein involved in malignant transformation in chronic myelogenous leukemia (CML).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
19538165-4	2009	However, imatinib can also target other tyrosine kinase proteins different from Bcr-Abl such as Kit, that is the suspected cause of gastrointestinal stromal tumor (GIST).	imatinib	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
19538165-7	2009	In this review we will discuss the in vitro and in vivo results obtained with the novel tyrosine kinase inhibitors developed to overcome imatinib resistance in Bcr-Abl expressing hematologiocal disorders.	imatinib	137-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-167
19785662-2	2009	It has been documented that ABCB1 and ABCG2 interact with several first-generation, small-molecule, tyrosine kinase inhibitors (TKIs), including the Bcr-Abl fusion kinase inhibitor imatinib, used for the treatment of chronic myeloid leukaemia.	imatinib	181-189	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	38-43
19749465-0	2009	Analysis of binding energy activity of imatinib and Abl tyrosine kinase domain based on simple consideration for conformational change: An explanation for variation in imatinib effect in mutated type.	imatinib	168-176	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-55
19801694-0	2009	BCR-ABL mutational studies for predicting the response of patients with chronic myeloid leukaemia to second-generation tyrosine kinase inhibitors after imatinib failure.	imatinib	152-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
19801694-2	2009	BCR-ABL kinase domain mutation is the commonest mechanism implicated in imatinib resistance.	imatinib	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
19801694-10	2009	Although BCR-ABL kinase domain mutational analysis has limitations as a means of predicting the clinical response to second-line tyrosine kinase inhibitors, it helps inform therapy decisions in the management of chronic myeloid leukaemia after imatinib failure.	imatinib	244-252	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
19737658-0	2009	Trisomy 8 in PDGFRB-negative cells in a patient with imatinib-sensitive chronic myelomonocytic leukemia and t(5;16)(q33;p13), PDGFRB-NDE1 fusion.	imatinib	53-61	platelet derived growth factor receptor beta	Homo sapiens	13-19
19793709-1	2009	The introduction of the BCR-ABL inhibitor imatinib revolutionized the treatment of patients with chronic myeloid leukemia (CML).	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
19793709-3	2009	Numerous mechanisms have been associated with imatinib resistance, including mutations to the BCR-ABL gene, increased production of BCR-ABL, and activation of BCR-ABL-independent pathways (e.g., SRC-family kinases [SFKs]).	imatinib	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
19793709-3	2009	Numerous mechanisms have been associated with imatinib resistance, including mutations to the BCR-ABL gene, increased production of BCR-ABL, and activation of BCR-ABL-independent pathways (e.g., SRC-family kinases [SFKs]).	imatinib	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
19793709-3	2009	Numerous mechanisms have been associated with imatinib resistance, including mutations to the BCR-ABL gene, increased production of BCR-ABL, and activation of BCR-ABL-independent pathways (e.g., SRC-family kinases [SFKs]).	imatinib	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
19793709-4	2009	Resistance to imatinib has driven the development of second-line therapies, such as dasatinib, a dual BCR-ABL/SFK inhibitor more potent than imatinib at targeting BCR-ABL.	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
19793709-4	2009	Resistance to imatinib has driven the development of second-line therapies, such as dasatinib, a dual BCR-ABL/SFK inhibitor more potent than imatinib at targeting BCR-ABL.	imatinib	141-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
19713230-0	2009	Chronic myeloid leukemia patients with the e13a2 BCR-ABL fusion transcript have inferior responses to imatinib compared to patients with the e14a2 transcript.	imatinib	102-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
19713230-2	2009	The clinical significance of the type of BCR-ABL transcript in newly diagnosed patients in chronic phase treated with imatinib 400 mg from initial diagnosis remains unknown.	imatinib	118-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
19749465-1	2009	Imatinib is a clinically well-tolerated small molecule inhibitor that exerts selective, dual inhibition on the transforming growth factor beta and platelet-derived growth factor pathways.	imatinib	0-8	transforming growth factor beta 1	Homo sapiens	111-142
19749465-2	2009	The recognition of an inactive conformation of Abl, in which a catalytically important Asp-Phe-Gly motif is flipped by approximately 180 degrees with respect to the active conformation, underlies the specificity of the cancer drug imatinib, which is used to treat chronic myelogenous leukemia.	imatinib	231-239	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
19474800-4	2009	In addition to inhibiting the BCR-ABL kinase, imatinib and nilotinib target the same array of other tyrosine kinases, including c-KIT and platelet-derived growth factor receptor (PDGFR), albeit with differing potencies.	imatinib	46-54	platelet derived growth factor receptor beta	Homo sapiens	138-177
19878642-1	2009	The discovery of molecularly targeted agents that selectively inhibit bcr-abl tyrosine kinase activity, such as imatinib, has revolutionized the treatment and natural history of chronic myelogenous leukemia (CML).	imatinib	112-120	BCR activator of RhoGEF and GTPase	Homo sapiens	70-73
19474800-4	2009	In addition to inhibiting the BCR-ABL kinase, imatinib and nilotinib target the same array of other tyrosine kinases, including c-KIT and platelet-derived growth factor receptor (PDGFR), albeit with differing potencies.	imatinib	46-54	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	128-133
19732238-8	2009	However, both acute and prolonged inhibition of this receptor with the c-kit antagonist imatinib mesylate does not appear to affect the spontaneous contractility of myometrium.	imatinib	88-105	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	71-76
19636292-4	2009	Imatinib of 100 microg/g body weight was administered to heterozygous (KIT-Asp818Tyr/+) mice orally for 7, 14 and 28 days, and cecal tumors were dissected.	imatinib	0-8	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	71-74
19636292-7	2009	Western blotting and real-time PCR revealed that KIT expression was almost equivalent, but KIT phosphorylation was significantly but not completely inhibited in tumor tissues after 7, 14 and 28 days of imatinib administration when compared with that before imatinib administration.	imatinib	202-210	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	91-94
19636292-8	2009	Phosphorylation of Akt and Stat1 was accordingly inhibited after imatinib administration.	imatinib	65-73	thymoma viral proto-oncogene 1	Mus musculus	19-22
19636292-8	2009	Phosphorylation of Akt and Stat1 was accordingly inhibited after imatinib administration.	imatinib	65-73	signal transducer and activator of transcription 1	Mus musculus	27-32
19474800-4	2009	In addition to inhibiting the BCR-ABL kinase, imatinib and nilotinib target the same array of other tyrosine kinases, including c-KIT and platelet-derived growth factor receptor (PDGFR), albeit with differing potencies.	imatinib	46-54	platelet derived growth factor receptor beta	Homo sapiens	179-184
19617878-14	2009	Our study raises a prospect of correlation of c-kit mutation and a potential treatment of adenoid cystic carcinoma with tyrosine kinase inhibitor (imatinib).	imatinib	147-155	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	46-51
19657955-0	2009	Plerixafor inhibits chemotaxis toward SDF-1 and CXCR4-mediated stroma contact in a dose-dependent manner resulting in increased susceptibility of BCR-ABL+ cell to Imatinib and Nilotinib.	imatinib	163-171	chemokine (C-X-C motif) ligand 12	Mus musculus	38-43
19657955-0	2009	Plerixafor inhibits chemotaxis toward SDF-1 and CXCR4-mediated stroma contact in a dose-dependent manner resulting in increased susceptibility of BCR-ABL+ cell to Imatinib and Nilotinib.	imatinib	163-171	chemokine (C-X-C motif) receptor 4	Mus musculus	48-53
19657955-7	2009	In addition, we could show that exposure of BCR-ABL(+) cells to Imatinib or Nilotinib induced an increase in surface CXCR4 expression.	imatinib	64-72	chemokine (C-X-C motif) receptor 4	Mus musculus	117-122
19492322-5	2009	He remained in chronic phase CML since diagnosis however recent molecular monitoring revealed increased BCR/ABL transcripts necessitating a change in therapy to imatinib.	imatinib	161-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
19783996-6	2009	Treatment with the c-Abl kinase inhibitor imatinib counteracts these cisplatin-induced effects.	imatinib	42-50	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	19-24
19920925-2	2009	The BCR-ABL inhibitor imatinib mesylate (IM) has improved survival in all phases of CML and is the standard of care for newly diagnosed patients in chronic phase.	imatinib	22-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
19625707-0	2009	Determining the rise in BCR-ABL RNA that optimally predicts a kinase domain mutation in patients with chronic myeloid leukemia on imatinib.	imatinib	130-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
19625707-1	2009	In imatinib-treated chronic myeloid leukemia (CML), secondary drug resistance is often caused by mutations in the BCR-ABL kinase domain (KD).	imatinib	3-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
19722748-3	2009	c-KIT (CD117)-positive mast cells have been associated with chronic fibrosing diseases and may potentially be treated with imatinib (Gleevec), a c-KIT blocker.	imatinib	123-131	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-5
19536906-2	2009	Imatinib dose escalation was the main treatment option before dasatinib, which has 325-fold more potent inhibition than imatinib against unmutated Bcr-Abl in vitro.	imatinib	120-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-154
19737945-8	2009	Phosphorylated receptor tyrosine kinase profiling showed a specific activation of platelet-derived growth factor receptor alpha/beta in EGFRvIII-transduced pediatric glioblastoma cells, and targeted coinhibition with erlotinib and imatinib leads to enhanced efficacy in this model.	imatinib	231-239	platelet derived growth factor receptor alpha	Homo sapiens	82-127
19737946-11	2009	CONCLUSION: Cellular and molecular analyses showed that sunitinib clinical activity is associated with inhibition of KIT in GIST following imatinib failure, illustrating the rational approach used to develop a therapy aimed at the underlying oncogenic signaling pathway aberrancy.	imatinib	139-147	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	117-120
19737953-0	2009	Circulating levels of soluble KIT serve as a biomarker for clinical outcome in gastrointestinal stromal tumor patients receiving sunitinib following imatinib failure.	imatinib	149-157	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	30-33
19737953-1	2009	PURPOSE: To evaluate changes in circulating levels of soluble KIT (sKIT) extracellular domain as a potential biomarker for clinical outcome in gastrointestinal stromal tumor patients treated with the multitargeted tyrosine kinase inhibitor sunitinib following imatinib failure in a previously reported phase III study.	imatinib	260-268	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	62-65
19732723-5	2009	Importantly, our data uncover a causative role of AID activity in the acquisition of BCR-ABL1 mutations leading to Imatinib resistance, thus providing a rationale for the rapid development of drug resistance and blast crisis progression.	imatinib	115-123	activation induced cytidine deaminase	Homo sapiens	50-53
19732723-5	2009	Importantly, our data uncover a causative role of AID activity in the acquisition of BCR-ABL1 mutations leading to Imatinib resistance, thus providing a rationale for the rapid development of drug resistance and blast crisis progression.	imatinib	115-123	BCR activator of RhoGEF and GTPase	Homo sapiens	85-93
19660459-3	2009	This work investigates the conformational changes that accompany the binding of Gleevec, or imatinib mesylate, to the tyrosine kinases c-Kit and c-Abl.	imatinib	92-109	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	135-140
19660459-3	2009	This work investigates the conformational changes that accompany the binding of Gleevec, or imatinib mesylate, to the tyrosine kinases c-Kit and c-Abl.	imatinib	92-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-150
19567878-0	2009	Long-term outcome of patients with chronic myeloid leukemia treated with second-generation tyrosine kinase inhibitors after imatinib failure is predicted by the in vitro sensitivity of BCR-ABL kinase domain mutations.	imatinib	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	185-192
19567878-1	2009	Secondary imatinib resistance in chronic myeloid leukemia (CML) is associated in approximately 50% of cases with mutations in the BCR-ABL kinase domain, necessitating switch to one of several new tyrosine kinase inhibitors (TKIs) that act differentially on mutated BCR-ABL.	imatinib	10-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
19567878-1	2009	Secondary imatinib resistance in chronic myeloid leukemia (CML) is associated in approximately 50% of cases with mutations in the BCR-ABL kinase domain, necessitating switch to one of several new tyrosine kinase inhibitors (TKIs) that act differentially on mutated BCR-ABL.	imatinib	10-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	265-272
19959090-2	2009	The Bcr-Abl tyrosine kinase inhibitor imatinib mesylate represented a major therapeutic advance over conventional CML therapy, with more than 90% of patients obtaining complete haematologic response and 70-80% of patients achieving a complete cytogenetic response.	imatinib	38-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
19959090-3	2009	Resistance to imatinib represents a clinical challenge and is often a result of point mutations causing a conformation change in Bcr-Abl, which impairs imatinib binding.	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
19959090-3	2009	Resistance to imatinib represents a clinical challenge and is often a result of point mutations causing a conformation change in Bcr-Abl, which impairs imatinib binding.	imatinib	152-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
19959091-1	2009	Therapy for patients with chronic myeloid leukaemia has grown in complexity, first with the advent of the prototype ABL kinase inhibitor, imatinib, and subsequently with the availability of alternate (currently second-line) inhibitors.	imatinib	138-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-119
19722748-3	2009	c-KIT (CD117)-positive mast cells have been associated with chronic fibrosing diseases and may potentially be treated with imatinib (Gleevec), a c-KIT blocker.	imatinib	123-131	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	7-12
19722748-3	2009	c-KIT (CD117)-positive mast cells have been associated with chronic fibrosing diseases and may potentially be treated with imatinib (Gleevec), a c-KIT blocker.	imatinib	123-131	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	145-150
19722748-14	2009	The possible role of c-KIT inhibitors such as imatinib (Gleevec) in the progression of fibrosis preceding the development of obliterative bronchiolitis is discussed.	imatinib	46-54	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	21-26
19624538-0	2009	RQ-PCR based WT1 expression in comparison to BCR-ABL quantification can predict Philadelphia negative clonal evolution in patients with imatinib-treated chronic myeloid leukaemia.	imatinib	136-144	WT1 transcription factor	Homo sapiens	13-16
19959084-3	2009	An optimal response to imatinib is defined by complete HR and at least minimal CgR (Ph + < 95%) at 3 months, at least partial CgR (Ph + < 35%) at 6 months, complete CgR at 12 months and major MolR (BCR-ABL: ABL < or = 0.1%) at 18 months.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	204-211
19959084-3	2009	An optimal response to imatinib is defined by complete HR and at least minimal CgR (Ph + < 95%) at 3 months, at least partial CgR (Ph + < 35%) at 6 months, complete CgR at 12 months and major MolR (BCR-ABL: ABL < or = 0.1%) at 18 months.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	208-211
19959087-3	2009	Over 90 point mutations coding for single amino acid substitutions in the BCR-ABL kinase domain have been isolated from CML patients resistant to imatinib treatment.	imatinib	146-154	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
19959087-4	2009	These mutations affect amino acids involved in imatinib binding or in regulatory regions of the BCR-ABL kinase domain, resulting in decreased sensitivity to imatinib while retaining aberrant kinase activity.	imatinib	157-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
19624538-6	2009	Thus, increasing WT1 levels in molecular responders may indicate Ph-negative clonal cytogenetic evolution during imatinib treatment.	imatinib	113-121	WT1 transcription factor	Homo sapiens	17-20
19679008-4	2009	Newer multikinase inhibitors active against multiple ABL1 mutations are also under development for patients in any CML phase who have therapy failure on sequential imatinib and a second-generation tyrosine kinase inhibitor or carry the highly resistant T315I mutation and are not candidates for allogeneic stem cell transplantation.	imatinib	164-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-57
19706776-1	2009	Gastrointestinal stromal tumors (GIST) are characterized by activating mutations of KIT or platelet-derived growth factor receptor A (PDGFRA), and treatment with the tyrosine kinase inhibitor imatinib yields responses in the majority of patients.	imatinib	192-200	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	84-87
19706776-1	2009	Gastrointestinal stromal tumors (GIST) are characterized by activating mutations of KIT or platelet-derived growth factor receptor A (PDGFRA), and treatment with the tyrosine kinase inhibitor imatinib yields responses in the majority of patients.	imatinib	192-200	platelet derived growth factor receptor alpha	Homo sapiens	91-132
19706776-1	2009	Gastrointestinal stromal tumors (GIST) are characterized by activating mutations of KIT or platelet-derived growth factor receptor A (PDGFRA), and treatment with the tyrosine kinase inhibitor imatinib yields responses in the majority of patients.	imatinib	192-200	platelet derived growth factor receptor alpha	Homo sapiens	134-140
19706776-7	2009	SAHA and LBH589 induced apoptosis in KIT-positive GIST, and strong synergism with imatinib was observed at low concentrations of SAHA and LBH589.	imatinib	82-90	LBH regulator of WNT signaling pathway	Homo sapiens	9-12
19362466-2	2009	METHODS: Exploratory study on imatinib in tumours expressing, at least, one of the receptors KIT or platelet-derived growth factor receptor (PDGFR).	imatinib	30-38	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	93-139
19362466-2	2009	METHODS: Exploratory study on imatinib in tumours expressing, at least, one of the receptors KIT or platelet-derived growth factor receptor (PDGFR).	imatinib	30-38	platelet derived growth factor receptor beta	Homo sapiens	141-146
23675141-0	2009	Kinetics of BCR-ABL Transcripts in Imatinib Mesylate treated Chronic Phase CML (CPCML), A Predictor of Response and Progression Free Survival.	imatinib	35-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
19505817-1	2009	PURPOSE: To evaluate the safety, efficacy and pharmacokinetics of imatinib in children with recurrent or refractory central nervous system (CNS) tumours expressing KIT and/or PDGFRA.	imatinib	66-74	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	164-167
19505817-1	2009	PURPOSE: To evaluate the safety, efficacy and pharmacokinetics of imatinib in children with recurrent or refractory central nervous system (CNS) tumours expressing KIT and/or PDGFRA.	imatinib	66-74	platelet derived growth factor receptor alpha	Homo sapiens	175-181
19505817-9	2009	Our results suggest a possible relationship between KIT expression and maintenance of SD with imatinib treatment; KIT immunopositivity was seen in only 58% (11/19) of study participants overall, but in 100% of patients with SD at 38 weeks.	imatinib	94-102	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	52-55
19505817-13	2009	Demonstration of SD in previously progressing patients (KIT-expressing) suggests cytostatic activity of imatinib.	imatinib	104-112	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	56-59
20073450-2	2009	These novel antineoplastic agents include imatinib mesylate, a protein tyrosine kinase inhibitor that is encoded by the Bcr-Abl gen created by the Philadelphia chromosome abnormality in chronic myeloid leukemia.	imatinib	42-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
19761433-6	2009	Most importantly, patients with rearrangements of PDGFRA or PDGFRB can be efficiently treated with the kinase inhibitor imatinib.	imatinib	120-128	platelet derived growth factor receptor alpha	Homo sapiens	50-56
19761433-6	2009	Most importantly, patients with rearrangements of PDGFRA or PDGFRB can be efficiently treated with the kinase inhibitor imatinib.	imatinib	120-128	platelet derived growth factor receptor beta	Homo sapiens	60-66
19641527-1	2009	Dasatinib is a highly potent BCR-ABL inhibitor that has shown durable efficacy in patients with chronic phase (CP) chronic myeloid leukemia (CML) after resistance, suboptimal response, or intolerance to prior imatinib.	imatinib	209-217	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
19357699-3	2009	BCR-ABL directly inhibited c-Jun expression, as c-Jun downregulation in primary CML neutrophils and in the CML blast cell lines, KCL22 and K562, was reversed by the tyrosine kinase inhibitor imatinib.	imatinib	191-199	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
19357699-3	2009	BCR-ABL directly inhibited c-Jun expression, as c-Jun downregulation in primary CML neutrophils and in the CML blast cell lines, KCL22 and K562, was reversed by the tyrosine kinase inhibitor imatinib.	imatinib	191-199	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	27-32
19723893-3	2009	In vitro findings point out that L576P/KIT is constitutively activated, and shows poor imatinib sensitivity.	imatinib	87-95	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	39-42
19357699-3	2009	BCR-ABL directly inhibited c-Jun expression, as c-Jun downregulation in primary CML neutrophils and in the CML blast cell lines, KCL22 and K562, was reversed by the tyrosine kinase inhibitor imatinib.	imatinib	191-199	PYD and CARD domain containing	Homo sapiens	45-49
19357699-6	2009	Imatinib-induced c-Jun upregulation promoted the monocytic differentiation of KCL22/alpha cells.	imatinib	0-8	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	17-22
19357699-7	2009	c-Jun knockdown in KCL22/alpha cells by a short interfering RNA redirected their differentiation from the monocytic to the neutrophilic lineage, even after imatinib treatment.	imatinib	156-164	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	0-5
19371951-0	2009	Philadelphia chromosome-positive acute myeloid leukemia (Ph + AML) treated with imatinib mesylate (IM): a report with IM plasma concentration and bcr-abl transcripts.	imatinib	80-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	146-153
19723306-1	2009	The development of Imatinib Mesylate (IM), the first specific inhibitor of BCR-ABL1, has had a major impact in patients with Chronic Myeloid Leukemia (CML), establishing IM as the standard therapy for CML.	imatinib	19-36	BCR activator of RhoGEF and GTPase	Homo sapiens	75-83
19608684-0	2009	A co-operative evaluation of different methods of detecting BCR-ABL kinase domain mutations in patients with chronic myeloid leukemia on second-line dasatinib or nilotinib therapy after failure of imatinib.	imatinib	197-205	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
19608684-1	2009	BACKGROUND: Various techniques have been employed to detect BCR-ABL kinase domain mutations in patients with chronic myeloid leukemia who are resistant to imatinib.	imatinib	155-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
19723893-5	2009	In parallel, the affinities of wild-type, L576P/KIT, and Delta559/KIT for imatinib were estimated by in silico studies.	imatinib	74-82	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	66-69
19723893-8	2009	Computer modeling proved that L576P/KIT is two times less sensitive than the wild-type counterpart and considerably less affine to imatinib than the sensitive Delta559/KIT.	imatinib	131-139	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	36-39
19954617-0	2009	[Influence of hOCT1 polymorphism on imatinib mesylate effectiveness in chronic myelogenous leukemia patients].	imatinib	36-53	solute carrier family 22 member 1	Homo sapiens	14-19
19950608-0	2009	[Expression of hOCT1 in patients with chronic myelogeneous leukemia treated by imatinib mesylate].	imatinib	79-96	solute carrier family 22 member 1	Homo sapiens	15-20
19950608-1	2009	OBJECTIVE: To measure the expression of hOCT1 gene in patients with Chronic Myelogeneous Leukemia (CML) and to explore its role in the progress of the disease and responding to Imatinib Mesylate (IM) treatment.	imatinib	177-194	solute carrier family 22 member 1	Homo sapiens	40-45
19749982-3	2009	Quiescence of leukemic stem cells has been suggested as a mechanism conferring insensitivity to imatinib, and exposure to the Granulocyte-Colony Stimulating Factor (G-CSF), together with imatinib, has led to a significant reduction in leukemic stem cells in vitro.	imatinib	96-104	colony stimulating factor 3	Homo sapiens	126-163
19749982-3	2009	Quiescence of leukemic stem cells has been suggested as a mechanism conferring insensitivity to imatinib, and exposure to the Granulocyte-Colony Stimulating Factor (G-CSF), together with imatinib, has led to a significant reduction in leukemic stem cells in vitro.	imatinib	187-195	colony stimulating factor 3	Homo sapiens	126-163
19749982-5	2009	We find that the addition of G-CSF to an imatinib treatment protocol leads to observable effects only if the majority of leukemic stem cells are quiescent; otherwise it does not modulate the leukemic cell burden.	imatinib	41-49	colony stimulating factor 3	Homo sapiens	29-34
19954617-1	2009	OBJECTIVE: To explore the correlation between hOCT1 polymorphism and imatinib mesylate (IM) effectiveness in chronic myelogenous leukemia(CML) patients, and to provide for the clinical individual personalized therapy.	imatinib	69-86	solute carrier family 22 member 1	Homo sapiens	46-51
20079191-12	2009	The responsiveness to imatinib mesylate therapy correlates with the mutation status of c-kit gene.	imatinib	22-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	87-92
19494352-1	2009	Dasatinib is an oral potent adenosine triphosphate (ATP)-competitive inhibitor of BCR-ABL, cKIT, platelet-derived growth factor receptor, and SRC family kinases (SFKs), which has demonstrated high efficiency in patients with imatinib-resistant chronic myelogenous leukemia.	imatinib	225-233	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
19654305-6	2009	We additionally show sensitivity of imatinib-resistant BCR-ABL T315I cells to bortezomib.	imatinib	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
19541823-6	2009	In imatinib-resistant leukemia, KW-2449 contributed to release of the resistance by the simultaneous down-regulation of BCR/ABL and Aurora kinases.	imatinib	3-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
19693287-7	2009	In addition, imatinib regulation of PDGF- and insulin-induced PI 3-kinase/Akt survival signaling was determined by immunoblot analyses, immunoprecipitation, and in vitro PI 3-kinase assays.	imatinib	13-21	thymoma viral proto-oncogene 1	Mus musculus	74-77
19693287-11	2009	In addition, imatinib inhibited PDGF-induced downstream phosphorylation of Akt, GSK-3beta, and p70S6kinase.	imatinib	13-21	thymoma viral proto-oncogene 1	Mus musculus	75-78
19693287-11	2009	In addition, imatinib inhibited PDGF-induced downstream phosphorylation of Akt, GSK-3beta, and p70S6kinase.	imatinib	13-21	glycogen synthase kinase 3 beta	Mus musculus	80-89
19083009-1	2009	INTRODUCTION: The development of imatinib as a therapeutic agent targeting BCR-ABL has increased the treatment options for chronic myeloid leukemia (CML) by significantly impacting outcomes, and imatinib is recommended by treatment guidelines as the first-line therapy.	imatinib	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
19620409-0	2009	Residual and recurrent gastrointestinal stromal tumors with KIT mutations: findings at first follow-up CT after imatinib treatment.	imatinib	112-120	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	60-63
19620409-1	2009	OBJECTIVE: The purpose of this study was to correlate findings on the first follow-up CT after treatment with imatinib in patients with residual or recurrent gastrointestinal stromal tumors (GISTs) with the different types of KIT mutation present at initial resection.	imatinib	110-118	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	226-229
19620409-2	2009	CONCLUSION: Residual and recurrent GISTs with KIT mutation of exon 11 deletion more frequently showed both tumor shrinkage and cystic change on 2-month follow-up CT images after the start of imatinib treatment than did other mutation types.	imatinib	191-199	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	46-49
19617296-5	2009	Receptor tyrosine-kinase inhibitors (imatinib, dasatinib, sunitinib) may have a role in treatment of patients with melanoma harbouring c-Kit mutations.	imatinib	37-45	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	135-140
19602594-7	2009	PDGFR and Src kinases can be inhibited by imatinib and dasatinib, respectively.	imatinib	42-50	platelet derived growth factor receptor beta	Homo sapiens	0-5
19427998-2	2009	To determine whether an Abl kinase inhibitor, STI571 (Gleevec; imatinib mesylate) sensitizes breast cancer cells to chemotherapeutic agents, we treated three breast cancer cell lines (BT-549, MDA-MB-231, and MDA-MB-468) that have active Abl kinases, with STI571 in combination with several conventional chemotherapeutic drugs frequently used to treat breast cancer, and assessed the effect on cell viability, proliferation, and apoptosis.	imatinib	46-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-27
19427998-4	2009	Significantly, STI571 increased the ability of cisplatin to inhibit constitutive activation of PI3K/Akt in BT-549 cells, synergized with camptothecin to increase the stability of IkappaB in MDA-MB-231 cells, and in MDA-MB-468 cells, camptothecin and 5-fluorouracil inhibited STI571-dependent activation of STAT3.	imatinib	15-21	AKT serine/threonine kinase 1	Homo sapiens	100-103
19427998-4	2009	Significantly, STI571 increased the ability of cisplatin to inhibit constitutive activation of PI3K/Akt in BT-549 cells, synergized with camptothecin to increase the stability of IkappaB in MDA-MB-231 cells, and in MDA-MB-468 cells, camptothecin and 5-fluorouracil inhibited STI571-dependent activation of STAT3.	imatinib	15-21	signal transducer and activator of transcription 3	Homo sapiens	306-311
19563513-4	2009	Furthermore, when CML cells were treated with imatinib there was a 55% and 20% reduction of p210(BCR-ABL1) and p145(ABL1) binding to pericentrin, respectively.	imatinib	46-54	BCR activator of RhoGEF and GTPase	Homo sapiens	97-105
19563513-4	2009	Furthermore, when CML cells were treated with imatinib there was a 55% and 20% reduction of p210(BCR-ABL1) and p145(ABL1) binding to pericentrin, respectively.	imatinib	46-54	POM121 transmembrane nucleoporin	Homo sapiens	111-115
19563513-4	2009	Furthermore, when CML cells were treated with imatinib there was a 55% and 20% reduction of p210(BCR-ABL1) and p145(ABL1) binding to pericentrin, respectively.	imatinib	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-105
19563513-4	2009	Furthermore, when CML cells were treated with imatinib there was a 55% and 20% reduction of p210(BCR-ABL1) and p145(ABL1) binding to pericentrin, respectively.	imatinib	46-54	pericentrin	Homo sapiens	133-144
19602594-7	2009	PDGFR and Src kinases can be inhibited by imatinib and dasatinib, respectively.	imatinib	42-50	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	10-13
19506164-6	2009	The association of primary imatinib resistance with higher transcript levels of the drug metabolism gene PTGS1 was confirmed in a separate data set of 68 newly diagnosed, imatinib-treated CML (P = .008).	imatinib	27-35	prostaglandin-endoperoxide synthase 1	Homo sapiens	105-110
19289603-11	2009	Imatinib therapy for DMD may hold promise for ameliorating muscle necrosis, inflammation, and fibrosis by inhibiting c-abl and PDGFR signaling pathways and downstream inflammatory cytokine and fibrotic gene expression.	imatinib	0-8	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	117-122
19289603-11	2009	Imatinib therapy for DMD may hold promise for ameliorating muscle necrosis, inflammation, and fibrosis by inhibiting c-abl and PDGFR signaling pathways and downstream inflammatory cytokine and fibrotic gene expression.	imatinib	0-8	platelet derived growth factor receptor, beta polypeptide	Mus musculus	127-132
20523867-1	2009	PURPOSE: Imatinib is an efficacious drug against chronic myeloid leukemia (CML) and gastrointestinal stromal tumor (GIST) due to selective inhibition of c-KIT and BCR-ABL kinases.	imatinib	9-17	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	153-158
19635185-0	2009	Effect of LMO2 protein expression on survival in chronic myeloid leukemia patients treated with imatinib mesylate.	imatinib	96-113	LIM domain only 2	Homo sapiens	10-14
19635185-4	2009	We examined whether LMO2 protein expression can predict outcome CML patients undergoing tyrosine kinase inhibitor therapy, imatinib mesylate (IM).	imatinib	123-140	LIM domain only 2	Homo sapiens	20-24
19506164-6	2009	The association of primary imatinib resistance with higher transcript levels of the drug metabolism gene PTGS1 was confirmed in a separate data set of 68 newly diagnosed, imatinib-treated CML (P = .008).	imatinib	171-179	prostaglandin-endoperoxide synthase 1	Homo sapiens	105-110
19506164-7	2009	In contrast, up to 11 different genes were identified in a multivariate model that optimally discriminated secondary imatinib resistance lacking ABL1 kinase domain mutation from imatinib-responsive cases, likely related to the more complex pathogenesis of secondary resistance.	imatinib	117-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-149
19506164-7	2009	In contrast, up to 11 different genes were identified in a multivariate model that optimally discriminated secondary imatinib resistance lacking ABL1 kinase domain mutation from imatinib-responsive cases, likely related to the more complex pathogenesis of secondary resistance.	imatinib	178-186	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-149
19506164-8	2009	CONCLUSION: Gene expression profiling of CML at diagnosis for PTGS1 may be useful in predicting imatinib response and in selecting alternate therapy.	imatinib	96-104	prostaglandin-endoperoxide synthase 1	Homo sapiens	62-67
18990444-0	2009	A phase II trial of high-dose imatinib mesylate for relapsed or refractory c-kit positive and Bcr-Abl negative acute myeloid leukaemia: the AFR-15 trial.	imatinib	30-47	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	77-80
18990444-1	2009	This was a phase II investigation of high-dose imatinib in 15 adult patients with relapsed or refractory c-kit positive and Bcr-Abl negative acute myeloid leukaemia (AML).	imatinib	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
19167064-0	2009	Is it possible to discontinue imatinib mesylate therapy in Chronic Myeloid Leukemia patients with undetectable BCR/ABL?	imatinib	30-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
19118898-5	2009	Albeit observed infrequently in chronic phase CML, sFRP1 promoter methylation correlated with primary cytogenetic resistance to imatinib mesylate.	imatinib	128-145	secreted frizzled related protein 1	Homo sapiens	51-56
19144405-0	2009	Success of short-term, higher-dose imatinib mesylate to induce clinical response in FIP1L1-PDGFRalpha-negative hypereosinophilic syndrome.	imatinib	35-52	factor interacting with PAPOLA and CPSF1	Homo sapiens	84-90
19340007-0	2009	Inhibition of imatinib-mediated apoptosis by the caspase-cleaved form of the tyrosine kinase Lyn in chronic myelogenous leukemia cells.	imatinib	14-22	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	93-96
19340007-4	2009	We established that Lyn is cleaved in imatinib-treated parental K562 cells in a caspase-dependent manner.	imatinib	38-46	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	20-23
19340007-9	2009	LynDeltaN also inhibits imatinib-mediated caspase-3 activation in the small proportion of nilotinib-resistant K562 cells overexpressing Lyn that can engage an apoptotic program upon imatinib stimulation.	imatinib	24-32	caspase 3	Homo sapiens	42-51
19340007-9	2009	LynDeltaN also inhibits imatinib-mediated caspase-3 activation in the small proportion of nilotinib-resistant K562 cells overexpressing Lyn that can engage an apoptotic program upon imatinib stimulation.	imatinib	24-32	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	0-3
19144405-0	2009	Success of short-term, higher-dose imatinib mesylate to induce clinical response in FIP1L1-PDGFRalpha-negative hypereosinophilic syndrome.	imatinib	35-52	platelet derived growth factor receptor alpha	Homo sapiens	91-101
19340007-9	2009	LynDeltaN also inhibits imatinib-mediated caspase-3 activation in the small proportion of nilotinib-resistant K562 cells overexpressing Lyn that can engage an apoptotic program upon imatinib stimulation.	imatinib	182-190	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	0-3
19340007-11	2009	Taken together, our data show that the caspase-cleaved form of Lyn exerts a negative feedback on imatinib-mediated CML cell apoptosis that is entirely dependent on its kinase activity and likely on the BCR-ABL pathway.	imatinib	97-105	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	63-66
19144405-1	2009	Presence of the oncogenic mutation FIP1L1-PDGFRalpha in hypereosinophilic patients is predictive of hematologic response to imatinib mesylate.	imatinib	124-141	factor interacting with PAPOLA and CPSF1	Homo sapiens	35-41
19340007-11	2009	Taken together, our data show that the caspase-cleaved form of Lyn exerts a negative feedback on imatinib-mediated CML cell apoptosis that is entirely dependent on its kinase activity and likely on the BCR-ABL pathway.	imatinib	97-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	202-209
19144405-1	2009	Presence of the oncogenic mutation FIP1L1-PDGFRalpha in hypereosinophilic patients is predictive of hematologic response to imatinib mesylate.	imatinib	124-141	platelet derived growth factor receptor alpha	Homo sapiens	42-52
19144405-3	2009	A patient with FIP1L1-PDGFRalpha-negative HES who had intolerance of interferon alpha-2b and hydroxyurea was treated with escalating doses of imatinib.	imatinib	142-150	factor interacting with PAPOLA and CPSF1	Homo sapiens	15-21
19144405-3	2009	A patient with FIP1L1-PDGFRalpha-negative HES who had intolerance of interferon alpha-2b and hydroxyurea was treated with escalating doses of imatinib.	imatinib	142-150	platelet derived growth factor receptor alpha	Homo sapiens	22-32
19144405-3	2009	A patient with FIP1L1-PDGFRalpha-negative HES who had intolerance of interferon alpha-2b and hydroxyurea was treated with escalating doses of imatinib.	imatinib	142-150	interferon alpha 2	Homo sapiens	69-88
20021947-6	2009	CONCLUSION: The mechanism of imatinib mesylate resistance after initial treatment with this agent in gastrointestinal stromal tumors is a novel mutation development in kinase domain of c-kit.	imatinib	29-46	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	185-190
19671763-5	2009	Molecular modeling studies found that the L576P mutation induces structural changes in KIT that reduce the affinity for imatinib (DeltaDeltaGbind = -2.52 kcal/mol) but not for dasatinib (DeltaDeltaGbind = +0.32 kcal/mol).	imatinib	120-128	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	87-90
19544423-5	2009	The formation of the clusters could be completely blocked by adding a c-kit/tyrosine kinase inhibitor, Gleevec (imatinib mesylate; Novartis International, Basel, Switzerland, http://www.novartis.com), to the culture.	imatinib	103-110	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	70-75
19544423-5	2009	The formation of the clusters could be completely blocked by adding a c-kit/tyrosine kinase inhibitor, Gleevec (imatinib mesylate; Novartis International, Basel, Switzerland, http://www.novartis.com), to the culture.	imatinib	112-129	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	70-75
19602047-7	2009	Finally, interruption of c-Myc activity by 10058-F4 exerted an anti-leukaemia effect with a synergistic interaction with imatinib and overcame the anti-apoptosis rescued by IL-3 supplement.	imatinib	121-129	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	25-30
19423701-9	2009	Tyrosine 52 is further shown to be phosphorylated by c-Abl kinase, and the c-Abl inhibitor STI571 disrupts FAK interaction with RACK1.	imatinib	91-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-80
19423701-9	2009	Tyrosine 52 is further shown to be phosphorylated by c-Abl kinase, and the c-Abl inhibitor STI571 disrupts FAK interaction with RACK1.	imatinib	91-97	protein tyrosine kinase 2	Homo sapiens	107-110
19423701-9	2009	Tyrosine 52 is further shown to be phosphorylated by c-Abl kinase, and the c-Abl inhibitor STI571 disrupts FAK interaction with RACK1.	imatinib	91-97	receptor for activated C kinase 1	Homo sapiens	128-133
19584153-2	2009	Several cellular and genetic mechanisms of imatinib resistance have been proposed, including amplification and overexpression of the BCR/ABL gene, the tyrosine kinase domain point mutations, and MDR1 gene overexpression.	imatinib	43-51	ATP binding cassette subfamily B member 1	Homo sapiens	195-199
19487385-2	2009	Dasatinib, a potent inhibitor of BCR-ABL and SRC-family kinases, has efficacy in patients with CML-AP who have experienced treatment failure with imatinib.	imatinib	146-154	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
19508953-2	2009	We hypothesized that the administration of imatinib mesylate, an inhibitor of tyrosine kinase and TGF-beta pro-fibrogenic activity, could improve the muscular conditions in mdx mice.	imatinib	43-60	transforming growth factor, beta 1	Mus musculus	98-106
19508953-6	2009	Pro-inflammatory cytokines and TGF-beta were also reduced, while IL-10 was increased, suggesting an immunomodulatory effect of imatinib, which can ameliorate the dystrophic phenotype in mdx mice.	imatinib	127-135	interleukin 10	Mus musculus	65-70
19378338-0	2009	NF-kappaB inhibition triggers death of imatinib-sensitive and imatinib-resistant chronic myeloid leukemia cells including T315I Bcr-Abl mutants.	imatinib	39-47	nuclear factor kappa B subunit 1	Homo sapiens	0-9
19378338-0	2009	NF-kappaB inhibition triggers death of imatinib-sensitive and imatinib-resistant chronic myeloid leukemia cells including T315I Bcr-Abl mutants.	imatinib	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
19694363-4	2009	Data have recently shown that inhibiting platelet-derived growth factor receptors (PDGFR) with imatinib mesylate can induce high rates of clinical response in patients with unresectable or metastatic DFSP.	imatinib	95-112	platelet derived growth factor receptor beta	Homo sapiens	41-81
19378338-0	2009	NF-kappaB inhibition triggers death of imatinib-sensitive and imatinib-resistant chronic myeloid leukemia cells including T315I Bcr-Abl mutants.	imatinib	62-70	nuclear factor kappa B subunit 1	Homo sapiens	0-9
19378338-0	2009	NF-kappaB inhibition triggers death of imatinib-sensitive and imatinib-resistant chronic myeloid leukemia cells including T315I Bcr-Abl mutants.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
19378338-1	2009	The Bcr-Abl inhibitor imatinib is the current first-line therapy for all newly diagnosed chronic myeloid leukemia (CML).	imatinib	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
19378338-5	2009	Pharmacological blockade of NF-kappaB by the IKK2 inhibitor AS602868 prevented survival of BaF cells expressing either wild-type, M351T or T315I imatinib-resistant mutant forms of Bcr-Abl both in vitro and in vivo using a mouse xenograft model.	imatinib	145-153	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	28-37
19378338-5	2009	Pharmacological blockade of NF-kappaB by the IKK2 inhibitor AS602868 prevented survival of BaF cells expressing either wild-type, M351T or T315I imatinib-resistant mutant forms of Bcr-Abl both in vitro and in vivo using a mouse xenograft model.	imatinib	145-153	inhibitor of kappaB kinase beta	Mus musculus	45-49
19378338-5	2009	Pharmacological blockade of NF-kappaB by the IKK2 inhibitor AS602868 prevented survival of BaF cells expressing either wild-type, M351T or T315I imatinib-resistant mutant forms of Bcr-Abl both in vitro and in vivo using a mouse xenograft model.	imatinib	145-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	180-187
19378338-7	2009	Importantly, the IKK2 inhibitor strongly decreased in vitro survival and ability to form hematopoietic colonies of primary imatinib resistant CML cells including T315I cells.	imatinib	123-131	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	17-21
19378338-8	2009	Our data strongly support the targeting of NF-kappaB as a promising new therapeutic opportunity for the treatment of imatinib resistant CML patients in particular in the case of T315I patients.	imatinib	117-125	nuclear factor kappa B subunit 1	Homo sapiens	43-52
19584324-0	2009	JAK2 inhibitors: not the next imatinib but researchers see other possibilities.	imatinib	30-38	Janus kinase 2	Homo sapiens	0-4
19694363-4	2009	Data have recently shown that inhibiting platelet-derived growth factor receptors (PDGFR) with imatinib mesylate can induce high rates of clinical response in patients with unresectable or metastatic DFSP.	imatinib	95-112	platelet derived growth factor receptor beta	Homo sapiens	83-88
19324082-3	2009	The results indicate that p38 is a mediator of the STI-571-induced apoptosis, while C3G plays a negative role on STI-571-mediated p38 activation through a Rap1-dependent mechanism.	imatinib	51-58	mitogen-activated protein kinase 14	Homo sapiens	26-29
19246139-8	2009	In a group of patients, oncogenic tyrosine kinases (TK) such as FIP1L1/PDGFRA, can be employed as therapeutic targets by using imatinib or other TK-blocking agents.	imatinib	127-135	factor interacting with PAPOLA and CPSF1	Homo sapiens	64-70
19246139-8	2009	In a group of patients, oncogenic tyrosine kinases (TK) such as FIP1L1/PDGFRA, can be employed as therapeutic targets by using imatinib or other TK-blocking agents.	imatinib	127-135	platelet derived growth factor receptor alpha	Homo sapiens	71-77
19480935-3	2009	CML patients with an ABL1/ETV6 fusion historically have demonstrated a variable and sometimes transient response to treatment with imatinib mesylate, which was also the case in the present patient.	imatinib	131-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-25
19480935-3	2009	CML patients with an ABL1/ETV6 fusion historically have demonstrated a variable and sometimes transient response to treatment with imatinib mesylate, which was also the case in the present patient.	imatinib	131-148	ETS variant transcription factor 6	Homo sapiens	26-30
19324082-0	2009	C3G silencing enhances STI-571-induced apoptosis in CML cells through p38 MAPK activation, but it antagonizes STI-571 inhibitory effect on survival.	imatinib	23-30	Rap guanine nucleotide exchange factor 1	Homo sapiens	0-3
19324082-0	2009	C3G silencing enhances STI-571-induced apoptosis in CML cells through p38 MAPK activation, but it antagonizes STI-571 inhibitory effect on survival.	imatinib	110-117	Rap guanine nucleotide exchange factor 1	Homo sapiens	0-3
19591692-0	2009	Influence of the dual ABCB1 and ABCG2 inhibitor tariquidar on the disposition of oral imatinib in mice.	imatinib	86-94	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	22-27
19591692-1	2009	BACKGROUND: Imatinib, a tyrosine kinase inhibitor currently approved for treatment of several malignancies, has been shown to be a substrate for multiple efflux-transporter proteins, including ABCB1 (P-glycoprotein) and ABCG2 (BCRP).	imatinib	12-20	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	193-198
19591692-1	2009	BACKGROUND: Imatinib, a tyrosine kinase inhibitor currently approved for treatment of several malignancies, has been shown to be a substrate for multiple efflux-transporter proteins, including ABCB1 (P-glycoprotein) and ABCG2 (BCRP).	imatinib	12-20	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	220-225
19591692-1	2009	BACKGROUND: Imatinib, a tyrosine kinase inhibitor currently approved for treatment of several malignancies, has been shown to be a substrate for multiple efflux-transporter proteins, including ABCB1 (P-glycoprotein) and ABCG2 (BCRP).	imatinib	12-20	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	227-231
19548306-2	2009	High expression of bcr-abl in mRNA and protein levels, and other alterations were found in patients who experienced imatinib treatment failures and thus it is important to design alternative treatment strategies.	imatinib	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
19276970-2	2009	High frequency of reported KIT reactivity by immunohistochemistry (IHC) in part prompted the initiation of a phase 2 clinical trial of imatinib mesylate (Gleevec, Novartis Pharmaceuticals, East Hanover, NJ) for the treatment of advanced MCC.	imatinib	135-152	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	27-30
19402171-2	2009	Loss of response on imatinib is often because of BCR-ABL mutations.	imatinib	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
19383029-2	2009	Most of the constitutively active KIT can be inhibited by imatinib; D816V KIT cannot.	imatinib	58-66	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	34-37
19383029-5	2009	Imatinib-sensitive HMC-1.1 cells harboring the mutation V560G in the juxtamembrane domain of KIT, imatinib-resistant HMC-1.2 cells harboring both V560G and D816V mutations, and murine P815 cells, were treated with triptolide, and analyzed in terms of growth, apoptosis, and signal transduction.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	93-96
19383029-5	2009	Imatinib-sensitive HMC-1.1 cells harboring the mutation V560G in the juxtamembrane domain of KIT, imatinib-resistant HMC-1.2 cells harboring both V560G and D816V mutations, and murine P815 cells, were treated with triptolide, and analyzed in terms of growth, apoptosis, and signal transduction.	imatinib	98-106	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	93-96
19383029-7	2009	Our results demonstrated that triptolide potently inhibits the growth of both human and murine mast cells harboring not only imatinib-sensitive KIT mutation but also imatinib-resistant D816V KIT.	imatinib	125-133	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	144-147
19383029-7	2009	Our results demonstrated that triptolide potently inhibits the growth of both human and murine mast cells harboring not only imatinib-sensitive KIT mutation but also imatinib-resistant D816V KIT.	imatinib	166-174	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	191-194
19383029-11	2009	Our data demonstrate that triptolide inhibits imatinib-resistant mast cells harboring D816V KIT.	imatinib	46-54	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	92-95
19324082-3	2009	The results indicate that p38 is a mediator of the STI-571-induced apoptosis, while C3G plays a negative role on STI-571-mediated p38 activation through a Rap1-dependent mechanism.	imatinib	113-120	Rap guanine nucleotide exchange factor 1	Homo sapiens	84-87
19324082-3	2009	The results indicate that p38 is a mediator of the STI-571-induced apoptosis, while C3G plays a negative role on STI-571-mediated p38 activation through a Rap1-dependent mechanism.	imatinib	113-120	mitogen-activated protein kinase 14	Homo sapiens	130-133
19324082-3	2009	The results indicate that p38 is a mediator of the STI-571-induced apoptosis, while C3G plays a negative role on STI-571-mediated p38 activation through a Rap1-dependent mechanism.	imatinib	113-120	RAP1A, member of RAS oncogene family	Homo sapiens	155-159
19324082-6	2009	On the other hand, C3G knock-down reverts the STI-571-inhibitory effect on ERKs and Akt pathways in a Rap1-independent fashion.	imatinib	46-53	Rap guanine nucleotide exchange factor 1	Homo sapiens	19-22
19324082-6	2009	On the other hand, C3G knock-down reverts the STI-571-inhibitory effect on ERKs and Akt pathways in a Rap1-independent fashion.	imatinib	46-53	AKT serine/threonine kinase 1	Homo sapiens	84-87
19324082-6	2009	On the other hand, C3G knock-down reverts the STI-571-inhibitory effect on ERKs and Akt pathways in a Rap1-independent fashion.	imatinib	46-53	RAP1A, member of RAS oncogene family	Homo sapiens	102-106
19324082-7	2009	Moreover, C3G overexpression also increased both, basal and STI-571-induced apoptosis, in agreement with previous reports.	imatinib	60-67	Rap guanine nucleotide exchange factor 1	Homo sapiens	10-13
19291793-0	2009	Pml and TAp73 interacting at nuclear body mediate imatinib-induced p53-independent apoptosis of chronic myeloid leukemia cells.	imatinib	50-58	PML nuclear body scaffold	Homo sapiens	0-3
19695406-20	2009	CONCLUSIONS: In this pharmacokinetic study in Chinese patients with CML resistant to or intolerant of imatinib, nilotinib 400 mg BID was rapidly absorbed after a single dose and multiple doses.	imatinib	102-110	BH3 interacting domain death agonist	Homo sapiens	129-132
19403302-0	2009	Epigenetic down-regulation of BIM expression is associated with reduced optimal responses to imatinib treatment in chronic myeloid leukaemia.	imatinib	93-101	BCL2 like 11	Homo sapiens	30-33
19403302-1	2009	BACKGROUND: Expression of the pro-apoptotic BCL-2-interacting mediator (BIM) has recently been implicated in imatinib-induced apoptosis of BCR-ABL1(+) cells.	imatinib	109-117	BCL2 apoptosis regulator	Homo sapiens	44-49
19403302-1	2009	BACKGROUND: Expression of the pro-apoptotic BCL-2-interacting mediator (BIM) has recently been implicated in imatinib-induced apoptosis of BCR-ABL1(+) cells.	imatinib	109-117	BCL2 like 11	Homo sapiens	72-75
19403302-1	2009	BACKGROUND: Expression of the pro-apoptotic BCL-2-interacting mediator (BIM) has recently been implicated in imatinib-induced apoptosis of BCR-ABL1(+) cells.	imatinib	109-117	BCR activator of RhoGEF and GTPase	Homo sapiens	139-147
19403302-6	2009	RESULTS: We demonstrated that down-regulation of BIM expression was present in 36% of the patients and was significantly associated with a lack of optimal response to imatinib as indicated by the decrease in cytogenetic and molecular responses at 6, 12 and 18 months in comparison with patients with normal BIM expression (p<0.05).	imatinib	167-175	BCL2 like 11	Homo sapiens	49-52
19403302-8	2009	Using CML cell lines with low and normal expression of BIM we further demonstrated that the expression of BIM is required for imatinib-induced CML apoptosis.	imatinib	126-134	BCL2 like 11	Homo sapiens	55-58
19403302-8	2009	Using CML cell lines with low and normal expression of BIM we further demonstrated that the expression of BIM is required for imatinib-induced CML apoptosis.	imatinib	126-134	BCL2 like 11	Homo sapiens	106-109
19620796-5	2009	The therapy of choice for resectable GIST is still surgery, but at present we can use imatinib, a selective tyrosine kinase inhibitor for KIT, PDGFRs and Bcr-Abl, for such advanced GIST patients.	imatinib	86-94	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	138-141
19620796-5	2009	The therapy of choice for resectable GIST is still surgery, but at present we can use imatinib, a selective tyrosine kinase inhibitor for KIT, PDGFRs and Bcr-Abl, for such advanced GIST patients.	imatinib	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-161
19620796-7	2009	Secondary mutations of the c-kit gene in addition to primary c-kit gene mutation are a major cause of secondary resistance to imatinib.	imatinib	126-134	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	27-32
19620796-7	2009	Secondary mutations of the c-kit gene in addition to primary c-kit gene mutation are a major cause of secondary resistance to imatinib.	imatinib	126-134	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	61-66
19484334-4	2009	Anecdotal evidence suggests that imatinib mesylate, a selective tyrosine kinase inhibitor of ABL1, ARG, PDGFR, and KIT kinases has activity in PV.	imatinib	33-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-97
19484334-4	2009	Anecdotal evidence suggests that imatinib mesylate, a selective tyrosine kinase inhibitor of ABL1, ARG, PDGFR, and KIT kinases has activity in PV.	imatinib	33-50	platelet derived growth factor receptor beta	Homo sapiens	104-109
19291793-0	2009	Pml and TAp73 interacting at nuclear body mediate imatinib-induced p53-independent apoptosis of chronic myeloid leukemia cells.	imatinib	50-58	tumor protein p53	Homo sapiens	67-70
19291793-4	2009	As reported previously, p53(wild) CML was more resistant to imatinib than that lacking p53.	imatinib	60-68	tumor protein p53	Homo sapiens	24-27
19291793-5	2009	Here, we searched for an imatinib-induced p53 independent proapoptotic mechanism.	imatinib	25-33	tumor protein p53	Homo sapiens	42-45
19291793-6	2009	We found imatinib up-regulated phosphorylation of p38 mitogen-activated protein kinase (MAPK), checkpoint kinase 2 (chk2) and transactivation-competent (TA) p73; expression of pml and bax; formation of PML-nuclear body (NB); and co-localization of TAp73/PML-NB in p53-nonfunctioning K562 and p53(mutant) Meg-01 CML cells, but not in BCR-ABL(-) HL60 cells.	imatinib	9-17	mitogen-activated protein kinase 14	Homo sapiens	50-86
19291793-6	2009	We found imatinib up-regulated phosphorylation of p38 mitogen-activated protein kinase (MAPK), checkpoint kinase 2 (chk2) and transactivation-competent (TA) p73; expression of pml and bax; formation of PML-nuclear body (NB); and co-localization of TAp73/PML-NB in p53-nonfunctioning K562 and p53(mutant) Meg-01 CML cells, but not in BCR-ABL(-) HL60 cells.	imatinib	9-17	checkpoint kinase 2	Homo sapiens	95-114
19291793-6	2009	We found imatinib up-regulated phosphorylation of p38 mitogen-activated protein kinase (MAPK), checkpoint kinase 2 (chk2) and transactivation-competent (TA) p73; expression of pml and bax; formation of PML-nuclear body (NB); and co-localization of TAp73/PML-NB in p53-nonfunctioning K562 and p53(mutant) Meg-01 CML cells, but not in BCR-ABL(-) HL60 cells.	imatinib	9-17	checkpoint kinase 2	Homo sapiens	116-120
19291793-6	2009	We found imatinib up-regulated phosphorylation of p38 mitogen-activated protein kinase (MAPK), checkpoint kinase 2 (chk2) and transactivation-competent (TA) p73; expression of pml and bax; formation of PML-nuclear body (NB); and co-localization of TAp73/PML-NB in p53-nonfunctioning K562 and p53(mutant) Meg-01 CML cells, but not in BCR-ABL(-) HL60 cells.	imatinib	9-17	tumor protein p73	Homo sapiens	157-160
19291793-6	2009	We found imatinib up-regulated phosphorylation of p38 mitogen-activated protein kinase (MAPK), checkpoint kinase 2 (chk2) and transactivation-competent (TA) p73; expression of pml and bax; formation of PML-nuclear body (NB); and co-localization of TAp73/PML-NB in p53-nonfunctioning K562 and p53(mutant) Meg-01 CML cells, but not in BCR-ABL(-) HL60 cells.	imatinib	9-17	PML nuclear body scaffold	Homo sapiens	176-179
19291793-6	2009	We found imatinib up-regulated phosphorylation of p38 mitogen-activated protein kinase (MAPK), checkpoint kinase 2 (chk2) and transactivation-competent (TA) p73; expression of pml and bax; formation of PML-nuclear body (NB); and co-localization of TAp73/PML-NB in p53-nonfunctioning K562 and p53(mutant) Meg-01 CML cells, but not in BCR-ABL(-) HL60 cells.	imatinib	9-17	BCL2 associated X, apoptosis regulator	Homo sapiens	184-187
19291793-6	2009	We found imatinib up-regulated phosphorylation of p38 mitogen-activated protein kinase (MAPK), checkpoint kinase 2 (chk2) and transactivation-competent (TA) p73; expression of pml and bax; formation of PML-nuclear body (NB); and co-localization of TAp73/PML-NB in p53-nonfunctioning K562 and p53(mutant) Meg-01 CML cells, but not in BCR-ABL(-) HL60 cells.	imatinib	9-17	PML nuclear body scaffold	Homo sapiens	202-205
19291793-6	2009	We found imatinib up-regulated phosphorylation of p38 mitogen-activated protein kinase (MAPK), checkpoint kinase 2 (chk2) and transactivation-competent (TA) p73; expression of pml and bax; formation of PML-nuclear body (NB); and co-localization of TAp73/PML-NB in p53-nonfunctioning K562 and p53(mutant) Meg-01 CML cells, but not in BCR-ABL(-) HL60 cells.	imatinib	9-17	PML nuclear body scaffold	Homo sapiens	254-257
19291793-6	2009	We found imatinib up-regulated phosphorylation of p38 mitogen-activated protein kinase (MAPK), checkpoint kinase 2 (chk2) and transactivation-competent (TA) p73; expression of pml and bax; formation of PML-nuclear body (NB); and co-localization of TAp73/PML-NB in p53-nonfunctioning K562 and p53(mutant) Meg-01 CML cells, but not in BCR-ABL(-) HL60 cells.	imatinib	9-17	tumor protein p53	Homo sapiens	264-267
19291793-6	2009	We found imatinib up-regulated phosphorylation of p38 mitogen-activated protein kinase (MAPK), checkpoint kinase 2 (chk2) and transactivation-competent (TA) p73; expression of pml and bax; formation of PML-nuclear body (NB); and co-localization of TAp73/PML-NB in p53-nonfunctioning K562 and p53(mutant) Meg-01 CML cells, but not in BCR-ABL(-) HL60 cells.	imatinib	9-17	tumor protein p53	Homo sapiens	292-295
19291793-8	2009	Knockdown of either pml or TAp73 abolished the imatinib-induced apoptosis.	imatinib	47-55	PML nuclear body scaffold	Homo sapiens	20-23
19291793-10	2009	Conversely, interferon alpha-2a (IFNalpha), which increased phosphrylated TAp73 and TAp73/PML-NB co-localization, increased additively apoptosis with imatinib.	imatinib	150-158	interferon alpha 2	Homo sapiens	12-31
19291793-10	2009	Conversely, interferon alpha-2a (IFNalpha), which increased phosphrylated TAp73 and TAp73/PML-NB co-localization, increased additively apoptosis with imatinib.	imatinib	150-158	interferon alpha 2	Homo sapiens	33-41
19291793-11	2009	The imatinib-induced TAp73/PML-NB co-localization was accompanied by co-immpunoprecipitation of TAp73 with pml.	imatinib	4-12	PML nuclear body scaffold	Homo sapiens	27-30
19306298-4	2009	We found that AICD expression is decreased by treatment with STI-571, a c-Abl inhibitor, suggesting a modulation of AICD transcription by c-Abl kinase.	imatinib	61-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-77
19291793-11	2009	The imatinib-induced TAp73/PML-NB co-localization was accompanied by co-immpunoprecipitation of TAp73 with pml.	imatinib	4-12	PML nuclear body scaffold	Homo sapiens	107-110
19291793-12	2009	The imatinib-induced co-localization was also found in primary CML cells from 3 of 6 patients, including 2 with p53(mutant) and one with p53(wild).	imatinib	4-12	tumor protein p53	Homo sapiens	112-115
19291793-12	2009	The imatinib-induced co-localization was also found in primary CML cells from 3 of 6 patients, including 2 with p53(mutant) and one with p53(wild).	imatinib	4-12	tumor protein p53	Homo sapiens	137-140
19291793-13	2009	A novel p53-independent proapoptotic mechanism using p38 MAPK /pml/TAp73 axis with a step processing at PML-NB and probably with chk2 and bax being involved is hereby evident in some imatinib-treated CML cells.	imatinib	183-191	tumor protein p53	Homo sapiens	8-11
19291793-13	2009	A novel p53-independent proapoptotic mechanism using p38 MAPK /pml/TAp73 axis with a step processing at PML-NB and probably with chk2 and bax being involved is hereby evident in some imatinib-treated CML cells.	imatinib	183-191	PML nuclear body scaffold	Homo sapiens	63-66
19291793-13	2009	A novel p53-independent proapoptotic mechanism using p38 MAPK /pml/TAp73 axis with a step processing at PML-NB and probably with chk2 and bax being involved is hereby evident in some imatinib-treated CML cells.	imatinib	183-191	PML nuclear body scaffold	Homo sapiens	104-107
19291793-13	2009	A novel p53-independent proapoptotic mechanism using p38 MAPK /pml/TAp73 axis with a step processing at PML-NB and probably with chk2 and bax being involved is hereby evident in some imatinib-treated CML cells.	imatinib	183-191	checkpoint kinase 2	Homo sapiens	129-133
19291793-13	2009	A novel p53-independent proapoptotic mechanism using p38 MAPK /pml/TAp73 axis with a step processing at PML-NB and probably with chk2 and bax being involved is hereby evident in some imatinib-treated CML cells.	imatinib	183-191	BCL2 associated X, apoptosis regulator	Homo sapiens	138-141
19466505-1	2009	For relevant imatinib therapy against Philadelphia (Ph)-positive leukemias, it is essential to monitor mutations in the chimerical bcr-abl tyrosine kinase domain (TKD).	imatinib	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
19761684-0	2009	Effects of imatinib mesylate on renin-angiotensin system (RAS) activity during the clinical course of chronic myeloid leukaemia.	imatinib	11-28	renin	Homo sapiens	32-37
19561230-2	2009	Recently, a novel BRAF exon 15 mutation (V600E) was detected in imatinib-naive wild-type high-risk intestinal GISTs (4%).	imatinib	64-72	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	18-22
19761684-4	2009	De novo CML patients had increased ACE, angiotensinogen and renin mRNA levels and these expression levels decreased following administration of imatinib.	imatinib	144-152	angiotensin I converting enzyme	Homo sapiens	35-38
19761684-4	2009	De novo CML patients had increased ACE, angiotensinogen and renin mRNA levels and these expression levels decreased following administration of imatinib.	imatinib	144-152	angiotensinogen	Homo sapiens	40-55
19761684-4	2009	De novo CML patients had increased ACE, angiotensinogen and renin mRNA levels and these expression levels decreased following administration of imatinib.	imatinib	144-152	renin	Homo sapiens	60-65
19237191-3	2009	UPR inhibition using inositol-requiring enzyme 1alpha (IRE1alpha) or activating transcription factor 6 (ATF6) dominant-negative mutants diminished the ability of Bcr-Abl to protect the cells from etoposide- and imatinib-induced apoptosis.	imatinib	211-219	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-169
19234339-3	2009	This study was conducted to determine whether imatinib mesylate and AMN107 inhibit orbital fibroblast proliferation and hyaluronan production induced by PDGF-BB and TGF-beta(1) and whether expression of the genes PDGF-B and TGF-B(1) (growth factors suggested to play a role in GO) are increased in GO orbital tissues.	imatinib	46-63	transforming growth factor beta 1	Homo sapiens	165-176
19234339-3	2009	This study was conducted to determine whether imatinib mesylate and AMN107 inhibit orbital fibroblast proliferation and hyaluronan production induced by PDGF-BB and TGF-beta(1) and whether expression of the genes PDGF-B and TGF-B(1) (growth factors suggested to play a role in GO) are increased in GO orbital tissues.	imatinib	46-63	platelet derived growth factor subunit B	Homo sapiens	153-159
19567819-0	2009	Gene expression profiling of imatinib and PD166326-resistant CML cell lines identifies Fyn as a gene associated with resistance to BCR-ABL inhibitors.	imatinib	29-37	FYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	87-90
19567819-0	2009	Gene expression profiling of imatinib and PD166326-resistant CML cell lines identifies Fyn as a gene associated with resistance to BCR-ABL inhibitors.	imatinib	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
19567819-9	2009	Small interfering RNA experiments and pharmacologic approaches identified FYN as a candidate for resistance to imatinib.	imatinib	111-119	FYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	74-77
20641611-0	2004	[N-(11)C-methyl]-[4-[(4-Methyl-1-piperazinyl)methyl]-N-[4-methyl-3-[[4-(3-pyridyl)-2-pyrimidinyl]amino]phenyl]benzamide Imatinib ([4-[(4-methyl-1-piperazinyl)methyl]-N-[4-methyl-3-[[4-(3-pyridyl)-2-pyrimidinyl]amino]phenyl]benzamide) is a synthetic tyrosine kinase (TK) signal transduction inhibitor used for the treatment of a variety of chronic myeloid leukemia (CML) attributed to the Philadelphia chromosome-positive trait (1).	imatinib	120-128	TXK tyrosine kinase	Homo sapiens	249-264
19568437-0	2009	ERK2, but not ERK1, mediates acquired and "de novo" resistance to imatinib mesylate: implication for CML therapy.	imatinib	66-83	mitogen-activated protein kinase 1	Homo sapiens	0-4
19369231-1	2009	Dasatinib is the most potent BCR-ABL inhibitor, with 325-fold higher potency than imatinib against unmutated BCR-ABL in vitro.	imatinib	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
19369233-5	2009	Patients with a BCR-ABL1/ABL1 ratio greater than 1% to 10% after 3 months of imatinib had a 92% probability of achieving CCyR with continued therapy, similar to the 98% for those with 1% or less, but their risk of progression (11%) was almost 3-fold that of patients with a BCR-ABL1/ABL1 transcript ratio of 1% or less (4%) and similar to that of patients with transcript levels more than 10% (13%).	imatinib	77-85	BCR activator of RhoGEF and GTPase	Homo sapiens	16-24
19369233-5	2009	Patients with a BCR-ABL1/ABL1 ratio greater than 1% to 10% after 3 months of imatinib had a 92% probability of achieving CCyR with continued therapy, similar to the 98% for those with 1% or less, but their risk of progression (11%) was almost 3-fold that of patients with a BCR-ABL1/ABL1 transcript ratio of 1% or less (4%) and similar to that of patients with transcript levels more than 10% (13%).	imatinib	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-24
19369233-5	2009	Patients with a BCR-ABL1/ABL1 ratio greater than 1% to 10% after 3 months of imatinib had a 92% probability of achieving CCyR with continued therapy, similar to the 98% for those with 1% or less, but their risk of progression (11%) was almost 3-fold that of patients with a BCR-ABL1/ABL1 transcript ratio of 1% or less (4%) and similar to that of patients with transcript levels more than 10% (13%).	imatinib	77-85	BCR activator of RhoGEF and GTPase	Homo sapiens	274-282
19369233-5	2009	Patients with a BCR-ABL1/ABL1 ratio greater than 1% to 10% after 3 months of imatinib had a 92% probability of achieving CCyR with continued therapy, similar to the 98% for those with 1% or less, but their risk of progression (11%) was almost 3-fold that of patients with a BCR-ABL1/ABL1 transcript ratio of 1% or less (4%) and similar to that of patients with transcript levels more than 10% (13%).	imatinib	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-29
19509176-3	2009	EXPERIMENTAL DESIGN: We grafted the human GIST882 cell line with KIT exon 13 mutation and two biopsies from patients radiologically progressing under imatinib showing KIT exon11 and KIT exon9 mutations, respectively.	imatinib	150-158	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	167-170
19509176-3	2009	EXPERIMENTAL DESIGN: We grafted the human GIST882 cell line with KIT exon 13 mutation and two biopsies from patients radiologically progressing under imatinib showing KIT exon11 and KIT exon9 mutations, respectively.	imatinib	150-158	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	167-170
19509233-4	2009	Gleevec (STI571, imatinib mesylate), in addition to the bcr-abl oncogene in chronic myelogenous leukemia, inhibits c-kit and platelet-derived growth factor receptor (PDGFR) signaling, thereby expanding its use to several malignant and benign human diseases.	imatinib	17-34	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	115-120
19509233-4	2009	Gleevec (STI571, imatinib mesylate), in addition to the bcr-abl oncogene in chronic myelogenous leukemia, inhibits c-kit and platelet-derived growth factor receptor (PDGFR) signaling, thereby expanding its use to several malignant and benign human diseases.	imatinib	17-34	platelet derived growth factor receptor beta	Homo sapiens	125-164
19509233-4	2009	Gleevec (STI571, imatinib mesylate), in addition to the bcr-abl oncogene in chronic myelogenous leukemia, inhibits c-kit and platelet-derived growth factor receptor (PDGFR) signaling, thereby expanding its use to several malignant and benign human diseases.	imatinib	17-34	platelet derived growth factor receptor beta	Homo sapiens	166-171
21475882-0	2009	RUNX1T1 is overexpressed in imatinib mesylate-resistant cells.	imatinib	28-45	RUNX1 partner transcriptional co-repressor 1	Homo sapiens	0-7
21475882-3	2009	The development of imatinib mesylate (STI571, Gleevec ), a potent and selective BCR-ABL tyrosine kinase inhibitor, represents an important advance in cancer therapy.	imatinib	19-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
21475882-3	2009	The development of imatinib mesylate (STI571, Gleevec ), a potent and selective BCR-ABL tyrosine kinase inhibitor, represents an important advance in cancer therapy.	imatinib	38-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
21475882-5	2009	In order to identify the genes potentially related to these resistance mechanisms, we examined genes differentially expressed in BCR-ABL-positive cell lines resistant to imatinib mesylate.	imatinib	170-178	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
21475882-8	2009	Among these, RUNX1T1 was shown to be overexpressed in another resistant cell line and in patients resistant to imatinib mesylate.	imatinib	111-128	RUNX1 partner transcriptional co-repressor 1	Homo sapiens	13-20
21475882-9	2009	This suggests that RUNX1T1 is a putative candidate for the further study of imatinib mesylate resistance.	imatinib	76-93	RUNX1 partner transcriptional co-repressor 1	Homo sapiens	19-26
19258052-6	2009	Imatinib mesylate is a specific inhibitor of three tyrosine kinase receptors, two of which, PDGF-R and c-Kit, are implicated in the pathogenesis of intimal hyperplasia.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	92-98
19258052-6	2009	Imatinib mesylate is a specific inhibitor of three tyrosine kinase receptors, two of which, PDGF-R and c-Kit, are implicated in the pathogenesis of intimal hyperplasia.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	103-108
19469547-2	2009	Clinical treatment with imatinib targets the kinase domain of KIT, but tumor regrowth occurs as a result of the development of resistant mutations in the kinase active site.	imatinib	24-32	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	62-65
20641611-3	2004	In addition, imatinib has been shown to be an effective treatment against a variety of other conditions that are characterized by the expression of abl, c-kit, or PDGF TKs (3).	imatinib	13-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	153-158
20641611-0	2004	[N-(11)C-methyl]-[4-[(4-Methyl-1-piperazinyl)methyl]-N-[4-methyl-3-[[4-(3-pyridyl)-2-pyrimidinyl]amino]phenyl]benzamide Imatinib ([4-[(4-methyl-1-piperazinyl)methyl]-N-[4-methyl-3-[[4-(3-pyridyl)-2-pyrimidinyl]amino]phenyl]benzamide) is a synthetic tyrosine kinase (TK) signal transduction inhibitor used for the treatment of a variety of chronic myeloid leukemia (CML) attributed to the Philadelphia chromosome-positive trait (1).	imatinib	120-128	TXK tyrosine kinase	Homo sapiens	266-268
20641611-3	2004	In addition, imatinib has been shown to be an effective treatment against a variety of other conditions that are characterized by the expression of abl, c-kit, or PDGF TKs (3).	imatinib	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	148-151
19502190-1	2009	The BCR-ABL inhibitor imatinib is standard first-line therapy for patients with chronic myeloid leukemia (CML) and has revolutionized treatment of the disease.	imatinib	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
19210352-1	2009	BACKGROUND: The Fip1-like-1-platelet-derived growth factor receptor alpha (FIP1L1-PDGFRA) gene fusion is a common cause of chronic eosinophilic leukemia (CEL)/hypereosinophilic syndrome (HES), and patients suffering from this particular subgroup of CEL/HES respond to low-dose imatinib therapy.	imatinib	277-285	factor interacting with PAPOLA and CPSF1	Homo sapiens	75-81
19210352-1	2009	BACKGROUND: The Fip1-like-1-platelet-derived growth factor receptor alpha (FIP1L1-PDGFRA) gene fusion is a common cause of chronic eosinophilic leukemia (CEL)/hypereosinophilic syndrome (HES), and patients suffering from this particular subgroup of CEL/HES respond to low-dose imatinib therapy.	imatinib	277-285	platelet derived growth factor receptor alpha	Homo sapiens	82-88
19210352-3	2009	METHODS: In an imatinib resistant FIP1L1-PDGFRA positive patient, we analyzed the molecular structure of the fusion gene and analyzed the effect of several kinase inhibitors on FIP1L1-PDGFRA-mediated proliferative responses in vitro.	imatinib	15-23	factor interacting with PAPOLA and CPSF1	Homo sapiens	34-40
19210352-3	2009	METHODS: In an imatinib resistant FIP1L1-PDGFRA positive patient, we analyzed the molecular structure of the fusion gene and analyzed the effect of several kinase inhibitors on FIP1L1-PDGFRA-mediated proliferative responses in vitro.	imatinib	15-23	platelet derived growth factor receptor alpha	Homo sapiens	41-47
19210352-3	2009	METHODS: In an imatinib resistant FIP1L1-PDGFRA positive patient, we analyzed the molecular structure of the fusion gene and analyzed the effect of several kinase inhibitors on FIP1L1-PDGFRA-mediated proliferative responses in vitro.	imatinib	15-23	factor interacting with PAPOLA and CPSF1	Homo sapiens	177-183
19210352-3	2009	METHODS: In an imatinib resistant FIP1L1-PDGFRA positive patient, we analyzed the molecular structure of the fusion gene and analyzed the effect of several kinase inhibitors on FIP1L1-PDGFRA-mediated proliferative responses in vitro.	imatinib	15-23	platelet derived growth factor receptor alpha	Homo sapiens	184-190
19210352-7	2009	Structural modeling revealed that the newly identified S601P mutated form of PDGFRA destabilizes the inactive conformation of the kinase domain that is necessary to bind imatinib as well as sorafenib.	imatinib	170-178	platelet derived growth factor receptor alpha	Homo sapiens	77-83
19210352-8	2009	CONCLUSIONS: We identified a novel mutation in FIP1L1-PDGFRA resulting in both imatinib and sorafenib resistance.	imatinib	79-87	factor interacting with PAPOLA and CPSF1	Homo sapiens	47-53
19210352-8	2009	CONCLUSIONS: We identified a novel mutation in FIP1L1-PDGFRA resulting in both imatinib and sorafenib resistance.	imatinib	79-87	platelet derived growth factor receptor alpha	Homo sapiens	54-60
19010635-1	2009	AIM: The use of a non-toxic tyrosine kinase receptor inhibitor, Imatinib Mesylate (IM), has become an ever-more common therapeutic alternative in some Kit (CD117) over-expressing neoplasms.	imatinib	64-81	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	156-161
19519355-4	2009	Nilotinib is a second-generation tyrosine kinase inhibitor 30-50 fold more potent than imatinib with high affinity and selectivity on BCR/ABL, active against a wide range of mutant clones, except T315I mutation.	imatinib	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
19377081-4	2009	In this study we used flow cytometry to investigate the in vitro inhibition of Crkl phosphorylation by imatinib in CD34(+) cells in diagnostic samples from two groups of patients distinguished by their cytogenetic response.	imatinib	103-111	CRK like proto-oncogene, adaptor protein	Homo sapiens	79-83
19580708-2	2009	INTRODUCTION: GISTs, a new nosological entity recently described, represent a peculiar model of solid tumor: the identification of the molecular mechanism responsible for the oncogenesis led to the development of a new drug (imatinib) active on the specific molecular target, represented by the product of the mutated proto-oncogene c-kit which is a tyrosine kinase receptor that becomes constitutively active by mutation.	imatinib	225-233	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	318-338
19394750-1	2009	OBJECTIVE: To investigate the interaction of imatinib mesylate (IM) with the clinically relevant adenosine triphosphate-binding cassette efflux transporter MDR1 (ABCB1) in cells from patients with chronic myeloid leukemia (CML) and to explore whether inhibition of this transporter would improve IM"s efficacy in the elimination of CML CD34(+) cells by increasing cell-associated drug accumulation.	imatinib	45-62	ATP binding cassette subfamily B member 1	Homo sapiens	156-160
19394750-1	2009	OBJECTIVE: To investigate the interaction of imatinib mesylate (IM) with the clinically relevant adenosine triphosphate-binding cassette efflux transporter MDR1 (ABCB1) in cells from patients with chronic myeloid leukemia (CML) and to explore whether inhibition of this transporter would improve IM"s efficacy in the elimination of CML CD34(+) cells by increasing cell-associated drug accumulation.	imatinib	45-62	ATP binding cassette subfamily B member 1	Homo sapiens	162-167
19394750-1	2009	OBJECTIVE: To investigate the interaction of imatinib mesylate (IM) with the clinically relevant adenosine triphosphate-binding cassette efflux transporter MDR1 (ABCB1) in cells from patients with chronic myeloid leukemia (CML) and to explore whether inhibition of this transporter would improve IM"s efficacy in the elimination of CML CD34(+) cells by increasing cell-associated drug accumulation.	imatinib	45-62	CD34 molecule	Homo sapiens	336-340
19490758-7	2009	Imatinib and docetaxel induced apoptosis through caspase-3 enzyme activity and mitochondrial membrane potential.	imatinib	0-8	caspase 3	Homo sapiens	49-58
19377081-4	2009	In this study we used flow cytometry to investigate the in vitro inhibition of Crkl phosphorylation by imatinib in CD34(+) cells in diagnostic samples from two groups of patients distinguished by their cytogenetic response.	imatinib	103-111	CD34 molecule	Homo sapiens	115-119
19623482-6	2009	K562 cells stably transfected to express CCN3 showed enhanced apoptosis in response to treatment with the tyrosine kinase inhibitor, imatinib.	imatinib	133-141	cellular communication network factor 3	Homo sapiens	41-45
19455391-2	2009	Dasatinib is 325-fold more potent than imatinib in inhibiting BCR-ABL in vitro and is indicated for the treatment of chronic myeloid leukemia (CML) and Philadelphia chromosome-positive acute lymphoblastic leukemia resistant or intolerant to imatinib.	imatinib	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
19623482-9	2009	CCN3 restores growth regulation, regains sensitivity to the induction of apoptosis and enhances imatinib cell kill in CML cells.	imatinib	96-104	cellular communication network factor 3	Homo sapiens	0-4
19013640-0	2009	Imatinib has limited therapeutic activity for hypereosinophilic syndrome patients with unknown or negative PDGFRalpha mutation status.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	107-117
19013640-3	2009	Efficacy of imatinib mesylate is well established in CEL with FIP1L1-platelet-derived growth factor-alpha (PDGFRalpha) rearrangement.	imatinib	12-29	platelet derived growth factor receptor alpha	Homo sapiens	107-117
19013640-6	2009	Our results confirm low response rate to imatinib in HES patients with unknown or negative PDGFRalpha status, and underscore the need for new therapeutic options for this disorder.	imatinib	41-49	platelet derived growth factor receptor alpha	Homo sapiens	91-101
18951628-0	2009	Haemorrhagic complications associated with reduced alpha2-plasmin inhibitor during imatinib use in a patient with Philadelphia chromosome-positive acute lymphoblastic leukaemia.	imatinib	83-91	serpin family F member 2	Homo sapiens	51-75
19091403-0	2009	Molecular response to imatinib in patient with Ph negative p190 BCR-ABL transcript positive chronic myeloid leukemia with cyclic leukocytosis.	imatinib	22-30	contactin associated protein 1	Homo sapiens	59-63
19091403-0	2009	Molecular response to imatinib in patient with Ph negative p190 BCR-ABL transcript positive chronic myeloid leukemia with cyclic leukocytosis.	imatinib	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
19091403-4	2009	This is the first report of Philadelphia negative, p190 BCR-ABL positive CML with cyclic spontaneous oscillation of white blood cell count (WBC), and excellent response to imatinib treatment.	imatinib	172-180	contactin associated protein 1	Homo sapiens	51-55
19091403-4	2009	This is the first report of Philadelphia negative, p190 BCR-ABL positive CML with cyclic spontaneous oscillation of white blood cell count (WBC), and excellent response to imatinib treatment.	imatinib	172-180	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
19519539-0	2009	Basis for resistance to imatinib in 16 BCR-ABL mutants as determined using molecular dynamics.	imatinib	24-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
19519539-1	2009	Large-scale (approximately 36,000 atoms) long-time (30 ns each) molecular dynamics (MD) simulations on the complex of imatinib and 16 common mutants of the ABL tyrosine kinase domain have been performed to study the imatinib resistance mechanisms at the atomic level.	imatinib	216-224	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-159
19519539-2	2009	MD simulations show that long time computational simulations could offer insight information that static models, simple homology modeling methods, or short-time simulations cannot provide for the BCR-ABL imatinib resistance problem.	imatinib	204-212	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	196-203
19519539-3	2009	Three possible types of mutational effects from those mutants are found: the direct effect on the contact interaction with imatinib (e.g. some P-loop mutations), the effect on the conformation of a remote region contacting with imatinib (e.g. T315I), and the effect on interaction between two regions within the BCR-ABL domain (e.g. H396P).	imatinib	123-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	312-319
19519539-3	2009	Three possible types of mutational effects from those mutants are found: the direct effect on the contact interaction with imatinib (e.g. some P-loop mutations), the effect on the conformation of a remote region contacting with imatinib (e.g. T315I), and the effect on interaction between two regions within the BCR-ABL domain (e.g. H396P).	imatinib	228-236	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	312-319
19961019-8	2009	The mutations of c-kit influences the therapeutic effects of imatinib.	imatinib	61-69	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	17-22
19951530-9	2009	CONCLUSION: Imatinib in treatment of MPN with eosinophilia and positive FIP1L1-PDGFR alpha gene patients can induce high hematologic and molecular remission.	imatinib	12-20	factor interacting with PAPOLA and CPSF1	Homo sapiens	72-78
19248046-1	2009	BACKGROUND: This study determined the maximum tolerated dose (MTD) and dose-limiting toxicities (DLT) of the oral vascular endothelial growth factor receptor (VEGFR) inhibitor, vatalanib, when administered with imatinib and hydroxyurea on a continuous daily schedule among recurrent malignant glioma patients.	imatinib	211-219	kinase insert domain receptor	Homo sapiens	114-157
19951530-9	2009	CONCLUSION: Imatinib in treatment of MPN with eosinophilia and positive FIP1L1-PDGFR alpha gene patients can induce high hematologic and molecular remission.	imatinib	12-20	platelet derived growth factor receptor alpha	Homo sapiens	79-90
19951536-12	2009	mRNA expression of Gfi-1B, GPA and gamma-globin gene and the expression of GPA protein on cell surface were all significantly decreased after being exposed to 0.2 micromol/L imatinib for 48 hours in K562-shRNA-IER3IP1 group (P<0.01).	imatinib	174-182	immediate early response 3 interacting protein 1	Homo sapiens	210-217
19951536-13	2009	During the erythroid differentiation induced by imatinib, mRNA expression of IER3IP1 obviously increased at the 3 h, and decreased from 6 h to 48 h. CONCLUSIONS: Inhibition of expression of IER3IP1 gene can inhibit erythroid differentiation and elevate the proliferation of K562 cells.	imatinib	48-56	immediate early response 3 interacting protein 1	Homo sapiens	77-84
19951536-13	2009	During the erythroid differentiation induced by imatinib, mRNA expression of IER3IP1 obviously increased at the 3 h, and decreased from 6 h to 48 h. CONCLUSIONS: Inhibition of expression of IER3IP1 gene can inhibit erythroid differentiation and elevate the proliferation of K562 cells.	imatinib	48-56	immediate early response 3 interacting protein 1	Homo sapiens	190-197
19248046-1	2009	BACKGROUND: This study determined the maximum tolerated dose (MTD) and dose-limiting toxicities (DLT) of the oral vascular endothelial growth factor receptor (VEGFR) inhibitor, vatalanib, when administered with imatinib and hydroxyurea on a continuous daily schedule among recurrent malignant glioma patients.	imatinib	211-219	kinase insert domain receptor	Homo sapiens	159-164
19401345-0	2009	Abnormalities in glucose uptake and metabolism in imatinib-resistant human BCR-ABL-positive cells.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
19401345-5	2009	Our results show that sensitive K562-s and LAMA84-s BCR-ABL-positive cells have decreased glucose uptake, decreased lactate production, and an improved oxidative TCA cycle following imatinib treatment.	imatinib	182-190	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
19401345-10	2009	The changes in glucose uptake and metabolism were accompanied by intracellular translocation of GLUT-1 from the plasma membrane into the intracellular fraction in sensitive cells treated with imatinib, whereas GLUT-1 remained located at the plasma membrane in LAMA84-r and K562-r cells.	imatinib	192-200	solute carrier family 2 member 1	Homo sapiens	96-102
19401345-7	2009	In addition, oxidative synthesis of RNA ribose from (13)C-glucose via glucose-6-phosphate dehydrogenase was decreased, and RNA synthesis via the nonoxidative transketolase pathway was increased in imatinib-resistant cells.	imatinib	197-205	glucose-6-phosphate dehydrogenase	Homo sapiens	70-103
19401345-12	2009	In summary, elevated glucose uptake and nonoxidative glycolytic metabolic phenotype can be used as sensitive markers for early detection of imatinib resistance in BCR-ABL-positive cells.	imatinib	140-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
19358301-6	2009	In addition, FAK silencing enhanced in vitro and in vivo efficacy of ABL tyrosine kinase inhibitor imatinib in BCR/ABL-BaF3 cells.	imatinib	99-107	PTK2 protein tyrosine kinase 2	Mus musculus	13-16
19306355-5	2009	Newer Bcr-Abl tyrosine kinase inhibitors can induce responses in patients with all phases of imatinib-resistant CML, even those with imatinib-resistant mutations in the BCR-ABL gene.	imatinib	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-13
19306355-5	2009	Newer Bcr-Abl tyrosine kinase inhibitors can induce responses in patients with all phases of imatinib-resistant CML, even those with imatinib-resistant mutations in the BCR-ABL gene.	imatinib	133-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-13
19306355-5	2009	Newer Bcr-Abl tyrosine kinase inhibitors can induce responses in patients with all phases of imatinib-resistant CML, even those with imatinib-resistant mutations in the BCR-ABL gene.	imatinib	133-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	169-176
19358301-6	2009	In addition, FAK silencing enhanced in vitro and in vivo efficacy of ABL tyrosine kinase inhibitor imatinib in BCR/ABL-BaF3 cells.	imatinib	99-107	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	69-72
19358301-6	2009	In addition, FAK silencing enhanced in vitro and in vivo efficacy of ABL tyrosine kinase inhibitor imatinib in BCR/ABL-BaF3 cells.	imatinib	99-107	BCR activator of RhoGEF and GTPase	Mus musculus	111-114
19358301-6	2009	In addition, FAK silencing enhanced in vitro and in vivo efficacy of ABL tyrosine kinase inhibitor imatinib in BCR/ABL-BaF3 cells.	imatinib	99-107	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	115-118
19451502-4	2009	The histiocytes were positive for platelet-derived growth factor receptor alpha, the target molecule for imatinib.	imatinib	105-113	platelet derived growth factor receptor alpha	Homo sapiens	34-79
19442606-8	2009	Quantitative RT-PCR analysis showed that Imatinib treatment decreased expression of the cartilage and bone related genes, Col2a1 and osteocalcin, respectively.	imatinib	41-49	collagen type II alpha 1 chain	Rattus norvegicus	122-128
19344397-0	2009	Does a rise in the BCR-ABL1 transcript level identify chronic phase CML patients responding to imatinib who have a high risk of cytogenetic relapse?	imatinib	95-103	BCR activator of RhoGEF and GTPase	Homo sapiens	19-27
19344397-1	2009	BCR-ABL1 transcript numbers were monitored in 161 patients who started treatment with imatinib early after diagnosis of chronic myeloid leukaemia in chronic phase and achieved complete cytogenetic responses (CCyR).	imatinib	86-94	BCR activator of RhoGEF and GTPase	Homo sapiens	0-8
19442606-8	2009	Quantitative RT-PCR analysis showed that Imatinib treatment decreased expression of the cartilage and bone related genes, Col2a1 and osteocalcin, respectively.	imatinib	41-49	bone gamma-carboxyglutamate protein	Rattus norvegicus	133-144
19360458-3	2009	We show here that the expression of Gfi1b is strongly elevated in CML and AML patients compared to normal healthy controls and that imatinib, a drug widely used to treat CML, further enhances Gfi1b expression in patients even after remission.	imatinib	132-140	growth factor independent 1B transcriptional repressor	Homo sapiens	36-41
19366808-1	2009	Although the BCR/ABL tyrosine kinase inhibitor imatinib is highly effective for treatment of chronic myelogenous leukemia and Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia, relapse with emerging imatinib resistance mutations in the BCR/ABL kinase domain poses a significant problem.	imatinib	47-55	BCR activator of RhoGEF and GTPase	Homo sapiens	13-16
19366808-1	2009	Although the BCR/ABL tyrosine kinase inhibitor imatinib is highly effective for treatment of chronic myelogenous leukemia and Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia, relapse with emerging imatinib resistance mutations in the BCR/ABL kinase domain poses a significant problem.	imatinib	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-20
19366808-1	2009	Although the BCR/ABL tyrosine kinase inhibitor imatinib is highly effective for treatment of chronic myelogenous leukemia and Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia, relapse with emerging imatinib resistance mutations in the BCR/ABL kinase domain poses a significant problem.	imatinib	47-55	BCR activator of RhoGEF and GTPase	Homo sapiens	254-257
19366808-1	2009	Although the BCR/ABL tyrosine kinase inhibitor imatinib is highly effective for treatment of chronic myelogenous leukemia and Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia, relapse with emerging imatinib resistance mutations in the BCR/ABL kinase domain poses a significant problem.	imatinib	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	258-261
19366808-1	2009	Although the BCR/ABL tyrosine kinase inhibitor imatinib is highly effective for treatment of chronic myelogenous leukemia and Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia, relapse with emerging imatinib resistance mutations in the BCR/ABL kinase domain poses a significant problem.	imatinib	217-225	BCR activator of RhoGEF and GTPase	Homo sapiens	13-16
19366808-1	2009	Although the BCR/ABL tyrosine kinase inhibitor imatinib is highly effective for treatment of chronic myelogenous leukemia and Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia, relapse with emerging imatinib resistance mutations in the BCR/ABL kinase domain poses a significant problem.	imatinib	217-225	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-20
19366808-1	2009	Although the BCR/ABL tyrosine kinase inhibitor imatinib is highly effective for treatment of chronic myelogenous leukemia and Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia, relapse with emerging imatinib resistance mutations in the BCR/ABL kinase domain poses a significant problem.	imatinib	217-225	BCR activator of RhoGEF and GTPase	Homo sapiens	254-257
19366808-1	2009	Although the BCR/ABL tyrosine kinase inhibitor imatinib is highly effective for treatment of chronic myelogenous leukemia and Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia, relapse with emerging imatinib resistance mutations in the BCR/ABL kinase domain poses a significant problem.	imatinib	217-225	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	258-261
19366808-3	2009	The increased sensitivity to sorafenib was also observed in cells inducibly expressing BCR/ABL with the imatinib-resistant E255K or T315I mutation.	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
19225039-2	2009	Four drugs, flavopiridol, imatinib mesylate (Gleevec), PF-407288, and prazosin, with different transport specificity for BCRP/Bcrp and MDR1/Mdr1a were selected, and the drug levels in plasma, cerebrospinal fluid, and brain of mice were determined.	imatinib	26-43	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	121-125
19225039-2	2009	Four drugs, flavopiridol, imatinib mesylate (Gleevec), PF-407288, and prazosin, with different transport specificity for BCRP/Bcrp and MDR1/Mdr1a were selected, and the drug levels in plasma, cerebrospinal fluid, and brain of mice were determined.	imatinib	26-43	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	126-130
19225039-2	2009	Four drugs, flavopiridol, imatinib mesylate (Gleevec), PF-407288, and prazosin, with different transport specificity for BCRP/Bcrp and MDR1/Mdr1a were selected, and the drug levels in plasma, cerebrospinal fluid, and brain of mice were determined.	imatinib	26-43	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	135-139
19225039-2	2009	Four drugs, flavopiridol, imatinib mesylate (Gleevec), PF-407288, and prazosin, with different transport specificity for BCRP/Bcrp and MDR1/Mdr1a were selected, and the drug levels in plasma, cerebrospinal fluid, and brain of mice were determined.	imatinib	45-52	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	121-125
19225039-2	2009	Four drugs, flavopiridol, imatinib mesylate (Gleevec), PF-407288, and prazosin, with different transport specificity for BCRP/Bcrp and MDR1/Mdr1a were selected, and the drug levels in plasma, cerebrospinal fluid, and brain of mice were determined.	imatinib	45-52	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	126-130
19225039-2	2009	Four drugs, flavopiridol, imatinib mesylate (Gleevec), PF-407288, and prazosin, with different transport specificity for BCRP/Bcrp and MDR1/Mdr1a were selected, and the drug levels in plasma, cerebrospinal fluid, and brain of mice were determined.	imatinib	45-52	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	135-139
19225039-5	2009	For imatinib, a better substrate of P-gp than Bcrp, the B/P ratios in Bcrp(-/-) were comparable to those in FVB mice, whereas the B/P ratios in Mdr1a/1b(-/-), (-/-) and Mdr1a/1b(-/-), (-/-)Bcrp(-/-) mice were more than 4- and 28-fold of those in FVB mice at both time points, respectively.	imatinib	4-12	phosphoglycolate phosphatase	Mus musculus	36-40
19205737-11	2009	With Imatinib, a selective PDGFR tyrosin kinase inhibitor, partial and complete remissions of DFSP could be achieved.	imatinib	5-13	platelet derived growth factor receptor beta	Homo sapiens	27-32
19380743-1	2009	The tyrosine kinase Bcr-Abl causes chronic myeloid leukemia and is the cognate target of tyrosine kinase inhibitors like imatinib.	imatinib	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
19325470-14	2009	In cultured human lung fibroblasts, TGF-beta1 suppressed KGF messenger RNA and protein expression, which were reversed by SB431542 and by the c-Abl inhibitor, imatinib mesylate, but not by the p38 map kinase inhibitor, SB203580.	imatinib	159-176	transforming growth factor beta 1	Homo sapiens	36-45
19325470-14	2009	In cultured human lung fibroblasts, TGF-beta1 suppressed KGF messenger RNA and protein expression, which were reversed by SB431542 and by the c-Abl inhibitor, imatinib mesylate, but not by the p38 map kinase inhibitor, SB203580.	imatinib	159-176	fibroblast growth factor 7	Homo sapiens	57-60
19325470-14	2009	In cultured human lung fibroblasts, TGF-beta1 suppressed KGF messenger RNA and protein expression, which were reversed by SB431542 and by the c-Abl inhibitor, imatinib mesylate, but not by the p38 map kinase inhibitor, SB203580.	imatinib	159-176	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-147
19343480-4	2009	In contrast, in a case of Philadelphia chromosome-positive acute lymphoid leukemia being treated with chemotherapy including imatinib, we monitored both wild-type and T315I bcr-abl transcripts, and found increased levels of T315I transcripts during relapse (0% at the time of diagnosis and 54.8% at relapse).	imatinib	125-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	173-180
19360458-3	2009	We show here that the expression of Gfi1b is strongly elevated in CML and AML patients compared to normal healthy controls and that imatinib, a drug widely used to treat CML, further enhances Gfi1b expression in patients even after remission.	imatinib	132-140	growth factor independent 1B transcriptional repressor	Homo sapiens	192-197
19360458-4	2009	Our data suggest that Gfi1b may be an important factor to establish or maintain myeloid leukemia and myeloproliferative diseases and that, high expression levels of Gfi1b might be associated with the emergence of Philadelphia chromosome negative myeloid malignancies after imatinib withdrawal or after the development of imatinib resistance.	imatinib	273-281	growth factor independent 1B transcriptional repressor	Homo sapiens	165-170
19360458-4	2009	Our data suggest that Gfi1b may be an important factor to establish or maintain myeloid leukemia and myeloproliferative diseases and that, high expression levels of Gfi1b might be associated with the emergence of Philadelphia chromosome negative myeloid malignancies after imatinib withdrawal or after the development of imatinib resistance.	imatinib	321-329	growth factor independent 1B transcriptional repressor	Homo sapiens	165-170
19363292-1	2009	Imatinib mesylate (IM), a potent inhibitor of the BCR/ABL tyrosine kinase, has become standard first-line therapy for patients with chronic myeloid leukemia (CML), but the frequency of resistance increases in advancing stages of disease.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
19363292-1	2009	Imatinib mesylate (IM), a potent inhibitor of the BCR/ABL tyrosine kinase, has become standard first-line therapy for patients with chronic myeloid leukemia (CML), but the frequency of resistance increases in advancing stages of disease.	imatinib	19-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
19242505-5	2009	Imatinib-treated rats had a significant reduction in glomerular macrophage accumulation and reduced renal cortical PDGFR-beta and M-CSF receptor mRNA expression.	imatinib	0-8	platelet derived growth factor receptor beta	Rattus norvegicus	115-125
18977528-5	2009	The resistant indexes (IC(50)(K562-Vinc)/IC(50)(K562-WT)) for structurally unrelated drugs like imatinib, doxorubicin and colchicine were 8.0+/-0.3, 2.8+/-0.4 and 44.8+/-8.8, respectively.	imatinib	96-104	nuclear paraspeckle assembly transcript 1	Homo sapiens	35-39
19041155-0	2009	Imatinib inhibits in vitro proliferation of cells derived from a pleural solitary fibrous tumor expressing platelet-derived growth factor receptor-beta.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	107-151
18977528-6	2009	The imatinib resistance was reversed by P-gp blockade suggesting the involvement of P-gp in imatinib transport.	imatinib	4-12	phosphoglycolate phosphatase	Homo sapiens	40-44
18977528-6	2009	The imatinib resistance was reversed by P-gp blockade suggesting the involvement of P-gp in imatinib transport.	imatinib	4-12	phosphoglycolate phosphatase	Homo sapiens	84-88
18977528-6	2009	The imatinib resistance was reversed by P-gp blockade suggesting the involvement of P-gp in imatinib transport.	imatinib	92-100	phosphoglycolate phosphatase	Homo sapiens	40-44
18977528-6	2009	The imatinib resistance was reversed by P-gp blockade suggesting the involvement of P-gp in imatinib transport.	imatinib	92-100	phosphoglycolate phosphatase	Homo sapiens	84-88
18977528-8	2009	The inhibition of NF-kappaB with BAY 11-7082 increased the cytotoxicity of imatinib in K562-Vinc cells but not in K562-WT.	imatinib	75-83	nuclear factor kappa B subunit 1	Homo sapiens	18-27
18977528-8	2009	The inhibition of NF-kappaB with BAY 11-7082 increased the cytotoxicity of imatinib in K562-Vinc cells but not in K562-WT.	imatinib	75-83	nuclear paraspeckle assembly transcript 1	Homo sapiens	92-96
18977528-12	2009	Our results indicate that the vincristine-resistant K562 cells which developed MDR phenotype, exhibited resistance to imatinib associated with a functional P-gp over-expression.	imatinib	118-126	phosphoglycolate phosphatase	Homo sapiens	156-160
19151780-0	2009	Nuclear entrapment of BCR-ABL by combining imatinib mesylate with leptomycin B does not eliminate CD34+ chronic myeloid leukaemia cells.	imatinib	43-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
19212337-2	2009	Most FIP1L1-PDGFRA positive patients enjoy durable and complete molecular responses to low-dose imatinib (Glivec/Gleevec).	imatinib	96-104	factor interacting with PAPOLA and CPSF1	Homo sapiens	5-11
19212337-2	2009	Most FIP1L1-PDGFRA positive patients enjoy durable and complete molecular responses to low-dose imatinib (Glivec/Gleevec).	imatinib	96-104	platelet derived growth factor receptor alpha	Homo sapiens	12-18
19212337-7	2009	In vitro, the novel FIP1L1-PDGFRalpha D842V mutant is highly resistant to sorafenib, imatinib, dasatinib (Sprycell) and PKC412 (Midostaurin).	imatinib	85-93	factor interacting with PAPOLA and CPSF1	Homo sapiens	20-26
19212337-8	2009	Thus, sorafenib is clinically active in imatinib-resistant FIP1L1-PDGFRalpha T674I CEL, but the rapid emergence of other mutants may limit the response duration.	imatinib	40-48	factor interacting with PAPOLA and CPSF1	Homo sapiens	59-65
19041155-8	2009	With the limit of experimental findings, our results support a possible future application of imatinib as a candidate molecule in the target therapy of malignant SFTs over-expressing wild-type PDGFR.	imatinib	94-102	platelet derived growth factor receptor beta	Homo sapiens	193-198
19041155-1	2009	We examined the in vitro effects of imatinib (Novartis Pharma AG, Basel, Switzerland) as a possible inhibitor of PDGFR pathway on cells derived from a recurrence of a pleural malignant solitary fibrous tumor (SFT).	imatinib	36-44	platelet derived growth factor receptor beta	Homo sapiens	113-118
19062090-3	2009	Here, we describe five cases of CML in late CP, which were switched to imatinib while in CCR after interferon alpha (IFN alpha) and reached complete and stable molecular remission with intermittent drug administration at 400mg/every 20 days/month.	imatinib	71-79	interferon alpha 1	Homo sapiens	117-126
19041155-7	2009	Western blotting showed that PDGFR-beta was highly expressed and phosphorylated in SFT-derived cells and imatinib treatment reduced PDGFR-beta phosphorylation and SMA expression.	imatinib	105-113	platelet derived growth factor receptor beta	Homo sapiens	132-142
19268365-3	2009	Bcl-6 expression is induced in Bcr-Abl expressing lymphoid cell lines by the tyrosine kinase inhibitor, imatinib.	imatinib	104-112	BCL6 transcription repressor	Homo sapiens	0-5
19131110-0	2009	Compound 48, a novel dual PPAR alpha/gamma ligand, inhibits the growth of human CML cell lines and enhances the anticancer-effects of imatinib.	imatinib	134-142	peroxisome proliferator activated receptor alpha	Homo sapiens	26-36
19131110-6	2009	Overall, our data suggest that the PPAR alpha/gamma ligands may have potentials in the treatment of CML in an adjuvant setting either before or after the development of imatinib resistance.	imatinib	169-177	peroxisome proliferator activated receptor alpha	Homo sapiens	35-45
19268365-4	2009	We show that p38 MAPK mediates induction of Bcl-6 following inhibition of Bcr-Abl by imatinib.	imatinib	85-93	mitogen-activated protein kinase 14	Homo sapiens	13-16
19268365-4	2009	We show that p38 MAPK mediates induction of Bcl-6 following inhibition of Bcr-Abl by imatinib.	imatinib	85-93	BCL6 transcription repressor	Homo sapiens	44-49
21475850-0	2009	Secondary resistance to imatinib in patients with gastrointestinal stromal tumors through an acquired KIT exon 17 mutation.	imatinib	24-32	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	102-105
19417143-0	2009	Imatinib blocks migration and invasion of medulloblastoma cells by concurrently inhibiting activation of platelet-derived growth factor receptor and transactivation of epidermal growth factor receptor.	imatinib	0-8	epidermal growth factor receptor	Homo sapiens	168-200
19417143-7	2009	Imatinib (1 mumol/L) treatment of DAOY and D556 cells inhibited PDGF-BB- and serum-mediated migration and invasion at 24 and 48 h, respectively, and concomitantly inhibited PDGF-BB activation of PDGFRB, Akt, and ERK but increased PTEN expression and activity.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	195-201
19417143-7	2009	Imatinib (1 mumol/L) treatment of DAOY and D556 cells inhibited PDGF-BB- and serum-mediated migration and invasion at 24 and 48 h, respectively, and concomitantly inhibited PDGF-BB activation of PDGFRB, Akt, and ERK but increased PTEN expression and activity.	imatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	203-206
19417143-7	2009	Imatinib (1 mumol/L) treatment of DAOY and D556 cells inhibited PDGF-BB- and serum-mediated migration and invasion at 24 and 48 h, respectively, and concomitantly inhibited PDGF-BB activation of PDGFRB, Akt, and ERK but increased PTEN expression and activity.	imatinib	0-8	mitogen-activated protein kinase 1	Homo sapiens	212-215
19417143-7	2009	Imatinib (1 mumol/L) treatment of DAOY and D556 cells inhibited PDGF-BB- and serum-mediated migration and invasion at 24 and 48 h, respectively, and concomitantly inhibited PDGF-BB activation of PDGFRB, Akt, and ERK but increased PTEN expression and activity.	imatinib	0-8	phosphatase and tensin homolog	Homo sapiens	230-234
19417143-8	2009	Imatinib treatment also induced DAOY cell apoptosis at 72 h and inhibited DAOY and D556 cell proliferation at 48 h. siRNA silencing of PDGFRB similarly inhibited signaling, migration, and survival and both siRNA and imatinib treatment inhibited PDGF-BB-mediated EGFR transactivation, indicating that the effects of imatinib treatment are specific to PDGFRB target inhibition.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	135-141
19417143-8	2009	Imatinib treatment also induced DAOY cell apoptosis at 72 h and inhibited DAOY and D556 cell proliferation at 48 h. siRNA silencing of PDGFRB similarly inhibited signaling, migration, and survival and both siRNA and imatinib treatment inhibited PDGF-BB-mediated EGFR transactivation, indicating that the effects of imatinib treatment are specific to PDGFRB target inhibition.	imatinib	0-8	epidermal growth factor receptor	Homo sapiens	262-266
19417143-8	2009	Imatinib treatment also induced DAOY cell apoptosis at 72 h and inhibited DAOY and D556 cell proliferation at 48 h. siRNA silencing of PDGFRB similarly inhibited signaling, migration, and survival and both siRNA and imatinib treatment inhibited PDGF-BB-mediated EGFR transactivation, indicating that the effects of imatinib treatment are specific to PDGFRB target inhibition.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	350-356
19417143-8	2009	Imatinib treatment also induced DAOY cell apoptosis at 72 h and inhibited DAOY and D556 cell proliferation at 48 h. siRNA silencing of PDGFRB similarly inhibited signaling, migration, and survival and both siRNA and imatinib treatment inhibited PDGF-BB-mediated EGFR transactivation, indicating that the effects of imatinib treatment are specific to PDGFRB target inhibition.	imatinib	216-224	platelet derived growth factor receptor beta	Homo sapiens	135-141
19417143-8	2009	Imatinib treatment also induced DAOY cell apoptosis at 72 h and inhibited DAOY and D556 cell proliferation at 48 h. siRNA silencing of PDGFRB similarly inhibited signaling, migration, and survival and both siRNA and imatinib treatment inhibited PDGF-BB-mediated EGFR transactivation, indicating that the effects of imatinib treatment are specific to PDGFRB target inhibition.	imatinib	315-323	platelet derived growth factor receptor beta	Homo sapiens	135-141
19417143-9	2009	These results indicate that PDGFRB tyrosine kinase activity is critical for migration and invasion of medulloblastoma cells possibly by transactivating EGFR; thus, imatinib may represent an important novel therapeutic agent for the treatment of medulloblastoma.	imatinib	164-172	platelet derived growth factor receptor beta	Homo sapiens	28-34
19417143-9	2009	These results indicate that PDGFRB tyrosine kinase activity is critical for migration and invasion of medulloblastoma cells possibly by transactivating EGFR; thus, imatinib may represent an important novel therapeutic agent for the treatment of medulloblastoma.	imatinib	164-172	epidermal growth factor receptor	Homo sapiens	152-156
21475850-7	2009	In conclusion, the exon 17 missense mutation T2467G in the tyrosine kinase domain of the KIT gene is correlated with imatinib resistance.	imatinib	117-125	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	89-92
19299048-6	2009	Inhibitors of KIT, a membrane receptor, are mainly represented by imatinib, an inhibitor of tyrosine kinase.	imatinib	66-74	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-17
19411681-14	2009	Compared with previous studies in western populations, these results suggest that ethnic differences may influence the relationship between KIT genotype and clinical outcome to imatinib.	imatinib	177-185	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	140-143
19203346-9	2009	Taken together, our results demonstrated for the first time that the loss of Bcr-Abl in imatinib-resistant cells led to the down-regulation of c-FLIP and subsequent increase of TRAIL sensitivity, suggesting that TRAIL could be an effective strategy for the treatment of imatinib-resistant CML with loss of Bcr-Abl.	imatinib	270-278	CASP8 and FADD like apoptosis regulator	Homo sapiens	143-149
19203346-0	2009	Sensitization of imatinib-resistant CML cells to TRAIL-induced apoptosis is mediated through down-regulation of Bcr-Abl as well as c-FLIP.	imatinib	17-25	TNF superfamily member 10	Homo sapiens	49-54
19203346-9	2009	Taken together, our results demonstrated for the first time that the loss of Bcr-Abl in imatinib-resistant cells led to the down-regulation of c-FLIP and subsequent increase of TRAIL sensitivity, suggesting that TRAIL could be an effective strategy for the treatment of imatinib-resistant CML with loss of Bcr-Abl.	imatinib	270-278	TNF superfamily member 10	Homo sapiens	212-217
19203346-0	2009	Sensitization of imatinib-resistant CML cells to TRAIL-induced apoptosis is mediated through down-regulation of Bcr-Abl as well as c-FLIP.	imatinib	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
19203346-0	2009	Sensitization of imatinib-resistant CML cells to TRAIL-induced apoptosis is mediated through down-regulation of Bcr-Abl as well as c-FLIP.	imatinib	17-25	PYD and CARD domain containing	Homo sapiens	128-132
19301902-0	2009	Design of chimeric histone deacetylase- and tyrosine kinase-inhibitors: a series of imatinib hybrides as potent inhibitors of wild-type and mutant BCR-ABL, PDGF-Rbeta, and histone deacetylases.	imatinib	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-154
19203346-1	2009	Resistance to imatinib is commonly associated with reactivation of Bcr-Abl signalling.	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
19203346-2	2009	However, Bcr-Abl-independent signalling pathways may be activated and contributed to imatinib resistance in some CML (chronic myelogenous leukaemia) patients.	imatinib	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
19203346-3	2009	We had isolated three imatinib-resistant K562/R1, R2 and R3 variants with gradual loss of Bcr-Abl from K562 cells to develop effective therapeutic strategies for imatinib-resistant CML.	imatinib	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
19203346-6	2009	These results were accompanied by down-regulation of c-FLIP {cellular FLICE [FADD (Fas-associated death domain)-like interleukin 1beta-converting enzyme]-inhibitory protein} in imatinib-resistant K562 variants compared with K562 cells.	imatinib	177-185	CASP8 and FADD like apoptosis regulator	Homo sapiens	53-59
19203346-6	2009	These results were accompanied by down-regulation of c-FLIP {cellular FLICE [FADD (Fas-associated death domain)-like interleukin 1beta-converting enzyme]-inhibitory protein} in imatinib-resistant K562 variants compared with K562 cells.	imatinib	177-185	caspase 8	Homo sapiens	70-75
19203346-9	2009	Taken together, our results demonstrated for the first time that the loss of Bcr-Abl in imatinib-resistant cells led to the down-regulation of c-FLIP and subsequent increase of TRAIL sensitivity, suggesting that TRAIL could be an effective strategy for the treatment of imatinib-resistant CML with loss of Bcr-Abl.	imatinib	88-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
19203346-9	2009	Taken together, our results demonstrated for the first time that the loss of Bcr-Abl in imatinib-resistant cells led to the down-regulation of c-FLIP and subsequent increase of TRAIL sensitivity, suggesting that TRAIL could be an effective strategy for the treatment of imatinib-resistant CML with loss of Bcr-Abl.	imatinib	88-96	CASP8 and FADD like apoptosis regulator	Homo sapiens	143-149
19203346-9	2009	Taken together, our results demonstrated for the first time that the loss of Bcr-Abl in imatinib-resistant cells led to the down-regulation of c-FLIP and subsequent increase of TRAIL sensitivity, suggesting that TRAIL could be an effective strategy for the treatment of imatinib-resistant CML with loss of Bcr-Abl.	imatinib	88-96	TNF superfamily member 10	Homo sapiens	177-182
19203346-9	2009	Taken together, our results demonstrated for the first time that the loss of Bcr-Abl in imatinib-resistant cells led to the down-regulation of c-FLIP and subsequent increase of TRAIL sensitivity, suggesting that TRAIL could be an effective strategy for the treatment of imatinib-resistant CML with loss of Bcr-Abl.	imatinib	88-96	TNF superfamily member 10	Homo sapiens	212-217
19203346-9	2009	Taken together, our results demonstrated for the first time that the loss of Bcr-Abl in imatinib-resistant cells led to the down-regulation of c-FLIP and subsequent increase of TRAIL sensitivity, suggesting that TRAIL could be an effective strategy for the treatment of imatinib-resistant CML with loss of Bcr-Abl.	imatinib	88-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	306-313
19203346-9	2009	Taken together, our results demonstrated for the first time that the loss of Bcr-Abl in imatinib-resistant cells led to the down-regulation of c-FLIP and subsequent increase of TRAIL sensitivity, suggesting that TRAIL could be an effective strategy for the treatment of imatinib-resistant CML with loss of Bcr-Abl.	imatinib	270-278	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
19830137-6	2009	Conversion of the BCR-ABL status to negative and improvements in hematologic parameters were achieved when the brand medication, imatinib, was resumed at a dose of 600 mg per day.	imatinib	129-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
19351841-0	2009	Natural killer cell IFN-gamma levels predict long-term survival with imatinib mesylate therapy in gastrointestinal stromal tumor-bearing patients.	imatinib	69-86	interferon gamma	Homo sapiens	20-29
19229297-7	2009	Finally, we show that repression of 24p3R by BCR-ABL is a critical feature of the mechanism by which imatinib kills BCR-ABL(+) cells.	imatinib	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
19301902-0	2009	Design of chimeric histone deacetylase- and tyrosine kinase-inhibitors: a series of imatinib hybrides as potent inhibitors of wild-type and mutant BCR-ABL, PDGF-Rbeta, and histone deacetylases.	imatinib	84-92	platelet derived growth factor receptor beta	Homo sapiens	156-166
18704417-9	2009	Achieving CCgR within 12 months and maintaining it without an increase in BCR-ABL transcripts might indicate that low-dose imatinib therapy can produce acceptable outcomes without excess toxicity.	imatinib	123-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
19229297-7	2009	Finally, we show that repression of 24p3R by BCR-ABL is a critical feature of the mechanism by which imatinib kills BCR-ABL(+) cells.	imatinib	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
19234487-1	2009	Chronic myelogenous leukemia (CML) patients treated with imatinib mesylate (IM) become drug resistant by mutations within the kinase domain of Bcr-Abl, and by other changes that cause progression to advanced stage (blast crisis) and increased expression of the Lyn tyrosine kinase, the regulation of which is not understood yet.	imatinib	57-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-150
19234487-1	2009	Chronic myelogenous leukemia (CML) patients treated with imatinib mesylate (IM) become drug resistant by mutations within the kinase domain of Bcr-Abl, and by other changes that cause progression to advanced stage (blast crisis) and increased expression of the Lyn tyrosine kinase, the regulation of which is not understood yet.	imatinib	57-74	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	261-264
19225164-5	2009	There were significant increases in the phosphocontent of downstream PDGFR targets Akt and ERK1/2 (5.3-fold and 2.4-fold, respectively) that were inhibited by PDGF immunoneutralization or by the selective PDGFR inhibitor imatinib.	imatinib	221-229	platelet derived growth factor receptor beta	Homo sapiens	69-74
19225164-5	2009	There were significant increases in the phosphocontent of downstream PDGFR targets Akt and ERK1/2 (5.3-fold and 2.4-fold, respectively) that were inhibited by PDGF immunoneutralization or by the selective PDGFR inhibitor imatinib.	imatinib	221-229	AKT serine/threonine kinase 1	Homo sapiens	83-86
19225164-5	2009	There were significant increases in the phosphocontent of downstream PDGFR targets Akt and ERK1/2 (5.3-fold and 2.4-fold, respectively) that were inhibited by PDGF immunoneutralization or by the selective PDGFR inhibitor imatinib.	imatinib	221-229	mitogen-activated protein kinase 3	Homo sapiens	91-97
19225164-5	2009	There were significant increases in the phosphocontent of downstream PDGFR targets Akt and ERK1/2 (5.3-fold and 2.4-fold, respectively) that were inhibited by PDGF immunoneutralization or by the selective PDGFR inhibitor imatinib.	imatinib	221-229	platelet derived growth factor receptor beta	Homo sapiens	205-210
19225164-8	2009	Inhibition of PDGFR activation by MacCM, either by addition of imatinib or by PDGF immunodepletion of MacCM, effectively disrupted the prosurvival effect.	imatinib	63-71	platelet derived growth factor receptor beta	Homo sapiens	14-19
19338769-0	2009	bFGF rescues imatinib/STI571-induced apoptosis of sis-NIH3T3 fibroblasts.	imatinib	13-21	fibroblast growth factor 2	Homo sapiens	0-4
19338769-0	2009	bFGF rescues imatinib/STI571-induced apoptosis of sis-NIH3T3 fibroblasts.	imatinib	22-28	fibroblast growth factor 2	Homo sapiens	0-4
19195046-1	2009	Dasatinib is a highly potent Bcr-Abl inhibitor that is approved for the treatment of imatinib-resistant or -intolerant chronic myeloid leukemia (CML) and Philadelphia chromosome-positive acute lymphoblastic leukemia.	imatinib	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
19120352-0	2009	Weekly imatinib dosage for chronic eosinophilic leukaemia expressing FIP1L1-PDGFRA fusion transcript: extended follow-up.	imatinib	7-15	factor interacting with PAPOLA and CPSF1	Homo sapiens	69-75
19120352-0	2009	Weekly imatinib dosage for chronic eosinophilic leukaemia expressing FIP1L1-PDGFRA fusion transcript: extended follow-up.	imatinib	7-15	platelet derived growth factor receptor alpha	Homo sapiens	76-82
19276246-1	2009	PURPOSE: Imatinib, a BCR-ABL tyrosine kinase inhibitor, is a substrate of the efflux transporters P-glycoprotein (P-gp; ABCB1) and ABCG2 (breast cancer resistance protein), and its brain accumulation is restricted by both transporters.	imatinib	9-17	phosphoglycolate phosphatase	Mus musculus	98-112
19318579-9	2009	Furthermore, imatinib-resistant Bcr-Abl-positive cell lines were found to spontaneously overexpress GAPDH.	imatinib	13-21	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	100-105
19318579-10	2009	Finally, we showed that a GAPDH partial knockdown, using specific short hairpin RNAs, was sufficient to resensitize those resistant cells to imatinib-induced cell death.	imatinib	141-149	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	26-31
19318579-12	2009	We also established that GAPDH overexpression can be found in imatinib-resistant Bcr-Abl-positive cells and that its down-regulation can resensitize those resistant cells to imatinib-induced death.	imatinib	62-70	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	25-30
19318579-12	2009	We also established that GAPDH overexpression can be found in imatinib-resistant Bcr-Abl-positive cells and that its down-regulation can resensitize those resistant cells to imatinib-induced death.	imatinib	174-182	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	25-30
19298600-14	2009	ADAM17, as a major sheddase in GIST, could be potentially a suitable target in anticancer treatment of imatinib-resistant GISTs.	imatinib	103-111	ADAM metallopeptidase domain 17	Homo sapiens	0-6
19417561-0	2009	Cas-L was overexpressed in imatinib-resistant gastrointestinal stromal tumor cells.	imatinib	27-35	neural precursor cell expressed, developmentally down-regulated 9	Homo sapiens	0-5
19417561-4	2009	In GIST-T1 IR cells, KIT and its downstream signaling molecules remained phosphorylated with the presence of 1 microM imatinib, and no new mutations were found in KIT, PDGFRA, PKCtheta and JAK2.	imatinib	118-126	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	21-24
19417561-7	2009	Interestingly, GIST-T1 IR cells transfected with Cas-L siRNA turned out to become again sensitive to imatinib.	imatinib	101-109	neural precursor cell expressed, developmentally down-regulated 9	Homo sapiens	49-54
19417561-8	2009	Imatinib or PP1, a SRC inhibitor, alone was not enough to suppress the activation of KIT and its downstream signaling molecules, but the combination of them showed strong inhibitory effects on those in the resistant cells.	imatinib	0-8	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	19-22
19417561-9	2009	We report for the first time that the mechanism of imatinib-resistant GISTs, at least in one cell line, involves KIT/Cas-L/SRC signaling.	imatinib	51-59	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	113-116
19417561-9	2009	We report for the first time that the mechanism of imatinib-resistant GISTs, at least in one cell line, involves KIT/Cas-L/SRC signaling.	imatinib	51-59	neural precursor cell expressed, developmentally down-regulated 9	Homo sapiens	117-122
19417561-9	2009	We report for the first time that the mechanism of imatinib-resistant GISTs, at least in one cell line, involves KIT/Cas-L/SRC signaling.	imatinib	51-59	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	123-126
19417561-10	2009	Cas-L depletion sensitized the resistant GIST-T1 IR cells to imatinib.	imatinib	61-69	neural precursor cell expressed, developmentally down-regulated 9	Homo sapiens	0-5
19276246-1	2009	PURPOSE: Imatinib, a BCR-ABL tyrosine kinase inhibitor, is a substrate of the efflux transporters P-glycoprotein (P-gp; ABCB1) and ABCG2 (breast cancer resistance protein), and its brain accumulation is restricted by both transporters.	imatinib	9-17	phosphoglycolate phosphatase	Mus musculus	114-118
19276246-1	2009	PURPOSE: Imatinib, a BCR-ABL tyrosine kinase inhibitor, is a substrate of the efflux transporters P-glycoprotein (P-gp; ABCB1) and ABCG2 (breast cancer resistance protein), and its brain accumulation is restricted by both transporters.	imatinib	9-17	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	120-125
19276246-1	2009	PURPOSE: Imatinib, a BCR-ABL tyrosine kinase inhibitor, is a substrate of the efflux transporters P-glycoprotein (P-gp; ABCB1) and ABCG2 (breast cancer resistance protein), and its brain accumulation is restricted by both transporters.	imatinib	9-17	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	131-136
19217274-1	2009	As an inhibitor of the tyrosine kinase activity of the BCR-Abl oncoprotein, imatinib sets a new paradigm for the treatment of cancer with molecularly targeted therapies.	imatinib	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
19337284-6	2009	Imatinib mesylate and related tyrosine kinase inhibitors also block TGF-beta pathways and abrogate fibrotic responses.	imatinib	0-17	transforming growth factor beta 1	Homo sapiens	68-76
19191867-3	2009	Resistance to imatinib is mainly associated with three mechanisms: acquired mutations in the kinase domain of BCR-ABL protein, genetic amplification, and transcript overexpression of BCR-ABL rearrangement.	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
19335275-3	2009	With prolonged treatment imatinib resistance can develop, most likely due to secondary KIT mutations.	imatinib	25-33	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	87-90
19158834-1	2009	Imatinib is an effective first-line therapy for chronic myelogenous leukemia (CML) that acts by targeting the tyrosine kinase activity of BCR-ABL.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
19158834-3	2009	Among these, nilotinib is more potent against BCR-ABL than imatinib, and is effective against many imatinib-resistant BCR-ABL mutants.	imatinib	99-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
19191867-3	2009	Resistance to imatinib is mainly associated with three mechanisms: acquired mutations in the kinase domain of BCR-ABL protein, genetic amplification, and transcript overexpression of BCR-ABL rearrangement.	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	183-190
19381023-6	2009	Inhibition of the KIT gene cis-mutations and antiangiogenesis activities may be essential for the strategy for Imatinib/Sunitinibresistant GIST.	imatinib	111-119	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	18-21
19390946-4	2009	RESULTS: All imatinib- as well as sunitinib-resistant lesions showed viable tumor cells strongly re-expressing the KIT protein.	imatinib	13-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	115-118
19404005-3	2009	Most of molecular targeting small compounds are the inhibitors of tyrosine kinases, including pioneering imatinib which inhibits the receptor for platelet-derived growth factor (PDGF), c-Abl, etc.	imatinib	105-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	185-190
19404005-7	2009	Since established treatments had not been found for fibrotic lesion before, imatinib, a dual inhibitor of both transforming growth factor beta-, and PDGF-signaling, is likely to be a potent drug against fibrosis.	imatinib	76-84	transforming growth factor beta 1	Homo sapiens	111-142
19303137-2	2009	Imatinib mesylate is a small molecule that inhibits activation of the KIT and platelet-derived growth factor receptor alpha proteins, and is effective in first-line treatment of metastatic gastrointestinal stromal tumour.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	70-73
19201511-8	2009	Imatinib mesylate dramatically improves chronic eosinophilic leukaemias associated with PDGFR abnormalities, while corticosteroids are still the main treatment for the other patients.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	88-93
19536317-2	2009	Imatinib mesylate, a BCR-ABL TK inhibitor, is the frontline therapy for CML.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
19621544-6	2009	Cellular influx of imatinib is mediated by the OCT-1 protein, and patients with low OCT-1 activity may benefit from dose-intensive therapy.	imatinib	19-27	solute carrier family 22 member 1	Homo sapiens	47-52
19621544-6	2009	Cellular influx of imatinib is mediated by the OCT-1 protein, and patients with low OCT-1 activity may benefit from dose-intensive therapy.	imatinib	19-27	solute carrier family 22 member 1	Homo sapiens	84-89
19621546-1	2009	In patients with chronic myeloid leukemia (CML) resistant to imatinib, resistance is commonly associated with mutations in the BCR-ABL protein.	imatinib	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
19621546-2	2009	Approximately 85% to 90% of resistance-associated mutations occur within the ABL kinase domain, and confer resistance either directly, by blocking imatinib binding, or indirectly, by altering the conformation of BCR-ABL.	imatinib	147-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	212-219
19303137-2	2009	Imatinib mesylate is a small molecule that inhibits activation of the KIT and platelet-derived growth factor receptor alpha proteins, and is effective in first-line treatment of metastatic gastrointestinal stromal tumour.	imatinib	0-17	platelet derived growth factor receptor alpha	Homo sapiens	78-123
19276351-1	2009	Imatinib is an inhibitor of the Abl tyrosine kinase domain that is effective in the treatment of chronic myelogenic leukemia.	imatinib	0-8	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	32-35
19259085-1	2009	The goal of this study was to evaluate the time course of metabolic changes in leukaemia cells treated with the Bcr-Abl tyrosine kinase inhibitor imatinib.	imatinib	146-154	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
19259085-4	2009	Initially, imatinib treatment completely inhibited the activity of Bcr-Abl tyrosine kinase, followed by the inhibition of cell glycolytic activity and glucose uptake.	imatinib	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
19276351-2	2009	Although imatinib binds tightly to the Abl kinase domain, its affinity for the closely related kinase domain of c-Src is at least 2,000-fold lower.	imatinib	9-17	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	39-42
19276351-4	2009	The inability of c-Src to readily adopt this flipped DFG conformation was thought to underlie the selectivity of imatinib for Abl over c-Src.	imatinib	113-121	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	126-129
19276351-7	2009	The origin of the high affinity of these compounds for c-Src is suggested by the fact that they also inhibit clinically relevant Abl variants bearing mutations in a structural element, the P-loop, that normally interacts with the phosphate groups of ATP but is folded over a substructure of imatinib in Abl.	imatinib	291-299	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	129-132
19276351-8	2009	Importantly, several of the DSA compounds block the growth of Ba/F3 cells harboring imatinib-resistant BCR-ABL mutants, including the Thr315Ile "gatekeeper" mutation, but do not suppress the growth of parental Ba/F3 cells.	imatinib	84-92	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	107-110
18797870-12	2009	Imatinib mimicked effects of selective FLT3 inhibition.	imatinib	0-8	fms related receptor tyrosine kinase 3	Homo sapiens	39-43
19208803-0	2009	A systems biology understanding of the synergistic effects of arsenic sulfide and Imatinib in BCR/ABL-associated leukemia.	imatinib	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
19208803-1	2009	In this study, we show that combined use of Imatinib (IM) and arsenic sulfide [As(4)S(4) (AS)] exerts more profound therapeutic effects in a BCR/ABL-positive mouse model of chronic myeloid leukemia (CML) than either drug as a single agent.	imatinib	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-148
19151753-8	2009	Collectively, these results position Egr-1 downstream of c-Abl in the fibrotic response, delineate a novel Egr-1-dependent intracellular signaling mechanism that underlies the involvement of c-Abl in certain TGF-beta responses, and identify Egr-1 as a target of inhibition by imatinib.	imatinib	276-284	early growth response 1	Mus musculus	107-112
19151753-8	2009	Collectively, these results position Egr-1 downstream of c-Abl in the fibrotic response, delineate a novel Egr-1-dependent intracellular signaling mechanism that underlies the involvement of c-Abl in certain TGF-beta responses, and identify Egr-1 as a target of inhibition by imatinib.	imatinib	276-284	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	191-196
19151753-8	2009	Collectively, these results position Egr-1 downstream of c-Abl in the fibrotic response, delineate a novel Egr-1-dependent intracellular signaling mechanism that underlies the involvement of c-Abl in certain TGF-beta responses, and identify Egr-1 as a target of inhibition by imatinib.	imatinib	276-284	transforming growth factor, beta 1	Mus musculus	208-216
19151753-8	2009	Collectively, these results position Egr-1 downstream of c-Abl in the fibrotic response, delineate a novel Egr-1-dependent intracellular signaling mechanism that underlies the involvement of c-Abl in certain TGF-beta responses, and identify Egr-1 as a target of inhibition by imatinib.	imatinib	276-284	early growth response 1	Mus musculus	107-112
18797870-13	2009	In conclusion, FLT3 and its ligand regulate proliferation of hematopoietic progenitor cells in an autocrine/paracrine manner Nonspecific inhibition of FLT3 may contribute to hematotoxicity caused by imatinib treatment.	imatinib	199-207	fms related receptor tyrosine kinase 3	Homo sapiens	15-19
19153832-0	2009	N-acetyl cysteine enhances imatinib-induced apoptosis of Bcr-Abl+ cells by endothelial nitric oxide synthase-mediated production of nitric oxide.	imatinib	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
18797870-13	2009	In conclusion, FLT3 and its ligand regulate proliferation of hematopoietic progenitor cells in an autocrine/paracrine manner Nonspecific inhibition of FLT3 may contribute to hematotoxicity caused by imatinib treatment.	imatinib	199-207	fms related receptor tyrosine kinase 3	Homo sapiens	151-155
19383237-2	2009	In this study, inhibition of Bcr-Abl tyrosine kinase activity by imatinib significantly decreased VEGF expression in Bcr-Abl-positive K562 cells in vitro.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
19153832-0	2009	N-acetyl cysteine enhances imatinib-induced apoptosis of Bcr-Abl+ cells by endothelial nitric oxide synthase-mediated production of nitric oxide.	imatinib	27-35	nitric oxide synthase 3	Homo sapiens	75-108
19153832-1	2009	INTRODUCTION: Imatinib, a small-molecule inhibitor of the Bcr-Abl kinase, is a successful drug for treating chronic myeloid leukemia (CML).	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
19153832-6	2009	We report that imatinib-induced apoptosis of imatinib-resistant and imatinib-sensitive Bcr-Abl(+) CML cell lines and primary cells from CML patients is significantly enhanced by co-treatment with NAC compared to imatinib treatment alone.	imatinib	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
19153832-11	2009	Indeed, NO donor sodium nitroprusside (SNP) also enhanced imatinib-mediated apoptosis of Bcr-Abl(+) cells.	imatinib	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
19153832-12	2009	CONCLUSION: NAC enhances imatinib-induced apoptosis of Bcr-Abl(+) cells by endothelial nitric oxide synthase-mediated production of nitric oxide.	imatinib	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
19153832-12	2009	CONCLUSION: NAC enhances imatinib-induced apoptosis of Bcr-Abl(+) cells by endothelial nitric oxide synthase-mediated production of nitric oxide.	imatinib	25-33	nitric oxide synthase 3	Homo sapiens	75-108
19150257-4	2009	We found that p21-deficient cells were dramatically more sensitive towards imatinib and gefitinib than parental cells.	imatinib	75-83	cyclin dependent kinase inhibitor 1A	Homo sapiens	14-17
19150257-10	2009	Consistently, HCT116p53(-/-) cells are more resistant to imatinib than parental cells, suggesting that imatinib activity is partly dependent on p53 in colon cancer cells.	imatinib	57-65	tumor protein p53	Homo sapiens	20-23
19150257-10	2009	Consistently, HCT116p53(-/-) cells are more resistant to imatinib than parental cells, suggesting that imatinib activity is partly dependent on p53 in colon cancer cells.	imatinib	103-111	tumor protein p53	Homo sapiens	20-23
19048625-8	2009	Suppression of imatinib-induced autophagy by 3-methyladenine or small interfering RNA against Atg5, which inhibit autophagy at an early stage, attenuated the imatinib-induced cytotoxicity.	imatinib	15-23	autophagy related 5	Homo sapiens	94-98
19048625-8	2009	Suppression of imatinib-induced autophagy by 3-methyladenine or small interfering RNA against Atg5, which inhibit autophagy at an early stage, attenuated the imatinib-induced cytotoxicity.	imatinib	158-166	autophagy related 5	Homo sapiens	94-98
19058199-1	2009	Imatinib is currently in early clinical trials as targeted therapy for relapsed neuroblastomas and other childhood solid tumors expressing platelet-derived growth factor receptors (PDGFR) or c-Kit.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	139-179
19058199-1	2009	Imatinib is currently in early clinical trials as targeted therapy for relapsed neuroblastomas and other childhood solid tumors expressing platelet-derived growth factor receptors (PDGFR) or c-Kit.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	181-186
19058199-1	2009	Imatinib is currently in early clinical trials as targeted therapy for relapsed neuroblastomas and other childhood solid tumors expressing platelet-derived growth factor receptors (PDGFR) or c-Kit.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	191-196
19058199-8	2009	Low-dose imatinib was synergistic in combination with doxorubicin and caused increased G2/M- and S-phase arrest and apoptosis as evidenced by enhanced caspase-3 activation and sub-G1 DNA accumulation.	imatinib	9-17	caspase 3	Homo sapiens	151-160
18937342-5	2009	Treatment of animals with anti-CD117 or imatinib mesylate (Gleevec) reduced MC accumulation at the edge of healing wounds in mice and nonhuman primates, respectively.	imatinib	59-66	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	31-36
19056916-9	2009	The nucleoside substrates zidovudine and abacavir seem to bind to a region on BCRP that may have little or no overlap with the binding regions of either prazosin or imatinib.	imatinib	165-173	ATP binding cassette subfamily G member 2	Canis lupus familiaris	78-82
19135770-12	2009	The proliferating bcr/abl- and etv6/abl-positive cells displayed sensitivity to imatinib, demonstrating that their proliferation depended on the activity of these oncoproteins.	imatinib	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-25
19135770-12	2009	The proliferating bcr/abl- and etv6/abl-positive cells displayed sensitivity to imatinib, demonstrating that their proliferation depended on the activity of these oncoproteins.	imatinib	80-88	ETS variant transcription factor 6	Homo sapiens	31-35
19135770-12	2009	The proliferating bcr/abl- and etv6/abl-positive cells displayed sensitivity to imatinib, demonstrating that their proliferation depended on the activity of these oncoproteins.	imatinib	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-39
19135772-1	2009	OBJECTIVE: The recent success in treating chronic myeloid leukemia (CML) with tyrosine kinase inhibitors (TKI), such as imatinib mesylate (IM), has created a demand for reproducible methods to accurately assess inhibition of BCR-ABL activity within CML cells, including rare stem and progenitor cells, either in vitro or in vivo.	imatinib	120-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	225-232
19157685-6	2009	In addition, we have found that Bcr-Abl-positive cells are more sensitive than Bcr-Abl-negative cells to induction of apoptosis by the proteasome inhibitor BzLLLCOCHO, and that sequential addition of imatinib followed by BzLLLCOCHO has an additive effect on the induction of apoptosis in Bcr-Abl-positive cells.	imatinib	200-208	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
19006173-0	2009	c-Jun blocks cell differentiation but not growth inhibition or apoptosis of chronic myelogenous leukemia cells induced by STI571 and by histone deacetylase inhibitors.	imatinib	122-128	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	0-5
19006173-8	2009	Endogenous c-Jun expression was analyzed to determine the effective concentration of STI571 for inhibiting Bcr-Abl signaling.	imatinib	85-91	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	11-16
19006173-8	2009	Endogenous c-Jun expression was analyzed to determine the effective concentration of STI571 for inhibiting Bcr-Abl signaling.	imatinib	85-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
19006173-9	2009	Western blots show that STI571 inhibited c-Jun expression in a dose-dependent manner, reaching a maximum inhibition at 1 microM.	imatinib	24-30	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	41-46
19006173-10	2009	STI571 could inhibit c-Jun expression in K562 cells, but not in c-Jun-overexpression cells.	imatinib	0-6	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	21-26
19006173-11	2009	c-Jun did not alter growth inhibition and apoptotic induction by STI571 treatment, but inhibited STI571-induced erythroid differentiation.	imatinib	97-103	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	0-5
19383237-2	2009	In this study, inhibition of Bcr-Abl tyrosine kinase activity by imatinib significantly decreased VEGF expression in Bcr-Abl-positive K562 cells in vitro.	imatinib	65-73	vascular endothelial growth factor A	Homo sapiens	98-102
19383237-2	2009	In this study, inhibition of Bcr-Abl tyrosine kinase activity by imatinib significantly decreased VEGF expression in Bcr-Abl-positive K562 cells in vitro.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
19383237-5	2009	Combined treatment with imatinib and Bcr-Abl-targeting siRNAs resulted in an enhanced effect on VEGF suppression in K562 cells.	imatinib	24-32	vascular endothelial growth factor A	Homo sapiens	96-100
18466968-0	2009	Long-term remission in a patient with BCR/ABL-positive acute myeloid leukaemia on maintenance therapy with imatinib.	imatinib	107-115	BCR activator of RhoGEF and GTPase	Homo sapiens	38-41
18783828-5	2009	Here, we report that the serine/threonine kinase mTOR (the mammalian target of rapamycin) inhibitor, rapamycin, inhibits the growth of not only the Bcr-Abl-positive lymphoid leukemic cell line, SU-Ph2, established from Ph(+)ALL patients, but also the imatinib-resistant cell line, SU/SR, that has acquired T315I.	imatinib	251-259	mechanistic target of rapamycin kinase	Homo sapiens	49-53
18783828-5	2009	Here, we report that the serine/threonine kinase mTOR (the mammalian target of rapamycin) inhibitor, rapamycin, inhibits the growth of not only the Bcr-Abl-positive lymphoid leukemic cell line, SU-Ph2, established from Ph(+)ALL patients, but also the imatinib-resistant cell line, SU/SR, that has acquired T315I.	imatinib	251-259	mechanistic target of rapamycin kinase	Homo sapiens	59-88
18848355-0	2009	Supplemental results of the detection of splicing variant with c-ABL exon 7 deletion by direct sequencing Comment on "A recurrent splicing variant without c-ABL Exon 7 in Imatinib-resistant patients" by Curvo et al.	imatinib	171-179	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-68
19347730-1	2009	FB2 is a novel Abl/Src dual tyrosine kinase inhibitor which is designed to overcome imatinib resistance.	imatinib	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-18
19347730-1	2009	FB2 is a novel Abl/Src dual tyrosine kinase inhibitor which is designed to overcome imatinib resistance.	imatinib	84-92	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	19-22
19304540-12	2009	Imatinib treatment and allo-HSCT can both improve the OSs of 2-yrs of the patients with BCR/ABL(+)-ALL.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
19771231-5	2009	Thus RNAi targeted against Kit or its mutant form could be considered as a new antiproliferative agent against human mast leukemia cell lines, especially HMC1.2 cells which are resistant to the Kit tyrosine kinase inhibitor, imatinib mesylate.	imatinib	225-242	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	27-30
19236716-2	2009	Dasatinib is a tyrosine kinase inhibitor that has 325-fold greater in vitro activity against native BCR-ABL (breakpoint cluster region-Abelson leukemia virus) compared with imatinib and can overcome primary (intrinsic) and secondary (acquired) imatinib resistance.	imatinib	244-252	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
19236722-0	2009	The structure of the leukemia drug imatinib bound to human quinone reductase 2 (NQO2).	imatinib	35-43	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	59-78
19236722-0	2009	The structure of the leukemia drug imatinib bound to human quinone reductase 2 (NQO2).	imatinib	35-43	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	80-84
19236722-1	2009	BACKGROUND: Imatinib represents the first in a class of drugs targeted against chronic myelogenous leukemia to enter the clinic, showing excellent efficacy and specificity for Abl, Kit, and PDGFR kinases.	imatinib	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	176-179
19236722-1	2009	BACKGROUND: Imatinib represents the first in a class of drugs targeted against chronic myelogenous leukemia to enter the clinic, showing excellent efficacy and specificity for Abl, Kit, and PDGFR kinases.	imatinib	12-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	181-184
19236722-1	2009	BACKGROUND: Imatinib represents the first in a class of drugs targeted against chronic myelogenous leukemia to enter the clinic, showing excellent efficacy and specificity for Abl, Kit, and PDGFR kinases.	imatinib	12-20	platelet derived growth factor receptor beta	Homo sapiens	190-195
19236722-2	2009	Recent screens carried out to find off-target proteins that bind to imatinib identified the oxidoreductase NQO2, a flavoprotein that is phosphorylated in a chronic myelogenous leukemia cell line.	imatinib	68-76	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	107-111
19236722-3	2009	RESULTS: We examined the inhibition of NQO2 activity by the Abl kinase inhibitors imatinib, nilotinib, and dasatinib, and obtained IC50 values of 80 nM, 380 nM, and >100 microM, respectively.	imatinib	82-90	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	39-43
19236722-3	2009	RESULTS: We examined the inhibition of NQO2 activity by the Abl kinase inhibitors imatinib, nilotinib, and dasatinib, and obtained IC50 values of 80 nM, 380 nM, and >100 microM, respectively.	imatinib	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-63
19236722-4	2009	Using electronic absorption spectroscopy, we show that imatinib binding results in a perturbation of the protein environment around the flavin prosthetic group in NQO2.	imatinib	55-63	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	163-167
19236722-5	2009	We have determined the crystal structure of the complex of imatinib with human NQO2 at 1.75 A resolution, which reveals that imatinib binds in the enzyme active site, adjacent to the flavin isoalloxazine ring.	imatinib	59-67	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	79-83
19236722-5	2009	We have determined the crystal structure of the complex of imatinib with human NQO2 at 1.75 A resolution, which reveals that imatinib binds in the enzyme active site, adjacent to the flavin isoalloxazine ring.	imatinib	125-133	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	79-83
19236722-7	2009	CONCLUSION: The structure of the imatinib-NQO2 complex demonstrates that imatinib inhibits NQO2 activity by competing with substrate for the active site.	imatinib	33-41	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	42-46
19236722-7	2009	CONCLUSION: The structure of the imatinib-NQO2 complex demonstrates that imatinib inhibits NQO2 activity by competing with substrate for the active site.	imatinib	33-41	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	91-95
19236722-8	2009	The overall conformation of imatinib when bound to NQO2 resembles the folded conformation observed in some kinase complexes.	imatinib	28-36	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	51-55
19236722-9	2009	Interactions made by imatinib with residues at the rim of the active site provide an explanation for the binding selectivity of NQO2 for imatinib, nilotinib, and dasatinib.	imatinib	21-29	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	128-132
19236722-9	2009	Interactions made by imatinib with residues at the rim of the active site provide an explanation for the binding selectivity of NQO2 for imatinib, nilotinib, and dasatinib.	imatinib	137-145	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	128-132
19236722-11	2009	Taken together, these studies provide insight into the mechanism of NQO2 inhibition by imatinib, with potential implications for drug design and treatment of chronic myelogenous leukemia in patients.	imatinib	87-95	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	68-72
18827185-2	2009	Decades of research zeroing in on the role of BCR-ABL1 kinase in the pathogenesis of CML have culminated in the development of highly efficacious therapeutics that, like imatinib mesylate, target the oncogenic kinase activity of BCR-ABL1.	imatinib	170-187	BCR activator of RhoGEF and GTPase	Homo sapiens	46-54
18827185-2	2009	Decades of research zeroing in on the role of BCR-ABL1 kinase in the pathogenesis of CML have culminated in the development of highly efficacious therapeutics that, like imatinib mesylate, target the oncogenic kinase activity of BCR-ABL1.	imatinib	170-187	BCR activator of RhoGEF and GTPase	Homo sapiens	229-237
19176456-2	2009	Patients who become resistant to imatinib treatment often develop secondary mutations, the most common of which results in a substitution of isoleucine for threonine at the same location in the ATP-binding domain in all three kinases (in KIT this occurs at amino acid 670).	imatinib	33-41	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	238-241
19164557-0	2009	KIT kinase mutants show unique mechanisms of drug resistance to imatinib and sunitinib in gastrointestinal stromal tumor patients.	imatinib	64-72	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
19164557-2	2009	The efficacy of the inhibitors imatinib mesylate and sunitinib malate in GIST patients has been linked to their inhibition of these mutant KIT proteins.	imatinib	31-48	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	139-142
19164557-3	2009	However, patients on imatinib can acquire secondary KIT mutations that render the protein insensitive to the inhibitor.	imatinib	21-29	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	52-55
19035443-1	2009	Recent studies showed KIT gene aberrations in a substantial number of melanomas on acral skin and mucosa, suggesting the therapeutic benefit of tyrosine kinase inhibitors, such as imatinib.	imatinib	180-188	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	22-25
19920910-6	2009	Nilotinib (Tasigna, AMN107, Novartis) is a close analog of imatinib with approximately 20-fold higher potency for BCR-ABL kinase inhibition.	imatinib	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
19176456-5	2009	The resulting mutant KIT proteins were transiently expressed in COS1 African green monkey kidney cells grown with and without imatinib, and cell extracts were analyzed for KIT activation by immunoprecipitation and immunoblotting to determine autophosphorylation levels.	imatinib	126-134	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	21-24
19176456-6	2009	We also performed molecular modeling to estimate the relative affinities of wild-type (Thr670) KIT and the KIT mutants for ATP and imatinib.	imatinib	131-139	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	95-98
19187542-1	2009	BACKGROUND: Primary eosinophlia associated with the FIP1L1-PDGFRA rearrangement represents a subset of chronic eosinophilic leukaemia (CEL) and affected patients are very sensitive to imatinib treatment.	imatinib	184-192	factor interacting with PAPOLA and CPSF1	Homo sapiens	52-58
19176456-6	2009	We also performed molecular modeling to estimate the relative affinities of wild-type (Thr670) KIT and the KIT mutants for ATP and imatinib.	imatinib	131-139	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	107-110
19176456-10	2009	CONCLUSIONS: This combination of in vitro and molecular modeling analyses shows why, among all possible amino acid substitutions at position 670 of KIT, only Ile is naturally selected as a resistance mutant in imatinib-treated GIST patients.	imatinib	210-218	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	148-151
19187542-1	2009	BACKGROUND: Primary eosinophlia associated with the FIP1L1-PDGFRA rearrangement represents a subset of chronic eosinophilic leukaemia (CEL) and affected patients are very sensitive to imatinib treatment.	imatinib	184-192	platelet derived growth factor receptor alpha	Homo sapiens	59-65
19552835-0	2009	[Major molecular response to imatinib in a patient with acute mixed lineage leukemia expressing a novel BCR/ABL transcript].	imatinib	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
19552835-1	2009	OBJECTIVE: To identify the novel BCR/ABL transcript in a patient with acute mixed lineage leukemia (AMLL), and to evaluate the imatinib treatment response by quantitatively monitoring the aberrant BCR/ABL.	imatinib	127-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	197-204
19552835-9	2009	The patient was then treated with imatinib and hematological remission was soon achieved, and 5 months after the imatinib treatment the quantity of the aberrant BCR/ABL was gradually decreased to negative.	imatinib	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-168
19552835-9	2009	The patient was then treated with imatinib and hematological remission was soon achieved, and 5 months after the imatinib treatment the quantity of the aberrant BCR/ABL was gradually decreased to negative.	imatinib	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-168
19552835-13	2009	CONCLUSION: The aberrant BCR/ABL may contribute to the clinical features of AMLL and the AMLL patients that have aberrant BCR/ABL may be sensitive to Imatinib.	imatinib	150-158	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
18607592-5	2009	There is an interest to use imatinib mesylate in the treatment of c-kit positive ESS.	imatinib	28-45	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	66-71
19180499-3	2009	Immunohistochemical analyses of skin biopsy specimens demonstrated reductions of phosphorylated PDGFRbeta and Abl with imatinib therapy.	imatinib	119-127	platelet derived growth factor receptor beta	Homo sapiens	96-105
19180499-3	2009	Immunohistochemical analyses of skin biopsy specimens demonstrated reductions of phosphorylated PDGFRbeta and Abl with imatinib therapy.	imatinib	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-113
19014913-1	2009	The Bcr-Abl kinase inhibitor, STI571, is the first line treatment for chronic myeloid leukaemia (CML), but the recent emergence of STI571 resistance has led to the examination of combination therapies.	imatinib	30-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
19222892-2	2009	These tumors are characterized by somatic mutations of c-KIT (CD117), a proto-oncogene that encodes a receptor tyrosine kinase normally expressed in the interstitial cell of Cajal that control the GI smooth muscle peristalsis, and an exquisite sensitivity to the action of the tyrokinase inhibitor imatinib mesylate (STI571; Gleevec).	imatinib	298-315	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	55-60
19167615-0	2009	Development of AML with t(8;21)(q22;q22) and RUNX1-RUNX1T1 fusion following Philadelphia-negative clonal evolution during treatment of CML with Imatinib.	imatinib	144-152	RUNX family transcription factor 1	Homo sapiens	45-50
19117346-9	2009	A reduction in BCR-ABL transcript levels of at least 3 log after the first 4-week imatinib therapy was identified as the most powerful predictor of lower relapse (12.1% vs 45.1%, P = .011) and better disease-free survival (82.1% vs 41.7%, P = .009) rates.	imatinib	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
19182535-1	2009	The tyrosine kinase (TK) inhibitor, imatinib, has revolutionized therapy of malignancies that are addicted to one of its target kinases, c-abl, c-kit and PDGF-R.	imatinib	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-142
19182535-1	2009	The tyrosine kinase (TK) inhibitor, imatinib, has revolutionized therapy of malignancies that are addicted to one of its target kinases, c-abl, c-kit and PDGF-R.	imatinib	36-44	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	144-149
19182535-1	2009	The tyrosine kinase (TK) inhibitor, imatinib, has revolutionized therapy of malignancies that are addicted to one of its target kinases, c-abl, c-kit and PDGF-R.	imatinib	36-44	platelet derived growth factor receptor beta	Homo sapiens	154-160
19167615-0	2009	Development of AML with t(8;21)(q22;q22) and RUNX1-RUNX1T1 fusion following Philadelphia-negative clonal evolution during treatment of CML with Imatinib.	imatinib	144-152	RUNX1 partner transcriptional co-repressor 1	Homo sapiens	51-58
19222892-2	2009	These tumors are characterized by somatic mutations of c-KIT (CD117), a proto-oncogene that encodes a receptor tyrosine kinase normally expressed in the interstitial cell of Cajal that control the GI smooth muscle peristalsis, and an exquisite sensitivity to the action of the tyrokinase inhibitor imatinib mesylate (STI571; Gleevec).	imatinib	298-315	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	62-67
19222892-2	2009	These tumors are characterized by somatic mutations of c-KIT (CD117), a proto-oncogene that encodes a receptor tyrosine kinase normally expressed in the interstitial cell of Cajal that control the GI smooth muscle peristalsis, and an exquisite sensitivity to the action of the tyrokinase inhibitor imatinib mesylate (STI571; Gleevec).	imatinib	317-323	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	55-60
19222892-2	2009	These tumors are characterized by somatic mutations of c-KIT (CD117), a proto-oncogene that encodes a receptor tyrosine kinase normally expressed in the interstitial cell of Cajal that control the GI smooth muscle peristalsis, and an exquisite sensitivity to the action of the tyrokinase inhibitor imatinib mesylate (STI571; Gleevec).	imatinib	317-323	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	62-67
19171749-10	2009	Insulin receptor substrate-1 tyrosine phosphorylation and Akt phosphorylation after insulin administration were improved by imatinib.	imatinib	124-132	insulin receptor substrate 1	Mus musculus	0-28
19188143-5	2009	Moreover, clinically used drugs like paclitaxel, imatinib, and doxorubicin have been shown to achieve their therapeutic effects through activation of FOXO3a and FOXO3a targets.	imatinib	49-57	forkhead box O3	Homo sapiens	150-156
19188143-5	2009	Moreover, clinically used drugs like paclitaxel, imatinib, and doxorubicin have been shown to achieve their therapeutic effects through activation of FOXO3a and FOXO3a targets.	imatinib	49-57	forkhead box O3	Homo sapiens	161-167
19006078-5	2009	Patients with PDGFRB fusions genes are excellent candidates for treatment with imatinib; complete cytogenetic and even molecular remissions are common while primary or secondary resistance seems to be very rare.	imatinib	79-87	platelet derived growth factor receptor beta	Homo sapiens	14-20
19248972-2	2009	Although surgery remains the principle treatment of primary localized GIST, imatinib mesylate, a selective inhibitor of KIT protein, achieves dramatic responses in metastatic GIST.	imatinib	76-93	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	120-123
18971950-0	2009	Imatinib sensitivity as a consequence of a CSF1R-Y571D mutation and CSF1/CSF1R signaling abnormalities in the cell line GDM1.	imatinib	0-8	colony stimulating factor 1 receptor	Homo sapiens	43-48
18449471-0	2009	The effect of P-gp (Mdr1a/1b), BCRP (Bcrp1) and P-gp/BCRP inhibitors on the in vivo absorption, distribution, metabolism and excretion of imatinib.	imatinib	138-146	phosphoglycolate phosphatase	Mus musculus	14-18
18449471-0	2009	The effect of P-gp (Mdr1a/1b), BCRP (Bcrp1) and P-gp/BCRP inhibitors on the in vivo absorption, distribution, metabolism and excretion of imatinib.	imatinib	138-146	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	31-35
18449471-0	2009	The effect of P-gp (Mdr1a/1b), BCRP (Bcrp1) and P-gp/BCRP inhibitors on the in vivo absorption, distribution, metabolism and excretion of imatinib.	imatinib	138-146	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	37-42
18449471-0	2009	The effect of P-gp (Mdr1a/1b), BCRP (Bcrp1) and P-gp/BCRP inhibitors on the in vivo absorption, distribution, metabolism and excretion of imatinib.	imatinib	138-146	phosphoglycolate phosphatase	Mus musculus	48-52
18449471-0	2009	The effect of P-gp (Mdr1a/1b), BCRP (Bcrp1) and P-gp/BCRP inhibitors on the in vivo absorption, distribution, metabolism and excretion of imatinib.	imatinib	138-146	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	53-57
18449471-1	2009	Imatinib is transported by P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP), however, the exact impact of these transporters on absorption, distribution, metabolism and excretion (ADME) of imatinib is not fully understood due to incomplete data.	imatinib	0-8	phosphoglycolate phosphatase	Mus musculus	27-41
18449471-1	2009	Imatinib is transported by P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP), however, the exact impact of these transporters on absorption, distribution, metabolism and excretion (ADME) of imatinib is not fully understood due to incomplete data.	imatinib	0-8	phosphoglycolate phosphatase	Mus musculus	43-47
18449471-1	2009	Imatinib is transported by P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP), however, the exact impact of these transporters on absorption, distribution, metabolism and excretion (ADME) of imatinib is not fully understood due to incomplete data.	imatinib	0-8	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	53-85
18449471-1	2009	Imatinib is transported by P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP), however, the exact impact of these transporters on absorption, distribution, metabolism and excretion (ADME) of imatinib is not fully understood due to incomplete data.	imatinib	0-8	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	87-91
18449471-1	2009	Imatinib is transported by P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP), however, the exact impact of these transporters on absorption, distribution, metabolism and excretion (ADME) of imatinib is not fully understood due to incomplete data.	imatinib	206-214	phosphoglycolate phosphatase	Mus musculus	27-41
18449471-1	2009	Imatinib is transported by P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP), however, the exact impact of these transporters on absorption, distribution, metabolism and excretion (ADME) of imatinib is not fully understood due to incomplete data.	imatinib	206-214	phosphoglycolate phosphatase	Mus musculus	43-47
18449471-1	2009	Imatinib is transported by P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP), however, the exact impact of these transporters on absorption, distribution, metabolism and excretion (ADME) of imatinib is not fully understood due to incomplete data.	imatinib	206-214	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	53-85
18449471-1	2009	Imatinib is transported by P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP), however, the exact impact of these transporters on absorption, distribution, metabolism and excretion (ADME) of imatinib is not fully understood due to incomplete data.	imatinib	206-214	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	87-91
18449471-2	2009	We have performed a comprehensive ADME study of imatinib given as single agent or in combination with the well known BCRP/P-gp inhibitors, elacridar and pantoprazole, in wild-type and P-gp and/or BCRP knockout mice.	imatinib	48-56	phosphoglycolate phosphatase	Mus musculus	184-188
18449471-2	2009	We have performed a comprehensive ADME study of imatinib given as single agent or in combination with the well known BCRP/P-gp inhibitors, elacridar and pantoprazole, in wild-type and P-gp and/or BCRP knockout mice.	imatinib	48-56	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	196-200
18449471-5	2009	Both elacridar and pantoprazole significantly increased the AUC of orally administered imatinib in wild-type but also in P-gp/BCRP knockout mice.	imatinib	87-95	phosphoglycolate phosphatase	Mus musculus	121-125
18449471-5	2009	Both elacridar and pantoprazole significantly increased the AUC of orally administered imatinib in wild-type but also in P-gp/BCRP knockout mice.	imatinib	87-95	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	126-130
18449471-8	2009	In conclusion, P-gp and BCRP have only a modest effect on the ADME of imatinib in comparison to metabolic elimination.	imatinib	70-78	phosphoglycolate phosphatase	Mus musculus	15-19
18449471-8	2009	In conclusion, P-gp and BCRP have only a modest effect on the ADME of imatinib in comparison to metabolic elimination.	imatinib	70-78	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	24-28
18685617-0	2009	Acetylation of FOXO3a transcription factor in response to imatinib of chronic myeloid leukemia.	imatinib	58-66	forkhead box O3	Homo sapiens	15-21
18835038-0	2009	Renal failure and recovery associated with second-generation Bcr-Abl kinase inhibitors in imatinib-resistant chronic myelogenous leukemia.	imatinib	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
18971950-0	2009	Imatinib sensitivity as a consequence of a CSF1R-Y571D mutation and CSF1/CSF1R signaling abnormalities in the cell line GDM1.	imatinib	0-8	colony stimulating factor 1	Homo sapiens	43-47
18971950-0	2009	Imatinib sensitivity as a consequence of a CSF1R-Y571D mutation and CSF1/CSF1R signaling abnormalities in the cell line GDM1.	imatinib	0-8	colony stimulating factor 1 receptor	Homo sapiens	73-78
18971950-1	2009	Imatinib is usually a highly effective treatment for myeloproliferative neoplasms (MPNs) associated with ABL, PDGFRA or PDGFRB gene fusions; however, occasional imatinib-responsive patients have been reported without abnormalities of these genes.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-108
18971950-1	2009	Imatinib is usually a highly effective treatment for myeloproliferative neoplasms (MPNs) associated with ABL, PDGFRA or PDGFRB gene fusions; however, occasional imatinib-responsive patients have been reported without abnormalities of these genes.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	110-116
18971950-1	2009	Imatinib is usually a highly effective treatment for myeloproliferative neoplasms (MPNs) associated with ABL, PDGFRA or PDGFRB gene fusions; however, occasional imatinib-responsive patients have been reported without abnormalities of these genes.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	120-126
18971950-2	2009	To identify novel imatinib-sensitive lesions, we screened 11 BCR-ABL-negative cell lines and identified GDM1, derived from a patient with an atypical MPN (aMPN), as being responsive to imatinib.	imatinib	18-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-68
18971950-3	2009	Screening of genes encoding known imatinib targets revealed an exon 12 mutation in the colony-stimulating factor 1 receptor (CSF1R; c-FMS) with a predicted Y571D amino-acid substitution.	imatinib	34-42	colony stimulating factor 1 receptor	Homo sapiens	87-123
18971950-3	2009	Screening of genes encoding known imatinib targets revealed an exon 12 mutation in the colony-stimulating factor 1 receptor (CSF1R; c-FMS) with a predicted Y571D amino-acid substitution.	imatinib	34-42	colony stimulating factor 1 receptor	Homo sapiens	125-130
18971950-3	2009	Screening of genes encoding known imatinib targets revealed an exon 12 mutation in the colony-stimulating factor 1 receptor (CSF1R; c-FMS) with a predicted Y571D amino-acid substitution.	imatinib	34-42	colony stimulating factor 1 receptor	Homo sapiens	132-137
18971950-4	2009	CSF1R in GDM1 was constitutively phosphorylated, but rapidly dephosphorylated on exposure to imatinib.	imatinib	93-101	colony stimulating factor 1 receptor	Homo sapiens	0-5
19075254-0	2009	Activity of bosutinib, dasatinib, and nilotinib against 18 imatinib-resistant BCR/ABL mutants.	imatinib	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
19186237-2	2009	Although rare as a clinical entity, there is much interest in the pathology and treatment because the KIT protooncogene mutation common to most GISTs can be inhibited by imatinib mesylate.	imatinib	170-187	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	102-105
19111841-7	2009	Intriguingly, recently developed molecular targeted cancer drugs, such as the tyrosine kinase inhibitors imatinib mesylate, gefitinib and others, can also interact with BCRP.	imatinib	105-122	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	169-173
19296866-10	2009	Imatinib (Glivec), the most successful of protein kinase inhibitors, targets the inactive conformation of ABL tyrosine kinase.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-109
19296866-10	2009	Imatinib (Glivec), the most successful of protein kinase inhibitors, targets the inactive conformation of ABL tyrosine kinase.	imatinib	10-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-109
18971393-8	2009	In support of this, the cellular response to doxorubicin, tamoxifen, imatinib, trichostatin A, and flutamide increased in the presence of the cathepsin L inhibitor.	imatinib	69-77	cathepsin L	Mus musculus	142-153
18809244-0	2009	Combination of imatinib and vinorelbine enhances cell growth inhibition in breast cancer cells via PDGFR beta signalling.	imatinib	15-23	platelet derived growth factor receptor beta	Homo sapiens	99-109
18809244-1	2009	INTRODUCTION: Imatinib mesylate is a tyrosine kinase receptor inhibitor targeted against PDGFR alpha and beta, c-kit and bcr-abl.	imatinib	14-31	platelet derived growth factor receptor alpha	Homo sapiens	89-100
18809244-1	2009	INTRODUCTION: Imatinib mesylate is a tyrosine kinase receptor inhibitor targeted against PDGFR alpha and beta, c-kit and bcr-abl.	imatinib	14-31	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	111-116
18809244-1	2009	INTRODUCTION: Imatinib mesylate is a tyrosine kinase receptor inhibitor targeted against PDGFR alpha and beta, c-kit and bcr-abl.	imatinib	14-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
18809244-3	2009	This study was performed to evaluate the effects of imatinib on breast cancer cell lines with respect to the activity of PDGFR beta and Akt: a downstream modulator of cell growth and survival.	imatinib	52-60	platelet derived growth factor receptor beta	Homo sapiens	121-131
18809244-3	2009	This study was performed to evaluate the effects of imatinib on breast cancer cell lines with respect to the activity of PDGFR beta and Akt: a downstream modulator of cell growth and survival.	imatinib	52-60	AKT serine/threonine kinase 1	Homo sapiens	136-139
18809244-9	2009	CONCLUSIONS: The growth inhibitory effect of imatinib on breast cell lines may be caused by inhibiting the activity of the tyrosine kinases PDGFR beta and Akt.	imatinib	45-53	platelet derived growth factor receptor beta	Homo sapiens	140-150
18809244-9	2009	CONCLUSIONS: The growth inhibitory effect of imatinib on breast cell lines may be caused by inhibiting the activity of the tyrosine kinases PDGFR beta and Akt.	imatinib	45-53	AKT serine/threonine kinase 1	Homo sapiens	155-158
19149483-5	2009	The most successful example of kinase blockers is Imatinib (Imatinib mesylate, Gleevec, STI571), the inhibitor of Bcr/Abl oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
19149483-5	2009	The most successful example of kinase blockers is Imatinib (Imatinib mesylate, Gleevec, STI571), the inhibitor of Bcr/Abl oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.	imatinib	60-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
19707409-4	2009	Mechanisms of imatinib resistance include BCR-ABL point mutations resulting in decreased imatinib binding, as well as mutation-independent causes of resistance such as SRC family kinase dysregulation, BCR-ABL gene amplification, drug influx/efflux mechanisms and other poorly understood processes.	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
19052872-5	2009	Pretreatment with the c-Abl inhibitor STI571 and transfection with siRNA specific to c-Abl and p53 prior to irradiation reduced A2E/blue light-induced cell death.	imatinib	38-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-27
18398615-2	2009	Population pharmacokinetic (PPK) studies evaluating the effect of population covariates on the pharmacokinetics of imatinib and its active metabolite have been developed in adults with chronic myeloid leukemia (CML) and gastrointestinal stromal tumor (GIST).	imatinib	115-123	kallikrein B1	Homo sapiens	28-31
20877672-18	2009	Imatinib inhibits PDGFR and c-kit.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	18-23
20877672-18	2009	Imatinib inhibits PDGFR and c-kit.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	28-33
18398615-4	2009	PURPOSE: The objectives of the analysis were to develop a PPK model of imatinib and its active metabolite, CGP74588, to describe exposure in children and young adults and to identify covariates that are predictors of variability in disposition.	imatinib	71-79	kallikrein B1	Homo sapiens	58-61
19039816-0	2009	C6-unsubstituted pyrazolo[3,4-d]pyrimidines are dual Src/Abl inhibitors effective against imatinib mesylate resistant chronic myeloid leukemia cell lines.	imatinib	90-107	Rous sarcoma oncogene	Mus musculus	53-56
19028701-3	2009	Here, we identified human brain expressed X-linked 1 (hBex1) as a downstream target of the p75 neurotrophin receptor pathway in imatinib-resistant K562 cells by comparing the gene expression profiles with the parent K562 cells.	imatinib	128-136	brain expressed X-linked 1	Homo sapiens	26-52
19028701-3	2009	Here, we identified human brain expressed X-linked 1 (hBex1) as a downstream target of the p75 neurotrophin receptor pathway in imatinib-resistant K562 cells by comparing the gene expression profiles with the parent K562 cells.	imatinib	128-136	brain expressed X-linked 1	Homo sapiens	54-59
19028701-4	2009	Silencing hBex1 inhibited imatinib-induced cell apoptosis and overexpression of hBex1-sensitized cells to imatinib-induced apoptosis.	imatinib	26-34	brain expressed X-linked 1	Homo sapiens	10-15
19028701-4	2009	Silencing hBex1 inhibited imatinib-induced cell apoptosis and overexpression of hBex1-sensitized cells to imatinib-induced apoptosis.	imatinib	106-114	brain expressed X-linked 1	Homo sapiens	80-85
19028701-6	2009	Silencing of pcdh10 attenuated apoptosis induced by imatinib in hBex1 transfected cells, suggesting that, in addition to Mdr and Bcl-2 family members, reduced expression of hBex1 can also inhibit imatinib-induced apoptosis.	imatinib	52-60	protocadherin 10	Homo sapiens	13-19
19028701-6	2009	Silencing of pcdh10 attenuated apoptosis induced by imatinib in hBex1 transfected cells, suggesting that, in addition to Mdr and Bcl-2 family members, reduced expression of hBex1 can also inhibit imatinib-induced apoptosis.	imatinib	52-60	brain expressed X-linked 1	Homo sapiens	64-69
19028701-6	2009	Silencing of pcdh10 attenuated apoptosis induced by imatinib in hBex1 transfected cells, suggesting that, in addition to Mdr and Bcl-2 family members, reduced expression of hBex1 can also inhibit imatinib-induced apoptosis.	imatinib	52-60	brain expressed X-linked 1	Homo sapiens	173-178
19028701-6	2009	Silencing of pcdh10 attenuated apoptosis induced by imatinib in hBex1 transfected cells, suggesting that, in addition to Mdr and Bcl-2 family members, reduced expression of hBex1 can also inhibit imatinib-induced apoptosis.	imatinib	196-204	protocadherin 10	Homo sapiens	13-19
19028701-6	2009	Silencing of pcdh10 attenuated apoptosis induced by imatinib in hBex1 transfected cells, suggesting that, in addition to Mdr and Bcl-2 family members, reduced expression of hBex1 can also inhibit imatinib-induced apoptosis.	imatinib	196-204	brain expressed X-linked 1	Homo sapiens	173-178
19115309-6	2009	The present protocol made a simple and reliable inhibition assay of recombinant c-Abl kinase by imatinib possible (IC(50(recombinant))=291 nM; STI571, Gleevec; Novartis Pharma).	imatinib	96-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-85
19039816-0	2009	C6-unsubstituted pyrazolo[3,4-d]pyrimidines are dual Src/Abl inhibitors effective against imatinib mesylate resistant chronic myeloid leukemia cell lines.	imatinib	90-107	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	57-60
19039816-1	2009	Docking simulations were used to predict the most favorable interaction between the T315I mutated form of Abl (invariably associated with resistance to the tyrosine kinase inhibitor imatinib mesylate, IM) and C6-unsubstituted and substituted pyrazolo[3,4-d]pyrimidines previously found to be dual Src/Abl inhibitors.	imatinib	182-199	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	106-109
19039816-1	2009	Docking simulations were used to predict the most favorable interaction between the T315I mutated form of Abl (invariably associated with resistance to the tyrosine kinase inhibitor imatinib mesylate, IM) and C6-unsubstituted and substituted pyrazolo[3,4-d]pyrimidines previously found to be dual Src/Abl inhibitors.	imatinib	182-199	Rous sarcoma oncogene	Mus musculus	297-300
19039816-1	2009	Docking simulations were used to predict the most favorable interaction between the T315I mutated form of Abl (invariably associated with resistance to the tyrosine kinase inhibitor imatinib mesylate, IM) and C6-unsubstituted and substituted pyrazolo[3,4-d]pyrimidines previously found to be dual Src/Abl inhibitors.	imatinib	182-199	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	301-304
20007107-7	2009	The most common mechanisms of resistance to imatinib include BCR-ABL kinase domain mutations, amplification, and overexpression of the BCR-ABL oncogene, and clonal evolution with activation of additional transformation pathways.	imatinib	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
19118061-2	2009	These findings suggest KIT as a potential target for therapy with imatinib mesylate in these melanomas.	imatinib	66-83	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	23-26
19118061-7	2009	This overexpression of both KIT and SCF suggests the clinical application of imatinib mesylate in metastatic UM.	imatinib	77-94	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	28-31
19118061-7	2009	This overexpression of both KIT and SCF suggests the clinical application of imatinib mesylate in metastatic UM.	imatinib	77-94	KIT ligand	Homo sapiens	36-39
20007107-7	2009	The most common mechanisms of resistance to imatinib include BCR-ABL kinase domain mutations, amplification, and overexpression of the BCR-ABL oncogene, and clonal evolution with activation of additional transformation pathways.	imatinib	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
20007109-2	2009	Although most patients respond satisfactorily to imatinib, a subset of patients develops resistance mainly because of the acquisition of mutations within the kinase domain of BCR-ABL1 that impair the ability of TKIs to block the activity of the enzyme.	imatinib	49-57	BCR activator of RhoGEF and GTPase	Homo sapiens	175-183
19810774-2	2009	The introduction of imatinib, a tyrosine kinase inhibitor mainly targeting BCR-ABL, c-KIT and PDGFR, has profoundly improved the prognosis of both entities, while being surprisingly well tolerated.	imatinib	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
19754423-5	2009	Typical CYP1A2 substrates generally contain planar ring that can fit the narrow and planar active site of the enzyme, such as propranolol, clozapine, guanabenz, flutamide, imatinib, thalidomide, carbamazepine, lidocaine, theophylline, tacrine, tizanidine, zolpidem, riluzole, zileuton, and leflunomide.	imatinib	172-180	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	8-14
19810774-2	2009	The introduction of imatinib, a tyrosine kinase inhibitor mainly targeting BCR-ABL, c-KIT and PDGFR, has profoundly improved the prognosis of both entities, while being surprisingly well tolerated.	imatinib	20-28	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	84-89
19810774-2	2009	The introduction of imatinib, a tyrosine kinase inhibitor mainly targeting BCR-ABL, c-KIT and PDGFR, has profoundly improved the prognosis of both entities, while being surprisingly well tolerated.	imatinib	20-28	platelet derived growth factor receptor beta	Homo sapiens	94-99
18814279-7	2009	Coimmunoprecipitation assays showed that imatinib inhibited the M-CSF-induced phosphorylation of c-Fms in osteoclast precursor cells as well as the PDGF-induced PDGFR phosphorylation in MDA-MB-231 human breast cancer cells.	imatinib	41-49	platelet derived growth factor receptor beta	Homo sapiens	161-166
20047122-2	2009	Cure can be obtained only by complete surgical removal of the GIST; however, imatinib, an inhibitor of KIT and PDGFRA, is indicated for advanced, recurrent, and/or metastatic GISTs.	imatinib	77-85	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	103-106
20047122-2	2009	Cure can be obtained only by complete surgical removal of the GIST; however, imatinib, an inhibitor of KIT and PDGFRA, is indicated for advanced, recurrent, and/or metastatic GISTs.	imatinib	77-85	platelet derived growth factor receptor alpha	Homo sapiens	111-117
20008223-4	2009	Second generation TKIs, eg, dasatinib and nilotinib, show activity against most of the bcr-abl tyrosine kinase domain (TKD) mutations involved in acquired imatinib resistance, but clinical benefit is generally short-lived.	imatinib	155-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
19093166-5	2009	Growing comprehension of the molecular mechanisms of resistance to imatinib has led to the development of novel BCR-ABL inhibitors that yield higher affinity for BCR-ABL and/or potent inhibitory activity against other target molecules such as SRC family kinases.	imatinib	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
18814279-0	2009	Imatinib mesylate suppresses bone metastases of breast cancer by inhibiting osteoclasts through the blockade of c-Fms signals.	imatinib	0-17	colony stimulating factor 1 receptor	Homo sapiens	112-117
18814279-1	2009	Imatinib mesylate (imatinib) is a potent and selective inhibitor of the tyrosine kinases, Bcr-Abl, c-Kit and platelet-derived growth factor receptors (PDGFRs).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
18814279-1	2009	Imatinib mesylate (imatinib) is a potent and selective inhibitor of the tyrosine kinases, Bcr-Abl, c-Kit and platelet-derived growth factor receptors (PDGFRs).	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	99-104
18814279-1	2009	Imatinib mesylate (imatinib) is a potent and selective inhibitor of the tyrosine kinases, Bcr-Abl, c-Kit and platelet-derived growth factor receptors (PDGFRs).	imatinib	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
18814279-1	2009	Imatinib mesylate (imatinib) is a potent and selective inhibitor of the tyrosine kinases, Bcr-Abl, c-Kit and platelet-derived growth factor receptors (PDGFRs).	imatinib	19-27	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	99-104
18814279-2	2009	Recently, it has been reported that imatinib also targets the macrophage colony-stimulating factor (M-CSF) receptor c-Fms.	imatinib	36-44	colony stimulating factor 1	Homo sapiens	62-98
18814279-2	2009	Recently, it has been reported that imatinib also targets the macrophage colony-stimulating factor (M-CSF) receptor c-Fms.	imatinib	36-44	colony stimulating factor 1	Homo sapiens	100-105
18814279-2	2009	Recently, it has been reported that imatinib also targets the macrophage colony-stimulating factor (M-CSF) receptor c-Fms.	imatinib	36-44	colony stimulating factor 1 receptor	Homo sapiens	116-121
18814279-7	2009	Coimmunoprecipitation assays showed that imatinib inhibited the M-CSF-induced phosphorylation of c-Fms in osteoclast precursor cells as well as the PDGF-induced PDGFR phosphorylation in MDA-MB-231 human breast cancer cells.	imatinib	41-49	colony stimulating factor 1	Homo sapiens	64-69
18814279-7	2009	Coimmunoprecipitation assays showed that imatinib inhibited the M-CSF-induced phosphorylation of c-Fms in osteoclast precursor cells as well as the PDGF-induced PDGFR phosphorylation in MDA-MB-231 human breast cancer cells.	imatinib	41-49	colony stimulating factor 1 receptor	Homo sapiens	97-102
18814279-13	2009	In conclusion, these results collectively suggest that imatinib reduced bone metastases, at least in part, by inhibiting osteoclastic bone destruction through the blockade of c-Fms signals.	imatinib	55-63	colony stimulating factor 1 receptor	Homo sapiens	175-180
19093166-5	2009	Growing comprehension of the molecular mechanisms of resistance to imatinib has led to the development of novel BCR-ABL inhibitors that yield higher affinity for BCR-ABL and/or potent inhibitory activity against other target molecules such as SRC family kinases.	imatinib	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-169
19096755-0	2009	Successful treatment of myeloid neoplasms associated with PDGFRA rearrangement with imatinib mesylate.	imatinib	84-101	platelet derived growth factor receptor alpha	Homo sapiens	58-64
19096755-3	2009	Despite patients with FIP1-like-1-platelet-derived growth factor alpha (FIP1L1-PDGFRA) associated HES (myeloid neoplasms associated with PDGFRA rearrangement) have been shown to respond to low-dose imatinib with a complete and durable hematological and cytogenetic remission, influences of imatinib on clinical manifestations related to hypereosinophilia heart involvement are variable.	imatinib	198-206	factor interacting with PAPOLA and CPSF1	Homo sapiens	72-78
19096755-3	2009	Despite patients with FIP1-like-1-platelet-derived growth factor alpha (FIP1L1-PDGFRA) associated HES (myeloid neoplasms associated with PDGFRA rearrangement) have been shown to respond to low-dose imatinib with a complete and durable hematological and cytogenetic remission, influences of imatinib on clinical manifestations related to hypereosinophilia heart involvement are variable.	imatinib	290-298	factor interacting with PAPOLA and CPSF1	Homo sapiens	72-78
19082496-4	2009	Therefore we studied the serum levels and expression of platelet-derived growth factor (PDGF) in HNSCC patients and in cell culture as well as the effect of a PDGF-receptor (PDGF-R) inhibition by Imatinib (Gleevec, STI571) on the secretion and expression activity of PDGF and vascular endothelial growth factor (VEGF) by postulating there is a correlation between the PDGF and VEGF networks.	imatinib	196-204	platelet derived growth factor receptor beta	Homo sapiens	159-172
19915299-0	2009	Successful treatment of KIT D816V-positive, imatinib-resistant systemic mastocytosis with interferon-alpha.	imatinib	44-52	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	24-27
19082496-4	2009	Therefore we studied the serum levels and expression of platelet-derived growth factor (PDGF) in HNSCC patients and in cell culture as well as the effect of a PDGF-receptor (PDGF-R) inhibition by Imatinib (Gleevec, STI571) on the secretion and expression activity of PDGF and vascular endothelial growth factor (VEGF) by postulating there is a correlation between the PDGF and VEGF networks.	imatinib	196-204	platelet derived growth factor receptor beta	Homo sapiens	174-180
19082496-7	2009	Treatment of the cell lines with Imatinib, a partially selective PDGF-R inhibitor, resulted in reduced secretion of PDGF and VEGF.	imatinib	33-41	platelet derived growth factor receptor beta	Homo sapiens	65-71
19082496-7	2009	Treatment of the cell lines with Imatinib, a partially selective PDGF-R inhibitor, resulted in reduced secretion of PDGF and VEGF.	imatinib	33-41	vascular endothelial growth factor A	Homo sapiens	125-129
19082496-10	2009	Although further studies must be performed for a more complete understanding of this interaction, a targeting therapy for the inhibition of PDGF-R tyrosine phosphorylation by Imatinib may be a promising strategy for future tumor therapy by autocrine and paracrine inhibition of tumor growth and angiogenesis, presumably through simultaneous down-regulation of PDGF and VEGF.	imatinib	175-183	platelet derived growth factor receptor beta	Homo sapiens	140-146
19082496-10	2009	Although further studies must be performed for a more complete understanding of this interaction, a targeting therapy for the inhibition of PDGF-R tyrosine phosphorylation by Imatinib may be a promising strategy for future tumor therapy by autocrine and paracrine inhibition of tumor growth and angiogenesis, presumably through simultaneous down-regulation of PDGF and VEGF.	imatinib	175-183	vascular endothelial growth factor A	Homo sapiens	369-373
19020005-1	2009	Imatinib is a receptor tyrosine kinase inhibitor that blocks the activity of c-Abl, c-Kit, and PDGF receptors.	imatinib	0-8	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	77-82
18835981-0	2009	Imatinib mesylate (STI571)-induced cell edge translocation of kinase-active and kinase-defective Abelson kinase: requirements of myristoylation and src homology 3 domain.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-111
19020005-1	2009	Imatinib is a receptor tyrosine kinase inhibitor that blocks the activity of c-Abl, c-Kit, and PDGF receptors.	imatinib	0-8	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	84-89
18814181-9	2009	SHIP2 PDR/AAA interference with PDGFR signaling was demonstrated using imatinib, an inhibitor of PDGFR tyrosine kinase.	imatinib	71-79	inositol polyphosphate phosphatase like 1	Homo sapiens	0-5
18814181-9	2009	SHIP2 PDR/AAA interference with PDGFR signaling was demonstrated using imatinib, an inhibitor of PDGFR tyrosine kinase.	imatinib	71-79	platelet derived growth factor receptor beta	Homo sapiens	32-37
18814181-9	2009	SHIP2 PDR/AAA interference with PDGFR signaling was demonstrated using imatinib, an inhibitor of PDGFR tyrosine kinase.	imatinib	71-79	platelet derived growth factor receptor beta	Homo sapiens	97-102
19301661-0	2009	Therapeutic targeting of gene expression by siRNAs directed against BCR-ABL transcripts in a patient with imatinib-resistant chronic myeloid leukemia.	imatinib	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
19301661-5	2009	Here we show that in vivo application of targeted nonvirally delivered synthetic bcr-abl siRNA in a female patient with recurrent Philadelphia chromosome positive chronic myeloid leukemia (CML) resistant to imatinib (Y253F mutation) and chemotherapy after allogeneic hematopoietic stem cell transplantation can silence the expression of bcr-abl gene.	imatinib	207-215	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
19139121-0	2009	Inhibition of focal adhesion kinase as a potential therapeutic strategy for imatinib-resistant gastrointestinal stromal tumor.	imatinib	76-84	PTK2 protein tyrosine kinase 2	Mus musculus	14-35
19139121-2	2009	GIST is well known to have a mutation to c-KIT; thus, a specific c-KIT inhibitor (imatinib) is recognized as the first-line chemotherapy for GIST, although a certain type of c-KIT mutation reveals a resistance to imatinib due to as yet uncertain molecular mechanisms.	imatinib	82-90	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	41-46
19139121-2	2009	GIST is well known to have a mutation to c-KIT; thus, a specific c-KIT inhibitor (imatinib) is recognized as the first-line chemotherapy for GIST, although a certain type of c-KIT mutation reveals a resistance to imatinib due to as yet uncertain molecular mechanisms.	imatinib	82-90	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	65-70
19139121-2	2009	GIST is well known to have a mutation to c-KIT; thus, a specific c-KIT inhibitor (imatinib) is recognized as the first-line chemotherapy for GIST, although a certain type of c-KIT mutation reveals a resistance to imatinib due to as yet uncertain molecular mechanisms.	imatinib	82-90	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	65-70
19139121-2	2009	GIST is well known to have a mutation to c-KIT; thus, a specific c-KIT inhibitor (imatinib) is recognized as the first-line chemotherapy for GIST, although a certain type of c-KIT mutation reveals a resistance to imatinib due to as yet uncertain molecular mechanisms.	imatinib	213-221	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	65-70
19139121-2	2009	GIST is well known to have a mutation to c-KIT; thus, a specific c-KIT inhibitor (imatinib) is recognized as the first-line chemotherapy for GIST, although a certain type of c-KIT mutation reveals a resistance to imatinib due to as yet uncertain molecular mechanisms.	imatinib	213-221	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	65-70
19139121-3	2009	To assess the c-KIT mutation-related variation of cellular responses to imatinib, murine lymphocyte-derived Ba/F3 cells, which are stably transduced with different types of c-KIT mutation, were treated with either imatinib or a FAK inhibitor (TAE226), and their antitumor effects were determined in vitro and in vivo.	imatinib	72-80	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	14-19
19139121-5	2009	KIT820Tyr cells appeared to maintain the activities of FAK and AKT under the imatinib treatment, suggesting that FAK might play a role in cell survival in imatinib-resistant cells.	imatinib	77-85	PTK2 protein tyrosine kinase 2	Mus musculus	55-58
19139121-5	2009	KIT820Tyr cells appeared to maintain the activities of FAK and AKT under the imatinib treatment, suggesting that FAK might play a role in cell survival in imatinib-resistant cells.	imatinib	77-85	thymoma viral proto-oncogene 1	Mus musculus	63-66
19139121-5	2009	KIT820Tyr cells appeared to maintain the activities of FAK and AKT under the imatinib treatment, suggesting that FAK might play a role in cell survival in imatinib-resistant cells.	imatinib	77-85	PTK2 protein tyrosine kinase 2	Mus musculus	113-116
19139121-5	2009	KIT820Tyr cells appeared to maintain the activities of FAK and AKT under the imatinib treatment, suggesting that FAK might play a role in cell survival in imatinib-resistant cells.	imatinib	155-163	thymoma viral proto-oncogene 1	Mus musculus	63-66
19139121-5	2009	KIT820Tyr cells appeared to maintain the activities of FAK and AKT under the imatinib treatment, suggesting that FAK might play a role in cell survival in imatinib-resistant cells.	imatinib	155-163	PTK2 protein tyrosine kinase 2	Mus musculus	113-116
19139121-8	2009	In summary, c-KIT mutation at exon 17 displayed a resistance to imatinib with maintained activations of FAK and subsequent survival signals.	imatinib	64-72	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	12-17
19139121-9	2009	Targeting FAK could be a potential therapeutic strategy for imatinib-resistant GISTs.	imatinib	60-68	PTK2 protein tyrosine kinase 2	Mus musculus	10-13
19435483-2	2009	A recent paper in BMC Structural Biology reports a 1.75 A crystal structure of imatinib bound to the oxidoreductase NQO2 and reveals insights into the binding specificity and the off-target effects of the inhibitor.	imatinib	79-87	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	116-120
18973210-0	2009	Oncogenic and ligand-dependent activation of KIT/PDGFRA in surgical samples of imatinib-treated gastrointestinal stromal tumours (GISTs).	imatinib	79-87	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	45-48
18973210-0	2009	Oncogenic and ligand-dependent activation of KIT/PDGFRA in surgical samples of imatinib-treated gastrointestinal stromal tumours (GISTs).	imatinib	79-87	platelet derived growth factor receptor alpha	Homo sapiens	49-55
19568828-0	2009	Imatinib mesylate inhibited rat adjuvant arthritis and PDGF-dependent growth of synovial fibroblast via interference with the Akt signaling pathway.	imatinib	0-17	AKT serine/threonine kinase 1	Rattus norvegicus	126-129
19568828-9	2009	Imatinib also inhibited PDGF-induced phosphorylation of the PDGF receptor and Akt, whereas constitutive activated extracellular signal-regulated kinase was not inhibited by imatinib.	imatinib	0-8	AKT serine/threonine kinase 1	Rattus norvegicus	78-81
19568828-11	2009	Oral administration of imatinib ameliorated adjuvant-induced arthritis in rats, and it inhibited PDGF-induced RASF proliferation through disruption of the PDGF-R to Akt kinase signaling pathway.	imatinib	23-31	AKT serine/threonine kinase 1	Rattus norvegicus	165-168
19139130-2	2009	Because imatinib (Gleevec) has been reported to reduce RAD51 protein levels, we tested the clonogenic survival for RT112, H1299, PANC1, and PC3 tumor cell lines of varying p53 status and normal GM05757 normal fibroblasts after exposure to single agent imatinib (0-20 micromol/L; 0-72 hours).	imatinib	8-16	RAD51 recombinase	Homo sapiens	55-60
18835981-0	2009	Imatinib mesylate (STI571)-induced cell edge translocation of kinase-active and kinase-defective Abelson kinase: requirements of myristoylation and src homology 3 domain.	imatinib	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-111
19139130-4	2009	We observed decreased nuclear expression and chromatin binding of RAD51 protein following imatinib treatment.	imatinib	90-98	RAD51 recombinase	Homo sapiens	66-71
19139130-5	2009	Imatinib also resulted in decreased error-free HR as determined by a flow cytometry-based integrated direct repeat-green fusion protein reporter system; this correlated to reduced RAD51 expression.	imatinib	0-8	RAD51 recombinase	Homo sapiens	180-185
18835981-4	2009	Here we present evidence of distinct STI571-induced modulation of abl functions using high-resolution live-cell imaging approaches.	imatinib	37-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-69
18835981-5	2009	Within lamellipodia of fibroblast cells, STI571 was found to induce rapid translocation of abl to the lamellipodium tip.	imatinib	41-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-94
18835981-6	2009	Quantitative analysis yielded 0.81 and 1.8 microM for EC(50) values of STI571-induced cell edge translocation of abl-KD-green fluorescent protein (GFP) and wild-type abl-GFP, respectively.	imatinib	71-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-116
18835981-6	2009	Quantitative analysis yielded 0.81 and 1.8 microM for EC(50) values of STI571-induced cell edge translocation of abl-KD-green fluorescent protein (GFP) and wild-type abl-GFP, respectively.	imatinib	71-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-169
18835981-7	2009	It also revealed adverse response of drug-resistant abl-T334I to STI571, suggesting that drug binding to abl-GFP triggers translocation.	imatinib	65-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-55
18835981-7	2009	It also revealed adverse response of drug-resistant abl-T334I to STI571, suggesting that drug binding to abl-GFP triggers translocation.	imatinib	65-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-108
18835981-10	2009	Moreover, single-molecule observation revealed an STI571-induced rapid increase in slow diffusive species of abl in both the tip and the body region of lamellipodia.	imatinib	50-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-112
18835981-11	2009	These results suggest that although activated abl translocates to the cell edge at its open state, STI571 can also bind and lock abl in the open and membrane-tethered conformation as long as the SH3 domain and the C-terminal region are intact.	imatinib	99-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-132
19580340-0	2009	WT1 expression in peripheral leukocytes of patients with chronic myeloid leukemia serves for the prediction of Imatinib resistance.	imatinib	111-119	WT1 transcription factor	Homo sapiens	0-3
19309222-8	2009	There was a high correlation between PGP, MRP1 and LRP expression and IC50 values for imatinib and etoposide.	imatinib	86-94	phosphoglycolate phosphatase	Homo sapiens	37-40
19309222-8	2009	There was a high correlation between PGP, MRP1 and LRP expression and IC50 values for imatinib and etoposide.	imatinib	86-94	ATP binding cassette subfamily C member 1	Homo sapiens	42-46
19309222-8	2009	There was a high correlation between PGP, MRP1 and LRP expression and IC50 values for imatinib and etoposide.	imatinib	86-94	LDL receptor related protein 1	Homo sapiens	51-54
19309222-10	2009	Rhodamine retention alone and in the presence of cyclosporine was the lowest in imatinib-resistant K-562R-0.1 cell line, what suggest high PGP activity in this cell line.	imatinib	80-88	phosphoglycolate phosphatase	Homo sapiens	139-142
19309222-12	2009	These data suggest that imatinib is a substrate for multidrug resistance proteins, and an increased expression of PGP, MRP1 and LRP play a role in resistance to imatinib in CML.	imatinib	161-169	phosphoglycolate phosphatase	Homo sapiens	114-117
19309222-12	2009	These data suggest that imatinib is a substrate for multidrug resistance proteins, and an increased expression of PGP, MRP1 and LRP play a role in resistance to imatinib in CML.	imatinib	161-169	ATP binding cassette subfamily C member 1	Homo sapiens	119-123
19309222-12	2009	These data suggest that imatinib is a substrate for multidrug resistance proteins, and an increased expression of PGP, MRP1 and LRP play a role in resistance to imatinib in CML.	imatinib	161-169	LDL receptor related protein 1	Homo sapiens	128-131
19580340-4	2009	The effect of Imatinib was characterized not only by the expression of WT1 but also by BCR-ABL, and proliferative factor Ki-67.	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
19580340-2	2009	The aim of this study was to evaluate if the responsiveness of Chronic Myeloid Leukemia (CML) patients to Imatinib therapy was predictable from WT1 gene expression in peripheral blood leukocytes.	imatinib	106-114	WT1 transcription factor	Homo sapiens	144-147
19580340-5	2009	<br />Our results showed that leukocytes of CML patients, clinically responsive to Imatinib treatment, significantly decreased WT1 expression after in vitro incubation with Imatinib.	imatinib	89-97	WT1 transcription factor	Homo sapiens	133-136
19580340-5	2009	<br />Our results showed that leukocytes of CML patients, clinically responsive to Imatinib treatment, significantly decreased WT1 expression after in vitro incubation with Imatinib.	imatinib	179-187	WT1 transcription factor	Homo sapiens	133-136
19580340-4	2009	The effect of Imatinib was characterized not only by the expression of WT1 but also by BCR-ABL, and proliferative factor Ki-67.	imatinib	14-22	WT1 transcription factor	Homo sapiens	71-74
18815156-3	2009	We hypothesized that a combination of immunosuppressive agents, e.g. cyclophosphamide (CYC) and imatinib (PDGFR inhibitor), might be useful for treating SSc-related ILD.	imatinib	96-104	platelet derived growth factor receptor beta	Homo sapiens	106-111
19936007-2	2009	The current frontline therapy in CML is the BCR-ABL tyrosine kinase inhibitor, Imatinib.	imatinib	79-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
19806784-0	2009	Hemin counteracts the repression of Bcl-2 and NrF2 genes and the cell killing induced by imatinib in human Bcr-Abl(+) CML cells.	imatinib	89-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
19806784-1	2009	Imatinib is a targeted selective inhibitor of chimaeric Bcr-Abl tyrosine kinase developed for effective therapy of chronic myelogenous leukemia (CML) and acute lymphocytic leukemia (ALL) patients.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
19225231-4	2009	This patient has shown a relapse based on transcription-mediated amplification-hybridization protection assay (TMA-HPA) to monitor BCR-ABL transcripts, highlighting the uncertainty of discontinuing imatinib therapy for five months.	imatinib	198-206	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
19690756-8	2009	The treatment of localized GISTs is surgical resection and that of advanced or unresecable GISTs is based on the use of targeted therapy, imatinib, which is a pharmacological antagonist of the c-kit protein.	imatinib	138-146	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	193-198
19096980-0	2009	Secondary C-kit mutation is a cause of acquired resistance to imatinib in gastrointestinal stromal tumor.	imatinib	62-70	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	10-15
19096980-2	2009	Imatinib is a selective tyrosine kinase inhibitor of KIT and achieves a partial response or stable disease in most patients with metastatic GIST, but there is increasing evidence of acquired resistance.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	53-56
19708570-4	2009	This study included 8 CML patients (7 in a chronic phase, 1 in acceleration phase) treated with BCR-ABL ITK inhibitors of the first (imatinib) and the second line (ITK-II).	imatinib	133-141	IL2 inducible T cell kinase	Homo sapiens	104-107
19100369-4	2009	In the formerly most unfavorable subgroup, Philadelphia chromosome (Ph)/BCR-ABL-positive ALL, survival now ranges from 40% to 50% after incorporating imatinib in combination chemotherapy.	imatinib	150-158	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
19343297-3	2009	The advent of imatinib, an inhibitor targeted specifically for BCR-ABL, represented a significant medical advance in CML therapy.	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
19696984-4	2009	Based upon currently available data, the Austrian GIST-Panel recommends adjuvant treatment with 400 mg Imatinib/day for 1 year for KIT positive GIST patients with a high or moderate risk of relapse (according to Joensuu) [10] following complete resection of the primary tumor.	imatinib	103-111	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	131-134
19251035-6	2009	Inhibition of c-Abl tyrosine kinase by STI571 attenuates the effect of insulin on Akt/GSK-3beta phosphorylation and glycogen synthesis, and at the same time, it enhances the effect of insulin on ERK activation, cell proliferation and migration.	imatinib	39-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
19251035-6	2009	Inhibition of c-Abl tyrosine kinase by STI571 attenuates the effect of insulin on Akt/GSK-3beta phosphorylation and glycogen synthesis, and at the same time, it enhances the effect of insulin on ERK activation, cell proliferation and migration.	imatinib	39-45	insulin	Homo sapiens	71-78
19251035-6	2009	Inhibition of c-Abl tyrosine kinase by STI571 attenuates the effect of insulin on Akt/GSK-3beta phosphorylation and glycogen synthesis, and at the same time, it enhances the effect of insulin on ERK activation, cell proliferation and migration.	imatinib	39-45	AKT serine/threonine kinase 1	Homo sapiens	82-85
19251035-6	2009	Inhibition of c-Abl tyrosine kinase by STI571 attenuates the effect of insulin on Akt/GSK-3beta phosphorylation and glycogen synthesis, and at the same time, it enhances the effect of insulin on ERK activation, cell proliferation and migration.	imatinib	39-45	glycogen synthase kinase 3 beta	Homo sapiens	86-95
19251035-6	2009	Inhibition of c-Abl tyrosine kinase by STI571 attenuates the effect of insulin on Akt/GSK-3beta phosphorylation and glycogen synthesis, and at the same time, it enhances the effect of insulin on ERK activation, cell proliferation and migration.	imatinib	39-45	insulin	Homo sapiens	184-191
19251035-7	2009	This effect of STI571 is specific to c-Abl inhibition, because it does not occur in Abl-null cells and is restored in c-Abl-reconstituted cells.	imatinib	15-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-42
19251035-7	2009	This effect of STI571 is specific to c-Abl inhibition, because it does not occur in Abl-null cells and is restored in c-Abl-reconstituted cells.	imatinib	15-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-123
19091943-7	2008	We further used this approach to identify genes involved in the response of cancer cells to tumoricidal agents and found 4 genes required for the response of CML cells to imatinib treatment: PTPN1, NF1, SMARCB1, and SMARCE1, and 5 regulators of the response to FAS activation, FAS, FADD, CASP8, ARID1A and CBX1.	imatinib	171-179	protein tyrosine phosphatase non-receptor type 1	Homo sapiens	191-196
19563028-0	2009	[Arsenic trioxide inhibits cell growth in imatinib-resistant bcr-abl mutant cell lines in vitro].	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
19563028-1	2009	OBJECTIVE: To explore the effect of arsenic trioxide (As2O3) on the growth inhibition of imatinib (IM)-resistant bcr-abl mutant cell lines in vitro.	imatinib	89-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
19091943-7	2008	We further used this approach to identify genes involved in the response of cancer cells to tumoricidal agents and found 4 genes required for the response of CML cells to imatinib treatment: PTPN1, NF1, SMARCB1, and SMARCE1, and 5 regulators of the response to FAS activation, FAS, FADD, CASP8, ARID1A and CBX1.	imatinib	171-179	neurofibromin 1	Homo sapiens	198-201
19109573-9	2008	Imatinib or JAK2 inhibitors reversed inhibition of the pathway in cells from patients with CML and polycythemia vera, respectively, but not in cells from a patient with resistance to imatinib because of a mutation in the BCR-ABL kinase domain.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	221-228
19091943-7	2008	We further used this approach to identify genes involved in the response of cancer cells to tumoricidal agents and found 4 genes required for the response of CML cells to imatinib treatment: PTPN1, NF1, SMARCB1, and SMARCE1, and 5 regulators of the response to FAS activation, FAS, FADD, CASP8, ARID1A and CBX1.	imatinib	171-179	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily b, member 1	Homo sapiens	203-210
19091943-7	2008	We further used this approach to identify genes involved in the response of cancer cells to tumoricidal agents and found 4 genes required for the response of CML cells to imatinib treatment: PTPN1, NF1, SMARCB1, and SMARCE1, and 5 regulators of the response to FAS activation, FAS, FADD, CASP8, ARID1A and CBX1.	imatinib	171-179	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily e, member 1	Homo sapiens	216-223
19091943-7	2008	We further used this approach to identify genes involved in the response of cancer cells to tumoricidal agents and found 4 genes required for the response of CML cells to imatinib treatment: PTPN1, NF1, SMARCB1, and SMARCE1, and 5 regulators of the response to FAS activation, FAS, FADD, CASP8, ARID1A and CBX1.	imatinib	171-179	Fas associated via death domain	Homo sapiens	282-286
19091943-7	2008	We further used this approach to identify genes involved in the response of cancer cells to tumoricidal agents and found 4 genes required for the response of CML cells to imatinib treatment: PTPN1, NF1, SMARCB1, and SMARCE1, and 5 regulators of the response to FAS activation, FAS, FADD, CASP8, ARID1A and CBX1.	imatinib	171-179	caspase 8	Homo sapiens	288-293
19091943-7	2008	We further used this approach to identify genes involved in the response of cancer cells to tumoricidal agents and found 4 genes required for the response of CML cells to imatinib treatment: PTPN1, NF1, SMARCB1, and SMARCE1, and 5 regulators of the response to FAS activation, FAS, FADD, CASP8, ARID1A and CBX1.	imatinib	171-179	AT-rich interaction domain 1A	Homo sapiens	295-301
19091943-7	2008	We further used this approach to identify genes involved in the response of cancer cells to tumoricidal agents and found 4 genes required for the response of CML cells to imatinib treatment: PTPN1, NF1, SMARCB1, and SMARCE1, and 5 regulators of the response to FAS activation, FAS, FADD, CASP8, ARID1A and CBX1.	imatinib	171-179	chromobox 1	Homo sapiens	306-310
18938156-7	2008	Furthermore, the potent DDR1 and DDR2 inhibitory activity of imatinib, nilotinib and dasatinib may have therapeutic implications in a number of inflammatory, fibrotic and neoplastic diseases.	imatinib	61-69	discoidin domain receptor tyrosine kinase 1	Homo sapiens	24-28
18796631-6	2008	The antiapoptotic profile of CD40-triggered CLL resembled BCR-Abl-dependent changes seen in chronic myeloid leukemia (CML), which prompted application of c-Abl inhibitors imatinib or dasatinib.	imatinib	171-179	CD40 molecule	Homo sapiens	29-33
18796631-6	2008	The antiapoptotic profile of CD40-triggered CLL resembled BCR-Abl-dependent changes seen in chronic myeloid leukemia (CML), which prompted application of c-Abl inhibitors imatinib or dasatinib.	imatinib	171-179	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-159
19077273-8	2008	The Abl kinase inhibitor, STI571, blocked the inhibition of NMDA currents by Abl.	imatinib	26-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
19077273-8	2008	The Abl kinase inhibitor, STI571, blocked the inhibition of NMDA currents by Abl.	imatinib	26-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-80
19088049-2	2008	The effect of smoking on the pharmacokinetics of imatinib, which is metabolized by CYP3A4 and partly by CYP1A2, is unknown.	imatinib	49-57	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	83-89
19088049-2	2008	The effect of smoking on the pharmacokinetics of imatinib, which is metabolized by CYP3A4 and partly by CYP1A2, is unknown.	imatinib	49-57	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	104-110
19061839-2	2008	In vitro, transient potent BCR-ABL inhibition with either dasatinib or imatinib is cytotoxic to CML cell lines, as is transient potent EGFR inhibition with erlotinib in a lung cancer cell line.	imatinib	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
18938156-1	2008	Imatinib, nilotinib and dasatinib are protein kinase inhibitors which target the tyrosine kinase activity of the Breakpoint Cluster Region-Abelson kinase (BCR-ABL) and are used to treat chronic myelogenous leukemia.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-153
18938156-7	2008	Furthermore, the potent DDR1 and DDR2 inhibitory activity of imatinib, nilotinib and dasatinib may have therapeutic implications in a number of inflammatory, fibrotic and neoplastic diseases.	imatinib	61-69	discoidin domain receptor tyrosine kinase 2	Homo sapiens	33-37
18938156-1	2008	Imatinib, nilotinib and dasatinib are protein kinase inhibitors which target the tyrosine kinase activity of the Breakpoint Cluster Region-Abelson kinase (BCR-ABL) and are used to treat chronic myelogenous leukemia.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-162
18938156-3	2008	To further investigate the interaction of imatinib, nilotinib and dasatinib with DDR1 kinase we cloned and expressed human DDR1 and developed biochemical and cellular functional assays to assess their activity against DDR1 and the related receptor tyrosine kinase Discoidin Domain Receptor2 (DDR2).	imatinib	42-50	discoidin domain receptor tyrosine kinase 1	Homo sapiens	81-85
19075636-3	2008	These effects can be largely suppressed by TK inhibitor Imatinib mesylate, currently the leading drug in CML treatment.	imatinib	56-73	TXK tyrosine kinase	Homo sapiens	43-45
18950453-9	2008	These data confirmed the long-term efficacy of imatinib for PDGFR-rearranged CEL patients, and also showed that a minority of HES cases without known molecular aberrations may benefit from imatinib.	imatinib	47-55	platelet derived growth factor receptor beta	Homo sapiens	60-65
18762765-2	2008	Imatinib mesylate enables selective, dual inhibition of the transforming growth factor beta (TGFbeta) and PDGF pathways.	imatinib	0-17	transforming growth factor beta 1	Homo sapiens	60-91
18762765-2	2008	Imatinib mesylate enables selective, dual inhibition of the transforming growth factor beta (TGFbeta) and PDGF pathways.	imatinib	0-17	transforming growth factor beta 1	Homo sapiens	93-100
19047139-8	2008	In contrast, Imatinib inhibited only Bcr-Abl-dependent Src activity.	imatinib	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-44
19669326-1	2008	Imatinib (Gleevec, Novartis), an inhibitor of BCR-ABL, platelet-derived growth factor, and KIT receptor tyrosine kinases, is widely used in the treatment of chronic myelogenous leukemia and gastrointestinal stromal tumors.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
19047139-8	2008	In contrast, Imatinib inhibited only Bcr-Abl-dependent Src activity.	imatinib	13-21	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	55-58
19073506-1	2008	BACKGROUND: Imatinib mesylate is a potent inhibitor of the Bcr-Abl, c-Kit, and platelet-derived growth factor receptor (PDGFR) tyrosine kinases.	imatinib	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
19073506-1	2008	BACKGROUND: Imatinib mesylate is a potent inhibitor of the Bcr-Abl, c-Kit, and platelet-derived growth factor receptor (PDGFR) tyrosine kinases.	imatinib	12-29	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	68-73
19073506-1	2008	BACKGROUND: Imatinib mesylate is a potent inhibitor of the Bcr-Abl, c-Kit, and platelet-derived growth factor receptor (PDGFR) tyrosine kinases.	imatinib	12-29	platelet derived growth factor receptor beta	Homo sapiens	79-118
19073506-1	2008	BACKGROUND: Imatinib mesylate is a potent inhibitor of the Bcr-Abl, c-Kit, and platelet-derived growth factor receptor (PDGFR) tyrosine kinases.	imatinib	12-29	platelet derived growth factor receptor beta	Homo sapiens	120-125
18449950-5	2008	Of these, 54% (6/11) achieved a reduction of bcr-abl mRNA by > or = 2 log (n = 3) or > or = 3 log (n = 3) with 800 mg Imatinib.	imatinib	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
19047160-2	2008	Whereas imatinib, a selective inhibitor of Bcr-Abl tyrosine kinase, is now used in frontline therapy for CML, second-generation inhibitors of Bcr-Abl tyrosine kinase such as nilotinib or dasatinib have been developed for the treatment of imatinib-resistant or imatinib-intolerant disease.	imatinib	8-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
19047160-10	2008	Such mechanisms of resistance are close to those observed in imatinib-resistant cell lines and emphasize the critical role of Lyn in nilotinib resistance.	imatinib	61-69	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	126-129
19047099-0	2008	Imatinib targeting of KIT-mutant oncoprotein in melanoma.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	22-25
19047099-3	2008	We recently reported a patient with metastatic mucosal melanoma harboring a known KIT mutation treated with imatinib mesylate who experienced a major response.	imatinib	108-125	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	82-85
19047099-9	2008	RESULTS: Mucosal melanoma cells exhibited imatinib sensitivity correlating with KIT mutational status.	imatinib	42-50	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	80-83
19047099-10	2008	Imatinib dramatically decreased proliferation and was cytotoxic to a KIT mutated and amplified cell culture.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	69-72
19047099-13	2008	In vitro analyses revealed major sensitivity to KIT kinase inhibition by imatinib, with potent induction of melanoma cell apoptosis.	imatinib	73-81	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	48-51
19047110-11	2008	CONCLUSIONS: Hsp90 overexpression represents a poor prognosticator that correlates with several adverse parameters, highlighting its role in disease progression and alternative therapy for high-risk, imatinib-resistant gastrointestinal stromal tumors.	imatinib	200-208	heat shock protein 90 alpha family class A member 1	Homo sapiens	13-18
19669326-1	2008	Imatinib (Gleevec, Novartis), an inhibitor of BCR-ABL, platelet-derived growth factor, and KIT receptor tyrosine kinases, is widely used in the treatment of chronic myelogenous leukemia and gastrointestinal stromal tumors.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	91-94
19034614-10	2008	D816V c-kit mutation is frequent and associated with resistance against Imatinib.	imatinib	72-80	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	6-11
18551246-2	2008	Numerous preclinical data (for example, 75% of MUM express c-kit) suggest that imatinib mesylate (IM) may be a potential treatment of UMM.	imatinib	79-96	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	59-64
19039626-0	2008	Retention but significant reduction of BCR-ABL transcript in hematopoietic stem cells in chronic myelogenous leukemia after imatinib therapy.	imatinib	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
19039626-1	2008	Chronic myelogenous leukemia (CML) is effectively treated with imatinib mesylate (IM), a small molecule inhibitor of the BCR-ABL tyrosine kinase that is expressed in the entire hematopoietic compartment including stem cells (HSC) and progenitors in CML patients.	imatinib	63-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
18465140-1	2008	PURPOSE: Imatinib is a small molecule inhibiting the tyrosine kinases bcr-abl, c-kit, PDGFR-alpha and PDGFR-beta.	imatinib	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
18465140-1	2008	PURPOSE: Imatinib is a small molecule inhibiting the tyrosine kinases bcr-abl, c-kit, PDGFR-alpha and PDGFR-beta.	imatinib	9-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	79-84
18465140-1	2008	PURPOSE: Imatinib is a small molecule inhibiting the tyrosine kinases bcr-abl, c-kit, PDGFR-alpha and PDGFR-beta.	imatinib	9-17	platelet derived growth factor receptor alpha	Homo sapiens	86-97
18465140-1	2008	PURPOSE: Imatinib is a small molecule inhibiting the tyrosine kinases bcr-abl, c-kit, PDGFR-alpha and PDGFR-beta.	imatinib	9-17	platelet derived growth factor receptor beta	Homo sapiens	102-112
18465140-4	2008	METHODS: Expression patterns of abl, c-kit, PDGFR-alpha and PDGFR-beta (Imatinib targets) were studied in 5 cell lines and 111 tissue arrays by PCR and immunohistochemistry.	imatinib	72-80	platelet derived growth factor receptor beta	Homo sapiens	60-70
18571721-1	2008	Receptor activated tyrosine kinases such as c-kit, c-fms and PDGFR are known targets of inhibition by imatinib mesylate (Gleevec) and are expressed on AML blasts.	imatinib	102-119	colony stimulating factor 1 receptor	Homo sapiens	51-56
18486988-2	2008	In patients with GIST, overexpression of mutated KIT within the tumor is predictive of response to molecular targeted therapy using imatinib.	imatinib	132-140	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	49-52
18571721-1	2008	Receptor activated tyrosine kinases such as c-kit, c-fms and PDGFR are known targets of inhibition by imatinib mesylate (Gleevec) and are expressed on AML blasts.	imatinib	102-119	platelet derived growth factor receptor beta	Homo sapiens	61-66
18509354-0	2008	An activating KRAS mutation in imatinib-resistant chronic myeloid leukemia.	imatinib	31-39	KRAS proto-oncogene, GTPase	Homo sapiens	14-18
19052981-1	2008	Imatinib is a relatively specific inhibitor of the BCR/ABL tyrosine kinase, effective in chronic myeloid leukemia (CML).	imatinib	0-8	BCR activator of RhoGEF and GTPase	Homo sapiens	51-74
18754032-1	2008	Dasatinib is an inhibitor of BCR-ABL and SRC-family kinases for patients with imatinib-resistant or -intolerant chronic myelogenous leukemia (CML).	imatinib	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
18784740-5	2008	NUP214-ABL1 was more sensitive to imatinib (Glivec) than BCR-ABL1 in vitro and in cells, indicating a different activation state and conformation of the two ABL1 fusion kinases.	imatinib	34-42	nucleoporin 214	Homo sapiens	0-6
18514829-9	2008	Thus, both Bcr-Abl and Aurora kinase inhibition contribute to the efficacy of PHA-680626 against Imatinib-resistant BCR-ABL positive leukemias, particularly those harbouring the T315I mutation.	imatinib	97-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-18
18784740-5	2008	NUP214-ABL1 was more sensitive to imatinib (Glivec) than BCR-ABL1 in vitro and in cells, indicating a different activation state and conformation of the two ABL1 fusion kinases.	imatinib	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	7-11
18514829-9	2008	Thus, both Bcr-Abl and Aurora kinase inhibition contribute to the efficacy of PHA-680626 against Imatinib-resistant BCR-ABL positive leukemias, particularly those harbouring the T315I mutation.	imatinib	97-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
19056677-0	2008	BCR-ABL alternative splicing as a common mechanism for imatinib resistance: evidence from molecular dynamics simulations.	imatinib	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
19056677-3	2008	Sensitive PCR-based testing showed that 32 of 52 (62%) imatinib-resistant CML patients in chronic phase and 8 of 38 (21%) in accelerated or blast crisis expressed varying levels of the alternatively spliced BCR-ABL mRNA.	imatinib	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	207-214
18955451-9	2008	CONCLUSION: We confirmed the favorable impact of KIT exon 11 genotype when compared with KIT exon 9 and wild-type genotype for patients with advanced GIST who are treated with imatinib.	imatinib	176-184	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	49-52
19043528-6	2008	Sampling areas with different residual cellularity scores fromboth the imatinib-treated and untreated patients showed biochemical and immunohistochemical evidence of high levels of proautophagy beclin1/PI3KIII and low levels of antiautophagy beclin1/bcl2 complexes, together with the presence of LC3-II detected by Western blot analysis, thus supporting the presence of autophagy.	imatinib	71-79	beclin 1	Homo sapiens	194-201
19043528-6	2008	Sampling areas with different residual cellularity scores fromboth the imatinib-treated and untreated patients showed biochemical and immunohistochemical evidence of high levels of proautophagy beclin1/PI3KIII and low levels of antiautophagy beclin1/bcl2 complexes, together with the presence of LC3-II detected by Western blot analysis, thus supporting the presence of autophagy.	imatinib	71-79	peptidase inhibitor 3	Homo sapiens	202-205
19043528-6	2008	Sampling areas with different residual cellularity scores fromboth the imatinib-treated and untreated patients showed biochemical and immunohistochemical evidence of high levels of proautophagy beclin1/PI3KIII and low levels of antiautophagy beclin1/bcl2 complexes, together with the presence of LC3-II detected by Western blot analysis, thus supporting the presence of autophagy.	imatinib	71-79	beclin 1	Homo sapiens	242-249
19043528-6	2008	Sampling areas with different residual cellularity scores fromboth the imatinib-treated and untreated patients showed biochemical and immunohistochemical evidence of high levels of proautophagy beclin1/PI3KIII and low levels of antiautophagy beclin1/bcl2 complexes, together with the presence of LC3-II detected by Western blot analysis, thus supporting the presence of autophagy.	imatinib	71-79	BCL2 apoptosis regulator	Homo sapiens	250-254
18955451-9	2008	CONCLUSION: We confirmed the favorable impact of KIT exon 11 genotype when compared with KIT exon 9 and wild-type genotype for patients with advanced GIST who are treated with imatinib.	imatinib	176-184	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	89-92
18955458-1	2008	PURPOSE: Most gastrointestinal stromal tumors (GISTs) harbor mutant KIT or platelet-derived growth factor receptor alpha (PDGFRA) kinases, which are imatinib targets.	imatinib	149-157	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	68-71
18955458-1	2008	PURPOSE: Most gastrointestinal stromal tumors (GISTs) harbor mutant KIT or platelet-derived growth factor receptor alpha (PDGFRA) kinases, which are imatinib targets.	imatinib	149-157	platelet derived growth factor receptor alpha	Homo sapiens	75-120
18955458-1	2008	PURPOSE: Most gastrointestinal stromal tumors (GISTs) harbor mutant KIT or platelet-derived growth factor receptor alpha (PDGFRA) kinases, which are imatinib targets.	imatinib	149-157	platelet derived growth factor receptor alpha	Homo sapiens	122-128
18955458-5	2008	KIT/PDGFRA mutational status was determined for 78 patients by using tumor specimens obtained before and after prior imatinib therapy.	imatinib	117-125	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
18981115-0	2008	Imatinib mesylate inhibits CD4+ CD25+ regulatory T cell activity and enhances active immunotherapy against BCR-ABL- tumors.	imatinib	0-17	CD4 antigen	Mus musculus	27-30
18981115-0	2008	Imatinib mesylate inhibits CD4+ CD25+ regulatory T cell activity and enhances active immunotherapy against BCR-ABL- tumors.	imatinib	0-17	interleukin 2 receptor, alpha chain	Mus musculus	32-36
18981115-4	2008	In the current study, we have investigated the influence of imatinib mesylate on CD4(+)CD25(+)FoxP3(+) regulatory T cells (Treg), a critical population of lymphocytes that contributes to peripheral tolerance.	imatinib	60-77	CD4 antigen	Mus musculus	81-84
18981115-4	2008	In the current study, we have investigated the influence of imatinib mesylate on CD4(+)CD25(+)FoxP3(+) regulatory T cells (Treg), a critical population of lymphocytes that contributes to peripheral tolerance.	imatinib	60-77	interleukin 2 receptor, alpha chain	Mus musculus	87-91
18981115-4	2008	In the current study, we have investigated the influence of imatinib mesylate on CD4(+)CD25(+)FoxP3(+) regulatory T cells (Treg), a critical population of lymphocytes that contributes to peripheral tolerance.	imatinib	60-77	forkhead box P3	Mus musculus	94-99
18981115-5	2008	Used at concentrations achieved clinically, imatinib impaired Treg immunosuppressive function and FoxP3 expression but not production of IL-10 and TGF-beta in vitro.	imatinib	44-52	forkhead box P3	Mus musculus	98-103
18981115-6	2008	Imatinib significantly reduced the activation of the transcription factors STAT3 and STAT5 in Treg.	imatinib	0-8	signal transducer and activator of transcription 3	Mus musculus	75-80
18981115-6	2008	Imatinib significantly reduced the activation of the transcription factors STAT3 and STAT5 in Treg.	imatinib	0-8	signal transducer and activator of transcription 5A	Mus musculus	85-90
18981115-7	2008	Analysis of Treg TCR-induced signaling cascade indicated that imatinib inhibited phosphorylation of ZAP70 and LAT.	imatinib	62-70	zeta-chain (TCR) associated protein kinase	Mus musculus	100-105
18981115-7	2008	Analysis of Treg TCR-induced signaling cascade indicated that imatinib inhibited phosphorylation of ZAP70 and LAT.	imatinib	62-70	linker for activation of T cells	Mus musculus	110-113
18841158-1	2008	In a placebo-controlled randomised study of the platelet-derived growth factor receptor (PDGFR) inhibitor imatinib mesylate and docetaxel in metastatic prostate cancer with bone metastases (n=116), no significant differences in progression-free and overall survival were observed.	imatinib	106-123	platelet derived growth factor receptor beta	Homo sapiens	89-94
18635311-4	2008	However, the PU.1 suppression is abrogated in patients in remission, after interferon-alpha or imatinib treatment.	imatinib	95-103	Spi-1 proto-oncogene	Homo sapiens	13-17
18986386-0	2008	Prospective monitoring of BCR-ABL1 transcript levels in patients with Philadelphia chromosome-positive acute lymphoblastic leukaemia undergoing imatinib-combined chemotherapy.	imatinib	144-152	BCR activator of RhoGEF and GTPase	Homo sapiens	26-34
18827562-3	2008	In this study, we demonstrated through fluorescein isothiocyanate-labeled annexin V for apoptotic cells detection and western blotting that by inhibiting catalase activity, imatinib apoptosis induction was significantly enhanced (P<0.05) through diminishing survivin expression in K562 cells.	imatinib	173-181	annexin A5	Homo sapiens	74-83
18713947-4	2008	In this study, we found that the IRF-4 protein levels are increased in lymphoblastic cells transformed by the BCR/ABL oncogene in response to BCR/ABL tyrosine kinase inhibitor imatinib.	imatinib	176-184	interferon regulatory factor 4	Mus musculus	33-38
18713947-4	2008	In this study, we found that the IRF-4 protein levels are increased in lymphoblastic cells transformed by the BCR/ABL oncogene in response to BCR/ABL tyrosine kinase inhibitor imatinib.	imatinib	176-184	BCR activator of RhoGEF and GTPase	Mus musculus	110-117
18713947-4	2008	In this study, we found that the IRF-4 protein levels are increased in lymphoblastic cells transformed by the BCR/ABL oncogene in response to BCR/ABL tyrosine kinase inhibitor imatinib.	imatinib	176-184	BCR activator of RhoGEF and GTPase	Mus musculus	110-113
18713947-4	2008	In this study, we found that the IRF-4 protein levels are increased in lymphoblastic cells transformed by the BCR/ABL oncogene in response to BCR/ABL tyrosine kinase inhibitor imatinib.	imatinib	176-184	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	114-117
17584806-6	2008	Imatinib mesylate inhibited PDGF-mediated activation of signalling pathways (Src, extracellular signal-regulated kinase (ERK) and Akt phosphorylation) related to cell motility and survival, efficiently resulting in inhibition of PDGF-induced HTAMC responses.	imatinib	0-17	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	77-80
17584806-6	2008	Imatinib mesylate inhibited PDGF-mediated activation of signalling pathways (Src, extracellular signal-regulated kinase (ERK) and Akt phosphorylation) related to cell motility and survival, efficiently resulting in inhibition of PDGF-induced HTAMC responses.	imatinib	0-17	mitogen-activated protein kinase 1	Homo sapiens	82-119
17584806-6	2008	Imatinib mesylate inhibited PDGF-mediated activation of signalling pathways (Src, extracellular signal-regulated kinase (ERK) and Akt phosphorylation) related to cell motility and survival, efficiently resulting in inhibition of PDGF-induced HTAMC responses.	imatinib	0-17	mitogen-activated protein kinase 1	Homo sapiens	121-124
18679373-2	2008	To study the results of treatment with IM after IFN failure/intolerance versus allogeneic BMT (allo-BMT), we retrospectively analyzed 264 patients treated for CML in first chronic phase in three different institutions.	imatinib	39-41	interferon alpha 1	Homo sapiens	48-51
18795925-11	2008	Compared with cells expressing wild-type KIT at a similar level, M541L KIT-expressing cells displayed enhanced growth at low levels of SCF, and heightened sensitivity to the KIT inhibitor, imatinib mesylate.	imatinib	189-206	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	71-74
18795925-11	2008	Compared with cells expressing wild-type KIT at a similar level, M541L KIT-expressing cells displayed enhanced growth at low levels of SCF, and heightened sensitivity to the KIT inhibitor, imatinib mesylate.	imatinib	189-206	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	71-74
18980976-1	2008	PURPOSE: We recently identified a KIT exon 11 mutation in an anorectal melanoma of a patient who had an excellent response to treatment with imatinib.	imatinib	141-149	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	34-37
18974147-0	2008	Imatinib mesylate induces quiescence in gastrointestinal stromal tumor cells through the CDH1-SKP2-p27Kip1 signaling axis.	imatinib	0-17	cadherin 1	Homo sapiens	89-93
18974147-0	2008	Imatinib mesylate induces quiescence in gastrointestinal stromal tumor cells through the CDH1-SKP2-p27Kip1 signaling axis.	imatinib	0-17	S-phase kinase associated protein 2	Homo sapiens	94-98
18974147-0	2008	Imatinib mesylate induces quiescence in gastrointestinal stromal tumor cells through the CDH1-SKP2-p27Kip1 signaling axis.	imatinib	0-17	cyclin dependent kinase inhibitor 1B	Homo sapiens	99-106
18974147-5	2008	We report here that imatinib stimulates cellular quiescence in a proportion of GIST cells as evidenced by up-regulation of the CDK inhibitor p27(Kip1), loss of cyclin A, and reduced BrdUrd incorporation.	imatinib	20-28	interferon alpha inducible protein 27	Homo sapiens	141-144
18974147-5	2008	We report here that imatinib stimulates cellular quiescence in a proportion of GIST cells as evidenced by up-regulation of the CDK inhibitor p27(Kip1), loss of cyclin A, and reduced BrdUrd incorporation.	imatinib	20-28	cyclin dependent kinase inhibitor 1B	Homo sapiens	145-149
18974147-5	2008	We report here that imatinib stimulates cellular quiescence in a proportion of GIST cells as evidenced by up-regulation of the CDK inhibitor p27(Kip1), loss of cyclin A, and reduced BrdUrd incorporation.	imatinib	20-28	cyclin A2	Homo sapiens	160-168
18974147-6	2008	Mechanistically, these events are associated with an imatinib-induced modulation of the APC/CDH1 signaling axis.	imatinib	53-61	cadherin 1	Homo sapiens	92-96
18974147-7	2008	Specifically, we provide evidence that imatinib down-regulates SKP2 and that this event is associated with increased nuclear CDH1, an activator of the APC that has been shown to regulate SKP2 stability.	imatinib	39-47	S-phase kinase associated protein 2	Homo sapiens	63-67
18974147-7	2008	Specifically, we provide evidence that imatinib down-regulates SKP2 and that this event is associated with increased nuclear CDH1, an activator of the APC that has been shown to regulate SKP2 stability.	imatinib	39-47	S-phase kinase associated protein 2	Homo sapiens	187-191
18981009-7	2008	By adding genotype status to the final covariate imatinib model, a 22% reduction in CL/F was observed in heterozygous compared with wild-type patients corresponding to ABCG2 c.421C>A (P<0.05).	imatinib	49-57	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	168-173
18980976-8	2008	Almost all the KIT mutations were of the type predicted to be imatinib sensitive.	imatinib	62-70	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	15-18
19119132-5	2008	Hypopigmentation induced by imatinib mesylate with possible molecular blockage to a melanin-dependent KIT signal has been well documented; however, our case with repigmentation suggested that KIT signal of melanin formation would be much more sophisticated than we have believed.	imatinib	28-45	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	102-105
19119132-5	2008	Hypopigmentation induced by imatinib mesylate with possible molecular blockage to a melanin-dependent KIT signal has been well documented; however, our case with repigmentation suggested that KIT signal of melanin formation would be much more sophisticated than we have believed.	imatinib	28-45	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	192-195
18603297-5	2008	In order to understand the possible molecular mechanisms underlying STI571 resistance caused by ABL gene mutations, we investigated 19 patients (18 CML patients and 1 Ph (+) ALL patient) who either relapsed after initial response or had no response to STI571 treatment.	imatinib	68-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-99
18843283-3	2008	A few prospective trials have now better defined the natural history of imatinib-treated FIP1L1-PDGFRA-positive patients, from which some basic conclusions can be drawn: the prognosis is outstanding, acquired resistance is exceedingly rare, but ongoing imatinib treatment is likely required to prevent relapse.	imatinib	72-80	factor interacting with PAPOLA and CPSF1	Homo sapiens	89-95
18843283-3	2008	A few prospective trials have now better defined the natural history of imatinib-treated FIP1L1-PDGFRA-positive patients, from which some basic conclusions can be drawn: the prognosis is outstanding, acquired resistance is exceedingly rare, but ongoing imatinib treatment is likely required to prevent relapse.	imatinib	72-80	platelet derived growth factor receptor alpha	Homo sapiens	96-102
19021069-0	2008	OCT1 (SLC22A1) R61C polymorphism and response to imatinib treatment in chronic myeloid leukemia patients.	imatinib	49-57	solute carrier family 22 member 1	Homo sapiens	0-4
18956997-4	2008	Current treatment is aimed at inhibiting BCR and ABL kinase with novel agents, the first being imatinib in 2003, and more recently dasatinib in 2006.	imatinib	95-103	BCR activator of RhoGEF and GTPase	Homo sapiens	41-44
19021069-0	2008	OCT1 (SLC22A1) R61C polymorphism and response to imatinib treatment in chronic myeloid leukemia patients.	imatinib	49-57	solute carrier family 22 member 1	Homo sapiens	6-13
18765637-6	2008	AIB1/SRC-3-dependent transcription and phenotypic changes, such as cell growth and focus formation, can be reversed by an Abl kinase inhibitor, imatinib.	imatinib	144-152	nuclear receptor coactivator 3	Mus musculus	0-4
18765637-6	2008	AIB1/SRC-3-dependent transcription and phenotypic changes, such as cell growth and focus formation, can be reversed by an Abl kinase inhibitor, imatinib.	imatinib	144-152	nuclear receptor coactivator 3	Mus musculus	5-10
18956997-4	2008	Current treatment is aimed at inhibiting BCR and ABL kinase with novel agents, the first being imatinib in 2003, and more recently dasatinib in 2006.	imatinib	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-52
18956997-6	2008	It represents an aminopyrimidine derivative of imatinib with approximately 30 times more potency in vitro against imatinib-sensitive BCR-ABL-expressing cell lines and activity against 32 of 33 point mutations conferring resistance to imatinib.	imatinib	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
18956997-6	2008	It represents an aminopyrimidine derivative of imatinib with approximately 30 times more potency in vitro against imatinib-sensitive BCR-ABL-expressing cell lines and activity against 32 of 33 point mutations conferring resistance to imatinib.	imatinib	114-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
18956997-6	2008	It represents an aminopyrimidine derivative of imatinib with approximately 30 times more potency in vitro against imatinib-sensitive BCR-ABL-expressing cell lines and activity against 32 of 33 point mutations conferring resistance to imatinib.	imatinib	114-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
18936234-0	2008	AHI-1 interacts with BCR-ABL and modulates BCR-ABL transforming activity and imatinib response of CML stem/progenitor cells.	imatinib	77-85	Abelson helper integration site 1	Homo sapiens	0-5
19013895-2	2008	Indeed, imatinib mesylate inhibits KIT kinase activity and represents the front-line drug for the treatment of unresectable and metastatic GISTs.	imatinib	8-25	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	35-38
19080234-16	2008	CONCLUSION: The present case fulfilled the WHO diagnostic criteria of FIP1L1/PDGFRalpha(-) CEL which did not respond to routine treatment and imatinib.	imatinib	142-150	factor interacting with PAPOLA and CPSF1	Homo sapiens	70-76
19080234-16	2008	CONCLUSION: The present case fulfilled the WHO diagnostic criteria of FIP1L1/PDGFRalpha(-) CEL which did not respond to routine treatment and imatinib.	imatinib	142-150	platelet derived growth factor receptor alpha	Homo sapiens	77-87
18782571-12	2008	Using K562 cells, we analyzed the response of CML cells to low concentrations of DOXM when Bcr-Abl activity was reduced to various levels by its specific inhibitor, STI571.	imatinib	165-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
18782571-14	2008	A higher concentration of STI571 was required to diminish Bcr-Abl activity to the level which was sufficient to stimulate apoptotic cell death pathway in K562.	imatinib	26-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
18932293-1	2008	The molecular targets of sunitinib are receptor tyrosine kinases (RTKs), and this drug has also been known to exert blocking effects on the activation of KIT, which is similar to the mechanism of action of imatinib.	imatinib	206-214	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	154-157
18669873-1	2008	We have previously shown that imatinib uptake into chronic myeloid leukemia (CML) cells is dependent on human organic cation transporter 1 (hOCT1; SLC22A1), and that low hOCT1 expression is an important determinant of clinical outcome to imatinib treatment.	imatinib	30-38	solute carrier family 22 member 1	Homo sapiens	110-138
18940662-0	2008	Small molecule recognition of c-Src via the Imatinib-binding conformation.	imatinib	44-52	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	30-35
18940662-1	2008	The cancer drug, Imatinib, is a selective Abl kinase inhibitor that does not inhibit the closely related kinase c-Src.	imatinib	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-45
18940662-3	2008	A prominent hypothesis explaining the selectivity of Imatinib is that Abl has an intrinsic ability to adopt an inactive conformation (termed DFG-out), whereas c-Src appears to pay a high intrinsic energetic penalty for adopting this conformation, effectively excluding Imatinib from its ATP pocket.	imatinib	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-73
18940662-3	2008	A prominent hypothesis explaining the selectivity of Imatinib is that Abl has an intrinsic ability to adopt an inactive conformation (termed DFG-out), whereas c-Src appears to pay a high intrinsic energetic penalty for adopting this conformation, effectively excluding Imatinib from its ATP pocket.	imatinib	53-61	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	159-164
18940662-3	2008	A prominent hypothesis explaining the selectivity of Imatinib is that Abl has an intrinsic ability to adopt an inactive conformation (termed DFG-out), whereas c-Src appears to pay a high intrinsic energetic penalty for adopting this conformation, effectively excluding Imatinib from its ATP pocket.	imatinib	269-277	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	159-164
18940662-4	2008	This explanation of the difference in binding affinity of Imatinib for Abl versus c-Src makes the striking prediction that it would not be possible to design an inhibitor that binds to the DFG-out conformation of c-Src with high affinity.	imatinib	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-74
18940662-4	2008	This explanation of the difference in binding affinity of Imatinib for Abl versus c-Src makes the striking prediction that it would not be possible to design an inhibitor that binds to the DFG-out conformation of c-Src with high affinity.	imatinib	58-66	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	82-87
18940662-4	2008	This explanation of the difference in binding affinity of Imatinib for Abl versus c-Src makes the striking prediction that it would not be possible to design an inhibitor that binds to the DFG-out conformation of c-Src with high affinity.	imatinib	58-66	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	213-218
18940662-8	2008	Structural comparison between c-Src in complex with these inhibitors allows us to speculate on the differential selectivity of Imatinib for c-Src and Abl.	imatinib	127-135	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	30-35
18940662-8	2008	Structural comparison between c-Src in complex with these inhibitors allows us to speculate on the differential selectivity of Imatinib for c-Src and Abl.	imatinib	127-135	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	140-145
18940662-8	2008	Structural comparison between c-Src in complex with these inhibitors allows us to speculate on the differential selectivity of Imatinib for c-Src and Abl.	imatinib	127-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-153
18669873-7	2008	Both dasatinib and imatinib were transported from the basal to the apical layer, indicating that they were transported by ABCB1, which was confirmed using the ABCB1 inhibitor PSC833 (P = .001 and P < .001, respectively).	imatinib	19-27	ATP binding cassette subfamily B member 1	Homo sapiens	122-127
18669873-7	2008	Both dasatinib and imatinib were transported from the basal to the apical layer, indicating that they were transported by ABCB1, which was confirmed using the ABCB1 inhibitor PSC833 (P = .001 and P < .001, respectively).	imatinib	19-27	ATP binding cassette subfamily B member 1	Homo sapiens	159-164
18669873-10	2008	Dasatinib may therefore offer an advantage over imatinib in patients with low hOCT1 expression.	imatinib	48-56	solute carrier family 22 member 1	Homo sapiens	78-83
18669873-1	2008	We have previously shown that imatinib uptake into chronic myeloid leukemia (CML) cells is dependent on human organic cation transporter 1 (hOCT1; SLC22A1), and that low hOCT1 expression is an important determinant of clinical outcome to imatinib treatment.	imatinib	30-38	solute carrier family 22 member 1	Homo sapiens	140-145
18669873-1	2008	We have previously shown that imatinib uptake into chronic myeloid leukemia (CML) cells is dependent on human organic cation transporter 1 (hOCT1; SLC22A1), and that low hOCT1 expression is an important determinant of clinical outcome to imatinib treatment.	imatinib	30-38	solute carrier family 22 member 1	Homo sapiens	147-154
18669873-1	2008	We have previously shown that imatinib uptake into chronic myeloid leukemia (CML) cells is dependent on human organic cation transporter 1 (hOCT1; SLC22A1), and that low hOCT1 expression is an important determinant of clinical outcome to imatinib treatment.	imatinib	30-38	solute carrier family 22 member 1	Homo sapiens	170-175
18669873-1	2008	We have previously shown that imatinib uptake into chronic myeloid leukemia (CML) cells is dependent on human organic cation transporter 1 (hOCT1; SLC22A1), and that low hOCT1 expression is an important determinant of clinical outcome to imatinib treatment.	imatinib	238-246	solute carrier family 22 member 1	Homo sapiens	170-175
18663536-0	2008	A PDE model for imatinib-treated chronic myelogenous leukemia.	imatinib	16-24	aldehyde dehydrogenase 7 family member A1	Homo sapiens	2-5
20641266-0	2004	[(18)F]-N-(2-Chloro-6-methylphenyl)-2-(6-(4-(2-fluoroethyl)piperazin-1-yl)-2-methylpyrimidin-4-ylamino)thiazole-5-carboxamide Imatinib (4-[(4-methyl-1-piperazinyl)methyl]-N-[4-methyl-3-[[4-(3-pyridyl)-2-pyrimidinyl]amino]phenyl]benzamide) is a tyrosine kinase (TK) inhibitor used for the treatment of chronic myeloid leukemia (CML) attributed to the Philadelphia chromosome (Ph+) (1).	imatinib	126-134	TXK tyrosine kinase	Homo sapiens	244-259
20641266-0	2004	[(18)F]-N-(2-Chloro-6-methylphenyl)-2-(6-(4-(2-fluoroethyl)piperazin-1-yl)-2-methylpyrimidin-4-ylamino)thiazole-5-carboxamide Imatinib (4-[(4-methyl-1-piperazinyl)methyl]-N-[4-methyl-3-[[4-(3-pyridyl)-2-pyrimidinyl]amino]phenyl]benzamide) is a tyrosine kinase (TK) inhibitor used for the treatment of chronic myeloid leukemia (CML) attributed to the Philadelphia chromosome (Ph+) (1).	imatinib	126-134	TXK tyrosine kinase	Homo sapiens	261-263
20641266-3	2004	In addition, imatinib has been shown to be an effective treatment against a variety of other conditions that are characterized by the expression of Abl or c-Kit TKs (3).	imatinib	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	148-151
20641266-3	2004	In addition, imatinib has been shown to be an effective treatment against a variety of other conditions that are characterized by the expression of Abl or c-Kit TKs (3).	imatinib	13-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	155-160
20641266-5	2004	Dasatinib is a dual inhibitor of Src/Abl and c-Kit that was recently approved for treatment of imatinib-refractory CML and Ph+ acute lymphoblastic leukemia (ALL) (5, 6).	imatinib	95-103	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	33-36
20641266-5	2004	Dasatinib is a dual inhibitor of Src/Abl and c-Kit that was recently approved for treatment of imatinib-refractory CML and Ph+ acute lymphoblastic leukemia (ALL) (5, 6).	imatinib	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-40
20641266-5	2004	Dasatinib is a dual inhibitor of Src/Abl and c-Kit that was recently approved for treatment of imatinib-refractory CML and Ph+ acute lymphoblastic leukemia (ALL) (5, 6).	imatinib	95-103	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	45-50
18788725-1	2008	The liver-specific organic cation transport protein (OCT1; SLC22A1) transports several cationic drugs including the antidiabetic drug metformin and the anticancer agents oxaliplatin and imatinib.	imatinib	186-194	solute carrier family 22 member 1	Homo sapiens	53-57
18788725-1	2008	The liver-specific organic cation transport protein (OCT1; SLC22A1) transports several cationic drugs including the antidiabetic drug metformin and the anticancer agents oxaliplatin and imatinib.	imatinib	186-194	solute carrier family 22 member 1	Homo sapiens	59-66
18593226-6	2008	Currently, the BCR-ABL inhibitor imatinib mesylate (Gleevec) is being used as a first-line therapy for the treatment of CML.	imatinib	33-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
18645191-1	2008	PURPOSE: Kinase domain (KD) mutations in the BCR-ABL gene are associated with resistance to imatinib in chronic myeloid leukemia (CML) but their incidence and prognostic significance in chronic phase (CP) patients without resistance are unclear.	imatinib	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
18515258-0	2008	Imatinib mesylate (Gleevec) in advanced breast cancer-expressing C-Kit or PDGFR-beta: clinical activity and biological correlations.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	65-70
18515258-0	2008	Imatinib mesylate (Gleevec) in advanced breast cancer-expressing C-Kit or PDGFR-beta: clinical activity and biological correlations.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	74-84
18515258-0	2008	Imatinib mesylate (Gleevec) in advanced breast cancer-expressing C-Kit or PDGFR-beta: clinical activity and biological correlations.	imatinib	19-26	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	65-70
18515258-0	2008	Imatinib mesylate (Gleevec) in advanced breast cancer-expressing C-Kit or PDGFR-beta: clinical activity and biological correlations.	imatinib	19-26	platelet derived growth factor receptor beta	Homo sapiens	74-84
18515258-2	2008	Imatinib mesylate (Gleevec) inhibits several protein tyrosine kinases, including platelet-derived growth factor receptor (PDGFR) and c-kit, which are preferentially expressed in tumor cells.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	81-120
18515258-2	2008	Imatinib mesylate (Gleevec) inhibits several protein tyrosine kinases, including platelet-derived growth factor receptor (PDGFR) and c-kit, which are preferentially expressed in tumor cells.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	122-127
18515258-2	2008	Imatinib mesylate (Gleevec) inhibits several protein tyrosine kinases, including platelet-derived growth factor receptor (PDGFR) and c-kit, which are preferentially expressed in tumor cells.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	133-138
18515258-2	2008	Imatinib mesylate (Gleevec) inhibits several protein tyrosine kinases, including platelet-derived growth factor receptor (PDGFR) and c-kit, which are preferentially expressed in tumor cells.	imatinib	19-26	platelet derived growth factor receptor beta	Homo sapiens	81-120
18515258-2	2008	Imatinib mesylate (Gleevec) inhibits several protein tyrosine kinases, including platelet-derived growth factor receptor (PDGFR) and c-kit, which are preferentially expressed in tumor cells.	imatinib	19-26	platelet derived growth factor receptor beta	Homo sapiens	122-127
18515258-2	2008	Imatinib mesylate (Gleevec) inhibits several protein tyrosine kinases, including platelet-derived growth factor receptor (PDGFR) and c-kit, which are preferentially expressed in tumor cells.	imatinib	19-26	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	133-138
18515258-3	2008	We tested the activity of imatinib mesylate in MBC with overexpression of PDGFR or c-kit.	imatinib	26-43	platelet derived growth factor receptor beta	Homo sapiens	74-79
18515258-3	2008	We tested the activity of imatinib mesylate in MBC with overexpression of PDGFR or c-kit.	imatinib	26-43	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	83-88
18515258-14	2008	Immune studies showed imatinib inhibits interferon-gamma production by TCR-activated CD4(+) T cells.	imatinib	22-30	interferon gamma	Homo sapiens	40-56
18515258-14	2008	Immune studies showed imatinib inhibits interferon-gamma production by TCR-activated CD4(+) T cells.	imatinib	22-30	CD4 molecule	Homo sapiens	85-88
18671247-6	2008	Gene mutations of KIT or PDGFRA are critical in GISTs, because the aberrant versions not only are correlated with the specific cell morphology, histologic phenotype, metastasis, and prognosis, but also are the targets of therapy with imatinib and other agents.	imatinib	234-242	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	18-21
18671247-6	2008	Gene mutations of KIT or PDGFRA are critical in GISTs, because the aberrant versions not only are correlated with the specific cell morphology, histologic phenotype, metastasis, and prognosis, but also are the targets of therapy with imatinib and other agents.	imatinib	234-242	platelet derived growth factor receptor alpha	Homo sapiens	25-31
18829496-1	2008	PURPOSE: Although dual src-family kinase/BCR/ABL inhibitor, dasatinib (BMS-354825), provides therapeutic advantages to imatinib-resistant cells, the mechanism of dasatinib resistance was not fully known.	imatinib	119-127	BCR activator of RhoGEF and GTPase	Homo sapiens	23-48
18619723-4	2008	The tyrosine kinase (TK) inhibitor imatinib (STI571) has been described to counteract the TK activity of FIP1L1-PDGFRalpha in most patients.	imatinib	35-43	factor interacting with PAPOLA and CPSF1	Homo sapiens	105-111
18619726-4	2008	Western blotting analysis was performed to detect T-cell receptor (TCR), nuclear factor kappa B (NF-kappaB) and Src signaling events in T cells treated with dasatinib or imatinib.	imatinib	170-178	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	50-65
18657349-3	2008	Inhibitors of heat shock protein 90 (HSP90), a chaperone for which Kit is a client protein, have demonstrated activity against human cancers and evidence suggests they downregulate several mutated and imatinib-resistant forms of Kit.	imatinib	201-209	heat shock protein 90 alpha family class A member 1	Homo sapiens	14-35
18657349-3	2008	Inhibitors of heat shock protein 90 (HSP90), a chaperone for which Kit is a client protein, have demonstrated activity against human cancers and evidence suggests they downregulate several mutated and imatinib-resistant forms of Kit.	imatinib	201-209	heat shock protein 90 alpha family class A member 1	Homo sapiens	37-42
18657349-3	2008	Inhibitors of heat shock protein 90 (HSP90), a chaperone for which Kit is a client protein, have demonstrated activity against human cancers and evidence suggests they downregulate several mutated and imatinib-resistant forms of Kit.	imatinib	201-209	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	67-70
18619726-4	2008	Western blotting analysis was performed to detect T-cell receptor (TCR), nuclear factor kappa B (NF-kappaB) and Src signaling events in T cells treated with dasatinib or imatinib.	imatinib	170-178	nuclear factor kappa B subunit 1	Homo sapiens	73-95
18657349-3	2008	Inhibitors of heat shock protein 90 (HSP90), a chaperone for which Kit is a client protein, have demonstrated activity against human cancers and evidence suggests they downregulate several mutated and imatinib-resistant forms of Kit.	imatinib	201-209	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	229-232
18619723-4	2008	The tyrosine kinase (TK) inhibitor imatinib (STI571) has been described to counteract the TK activity of FIP1L1-PDGFRalpha in most patients.	imatinib	45-51	factor interacting with PAPOLA and CPSF1	Homo sapiens	105-111
18619726-4	2008	Western blotting analysis was performed to detect T-cell receptor (TCR), nuclear factor kappa B (NF-kappaB) and Src signaling events in T cells treated with dasatinib or imatinib.	imatinib	170-178	nuclear factor kappa B subunit 1	Homo sapiens	97-106
18619726-4	2008	Western blotting analysis was performed to detect T-cell receptor (TCR), nuclear factor kappa B (NF-kappaB) and Src signaling events in T cells treated with dasatinib or imatinib.	imatinib	170-178	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	112-115
18922118-1	2008	The BCR-ABL kinase inhibitor imatinib mesylate is currently the standard therapy for patients with chronic myeloid leukemia (CML).	imatinib	29-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
18619726-8	2008	Dasatinib proved to be more potent than imatinib on Src and TCR signaling events in Jurkat T cells.	imatinib	40-48	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	52-55
18619726-8	2008	Dasatinib proved to be more potent than imatinib on Src and TCR signaling events in Jurkat T cells.	imatinib	40-48	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	60-63
18922118-4	2008	Nilotinib is a tyrosine kinase inhibitor 30-fold more potent than imatinib against BCR-ABL kinase.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
18591368-5	2008	We used the NPC1 mouse model to evaluate c-Abl/p73 expression and activation in the cerebellum and the effect of therapy with the c-Abl-specific inhibitor imatinib.	imatinib	155-163	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	130-135
18591368-7	2008	Furthermore, inhibition of c-Abl with imatinib preserved Purkinje neurons and reduced general cell apoptosis in the cerebellum, improved neurological symptoms, and increased the survival of NPC mice.	imatinib	38-46	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	27-32
18591368-9	2008	Our results suggest that the c-Abl/p73 pathway is involved in NPC neurodegeneration and show that treatment with c-Abl inhibitors is useful in delaying progressive neurodegeneration, supporting the use of imatinib for clinical treatment of patients with NPC disease.	imatinib	205-213	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-34
18591368-9	2008	Our results suggest that the c-Abl/p73 pathway is involved in NPC neurodegeneration and show that treatment with c-Abl inhibitors is useful in delaying progressive neurodegeneration, supporting the use of imatinib for clinical treatment of patients with NPC disease.	imatinib	205-213	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-118
21083005-2	2008	The pivotal role of the Philadelphia chromosome, resulting from the breakpoint cluster region-Abelson (BCR-ABL) translocation, led to the development of imatinib mesylate, a tyrosine kinase inhibitor with significant activity against the BCR-ABL oncoprotein.	imatinib	153-170	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-101
21083005-2	2008	The pivotal role of the Philadelphia chromosome, resulting from the breakpoint cluster region-Abelson (BCR-ABL) translocation, led to the development of imatinib mesylate, a tyrosine kinase inhibitor with significant activity against the BCR-ABL oncoprotein.	imatinib	153-170	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
21083005-2	2008	The pivotal role of the Philadelphia chromosome, resulting from the breakpoint cluster region-Abelson (BCR-ABL) translocation, led to the development of imatinib mesylate, a tyrosine kinase inhibitor with significant activity against the BCR-ABL oncoprotein.	imatinib	153-170	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	238-245
18922118-5	2008	Nilotinib is active against a wide range of imatinib-resistant BCR-ABL mutant isoforms, except for T315I.	imatinib	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
18615681-0	2008	Chronic phase of ETV6-ABL1 positive CML responds to imatinib.	imatinib	52-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-26
18622894-2	2008	Imatinib mesylate offers an effective therapeutic option in patients with various types of malignancies by inhibiting tyrosine kinases such as c-kit.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	143-148
18571768-1	2008	Small molecule tyrosine kinase (TK) inhibitor, such as imatinib, is well established in the treatment of malignancy.	imatinib	55-63	TXK tyrosine kinase	Homo sapiens	15-30
18571768-1	2008	Small molecule tyrosine kinase (TK) inhibitor, such as imatinib, is well established in the treatment of malignancy.	imatinib	55-63	TXK tyrosine kinase	Homo sapiens	32-34
18571768-6	2008	The ability of several TK inhibitors, namely imatinib, to abrogate the activation of platelet-derived growth factor receptor-TK may entail their use in the treatment of SS and possibly more limited forms of sclerosis.	imatinib	45-53	TXK tyrosine kinase	Homo sapiens	23-25
18571768-6	2008	The ability of several TK inhibitors, namely imatinib, to abrogate the activation of platelet-derived growth factor receptor-TK may entail their use in the treatment of SS and possibly more limited forms of sclerosis.	imatinib	45-53	TXK tyrosine kinase	Homo sapiens	125-127
18615679-0	2008	Novel V600E BRAF mutations in imatinib-naive and imatinib-resistant gastrointestinal stromal tumors.	imatinib	30-38	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	12-16
18615679-0	2008	Novel V600E BRAF mutations in imatinib-naive and imatinib-resistant gastrointestinal stromal tumors.	imatinib	49-57	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	12-16
18816866-1	2008	The antivascular function of the platelet-derived growth factor receptor (PDGFR) inhibitor imatinib combined with paclitaxel has been demonstrated by invasive immunohistochemistry.	imatinib	91-99	platelet derived growth factor receptor beta	Homo sapiens	33-72
18615679-5	2008	Alterations in RAS/MEK/ERK pathway may also be involved in development of imatinib resistance in GIST, particularly in tumors lacking secondary KIT or PDGFRA mutations.	imatinib	74-82	mitogen-activated protein kinase kinase 7	Homo sapiens	19-22
18615679-5	2008	Alterations in RAS/MEK/ERK pathway may also be involved in development of imatinib resistance in GIST, particularly in tumors lacking secondary KIT or PDGFRA mutations.	imatinib	74-82	mitogen-activated protein kinase 1	Homo sapiens	23-26
18615679-10	2008	An identical V600E BRAF mutation was also identified in one of 28 imatinib resistant GIST lacking a defined mechanism of drug resistance.	imatinib	66-74	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	19-23
18615679-13	2008	A secondary V600E BRAF mutation could represent an alternative mechanism of imatinib resistance.	imatinib	76-84	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	18-22
18615681-0	2008	Chronic phase of ETV6-ABL1 positive CML responds to imatinib.	imatinib	52-60	ETS variant transcription factor 6	Homo sapiens	17-21
18433865-0	2008	JAK-2V617F mutation in RARS-t: a target for Imatinib therapy?	imatinib	44-52	arginyl-tRNA synthetase 1	Homo sapiens	23-27
18828913-1	2008	Imatinib was the first BCR-ABL-targeted agent approved for the treatment of patients with chronic myeloid leukemia (CML) and confers significant benefit for most patients; however, a substantial number of patients are either initially refractory or develop resistance.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
18816866-1	2008	The antivascular function of the platelet-derived growth factor receptor (PDGFR) inhibitor imatinib combined with paclitaxel has been demonstrated by invasive immunohistochemistry.	imatinib	91-99	platelet derived growth factor receptor beta	Homo sapiens	74-79
18816866-6	2008	Based on changes in PS, we hypothesized that imatinib interferes with the signaling pathway of vascular endothelial growth factor (VEGF).	imatinib	45-53	vascular endothelial growth factor A	Homo sapiens	95-129
18816866-6	2008	Based on changes in PS, we hypothesized that imatinib interferes with the signaling pathway of vascular endothelial growth factor (VEGF).	imatinib	45-53	vascular endothelial growth factor A	Homo sapiens	131-135
18816866-8	2008	It demonstrated reduced activation of both PDGFR-beta and VEGF receptor 2 (VEGFR2) in imatinib-treated mice.	imatinib	86-94	platelet derived growth factor receptor, beta polypeptide	Mus musculus	43-53
18816866-8	2008	It demonstrated reduced activation of both PDGFR-beta and VEGF receptor 2 (VEGFR2) in imatinib-treated mice.	imatinib	86-94	kinase insert domain protein receptor	Mus musculus	58-73
18816866-8	2008	It demonstrated reduced activation of both PDGFR-beta and VEGF receptor 2 (VEGFR2) in imatinib-treated mice.	imatinib	86-94	kinase insert domain protein receptor	Mus musculus	75-81
18928591-1	2008	This study was aimed to compare HHGV678 with imatinib (IM) in growth inhibition of Bcr-Abl wild type and IM-resistant cell lines, investigate the possibility of replacing IM with HHGV678 in treatment of chronic myeloid leukemia (CML) and IM-resistant CML patients.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
18694961-9	2008	Finally, we found a novel negative-feedback loop to the mitogen-activated protein kinase/Mnk pathway that is triggered by CGP57380 and demonstrated that an interruption of the loop further increased the activity of the combination against imatinib-sensitive and -resistant CML cells.	imatinib	239-247	ATPase copper transporting alpha	Homo sapiens	89-92
21127752-1	2008	The BCR-ABL kinase inhibitor imatinib mesylate is currently the standard therapy for patients with chronic myeloid leukemia (CML).	imatinib	29-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
18852120-1	2008	Imatinib mesylate is a potent, molecularly targeted therapy against the oncogenic tyrosine kinase BCR-ABL.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
18794084-2	2008	Imatinib efficiently inhibits the juxtamembrane PDGFRA mutations, whereas many tyrosine kinase domain activation loop PDGFRA mutations confer primary resistance to imatinib.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	48-54
18852120-8	2008	Finally, reducing Stat3 levels with small interfering RNA sensitized K562 cells cultured in CM to imatinib mesylate-induced cell death.	imatinib	98-115	signal transducer and activator of transcription 3	Homo sapiens	18-23
18852120-10	2008	Together, these data support a novel mechanism of BCR-ABL-independent imatinib mesylate resistance and provides preclinical rationale for using Stat3-inhibitors to increase the efficacy of imatinib mesylate within the context of the bone marrow microenvironment.	imatinib	189-197	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
18852120-10	2008	Together, these data support a novel mechanism of BCR-ABL-independent imatinib mesylate resistance and provides preclinical rationale for using Stat3-inhibitors to increase the efficacy of imatinib mesylate within the context of the bone marrow microenvironment.	imatinib	189-197	signal transducer and activator of transcription 3	Homo sapiens	144-149
18787413-6	2008	c-kit inhibition by imatinib mesylate (Gleevec) in DCs was previously shown to promote natural killer cell activation which may be due to dampening of IL-6 production by the DCs.	imatinib	20-37	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-5
18787413-6	2008	c-kit inhibition by imatinib mesylate (Gleevec) in DCs was previously shown to promote natural killer cell activation which may be due to dampening of IL-6 production by the DCs.	imatinib	20-37	interleukin 6	Homo sapiens	151-155
18794084-11	2008	CONCLUSIONS: Treatment with dasatinib or the heat shock protein 90 inhibitor IPI-504 may provide a therapeutic alternative for GIST patients whose tumors carry the imatinib-resistant PDGFRA(D842V) mutant isoform.	imatinib	164-172	platelet derived growth factor receptor alpha	Homo sapiens	183-189
18521081-1	2008	Oncogenic KIT or PDGFRA receptor tyrosine kinase mutations are compelling therapeutic targets in gastrointestinal stromal tumors (GISTs), and the KIT/PDGFRA kinase inhibitor, imatinib, is standard of care for patients with metastatic GIST.	imatinib	175-183	platelet derived growth factor receptor alpha	Homo sapiens	150-156
18521081-4	2008	Herein, we characterize biological functions of PKCtheta in imatinib-sensitive and imatinib-resistant GISTs, showing that lentivirus-mediated PKCtheta knockdown is accompanied by inhibition of KIT expression in three KIT+/PKCtheta+ GIST cell lines, but not in a comparator KIT+/PKCtheta- Ewing"s sarcoma cell line.	imatinib	60-68	protein kinase C theta	Homo sapiens	48-56
18521081-4	2008	Herein, we characterize biological functions of PKCtheta in imatinib-sensitive and imatinib-resistant GISTs, showing that lentivirus-mediated PKCtheta knockdown is accompanied by inhibition of KIT expression in three KIT+/PKCtheta+ GIST cell lines, but not in a comparator KIT+/PKCtheta- Ewing"s sarcoma cell line.	imatinib	60-68	protein kinase C theta	Homo sapiens	142-150
18521081-4	2008	Herein, we characterize biological functions of PKCtheta in imatinib-sensitive and imatinib-resistant GISTs, showing that lentivirus-mediated PKCtheta knockdown is accompanied by inhibition of KIT expression in three KIT+/PKCtheta+ GIST cell lines, but not in a comparator KIT+/PKCtheta- Ewing"s sarcoma cell line.	imatinib	60-68	protein kinase C theta	Homo sapiens	142-150
18521081-4	2008	Herein, we characterize biological functions of PKCtheta in imatinib-sensitive and imatinib-resistant GISTs, showing that lentivirus-mediated PKCtheta knockdown is accompanied by inhibition of KIT expression in three KIT+/PKCtheta+ GIST cell lines, but not in a comparator KIT+/PKCtheta- Ewing"s sarcoma cell line.	imatinib	83-91	protein kinase C theta	Homo sapiens	142-150
18521081-4	2008	Herein, we characterize biological functions of PKCtheta in imatinib-sensitive and imatinib-resistant GISTs, showing that lentivirus-mediated PKCtheta knockdown is accompanied by inhibition of KIT expression in three KIT+/PKCtheta+ GIST cell lines, but not in a comparator KIT+/PKCtheta- Ewing"s sarcoma cell line.	imatinib	83-91	protein kinase C theta	Homo sapiens	142-150
18794084-2	2008	Imatinib efficiently inhibits the juxtamembrane PDGFRA mutations, whereas many tyrosine kinase domain activation loop PDGFRA mutations confer primary resistance to imatinib.	imatinib	164-172	platelet derived growth factor receptor alpha	Homo sapiens	118-124
18794084-5	2008	EXPERIMENTAL DESIGN: Primary imatinib-resistant tumor cells and cell lines expressing imatinib-resistant PDGFRA(D842V) or imatinib-sensitive PDGFRA(DeltaDIM842-844) mutants were treated with different concentrations of dasatinib, sorafenib, nilotinib, and IPI-504.	imatinib	86-94	platelet derived growth factor receptor alpha	Homo sapiens	105-111
18794084-5	2008	EXPERIMENTAL DESIGN: Primary imatinib-resistant tumor cells and cell lines expressing imatinib-resistant PDGFRA(D842V) or imatinib-sensitive PDGFRA(DeltaDIM842-844) mutants were treated with different concentrations of dasatinib, sorafenib, nilotinib, and IPI-504.	imatinib	86-94	platelet derived growth factor receptor alpha	Homo sapiens	105-111
18794444-0	2008	Imatinib-mediated inactivation of Akt regulates ABCG2 function in head and neck squamous cell carcinoma.	imatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	34-37
18772113-1	2008	Resistance of Bcr-Abl-positive leukemic stem cells (LSCs) to imatinib treatment in patients with chronic myeloid leukemia (CML) can cause relapse of disease and might be the origin for emerging drug-resistant clones.	imatinib	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
18728664-9	2008	However, based on the characteristics of the responding tumour in our study, clinical activity of imatinib, specifically in patients with melanoma with certain c-kit aberrations, should be examined.	imatinib	98-106	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	160-165
18794444-0	2008	Imatinib-mediated inactivation of Akt regulates ABCG2 function in head and neck squamous cell carcinoma.	imatinib	0-8	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	48-53
18794444-1	2008	OBJECTIVE: To investigate whether the mechanism for the reversal of ABCG2 (also known as ABCP, MXR, and BCRP)-mediated drug resistance by imatinib mesylate (Gleevec, STI571; Novartis Pharmaceuticals Corp, East Hanover, New Jersey) is caused by the downregulation of Akt kinase.	imatinib	138-155	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	68-73
18794444-1	2008	OBJECTIVE: To investigate whether the mechanism for the reversal of ABCG2 (also known as ABCP, MXR, and BCRP)-mediated drug resistance by imatinib mesylate (Gleevec, STI571; Novartis Pharmaceuticals Corp, East Hanover, New Jersey) is caused by the downregulation of Akt kinase.	imatinib	138-155	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	89-93
18794444-1	2008	OBJECTIVE: To investigate whether the mechanism for the reversal of ABCG2 (also known as ABCP, MXR, and BCRP)-mediated drug resistance by imatinib mesylate (Gleevec, STI571; Novartis Pharmaceuticals Corp, East Hanover, New Jersey) is caused by the downregulation of Akt kinase.	imatinib	138-155	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	95-98
18794444-1	2008	OBJECTIVE: To investigate whether the mechanism for the reversal of ABCG2 (also known as ABCP, MXR, and BCRP)-mediated drug resistance by imatinib mesylate (Gleevec, STI571; Novartis Pharmaceuticals Corp, East Hanover, New Jersey) is caused by the downregulation of Akt kinase.	imatinib	138-155	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	104-108
18480468-10	2008	Ex vivo treatment of Kit+/+ uterine horns with imatinib resulted in a dose-dependent reduction of the frequency and amplitude of longitudinal myometrial contractions.	imatinib	47-55	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	21-24
18794444-1	2008	OBJECTIVE: To investigate whether the mechanism for the reversal of ABCG2 (also known as ABCP, MXR, and BCRP)-mediated drug resistance by imatinib mesylate (Gleevec, STI571; Novartis Pharmaceuticals Corp, East Hanover, New Jersey) is caused by the downregulation of Akt kinase.	imatinib	138-155	AKT serine/threonine kinase 1	Homo sapiens	266-269
18794444-3	2008	Recent studies show that imatinib reverses ABCG2-mediated drug resistance to topotecan hydrochloride and SN-38.	imatinib	25-33	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	43-48
18794444-4	2008	In addition, we have previously reported that imatinib downregulates Akt kinase activity, which is elevated in head and neck squamous cell carcinoma.	imatinib	46-54	AKT serine/threonine kinase 1	Homo sapiens	69-72
18794444-7	2008	Doxorubicin hydrochloride extrusion experiments also demonstrated 20% to 26% decrease in doxorubicin efflux on cells treated with imatinib, 1L6-hydroxymethyl-chiro-inositol 2-(R)-2-O-methyl-3-O-octadecylcarbonate, and transfection with siRNA Akt.	imatinib	130-138	AKT serine/threonine kinase 1	Homo sapiens	242-245
18794444-8	2008	With Western blot and immunofluorescence experiments, our data suggest that ABCG2 translocation is the mechanism by which imatinib and Akt regulate drug resistance.	imatinib	122-130	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	76-81
18794444-10	2008	CONCLUSION: Our findings demonstrate that imatinib confers greater doxorubicin retention, presumably via inhibition of Akt, which regulates ABCG2 function.	imatinib	42-50	AKT serine/threonine kinase 1	Homo sapiens	119-122
18794444-10	2008	CONCLUSION: Our findings demonstrate that imatinib confers greater doxorubicin retention, presumably via inhibition of Akt, which regulates ABCG2 function.	imatinib	42-50	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	140-145
18559370-3	2008	In the present study we investigated the therapeutic potential of the selective c-Abl inhibitor STI571 on both the intrahippocampal injection of Abeta(f) and APPsw/PSEN1DeltaE9 transgenic mice Alzheimer"s disease models.	imatinib	96-102	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	80-85
18567837-0	2008	Successful treatment of progressive cutaneous mastocytosis with imatinib in a 2-year-old boy carrying a somatic KIT mutation.	imatinib	64-72	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	112-115
18567837-3	2008	C-kit receptor mutations have been identified as causative for CM, some of which potentially respond to imatinib treatment as described for patients with systemic mastocytosis.	imatinib	104-112	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	2-5
18567837-5	2008	KIT gene analysis revealed not only a somatic deletion of codon 419 in exon 8 (c.1255_1257delGAC) which responds to imatinib therapy, but also a novel germ line p. Ser840Asn substitution encoded by exon 18 in the c-kit kinase domain.	imatinib	116-124	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
18004569-4	2008	RESULTS: Imatinib significantly inhibited F-ara-ATP accumulation in CD4(+) and CD8(+) T-lymphocytes in a concentration-dependent manner.	imatinib	9-17	CD4 molecule	Homo sapiens	68-71
18524988-0	2008	Multidrug resistance gene (MDR1) polymorphisms are associated with major molecular responses to standard-dose imatinib in chronic myeloid leukemia.	imatinib	110-118	ATP binding cassette subfamily B member 1	Homo sapiens	27-31
18524988-4	2008	We analyzed the 3 most relevant single nucleotide polymorphisms of MDR1 in 90 CML patients treated with imatinib.	imatinib	104-112	ATP binding cassette subfamily B member 1	Homo sapiens	67-71
18004569-4	2008	RESULTS: Imatinib significantly inhibited F-ara-ATP accumulation in CD4(+) and CD8(+) T-lymphocytes in a concentration-dependent manner.	imatinib	9-17	CD8a molecule	Homo sapiens	79-82
18559370-8	2008	Moreover, the intraperitoneal administration of STI571 rescued the cognitive decline in APPsw/PSEN1DeltaE9 mice, p73 phosphorylation, tau phosphorylation and caspase-3 activation in neurons around Abeta deposits.	imatinib	48-54	transformation related protein 73	Mus musculus	113-116
18004569-6	2008	The inhibition of F-ara-ATP by imatinib is likely due to inhibition of nucleoside transporters hENT1 and hENT2.	imatinib	31-39	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	95-100
18559370-8	2008	Moreover, the intraperitoneal administration of STI571 rescued the cognitive decline in APPsw/PSEN1DeltaE9 mice, p73 phosphorylation, tau phosphorylation and caspase-3 activation in neurons around Abeta deposits.	imatinib	48-54	caspase 3	Mus musculus	158-167
18004569-6	2008	The inhibition of F-ara-ATP by imatinib is likely due to inhibition of nucleoside transporters hENT1 and hENT2.	imatinib	31-39	solute carrier family 29 member 2	Homo sapiens	105-110
18559370-8	2008	Moreover, the intraperitoneal administration of STI571 rescued the cognitive decline in APPsw/PSEN1DeltaE9 mice, p73 phosphorylation, tau phosphorylation and caspase-3 activation in neurons around Abeta deposits.	imatinib	48-54	amyloid beta precursor protein	Homo sapiens	197-202
18573108-0	2008	Clinical imatinib mesylate treatment induces early normalisation of aberrant neutrophil leukotriene C4 synthase expression and activity in chronic myeloid leukaemia.	imatinib	9-26	leukotriene C4 synthase	Homo sapiens	88-111
18514495-1	2008	AIMS: Imatinib mesylate, a selective tyrosine kinase receptor inhibitor of KIT and PDGFRalpha, is currently licensed for the treatment of unresectable or metastatic gastrointestinal stromal tumours (GISTs), which are KIT positive.	imatinib	6-23	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	75-78
18757400-5	2008	Imatinib-mediated inhibition of BCR/ABL abrogated this effect, implicating a kinase-dependent mechanism.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
18757400-6	2008	Y253F, E255K, T315I, and H396P mutants of BCR/ABL that confer imatinib resistance also stimulated SSA.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
18641042-2	2008	BCR-ABL transcript levels decline over several years of imatinib treatment, and increasing numbers of patients have BCR-ABL transcripts at or below the limit of detection.	imatinib	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
18827790-5	2008	The degree of early reduction in BCR-ABL levels after commencing imatinib therapy is a good indicator of subsequent response.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
18514495-1	2008	AIMS: Imatinib mesylate, a selective tyrosine kinase receptor inhibitor of KIT and PDGFRalpha, is currently licensed for the treatment of unresectable or metastatic gastrointestinal stromal tumours (GISTs), which are KIT positive.	imatinib	6-23	platelet derived growth factor receptor alpha	Homo sapiens	83-93
18514495-1	2008	AIMS: Imatinib mesylate, a selective tyrosine kinase receptor inhibitor of KIT and PDGFRalpha, is currently licensed for the treatment of unresectable or metastatic gastrointestinal stromal tumours (GISTs), which are KIT positive.	imatinib	6-23	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	217-220
18781906-3	2008	Since CYP3A4 is the major isozyme involved in the metabolism of imatinib, we investigated the influence of EIAEDs on imatinib pharmacokinetics (pk).	imatinib	64-72	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	6-12
18998038-5	2008	Recently it has been shown that inhibiting PDGFR with imatinib can induce a high response rates in case of unresectable or metastatic disease.	imatinib	54-62	platelet derived growth factor receptor beta	Homo sapiens	43-48
18759691-1	2008	Treatment of chronic myeloid leukemia (CML) has changed drastically with the emergence of the Abl tyrosine kinase inhibitor (TKI), imatinib mesylate.	imatinib	131-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-97
18759691-3	2008	Point mutations within the Abl kinase domain that interfere with imatinib binding are the most critical cause of imatinib resistance.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-30
18759691-3	2008	Point mutations within the Abl kinase domain that interfere with imatinib binding are the most critical cause of imatinib resistance.	imatinib	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-30
18704194-8	2008	A dual inhibitor of PI3K and mTOR, PI-103, was more effective than rapamycin at suppressing proliferation of mouse pre-B-ALL and human CD19+CD34+)Ph+ ALL leukemia cells treated with the ABL kinase inhibitor imatinib.	imatinib	207-215	mechanistic target of rapamycin kinase	Mus musculus	29-33
18602920-0	2008	C-kit inhibition by imatinib mesylate attenuates progenitor cell expansion and inhibits liver tumor formation in mice.	imatinib	20-37	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	0-5
18602920-4	2008	Therefore, we hypothesized that the c-kit inhibitor imatinib mesylate (IM) would suppress LPC growth and, therefore, may exert antitumorigenic effects in the liver.	imatinib	52-69	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	36-41
18312355-4	2008	There are primary KIT or PDGFRA mutations diagnosed before imatinib treatment, linked to GIST pathogenesis, and secondary mutations detected during treatment, causing drug resistance.	imatinib	59-67	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	18-21
18312355-4	2008	There are primary KIT or PDGFRA mutations diagnosed before imatinib treatment, linked to GIST pathogenesis, and secondary mutations detected during treatment, causing drug resistance.	imatinib	59-67	platelet derived growth factor receptor alpha	Homo sapiens	25-31
18312355-7	2008	KIT exon 11 mutants respond well to imatinib.	imatinib	36-44	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
19097599-1	2008	Imatinib is a selective tyrosine kinase inhibitor which acts on breakpoint cluster region-Abelson fusion gene (BCR-ABL) positive leukemia including all phases of chronic myeloid leukemia and acute lymphoblastic leukemia.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
19097599-4	2008	We herein described an additional patient with BCR-ABL (ela2) positive acute lymphoblastic leukemia who developed tumor lysis syndrome after 10-day treatment with imatinib.	imatinib	163-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
19097599-4	2008	We herein described an additional patient with BCR-ABL (ela2) positive acute lymphoblastic leukemia who developed tumor lysis syndrome after 10-day treatment with imatinib.	imatinib	163-171	elastase, neutrophil expressed	Homo sapiens	56-60
18759727-8	2008	Up to 28% of patients may have to stop imatinib because of intolerance or disease resistance, mostly due to point mutations of BCR-ABL.	imatinib	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
18485676-1	2008	BACKGROUND: Imatinib mesylate has specific activity in inhibiting select tyrosine kinase receptors, including platelet-derived growth factor receptors (PDGFRs) and c-kit.	imatinib	12-29	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	164-169
18790751-7	2008	As structural mutations and/or gene amplification in Bcr-Abl can circumvent an otherwise potent anticancer drug such as imatinib, targeting Bcr-Abl expression as well as its kinase activity could be a novel additional therapeutic approach for the treatment of Bcr-Abl+ myeloid leukemia.	imatinib	120-128	BCR activator of RhoGEF and GTPase	Homo sapiens	53-56
18790751-7	2008	As structural mutations and/or gene amplification in Bcr-Abl can circumvent an otherwise potent anticancer drug such as imatinib, targeting Bcr-Abl expression as well as its kinase activity could be a novel additional therapeutic approach for the treatment of Bcr-Abl+ myeloid leukemia.	imatinib	120-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
18477770-1	2008	Although imatinib, a BCR-ABL tyrosine kinase inhibitor, is used to treat acute Philadelphia chromosome-positive (Ph(+)) leukemia, it does not prevent central nervous system (CNS) relapses resulting from poor drug penetration through the blood-brain barrier.	imatinib	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
18506689-0	2008	KIT overexpression induces proliferation in astrocytes in an imatinib-responsive manner and associates with proliferation index in gliomas.	imatinib	61-69	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	0-3
18492696-8	2008	CONCLUSIONS: The data demonstrated significant expression of PDGFR targets of imatinib mesylate in GCTs, whereas normal ovarian tissues had a complete absence of staining.This expression profile provides the rationale to investigate the role of imatinib mesylate in PDGFR-positive GCTs.	imatinib	78-95	platelet derived growth factor receptor beta	Homo sapiens	61-66
18492696-8	2008	CONCLUSIONS: The data demonstrated significant expression of PDGFR targets of imatinib mesylate in GCTs, whereas normal ovarian tissues had a complete absence of staining.This expression profile provides the rationale to investigate the role of imatinib mesylate in PDGFR-positive GCTs.	imatinib	78-95	platelet derived growth factor receptor beta	Homo sapiens	266-271
18492696-8	2008	CONCLUSIONS: The data demonstrated significant expression of PDGFR targets of imatinib mesylate in GCTs, whereas normal ovarian tissues had a complete absence of staining.This expression profile provides the rationale to investigate the role of imatinib mesylate in PDGFR-positive GCTs.	imatinib	78-86	platelet derived growth factor receptor beta	Homo sapiens	61-66
18492696-8	2008	CONCLUSIONS: The data demonstrated significant expression of PDGFR targets of imatinib mesylate in GCTs, whereas normal ovarian tissues had a complete absence of staining.This expression profile provides the rationale to investigate the role of imatinib mesylate in PDGFR-positive GCTs.	imatinib	78-86	platelet derived growth factor receptor beta	Homo sapiens	266-271
18506689-8	2008	Our results indicate that overexpression of KIT in mouse astrocytes promotes cell proliferation, and the increased proliferation is partly inhibited by imatinib treatment.	imatinib	152-160	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	44-47
18427551-4	2008	Upon stimulation with NGF, Erk and Akt are phosphorylated to a much greater degree in imatinib-treated cells than in untreated cells.	imatinib	86-94	nerve growth factor	Rattus norvegicus	22-25
18618737-15	2008	CONCLUSIONS: The combination imatinib and docetaxel was tolerated in patients with heavily pretreated EOC that expressed c-kit or PDGFRalpha.	imatinib	29-37	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	121-126
18618737-15	2008	CONCLUSIONS: The combination imatinib and docetaxel was tolerated in patients with heavily pretreated EOC that expressed c-kit or PDGFRalpha.	imatinib	29-37	platelet derived growth factor receptor alpha	Homo sapiens	130-140
18427551-4	2008	Upon stimulation with NGF, Erk and Akt are phosphorylated to a much greater degree in imatinib-treated cells than in untreated cells.	imatinib	86-94	Eph receptor B1	Rattus norvegicus	27-30
18427551-4	2008	Upon stimulation with NGF, Erk and Akt are phosphorylated to a much greater degree in imatinib-treated cells than in untreated cells.	imatinib	86-94	AKT serine/threonine kinase 1	Rattus norvegicus	35-38
18427551-6	2008	Imatinib treatment also enhanced NGF signaling in rat adrenal pheochromocytoma cell line PC12 that expresses TrkA and c-Abl, suggesting that it is not only restoration of responsiveness to NGF after blocking oncoprotein activity, but also c-Abl tyrosine kinase per se may be a negative regulator of growth factor signaling.	imatinib	0-8	nerve growth factor	Rattus norvegicus	33-36
18427551-6	2008	Imatinib treatment also enhanced NGF signaling in rat adrenal pheochromocytoma cell line PC12 that expresses TrkA and c-Abl, suggesting that it is not only restoration of responsiveness to NGF after blocking oncoprotein activity, but also c-Abl tyrosine kinase per se may be a negative regulator of growth factor signaling.	imatinib	0-8	neurotrophic receptor tyrosine kinase 1	Rattus norvegicus	109-113
18427551-6	2008	Imatinib treatment also enhanced NGF signaling in rat adrenal pheochromocytoma cell line PC12 that expresses TrkA and c-Abl, suggesting that it is not only restoration of responsiveness to NGF after blocking oncoprotein activity, but also c-Abl tyrosine kinase per se may be a negative regulator of growth factor signaling.	imatinib	0-8	nerve growth factor	Rattus norvegicus	189-192
18427551-9	2008	We found that NGF treatment induces cell survival in imatinib-treated CML cell lines, as well as colony formation of primary CD34+ CML cells, strongly suggesting that NGF/TrkA signaling contributes to aberrant signaling in CML.	imatinib	53-61	nerve growth factor	Rattus norvegicus	14-17
18427551-9	2008	We found that NGF treatment induces cell survival in imatinib-treated CML cell lines, as well as colony formation of primary CD34+ CML cells, strongly suggesting that NGF/TrkA signaling contributes to aberrant signaling in CML.	imatinib	53-61	neurotrophic receptor tyrosine kinase 1	Rattus norvegicus	171-175
18668566-0	2008	Smad1 pathway is activated in systemic sclerosis fibroblasts and is targeted by imatinib mesylate.	imatinib	80-97	SMAD family member 1	Homo sapiens	0-5
18668566-10	2008	Imatinib mesylate blocked activation of the Smad1 pathway in transforming growth factor beta-stimulated control fibroblasts and reversed activation of this pathway in SSc fibroblasts.	imatinib	0-17	SMAD family member 1	Homo sapiens	44-49
18668587-8	2008	Skin biopsies performed both before and after initial dosing of that patient revealed less fibrosis and less staining for type I procollagen after imatinib mesylate treatment, but essentially unchanged tissue gadolinium content.	imatinib	147-164	collagen type I alpha 2 chain	Homo sapiens	122-140
18668566-13	2008	Demonstration that the Smad1/CCN2 pathway is blocked by imatinib mesylate further clarifies the mechanism of the antifibrotic effects of this compound.	imatinib	56-73	SMAD family member 1	Homo sapiens	23-28
18668566-13	2008	Demonstration that the Smad1/CCN2 pathway is blocked by imatinib mesylate further clarifies the mechanism of the antifibrotic effects of this compound.	imatinib	56-73	cellular communication network factor 2	Homo sapiens	29-33
18668566-14	2008	This study suggests that SSc patients with activated Smad1 signaling may benefit from imatinib mesylate treatment.	imatinib	86-94	SMAD family member 1	Homo sapiens	53-58
18830516-7	2008	Patients on imatinib who cease responding may have mutations on their ABL gene.	imatinib	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-73
18422767-2	2008	Importantly, the resulting gene fusions can serve as specific therapeutic targets, as exemplified by the development of imatinib (Gleevec), which specifically inhibits the BCR-ABL gene fusion product that defines chronic myeloid leukaemia.	imatinib	120-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-179
18656692-5	2008	The cell line expressed ETV6/ABL1 fusion transcripts and displayed sensitivity to imatinib with an IC(50) of 0.1 microM.	imatinib	82-90	ETS variant transcription factor 6	Homo sapiens	24-28
18656692-5	2008	The cell line expressed ETV6/ABL1 fusion transcripts and displayed sensitivity to imatinib with an IC(50) of 0.1 microM.	imatinib	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-33
18808562-3	2008	Imatinib has been reported previously to be useful for treatment of hypereosinophilic syndrome and may work by selectively blocking protein-tyrosine kinases, such as platelet-derived growth factor receptor, and c-Kit.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	211-216
18665830-0	2008	Different kinetic patterns of BCR-ABL transcript levels in imatinib-treated chronic myeloid leukemia patients after achieving complete cytogenetic response.	imatinib	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
18665830-1	2008	Bone marrow BCR-ABL transcript levels were monitored serially by real-time quantitative PCR in 46 imatinib-treated chronic myeloid leukemia patients after achieving complete cytogenetic response (CCyR) for a median of 42 months (range: 9-53).	imatinib	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
18480061-3	2008	Instead, we discovered that disrupting c-Abl activity using STI571 (Gleevec, a c-Abl inhibitor) or stable c-Abl knockdown abolished MMR-dependent p73alpha stabilization, induction of GADD45alpha protein expression, and G(2) arrest.	imatinib	60-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-44
18305564-0	2008	Successful peripheral blood stem cell mobilization with granulocyte colony-stimulating factor in a patient with chronic myeloid leukemia achieving a complete cytogenetic remission with dasatinib after failing imatinib.	imatinib	209-217	colony stimulating factor 3	Homo sapiens	56-93
18670317-3	2008	Imatinib mesylate is a tyrosine kinase inhibitor targeting the platelet-derived growth factor (PDGFR-alpha and PDGFR-beta), the BCR-ABL, and c-KIT receptors.	imatinib	0-17	platelet derived growth factor receptor alpha	Homo sapiens	95-106
18670317-3	2008	Imatinib mesylate is a tyrosine kinase inhibitor targeting the platelet-derived growth factor (PDGFR-alpha and PDGFR-beta), the BCR-ABL, and c-KIT receptors.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	111-121
18670317-3	2008	Imatinib mesylate is a tyrosine kinase inhibitor targeting the platelet-derived growth factor (PDGFR-alpha and PDGFR-beta), the BCR-ABL, and c-KIT receptors.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	141-146
18670317-7	2008	Treatment with imatinib should be considered for patients with recurrent or unresectable MSFTs with PDGFR expression.	imatinib	15-23	platelet derived growth factor receptor beta	Homo sapiens	100-105
18282599-5	2008	Imatinib mesylate, a tyrosine kinase inhibitor that can target the M-CSF receptor, also prevented the effect of CM.	imatinib	0-17	colony stimulating factor 1	Homo sapiens	67-72
18472395-1	2008	Imatinib mesylate (Glivec, STI 571; Novartis), a small-molecular analog of ATP that potently inhibits the tyrosine kinase activities of Bcr-Abl, PDGFR-alpha, PDGFR-beta, c-Fms, Arg and c-kit, is one of the novel molecularly targeted agents being introduced into cancer therapy.	imatinib	0-17	platelet derived growth factor receptor alpha	Rattus norvegicus	145-156
18510589-0	2008	Dose-dependent, complete response to imatinib of a metastatic mucosal melanoma with a K642E KIT mutation.	imatinib	37-45	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	92-95
18626307-1	2008	Response to treatment with imatinib mesylate has been associated in preclinical models with the inhibition of two signaling pathways that promote cellular survival - the phosphatidylinositol 3-kinase/AKT pathway and the mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) pathway.	imatinib	27-44	AKT serine/threonine kinase 1	Homo sapiens	200-203
18626307-1	2008	Response to treatment with imatinib mesylate has been associated in preclinical models with the inhibition of two signaling pathways that promote cellular survival - the phosphatidylinositol 3-kinase/AKT pathway and the mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) pathway.	imatinib	27-44	mitogen-activated protein kinase 3	Homo sapiens	292-295
18626307-8	2008	A better understanding of the AKT and mitogen-activated protein kinase pathways is needed to optimize the clinical benefit of targeted therapy, such as imatinib.	imatinib	152-160	AKT serine/threonine kinase 1	Homo sapiens	30-33
18780518-1	2008	UNLABELLED: Imatinib is a tyrosine kinase inhibitor, which selectively antagonises the BCR-ABL molecular pathway which causes chronic myeloid leukaemia (CML).	imatinib	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
18472395-1	2008	Imatinib mesylate (Glivec, STI 571; Novartis), a small-molecular analog of ATP that potently inhibits the tyrosine kinase activities of Bcr-Abl, PDGFR-alpha, PDGFR-beta, c-Fms, Arg and c-kit, is one of the novel molecularly targeted agents being introduced into cancer therapy.	imatinib	0-17	platelet derived growth factor receptor beta	Rattus norvegicus	158-168
18472395-1	2008	Imatinib mesylate (Glivec, STI 571; Novartis), a small-molecular analog of ATP that potently inhibits the tyrosine kinase activities of Bcr-Abl, PDGFR-alpha, PDGFR-beta, c-Fms, Arg and c-kit, is one of the novel molecularly targeted agents being introduced into cancer therapy.	imatinib	0-17	colony stimulating factor 1 receptor	Rattus norvegicus	170-175
18628477-3	2008	Slug expression, inhibited by imatinib mesylate treatment, was knocked down in neuroblastoma cells by RNA interference, and the effects on invasion and apoptosis were evaluated in vitro.	imatinib	30-47	snail family transcriptional repressor 2	Homo sapiens	0-4
18718048-3	2008	The results indicated that after being cultured with 2.5 micromol/L imatinib mesylate for 0.5, 2, 6, 24 and 48 hours, the intensions of inhibiting SphK-1 activity were 0.007%, 38.9%, 34.6%, 28.1% and 76.1% resepectively.	imatinib	68-85	sphingosine kinase 1	Homo sapiens	147-153
18718048-4	2008	SphK-1 activity in CML cells also was reduced by 2.5 micromol/L imatinib mesylate (16.8% - 41.9% decrease).	imatinib	64-81	sphingosine kinase 1	Homo sapiens	0-6
18628477-12	2008	Animals injected with Slug-silenced cells had fewer tumors than controls and the inhibition of tumor growth was even higher in animals treated with imatinib mesylate.	imatinib	148-165	snail family transcriptional repressor 2	Homo sapiens	22-26
18234489-5	2008	Certain specific mutations in an exon (such as in exon 9) of the KIT gene result in GISTs that are relatively unresponsive to the Imatinib treatment.	imatinib	130-138	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	65-68
18602021-8	2008	Results obtained from these experiments indicate that STI571 decreases the efficacy of NER in leukemic cells expressing BCR/ABL.	imatinib	54-60	BCR activator of RhoGEF and GTPase	Mus musculus	120-127
18628453-2	2008	Mutations within the kinase domain of BCR-ABL1 constitute the most frequent mechanism of resistance in patients with chronic myelogenous leukemia treated with imatinib or the second generation tyrosine kinase inhibitors nilotinib and dasatinib.	imatinib	159-167	BCR activator of RhoGEF and GTPase	Homo sapiens	38-46
18628477-5	2008	RESULTS: Microarray analysis revealed that several genes, including Slug, were down-regulated by imatinib mesylate.	imatinib	97-114	snail family transcriptional repressor 2	Homo sapiens	68-72
18628477-10	2008	Slug down-regulation increased sensitivity to apoptosis induced by imatinib mesylate, etoposide, or doxorubicin.	imatinib	67-84	snail family transcriptional repressor 2	Homo sapiens	0-4
18718191-1	2008	Imatinib mesylate, a tyrosine kinase inhibitor targeting the Bcr-Abl protein, c-kit (KIT) and the platelet-derived growth factor receptors (PDGFR), is an important part of the therapeutic armamentarium used in chronic myelogenous leukemia and gastrointestinal stromal tumors.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
18632627-5	2008	Pharmacologic studies showed the KIT/CDK4-overexpressing subgroup to be resistant to BRAF inhibitors but sensitive to imatinib in both in vitro and in vivo melanoma models.	imatinib	118-126	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	33-36
18632627-5	2008	Pharmacologic studies showed the KIT/CDK4-overexpressing subgroup to be resistant to BRAF inhibitors but sensitive to imatinib in both in vitro and in vivo melanoma models.	imatinib	118-126	cyclin dependent kinase 4	Homo sapiens	37-41
18632627-6	2008	Mechanistically, imatinib treatment led to increased apoptosis and G(1) phase cell cycle arrest associated with the inhibition of phospho-ERK and increased expression of p27(KIP).	imatinib	17-25	interferon alpha inducible protein 27	Homo sapiens	170-173
18718191-1	2008	Imatinib mesylate, a tyrosine kinase inhibitor targeting the Bcr-Abl protein, c-kit (KIT) and the platelet-derived growth factor receptors (PDGFR), is an important part of the therapeutic armamentarium used in chronic myelogenous leukemia and gastrointestinal stromal tumors.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	78-83
18718191-1	2008	Imatinib mesylate, a tyrosine kinase inhibitor targeting the Bcr-Abl protein, c-kit (KIT) and the platelet-derived growth factor receptors (PDGFR), is an important part of the therapeutic armamentarium used in chronic myelogenous leukemia and gastrointestinal stromal tumors.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	85-88
18718191-1	2008	Imatinib mesylate, a tyrosine kinase inhibitor targeting the Bcr-Abl protein, c-kit (KIT) and the platelet-derived growth factor receptors (PDGFR), is an important part of the therapeutic armamentarium used in chronic myelogenous leukemia and gastrointestinal stromal tumors.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	98-138
18718191-1	2008	Imatinib mesylate, a tyrosine kinase inhibitor targeting the Bcr-Abl protein, c-kit (KIT) and the platelet-derived growth factor receptors (PDGFR), is an important part of the therapeutic armamentarium used in chronic myelogenous leukemia and gastrointestinal stromal tumors.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	140-145
18374481-4	2008	Of note, galangin caused a decrease in Bcl-2 levels and markedly increased the apoptotic activity of imatinib both in sensitive or imatinib-resistant Bcr-Abl+ cell lines.	imatinib	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
18612408-5	2008	In addition, AQP5 expression level increased with the emergence of imatinib mesylate resistance in paired samples (p = 0.047).	imatinib	67-75	aquaporin 5	Homo sapiens	13-17
18612157-9	2008	At least one target of imatinib (KIT, PDGFR-alpha, or PDGFR-beta) was expressed in all tumors, and most tumors expressed all three receptors.	imatinib	23-31	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	33-36
18612157-9	2008	At least one target of imatinib (KIT, PDGFR-alpha, or PDGFR-beta) was expressed in all tumors, and most tumors expressed all three receptors.	imatinib	23-31	platelet derived growth factor receptor alpha	Homo sapiens	38-49
18612157-9	2008	At least one target of imatinib (KIT, PDGFR-alpha, or PDGFR-beta) was expressed in all tumors, and most tumors expressed all three receptors.	imatinib	23-31	platelet derived growth factor receptor beta	Homo sapiens	54-64
18374481-0	2008	Galangin increases the cytotoxic activity of imatinib mesylate in imatinib-sensitive and imatinib-resistant Bcr-Abl expressing leukemia cells.	imatinib	45-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
18374481-0	2008	Galangin increases the cytotoxic activity of imatinib mesylate in imatinib-sensitive and imatinib-resistant Bcr-Abl expressing leukemia cells.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
18374481-1	2008	Resistance to imatinib mesylate is an emergent problem in the treatment of Bcr-Abl expressing myelogenous leukemias and additional therapeutic strategies are required.	imatinib	14-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
18420966-5	2008	The effects of imatinib on PDGF-B-induced proliferation and chemotaxis were tested on human PASMCs.	imatinib	15-23	platelet derived growth factor subunit B	Homo sapiens	27-33
18577744-0	2008	Persistent LYN signaling in imatinib-resistant, BCR-ABL-independent chronic myelogenous leukemia.	imatinib	28-36	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	11-14
18577747-0	2008	Association between imatinib-resistant BCR-ABL mutation-negative leukemia and persistent activation of LYN kinase.	imatinib	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
18577747-0	2008	Association between imatinib-resistant BCR-ABL mutation-negative leukemia and persistent activation of LYN kinase.	imatinib	20-28	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	103-106
18577747-2	2008	BCR-ABL mutations are associated with failure of imatinib treatment in many CML patients.	imatinib	49-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
18577747-3	2008	LYN kinase regulates survival and responsiveness of CML cells to inhibition of BCR-ABL kinase, and differences in LYN regulation have been found between imatinib-sensitive and -resistant CML cell lines.	imatinib	153-161	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	114-117
18577747-9	2008	RESULTS: Imatinib treatment suppressed LYN phosphorylation in cells from imatinib-sensitive CML patients and imatinib-sensitive cell lines.	imatinib	9-17	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	39-42
18577747-9	2008	RESULTS: Imatinib treatment suppressed LYN phosphorylation in cells from imatinib-sensitive CML patients and imatinib-sensitive cell lines.	imatinib	73-81	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	39-42
18577747-10	2008	Imatinib treatment blocked BCR-ABL signaling but did not suppress LYN phosphorylation in cells from imatinib-resistant patients, and persistent activation of LYN kinase was not associated with mutations in LYN kinase or its carboxyl-terminal regulatory domains.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
18577747-11	2008	Unique LYN phosphorylation sites (tyrosine-193 and tyrosine-459) and associated proteins (c-Cbl and p80) were identified in cells from imatinib-resistant patients.	imatinib	135-143	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	7-10
18577747-11	2008	Unique LYN phosphorylation sites (tyrosine-193 and tyrosine-459) and associated proteins (c-Cbl and p80) were identified in cells from imatinib-resistant patients.	imatinib	135-143	Cbl proto-oncogene	Homo sapiens	90-95
18577747-11	2008	Unique LYN phosphorylation sites (tyrosine-193 and tyrosine-459) and associated proteins (c-Cbl and p80) were identified in cells from imatinib-resistant patients.	imatinib	135-143	coilin	Homo sapiens	100-103
18577747-12	2008	Reducing LYN expression (siRNA) or activation (dasatinib) was associated with loss of cell survival and cytogenetic or complete hematologic responses in imatinib-resistant disease.	imatinib	153-161	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	9-12
18577747-13	2008	CONCLUSIONS: LYN activation was independent of BCR-ABL in cells from imatinib-resistant patients.	imatinib	69-77	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	13-16
18577747-14	2008	Thus, LYN kinase may be involved in imatinib resistance in CML patients with mutation-negative BCR-ABL and its direct inhibition is consistent with clinical responses in these patients.	imatinib	36-44	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	6-9
18577747-14	2008	Thus, LYN kinase may be involved in imatinib resistance in CML patients with mutation-negative BCR-ABL and its direct inhibition is consistent with clinical responses in these patients.	imatinib	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
18751412-1	2008	The case of a young man with stage IV chemoresistant pure seminoma overexpressing KIT, who achieved complete remission (CR) after the administration of imatinib mesylate (400 mg once daily), along with a third-line chemotherapy regimen, consisting of paclitaxel (150 mg/m2), oxaliplatin (100 mg/m2) and gemcitabine (800 mg/m2) every 2 weeks with granulocyte colony-stimulating factor (G-CSF) support is reported.	imatinib	152-169	colony stimulating factor 3	Homo sapiens	346-383
18525320-0	2008	Decrease of CD117 expression as possible prognostic marker for recurrence in the resected specimen after imatinib treatment in patients with initially unresectable gastrointestinal stromal tumors: a clinicopathological analysis.	imatinib	105-113	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	12-17
18525320-16	2008	Loss or decrease of CD117 expression in the resected specimen after imatinib treatment may be associated with disease recurrence.	imatinib	68-76	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	20-25
18751412-1	2008	The case of a young man with stage IV chemoresistant pure seminoma overexpressing KIT, who achieved complete remission (CR) after the administration of imatinib mesylate (400 mg once daily), along with a third-line chemotherapy regimen, consisting of paclitaxel (150 mg/m2), oxaliplatin (100 mg/m2) and gemcitabine (800 mg/m2) every 2 weeks with granulocyte colony-stimulating factor (G-CSF) support is reported.	imatinib	152-169	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	82-85
18066563-8	2008	Correct diagnosis is essential for proper management since GISTs specifically respond to the c-kit selective tyrosine kinase inhibitor, Imatinib mesylate.	imatinib	136-153	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	93-98
18751412-1	2008	The case of a young man with stage IV chemoresistant pure seminoma overexpressing KIT, who achieved complete remission (CR) after the administration of imatinib mesylate (400 mg once daily), along with a third-line chemotherapy regimen, consisting of paclitaxel (150 mg/m2), oxaliplatin (100 mg/m2) and gemcitabine (800 mg/m2) every 2 weeks with granulocyte colony-stimulating factor (G-CSF) support is reported.	imatinib	152-169	colony stimulating factor 3	Homo sapiens	385-390
18778561-2	2008	Imatinib provides targeted therapy for GIST by inhibiting the KIT and PDGFR-alpha tyrosine kinases.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	62-65
18540942-2	2008	The BCR/ABL kinase inhibitor imatinib is an effective agent in most patients and can now be regarded as front-line therapy.	imatinib	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
18540942-4	2008	While CML stem cells display primary resistance, stem cell subclones may, in addition, acquire imatinib-resistant mutants of BCR/ABL.	imatinib	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
18548219-1	2008	Imatinib is a tyrosine kinase inhibitor directed against the KIT and the PDGF-alpha receptors.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	61-64
18407462-6	2008	In addition, Wnt5a increased the nuclear beta-catenin level and treatment with imatinib or ionomycin, either of which blocks the beta-catenin pathway, reduced the anti-apoptotic activity of Wnt5a, together suggesting the simultaneous involvement of the beta-catenin-mediated pathway in the Wnt5a anti-apoptotic activity.	imatinib	79-87	catenin beta 1	Homo sapiens	129-141
18407462-6	2008	In addition, Wnt5a increased the nuclear beta-catenin level and treatment with imatinib or ionomycin, either of which blocks the beta-catenin pathway, reduced the anti-apoptotic activity of Wnt5a, together suggesting the simultaneous involvement of the beta-catenin-mediated pathway in the Wnt5a anti-apoptotic activity.	imatinib	79-87	Wnt family member 5A	Homo sapiens	190-195
18407462-6	2008	In addition, Wnt5a increased the nuclear beta-catenin level and treatment with imatinib or ionomycin, either of which blocks the beta-catenin pathway, reduced the anti-apoptotic activity of Wnt5a, together suggesting the simultaneous involvement of the beta-catenin-mediated pathway in the Wnt5a anti-apoptotic activity.	imatinib	79-87	catenin beta 1	Homo sapiens	129-141
18407462-6	2008	In addition, Wnt5a increased the nuclear beta-catenin level and treatment with imatinib or ionomycin, either of which blocks the beta-catenin pathway, reduced the anti-apoptotic activity of Wnt5a, together suggesting the simultaneous involvement of the beta-catenin-mediated pathway in the Wnt5a anti-apoptotic activity.	imatinib	79-87	Wnt family member 5A	Homo sapiens	190-195
18525340-1	2008	PURPOSE OF REVIEW: Gastrointestinal stromal tumour patients with exon 9 KIT mutations have a worse outcome, but progression-free survival is improved by treatment with imatinib 800 mg daily.	imatinib	168-176	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	72-75
18778561-4	2008	The mechanisms of acquired resistance to imatinib are heterogeneous, with most involving the emergence of secondary mutations in KIT exons 13, 14, or 17.	imatinib	41-49	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	129-132
18525340-8	2008	Patients with mutations in exon 9 of KIT should be considered for treatment with imatinib 800 mg daily, but current data do not indicate whether there is a survival advantage for immediate treatment at 800 mg.	imatinib	81-89	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	37-40
18452076-2	2008	New challenges have emerged with respect to induction of resistance to imatinib via ABL mutations.	imatinib	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-87
17983688-3	2008	Selectivity hereby seems to be conserved, as shown by the lack of activity on FLT3, a closely related class III receptor tyrosine kinase, which is not affected by the parent compound Imatinib.	imatinib	183-191	fms related receptor tyrosine kinase 3	Homo sapiens	78-82
18541900-1	2008	PURPOSE: Dasatinib is a BCR-ABL inhibitor, 325-fold more potent than imatinib against unmutated BCR-ABL in vitro.	imatinib	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
18061664-1	2008	Imatinib mesylate is a selective inhibitor of the bcr/abl, c-kit and PDGF receptor tyrosine kinases.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
18061664-1	2008	Imatinib mesylate is a selective inhibitor of the bcr/abl, c-kit and PDGF receptor tyrosine kinases.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	59-64
18549340-6	2008	RESULTS/CONCLUSION: The development of imatinib-resistant mutations in the FIP1L1-PDGFR-alpha kinase domain has spurred the development of an array of new tyrosine kinase inhibitors.	imatinib	39-47	factor interacting with PAPOLA and CPSF1	Homo sapiens	75-81
18549340-6	2008	RESULTS/CONCLUSION: The development of imatinib-resistant mutations in the FIP1L1-PDGFR-alpha kinase domain has spurred the development of an array of new tyrosine kinase inhibitors.	imatinib	39-47	platelet derived growth factor receptor alpha	Homo sapiens	82-93
18554156-2	2008	The first kinase inhibitor, imatinib mesilate (Gleevec, Novartis), came to market in 2001, an inhibitor of the breakpoint cluster region (BCR)/Abelson murine leukemia oncogene homolog (ABL) fusion, platelet-derived growth factor (PDGF) receptor, and c-kit kinases.	imatinib	28-45	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	143-175
18554156-2	2008	The first kinase inhibitor, imatinib mesilate (Gleevec, Novartis), came to market in 2001, an inhibitor of the breakpoint cluster region (BCR)/Abelson murine leukemia oncogene homolog (ABL) fusion, platelet-derived growth factor (PDGF) receptor, and c-kit kinases.	imatinib	28-45	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	185-188
18587017-1	2008	A significant minority of chronic myeloid leukaemia patients eventually develop resistance to imatinib, often as a result of point mutations within the BCR-ABL kinase domain.	imatinib	94-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-159
18587017-2	2008	Second-line tyrosine kinase inhibitors (TKIs) are effective against mutations that confer imatinib resistance; however, the T315I BCR-ABL mutant has proved resistant to all available TKIs.	imatinib	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
18564222-4	2008	HYPOTHESIS: Imatinib mesylate has activity against MCT in dogs, and response to treatment can be correlated to presence of mutation within exon 11 of c-kit.	imatinib	12-29	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	150-155
18564225-9	2008	Imatinib was administered if tumor-associated tyrosine kinase KIT was aberrant.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	62-65
18528425-4	2008	TKs are excellent drug targets as exemplified by the activity of imatinib in BCR-ABL1-positive disease, particularly chronic myeloid leukemia.	imatinib	65-73	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	81-85
18528425-5	2008	Resistance to imatinib is seen in a minority of cases and is often associated with the appearance of secondary point mutations within the TK domain of BCR-ABL1.	imatinib	14-22	BCR activator of RhoGEF and GTPase	Mus musculus	151-159
18548107-3	2008	BTK has been implicated in Bcr-Abl-mediated B-cell transformation and resistance to imatinib, implying that inhibiting BTK may be therapeutically beneficial.	imatinib	84-92	Bruton agammaglobulinemia tyrosine kinase	Mus musculus	0-3
18548107-3	2008	BTK has been implicated in Bcr-Abl-mediated B-cell transformation and resistance to imatinib, implying that inhibiting BTK may be therapeutically beneficial.	imatinib	84-92	Bruton agammaglobulinemia tyrosine kinase	Mus musculus	119-122
18548107-4	2008	We decided to test whether BTK is a critical node in Bcr-Abl transformation and potential drug target in imatinib-resistant Bcr-Abl-positive cells.	imatinib	105-113	Bruton agammaglobulinemia tyrosine kinase	Mus musculus	27-30
18346844-0	2008	MEK inhibitor enhances the inhibitory effect of imatinib on pancreatic cancer cell growth.	imatinib	48-56	mitogen-activated protein kinase kinase 7	Homo sapiens	0-3
18568034-5	2008	These effects are mediated through activation of PDGF-alpha receptors (PDGFR-alpha) on perivascular astrocytes, and treatment of mice with the PDGFR-alpha antagonist imatinib after ischemic stroke reduces both cerebrovascular permeability and hemorrhagic complications associated with late administration of thrombolytic tPA.	imatinib	166-174	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	71-82
18568034-5	2008	These effects are mediated through activation of PDGF-alpha receptors (PDGFR-alpha) on perivascular astrocytes, and treatment of mice with the PDGFR-alpha antagonist imatinib after ischemic stroke reduces both cerebrovascular permeability and hemorrhagic complications associated with late administration of thrombolytic tPA.	imatinib	166-174	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	143-154
18346844-1	2008	Imatinib mesylate (imatinib) inhibits the c-Kit-dependent tyrosine kinase activities and highly effective in the treatment of CML and GIST patients.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	42-47
18246120-1	2008	Bcr-Abl oncogene is responsible for the initial phase of chronic myelogenous leukemia (CML), which is effectively treated by the Bcr-Abl inhibitor imatinib.	imatinib	147-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
18346844-1	2008	Imatinib mesylate (imatinib) inhibits the c-Kit-dependent tyrosine kinase activities and highly effective in the treatment of CML and GIST patients.	imatinib	19-27	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	42-47
18246120-1	2008	Bcr-Abl oncogene is responsible for the initial phase of chronic myelogenous leukemia (CML), which is effectively treated by the Bcr-Abl inhibitor imatinib.	imatinib	147-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
18346844-6	2008	Western blot analysis demonstrated that 5 microM imatinib treatment for 1h activated the MEK-MAPK pathway and the activation was independent of Ras activation.	imatinib	49-57	mitogen-activated protein kinase kinase 7	Homo sapiens	89-92
18346844-7	2008	Administration of 5 microM imatinib and 1 microM U0126 (MEK inhibitor) significantly suppressed pancreatic cell growth.	imatinib	27-35	mitogen-activated protein kinase kinase 7	Homo sapiens	56-59
18550829-10	2008	We also demonstrate that the aberrant expression of IGF1R may be associated with oncogenesis in WT GISTs and suggest an alternative and/or complementary therapeutic regimen in the clinical management of all GISTs, especially in a subset of tumors that respond less favorably to imatinib-based therapy.	imatinib	278-286	insulin like growth factor 1 receptor	Homo sapiens	52-57
18366061-0	2008	Targeting of the N-terminal coiled coil oligomerization interface by a helix-2 peptide inhibits unmutated and imatinib-resistant BCR/ABL.	imatinib	110-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
18559609-4	2008	EXPERIMENTAL DESIGN: The effect of OCT inhibitors on [14C]dasatinib and [14C]imatinib IUR was compared using peripheral blood mononuclear cells from newly diagnosed CML patients.	imatinib	77-85	plexin A2	Homo sapiens	35-38
18559609-8	2008	Patients with high OCT-1 activity based on their imatinib uptake had IC50(dasatinib) values equivalent to patients with low OCT-1 activity.	imatinib	49-57	solute carrier family 22 member 1	Homo sapiens	19-24
18559609-1	2008	PURPOSE: The organic cation transporter OCT-1 mediates active transport of imatinib.	imatinib	75-83	solute carrier family 22 member 1	Homo sapiens	40-45
18559609-2	2008	We recently showed that low OCT-1 activity is a major contributor to suboptimal response in chronic myeloid leukemia (CML) patients treated with imatinib.	imatinib	145-153	solute carrier family 22 member 1	Homo sapiens	28-33
18366061-3	2008	The treatment of advanced Ph+ leukemia with selective ABL-kinase inhibitors such as Imatinib, Nilotinib and Dasatinib is initially effective but rapidly followed by resistance mainly because of specific mutations in BCR/ABL.	imatinib	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-57
18366061-3	2008	The treatment of advanced Ph+ leukemia with selective ABL-kinase inhibitors such as Imatinib, Nilotinib and Dasatinib is initially effective but rapidly followed by resistance mainly because of specific mutations in BCR/ABL.	imatinib	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	216-223
18366061-5	2008	Targeting the CC-domain forces BCR/ABL into a monomeric conformation reduces its kinase activity and increases the sensitivity for Imatinib.	imatinib	131-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
18366061-6	2008	We show that (i) targeting the tetramerization by a peptide representing the Helix-2 of the CC efficiently reduced the autophosphorylation of both unmutated and mutated BCR/ABL; (ii) Helix-2 inhibited the transformation potential of BCR/ABL independently of the presence of mutations; and (iii) Helix-2 efficiently cooperated with Imatinib as revealed by their effects on the transformation potential and the factor-independence related to BCR/ABL with the exception of mutant T315I.	imatinib	331-339	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	169-176
18366061-6	2008	We show that (i) targeting the tetramerization by a peptide representing the Helix-2 of the CC efficiently reduced the autophosphorylation of both unmutated and mutated BCR/ABL; (ii) Helix-2 inhibited the transformation potential of BCR/ABL independently of the presence of mutations; and (iii) Helix-2 efficiently cooperated with Imatinib as revealed by their effects on the transformation potential and the factor-independence related to BCR/ABL with the exception of mutant T315I.	imatinib	331-339	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	233-240
18366061-6	2008	We show that (i) targeting the tetramerization by a peptide representing the Helix-2 of the CC efficiently reduced the autophosphorylation of both unmutated and mutated BCR/ABL; (ii) Helix-2 inhibited the transformation potential of BCR/ABL independently of the presence of mutations; and (iii) Helix-2 efficiently cooperated with Imatinib as revealed by their effects on the transformation potential and the factor-independence related to BCR/ABL with the exception of mutant T315I.	imatinib	331-339	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	233-240
18366061-8	2008	These data provide evidence that the inhibition of tetramerization inhibits BCR/ABL-mediated transformation and can contribute to overcome Imatinib-resistance.	imatinib	139-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
18795086-3	2008	We report a case of a 28-year-old woman who delivered a healthy child of normal weight after having been treated with imatinib for Ph1-positive CML during the first four months of her pregnancy.	imatinib	118-126	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	131-134
18500834-9	2008	Microparticles were formulated with PK3, which encapsulated the anti-inflammatory drug, imatinib.	imatinib	88-96	pyruvate kinase M1/2	Homo sapiens	36-39
18500834-10	2008	In vivo experiments demonstrated that PK3 microparticles were able to significantly improve the efficacy of imatinib in treating acute liver failure.	imatinib	108-116	pyruvate kinase M1/2	Homo sapiens	38-41
18502845-0	2008	Imatinib mesylate for platelet-derived growth factor receptor-beta-positive Erdheim-Chester histiocytosis.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	22-66
18384443-6	2008	WHAT THIS STUDY ADDS: Co-administration of imatinib at 400 mg twice daily increased the plasma AUC of metoprolol by approximately 23% in 20 Chinese patients with chronic myeloid leukaemia (CML), about 17% increase in CYP2D6 intermediate metabolizers (IMs) (n = 6), 24% in extensive metabolizers (EMs) (n = 13), and 28% for the subject with unknown 2D6 status (n = 1) suggesting that imatinib has a weak to moderate inhibition on CYP2D6 in vivo.	imatinib	43-51	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	217-223
18384443-6	2008	WHAT THIS STUDY ADDS: Co-administration of imatinib at 400 mg twice daily increased the plasma AUC of metoprolol by approximately 23% in 20 Chinese patients with chronic myeloid leukaemia (CML), about 17% increase in CYP2D6 intermediate metabolizers (IMs) (n = 6), 24% in extensive metabolizers (EMs) (n = 13), and 28% for the subject with unknown 2D6 status (n = 1) suggesting that imatinib has a weak to moderate inhibition on CYP2D6 in vivo.	imatinib	43-51	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	429-435
18384443-8	2008	AIMS To investigate the effect of imatinib on the pharmacokinetics of a CYP2D6 substrate, metoprolol, in patients with chronic myeloid leukaemia (CML).	imatinib	34-42	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	72-78
18384443-17	2008	The oral clearance of imatinib was 11.0 +/- 2.0 l h(-1) and 11.8 +/- 4.1 l h(-1) for CYP2D6 IMs and EMs, respectively.	imatinib	22-30	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	85-91
19636920-1	2008	Imatinib (Glivec or Gleevec) potently inhibits the tyrosine kinase activity of BCR-ABL, a constitutively activated kinase, which causes chronic myelogenous leukemia (CML).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
18384443-18	2008	CONCLUSIONS: Co-administration of a high dose of imatinib resulted in a small or moderate increase in metoprolol plasma exposure in all patients regardless of CYP2D6 status.	imatinib	49-57	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	159-165
18503829-4	2008	The case illustrates that, although imatinib mesylate can be an effective treatment in eradication of the BCR-ABL fusion gene cells, the occurrence of additional specific abnormalities in Philadelphia-positive leukemias may pose a significant therapeutic challenge.	imatinib	36-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
18429956-5	2008	Combined treatment with VE-465 and imatinib caused more attenuation of the levels of phospho-AKT and c-Myc in K562 cells.	imatinib	35-43	AKT serine/threonine kinase 1	Homo sapiens	93-96
18429956-5	2008	Combined treatment with VE-465 and imatinib caused more attenuation of the levels of phospho-AKT and c-Myc in K562 cells.	imatinib	35-43	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	101-106
18515176-4	2008	Successful examples of personalizing molecularly targeted therapies based on biomarkers include the use of trastuzumab in HER-2 overexpressing breast cancer and imatinib in c-KIT expressing gastrointestinal stromal tumor.	imatinib	161-169	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	173-178
18533795-4	2008	Imatinib mesylate, an orally available tyrosine kinase inhibitor that targets Bcr-Abl, entered clinical evaluation in 1998.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
18491988-1	2008	Targeted therapy with the Abl kinase inhibitor imatinib has markedly improved the outlook for patients with chronic myeloid leukemia (CML).	imatinib	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-29
18338755-0	2008	Overcoming imatinib resistance using Src inhibitor CGP76030, Abl inhibitor nilotinib and Abl/Lyn inhibitor INNO-406 in newly established K562 variants with BCR-ABL gene amplification.	imatinib	11-19	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	37-40
18491988-4	2008	Despite excellent results in patients with imatinib-resistant or imatinib-intolerant CML treated with nilotinib or dasatinib, early indications suggest that: the cross-resistant Bcr-Abl(T315I) mutant is disproportionately represented among patients who relapse on these therapies; each Abl inhibitor exhibits vulnerabilities to certain kinase domain mutations.	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185
18491988-4	2008	Despite excellent results in patients with imatinib-resistant or imatinib-intolerant CML treated with nilotinib or dasatinib, early indications suggest that: the cross-resistant Bcr-Abl(T315I) mutant is disproportionately represented among patients who relapse on these therapies; each Abl inhibitor exhibits vulnerabilities to certain kinase domain mutations.	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-185
18491988-4	2008	Despite excellent results in patients with imatinib-resistant or imatinib-intolerant CML treated with nilotinib or dasatinib, early indications suggest that: the cross-resistant Bcr-Abl(T315I) mutant is disproportionately represented among patients who relapse on these therapies; each Abl inhibitor exhibits vulnerabilities to certain kinase domain mutations.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185
18491988-4	2008	Despite excellent results in patients with imatinib-resistant or imatinib-intolerant CML treated with nilotinib or dasatinib, early indications suggest that: the cross-resistant Bcr-Abl(T315I) mutant is disproportionately represented among patients who relapse on these therapies; each Abl inhibitor exhibits vulnerabilities to certain kinase domain mutations.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-185
18338755-0	2008	Overcoming imatinib resistance using Src inhibitor CGP76030, Abl inhibitor nilotinib and Abl/Lyn inhibitor INNO-406 in newly established K562 variants with BCR-ABL gene amplification.	imatinib	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-64
18338755-0	2008	Overcoming imatinib resistance using Src inhibitor CGP76030, Abl inhibitor nilotinib and Abl/Lyn inhibitor INNO-406 in newly established K562 variants with BCR-ABL gene amplification.	imatinib	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-92
18338755-0	2008	Overcoming imatinib resistance using Src inhibitor CGP76030, Abl inhibitor nilotinib and Abl/Lyn inhibitor INNO-406 in newly established K562 variants with BCR-ABL gene amplification.	imatinib	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
18553235-1	2008	BACKGROUND: Imatinib mesylate, an inhibitor of KIT, ABL protein, and platelet-derived growth factor receptor alpha (PDGFRalpha) tyrosine kinase, has recently been found to have a dramatic antitumor effect on gastrointestinal stromal tumor (GIST).	imatinib	12-29	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	47-50
18553235-1	2008	BACKGROUND: Imatinib mesylate, an inhibitor of KIT, ABL protein, and platelet-derived growth factor receptor alpha (PDGFRalpha) tyrosine kinase, has recently been found to have a dramatic antitumor effect on gastrointestinal stromal tumor (GIST).	imatinib	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-55
18338755-1	2008	Because imatinib (IM) resistance in chronic myeloid leukemia is primarily caused by the re-establishment of Abl kinase, new inhibitors may be efficacious.	imatinib	8-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-111
18553235-1	2008	BACKGROUND: Imatinib mesylate, an inhibitor of KIT, ABL protein, and platelet-derived growth factor receptor alpha (PDGFRalpha) tyrosine kinase, has recently been found to have a dramatic antitumor effect on gastrointestinal stromal tumor (GIST).	imatinib	12-29	platelet derived growth factor receptor alpha	Homo sapiens	69-114
18281615-13	2008	The combination of 17-DMAG with imatinib mesylate, the inhibitor of c-kit, had synergistic inhibitory effects on cell proliferation in WT B-Raf uveal melanoma cell lines.	imatinib	32-49	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	68-73
18553235-1	2008	BACKGROUND: Imatinib mesylate, an inhibitor of KIT, ABL protein, and platelet-derived growth factor receptor alpha (PDGFRalpha) tyrosine kinase, has recently been found to have a dramatic antitumor effect on gastrointestinal stromal tumor (GIST).	imatinib	12-29	platelet derived growth factor receptor alpha	Homo sapiens	116-126
18497981-2	2008	Recently, a selective Abl kinase inhibitor, Imatinib mesylate, was introduced as a first line therapy for CML.	imatinib	44-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-25
18497981-3	2008	Despite the initial response, CML patients develop a resistantance to Imatinib, which is mediated mainly by point mutations within the Abl protein.	imatinib	70-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-138
18497981-6	2008	The active fraction significantly inhibits the autophosphorylation of native and mutated Bcr-Abl, which are resistant to Imatinib treatment including the T315I mutation.	imatinib	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
18281615-13	2008	The combination of 17-DMAG with imatinib mesylate, the inhibitor of c-kit, had synergistic inhibitory effects on cell proliferation in WT B-Raf uveal melanoma cell lines.	imatinib	32-49	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	138-143
18381383-7	2008	Negative KIT expression was an independent prognostic factor in multivariate Cox regression analysis when the risk of aggressive behaviour and the status of imatinib treatment were adopted as covariates.	imatinib	157-165	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	9-12
18354488-1	2008	The BCR-ABL oncogenic tyrosine kinase causes chronic myeloid leukemia and is the target for imatinib therapy.	imatinib	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
18083230-0	2008	Imatinib-resistant K562 cells are more sensitive to celecoxib, a selective COX-2 inhibitor: role of COX-2 and MDR-1.	imatinib	0-8	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	75-80
18354488-2	2008	During imatinib treatment, cells are selected in some patients with BCR-ABL kinase domain mutations that render decreased drug sensitivity.	imatinib	7-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
18083230-0	2008	Imatinib-resistant K562 cells are more sensitive to celecoxib, a selective COX-2 inhibitor: role of COX-2 and MDR-1.	imatinib	0-8	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	100-105
18368071-0	2008	RNAi-mediated silencing of p190Bcr-Abl inactivates Stat5 and cooperates with imatinib mesylate and 17-allylamino-17-demetoxygeldanamycin in selective killing of p190Bcr-Abl-expressing leukemia cells.	imatinib	77-94	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	27-38
18401416-1	2008	Dasatinib, a potent inhibitor of BCR-ABL in vitro, is effective for patients with chronic myelogenous leukemia (CML) resistant or intolerant to imatinib.	imatinib	144-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
18368071-0	2008	RNAi-mediated silencing of p190Bcr-Abl inactivates Stat5 and cooperates with imatinib mesylate and 17-allylamino-17-demetoxygeldanamycin in selective killing of p190Bcr-Abl-expressing leukemia cells.	imatinib	77-94	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	161-172
18368071-6	2008	shRNA targeting p190 collaborated additively with imatinib and 17-AAG in growth inhibition of Ba/F3-p190wt and imatinib-resistant Ba/F3-p190Y253 H cells.	imatinib	50-58	RAS protein-specific guanine nucleotide-releasing factor 1	Mus musculus	16-20
18083230-0	2008	Imatinib-resistant K562 cells are more sensitive to celecoxib, a selective COX-2 inhibitor: role of COX-2 and MDR-1.	imatinib	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	110-115
18083230-4	2008	Further studies revealed the over-expression of COX-2 and MDR-1 in IR-K562 cells suggesting the possible involvement of COX-2 in the development of resistance to imatinib.	imatinib	162-170	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	48-53
18083230-4	2008	Further studies revealed the over-expression of COX-2 and MDR-1 in IR-K562 cells suggesting the possible involvement of COX-2 in the development of resistance to imatinib.	imatinib	162-170	ATP binding cassette subfamily B member 1	Homo sapiens	58-63
18083230-4	2008	Further studies revealed the over-expression of COX-2 and MDR-1 in IR-K562 cells suggesting the possible involvement of COX-2 in the development of resistance to imatinib.	imatinib	162-170	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	120-125
18368071-6	2008	shRNA targeting p190 collaborated additively with imatinib and 17-AAG in growth inhibition of Ba/F3-p190wt and imatinib-resistant Ba/F3-p190Y253 H cells.	imatinib	111-119	RAS protein-specific guanine nucleotide-releasing factor 1	Mus musculus	16-20
18569639-5	2008	Additionally, data also demonstrate that inhibition of telomerase was due to the direct action of imatinib on hTERT transcription, rather than an increase in cell death.	imatinib	98-106	telomerase reverse transcriptase	Homo sapiens	110-115
18359865-1	2008	We determined the maximum tolerated dose (MTD) and dose-limiting toxicity (DLT) of imatinib mesylate, an inhibitor of the receptor tyrosine kinases platelet-derived growth factor receptor (PDGFR), the proto-oncogene product c-kit, and the fusion protein Bcr-Abl, when administered for 8 days in combination with temozolomide (TMZ) to malignant glioma (MG) patients.	imatinib	83-100	platelet derived growth factor receptor beta	Homo sapiens	148-187
18359865-1	2008	We determined the maximum tolerated dose (MTD) and dose-limiting toxicity (DLT) of imatinib mesylate, an inhibitor of the receptor tyrosine kinases platelet-derived growth factor receptor (PDGFR), the proto-oncogene product c-kit, and the fusion protein Bcr-Abl, when administered for 8 days in combination with temozolomide (TMZ) to malignant glioma (MG) patients.	imatinib	83-100	platelet derived growth factor receptor beta	Homo sapiens	189-194
18359865-1	2008	We determined the maximum tolerated dose (MTD) and dose-limiting toxicity (DLT) of imatinib mesylate, an inhibitor of the receptor tyrosine kinases platelet-derived growth factor receptor (PDGFR), the proto-oncogene product c-kit, and the fusion protein Bcr-Abl, when administered for 8 days in combination with temozolomide (TMZ) to malignant glioma (MG) patients.	imatinib	83-100	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	224-229
18359865-1	2008	We determined the maximum tolerated dose (MTD) and dose-limiting toxicity (DLT) of imatinib mesylate, an inhibitor of the receptor tyrosine kinases platelet-derived growth factor receptor (PDGFR), the proto-oncogene product c-kit, and the fusion protein Bcr-Abl, when administered for 8 days in combination with temozolomide (TMZ) to malignant glioma (MG) patients.	imatinib	83-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	254-261
17914733-1	2008	BACKGROUND: Dasatinib, a dual inhibitor of the src and abl tyrosine kinases, was recently approved by the Federal Drug Administration for the treatment of imatinib mesylate-resistant chronic myeloid leukemia.	imatinib	155-172	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	47-50
19383325-0	2008	NESH protein expression switches to the adverse effect of imatinib mesylate.	imatinib	58-75	ABI family member 3	Homo sapiens	0-4
18600540-4	2008	Here we report that imatinib treatment decreased ENT1-dependent activity and mRNA expression.	imatinib	20-28	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	49-53
18600540-5	2008	Although, imatinib-resistant cells showed decreased levels of both ENT1 and ENT2 activity and expression, these cells remained sensitive to gemcitabine, suggesting that nucleoside analogs can be used as adjunctive therapy.	imatinib	10-18	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	67-71
18600540-5	2008	Although, imatinib-resistant cells showed decreased levels of both ENT1 and ENT2 activity and expression, these cells remained sensitive to gemcitabine, suggesting that nucleoside analogs can be used as adjunctive therapy.	imatinib	10-18	solute carrier family 29 member 2	Homo sapiens	76-80
18537751-3	2008	The introduction of imatinib mesylate (inhibiting KIT/PDGFRA (platelet-derived growth factor receptor-alpha) and their downstream signaling cascade) has revolutionized the therapy of advanced (inoperable and/or metastatic) GISTs.	imatinib	20-37	platelet derived growth factor receptor alpha	Homo sapiens	54-60
18623899-10	2008	Some myelodysplastic syndromes are associated with myeloproliferation and PDGFR gene rearrangements; imatinib is the first drug available for these patients.	imatinib	101-109	platelet derived growth factor receptor beta	Homo sapiens	74-79
18537751-3	2008	The introduction of imatinib mesylate (inhibiting KIT/PDGFRA (platelet-derived growth factor receptor-alpha) and their downstream signaling cascade) has revolutionized the therapy of advanced (inoperable and/or metastatic) GISTs.	imatinib	20-37	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	50-53
18537751-3	2008	The introduction of imatinib mesylate (inhibiting KIT/PDGFRA (platelet-derived growth factor receptor-alpha) and their downstream signaling cascade) has revolutionized the therapy of advanced (inoperable and/or metastatic) GISTs.	imatinib	20-37	platelet derived growth factor receptor alpha	Homo sapiens	62-107
18563733-6	2008	We recently reported the participation of Hsp70 overexpression in imatinib resistance whereas a role for Hsc70 has yet to be determined.	imatinib	66-74	heat shock protein family A (Hsp70) member 4	Homo sapiens	42-47
18563733-9	2008	This proteomic study therefore suggests opposing roles of Hsp70 and Hsc70 in imatinib resistance.	imatinib	77-85	heat shock protein family A (Hsp70) member 4	Homo sapiens	58-63
18563733-9	2008	This proteomic study therefore suggests opposing roles of Hsp70 and Hsc70 in imatinib resistance.	imatinib	77-85	heat shock protein family A (Hsp70) member 8	Homo sapiens	68-73
18706197-0	2008	FIP1L1-PDGFRalpha alone or with other genetic abnormalities reveals disease progression in chronic eosinophilic leukemia but good response to imatinib.	imatinib	142-150	factor interacting with PAPOLA and CPSF1	Homo sapiens	0-6
18706197-0	2008	FIP1L1-PDGFRalpha alone or with other genetic abnormalities reveals disease progression in chronic eosinophilic leukemia but good response to imatinib.	imatinib	142-150	platelet derived growth factor receptor alpha	Homo sapiens	7-17
18706197-1	2008	BACKGROUND: The FIP1L1-PDGFRalpha fusion gene plays an important role in the pathogenesis of chronic eosinophilic leukemia (CEL) and is a direct therapeutic target of the tyrosine kinase inhibitor imatinib mesylate.	imatinib	197-214	factor interacting with PAPOLA and CPSF1	Homo sapiens	16-22
18706197-1	2008	BACKGROUND: The FIP1L1-PDGFRalpha fusion gene plays an important role in the pathogenesis of chronic eosinophilic leukemia (CEL) and is a direct therapeutic target of the tyrosine kinase inhibitor imatinib mesylate.	imatinib	197-214	platelet derived growth factor receptor alpha	Homo sapiens	23-33
18706197-6	2008	Nevertheless, imatinib mesylate induced rapid and complete hematological responses in treated FIP1L1-PDGFRalpha cases, followed by molecular remission and reversal of myelofibrosis.	imatinib	14-31	factor interacting with PAPOLA and CPSF1	Homo sapiens	94-100
18706197-6	2008	Nevertheless, imatinib mesylate induced rapid and complete hematological responses in treated FIP1L1-PDGFRalpha cases, followed by molecular remission and reversal of myelofibrosis.	imatinib	14-31	platelet derived growth factor receptor alpha	Homo sapiens	101-111
18348294-1	2008	The majority of patients with chronic-phase (CP) chronic myeloid leukemia (CML) who are treated with Bcr-Abl tyrosine kinase inhibitors such as imatinib and dasatinib achieve cytogenetic disease remission (ie, Philadelphia chromosome-positive cells undetectable by cytogenetic evaluation).	imatinib	144-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
18483382-1	2008	PURPOSE: The activity of imatinib in leukemia has recently been linked with expression of the organic cation transporter 1 (OCT1) gene SLC22A1.	imatinib	25-33	solute carrier family 22 member 1	Homo sapiens	94-122
18483382-1	2008	PURPOSE: The activity of imatinib in leukemia has recently been linked with expression of the organic cation transporter 1 (OCT1) gene SLC22A1.	imatinib	25-33	solute carrier family 22 member 1	Homo sapiens	124-128
18483389-9	2008	In vitro studies showed that nilotinib, sunitinib, dasatinib, and sorafenib are more effective than imatinib against WT KIT.	imatinib	100-108	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	120-123
18483382-1	2008	PURPOSE: The activity of imatinib in leukemia has recently been linked with expression of the organic cation transporter 1 (OCT1) gene SLC22A1.	imatinib	25-33	solute carrier family 22 member 1	Homo sapiens	135-142
18483382-8	2008	Imatinib was confirmed to be a substrate for the three efflux transporters (P < 0.05) as well as for OATP1A2 (P = 0.0001).	imatinib	0-8	solute carrier organic anion transporter family member 1A2	Homo sapiens	104-111
18483382-9	2008	CONCLUSIONS: This study suggests that SLC22A1 expression is a composite surrogate for expression of various transporters relevant to imatinib IUR.	imatinib	133-141	solute carrier family 22 member 1	Homo sapiens	38-45
18071309-7	2008	The Bcr-Abl kinase inhibitor imatinib mesylate (1 microM) and two Jak2 kinase inhibitors strongly inhibited agar colony formation and the activation of Gab2 caused by Jak2.	imatinib	29-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
18483382-10	2008	This observation provides a mechanistic explanation for previous studies that have linked SLC22A1 with the antitumor activity of imatinib.	imatinib	129-137	solute carrier family 22 member 1	Homo sapiens	90-97
18071309-7	2008	The Bcr-Abl kinase inhibitor imatinib mesylate (1 microM) and two Jak2 kinase inhibitors strongly inhibited agar colony formation and the activation of Gab2 caused by Jak2.	imatinib	29-46	growth factor receptor bound protein 2-associated protein 2	Mus musculus	152-156
18483382-11	2008	Because of its high expression in the intestine, ciliary body, gliomas, and leukemia cells, OATP1A2 may play a key role in imatinib pharmacokinetics-pharmacodynamics.	imatinib	123-131	solute carrier organic anion transporter family member 1A2	Homo sapiens	92-99
18071309-7	2008	The Bcr-Abl kinase inhibitor imatinib mesylate (1 microM) and two Jak2 kinase inhibitors strongly inhibited agar colony formation and the activation of Gab2 caused by Jak2.	imatinib	29-46	Janus kinase 2	Mus musculus	167-171
18453565-0	2008	The critical role of IL-15 in the antitumor effects mediated by the combination therapy imatinib and IL-2.	imatinib	88-96	interleukin 15	Mus musculus	21-26
18172853-0	2008	Hemin reduces cellular sensitivity to imatinib and anthracyclins via Nrf2.	imatinib	38-46	NFE2 like bZIP transcription factor 2	Homo sapiens	69-73
18172853-3	2008	Hemin treatment of human BCR/ABL-positive KCL22 leukemia cells increased IC(50) values of imatinib, that is, the drug resistance, in a dose-dependent manner without any change in the BCR/ABL kinase activity.	imatinib	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
18172853-7	2008	Knockdown of Nrf2 expression by RNA interference largely abolished the effect of hemin on imatinib-treated cells, suggesting that Nrf2 recognition of MARE is essential for the hemin-mediated protective effect.	imatinib	90-98	NFE2 like bZIP transcription factor 2	Homo sapiens	13-17
18172853-7	2008	Knockdown of Nrf2 expression by RNA interference largely abolished the effect of hemin on imatinib-treated cells, suggesting that Nrf2 recognition of MARE is essential for the hemin-mediated protective effect.	imatinib	90-98	NFE2 like bZIP transcription factor 2	Homo sapiens	130-134
18453565-1	2008	The synergistic antitumor effects of the combination therapy imatinib mesylate (IM) and IL-2 depended upon NK1.1- expressing cells and were associated with the accumulation of CD11c(int)B220(+)NK1.1(+) IFN-producing killer dendritic cells (IKDC) into tumor beds.	imatinib	61-78	integrin alpha X	Mus musculus	176-181
18362061-3	2008	Since the tumor was weakly positive for c-kit, she was treated with imatinib mesylate for the recurrent liver tumors.	imatinib	68-85	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	40-45
18820368-1	2008	BACKGROUND: Imatinib mesylate (Gleevec, Novartis, Basel, Switzerland) is a small-molecule tyrosine kinase inhibitor with activity against ABL, BCR-ABL, c-KIT, and PDGFR alpha.	imatinib	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-141
18414381-1	2008	BACKGROUND AND PURPOSE: Effects of imatinib mesylate, a Kit receptor tyrosine kinase inhibitor, on spontaneous activity of interstitial cells of Cajal (ICC) and smooth muscles in the stomach were investigated.	imatinib	35-52	mast/stem cell growth factor receptor Kit	Cavia porcellus	56-59
18474303-0	2008	Imatinib resistance in a novel translocation der(17)t(1;17)(q25;p13) with loss of TP53 but without BCR/ABL kinase domain mutation in chronic myelogenous leukemia.	imatinib	0-8	H3 histone pseudogene 6	Homo sapiens	64-67
18474303-0	2008	Imatinib resistance in a novel translocation der(17)t(1;17)(q25;p13) with loss of TP53 but without BCR/ABL kinase domain mutation in chronic myelogenous leukemia.	imatinib	0-8	tumor protein p53	Homo sapiens	82-86
18820368-1	2008	BACKGROUND: Imatinib mesylate (Gleevec, Novartis, Basel, Switzerland) is a small-molecule tyrosine kinase inhibitor with activity against ABL, BCR-ABL, c-KIT, and PDGFR alpha.	imatinib	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-150
18820368-1	2008	BACKGROUND: Imatinib mesylate (Gleevec, Novartis, Basel, Switzerland) is a small-molecule tyrosine kinase inhibitor with activity against ABL, BCR-ABL, c-KIT, and PDGFR alpha.	imatinib	12-29	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	152-157
18820368-1	2008	BACKGROUND: Imatinib mesylate (Gleevec, Novartis, Basel, Switzerland) is a small-molecule tyrosine kinase inhibitor with activity against ABL, BCR-ABL, c-KIT, and PDGFR alpha.	imatinib	12-29	platelet derived growth factor receptor alpha	Homo sapiens	163-174
18487909-5	2008	Imatinib (gleevec) is an oral agent that selectively inhibits c-Kit, whose efficacy proves that a specific inhibitor can counteract the effects of a genetic defect responsible for cancer.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	62-67
18451237-11	2008	One patient with systemic mastocytosis and a partial response to therapy had a novel imatinib-sensitive KIT mutation (D816T).	imatinib	85-93	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	104-107
18323796-2	2008	The central role played by BCR-ABL1 in the pathogenesis of CML facilitated the development of the tyrosine kinase inhibitor (TKI) imatinib mesylate, the first actual targeted therapy in cancer history.	imatinib	130-147	BCR activator of RhoGEF and GTPase	Homo sapiens	27-35
18401414-0	2008	Sphingosine kinase-1 is a downstream regulator of imatinib-induced apoptosis in chronic myeloid leukemia cells.	imatinib	50-58	sphingosine kinase 1	Homo sapiens	0-20
18401414-1	2008	We examined the involvement of sphingosine kinase-1 (SphK1), which governs the ceramide/sphingosine-1-phosphate balance, in susceptibility to imatinib of either sensitive or resistant chronic myeloid leukemia cells.	imatinib	142-150	sphingosine kinase 1	Homo sapiens	31-51
18401414-1	2008	We examined the involvement of sphingosine kinase-1 (SphK1), which governs the ceramide/sphingosine-1-phosphate balance, in susceptibility to imatinib of either sensitive or resistant chronic myeloid leukemia cells.	imatinib	142-150	sphingosine kinase 1	Homo sapiens	53-58
18367480-1	2008	BACKGROUND: Resistance to imatinib is an important clinical issue in the treatment of Philadelphia chromosome-positive leukemias which is being tackled by the development of new, more potent drugs, such as the dual Src/Abl tyrosine kinase inhibitors dasatinib and bosutinib and the imatinib analog nilotinib.	imatinib	26-34	Rous sarcoma oncogene	Mus musculus	215-218
18367480-1	2008	BACKGROUND: Resistance to imatinib is an important clinical issue in the treatment of Philadelphia chromosome-positive leukemias which is being tackled by the development of new, more potent drugs, such as the dual Src/Abl tyrosine kinase inhibitors dasatinib and bosutinib and the imatinib analog nilotinib.	imatinib	26-34	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	219-222
18367480-1	2008	BACKGROUND: Resistance to imatinib is an important clinical issue in the treatment of Philadelphia chromosome-positive leukemias which is being tackled by the development of new, more potent drugs, such as the dual Src/Abl tyrosine kinase inhibitors dasatinib and bosutinib and the imatinib analog nilotinib.	imatinib	282-290	Rous sarcoma oncogene	Mus musculus	215-218
18367480-1	2008	BACKGROUND: Resistance to imatinib is an important clinical issue in the treatment of Philadelphia chromosome-positive leukemias which is being tackled by the development of new, more potent drugs, such as the dual Src/Abl tyrosine kinase inhibitors dasatinib and bosutinib and the imatinib analog nilotinib.	imatinib	282-290	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	219-222
18367481-0	2008	Phospho-CRKL monitoring for the assessment of BCR-ABL activity in imatinib-resistant chronic myeloid leukemia or Ph+ acute lymphoblastic leukemia patients treated with nilotinib.	imatinib	66-74	CRK like proto-oncogene, adaptor protein	Homo sapiens	8-12
18367481-0	2008	Phospho-CRKL monitoring for the assessment of BCR-ABL activity in imatinib-resistant chronic myeloid leukemia or Ph+ acute lymphoblastic leukemia patients treated with nilotinib.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
18367481-1	2008	Actual BCR-ABL kinase inhibition in vivo as determined by phospho-CRKL (pCRKL) monitoring has been recognized as a prognostic parameter in patients with chronic myelogenous leukemia treated with imatinib.	imatinib	195-203	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	7-14
18367481-1	2008	Actual BCR-ABL kinase inhibition in vivo as determined by phospho-CRKL (pCRKL) monitoring has been recognized as a prognostic parameter in patients with chronic myelogenous leukemia treated with imatinib.	imatinib	195-203	CRK like proto-oncogene, adaptor protein	Homo sapiens	66-70
18367481-3	2008	A minimum dose (200 mg) required for effective BCR-ABL inhibition in imatinib resistant/intolerant leukemia was determined.	imatinib	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
17942153-0	2008	Resistance to Imatinib Mesylate-induced apoptosis in acute lymphoblastic leukemia is associated with PTEN down-regulation due to promoter hypermethylation.	imatinib	14-31	phosphatase and tensin homolog	Homo sapiens	101-105
17942153-6	2008	These results suggest that Imatinib resistance in patients with ALL may be dependent at least in part to PTEN down-regulation due to the abnormal promoter hypermethylation and support the potential role of de-methylating agents for the treatment of patients with Ph+ ALL.	imatinib	27-35	phosphatase and tensin homolog	Homo sapiens	105-109
18401414-2	2008	Imatinib-sensitive LAMA84-s displayed marked SphK1 inhibition coupled with increased content of ceramide and decreased pro-survival sphingosine-1-phosphate.	imatinib	0-8	sphingosine kinase 1	Homo sapiens	45-50
18401414-4	2008	Overcoming imatinib resistance in LAMA84-r with farnesyltransferase or MEK/ERK inhibitors as well as with cytosine arabinoside led to SphK1 inhibition.	imatinib	11-19	mitogen-activated protein kinase kinase 7	Homo sapiens	71-74
18401414-4	2008	Overcoming imatinib resistance in LAMA84-r with farnesyltransferase or MEK/ERK inhibitors as well as with cytosine arabinoside led to SphK1 inhibition.	imatinib	11-19	mitogen-activated protein kinase 1	Homo sapiens	75-78
18323796-3	2008	Imatinib competes with ATP at the active site of BCR-ABL1 kinase.	imatinib	0-8	BCR activator of RhoGEF and GTPase	Homo sapiens	49-57
18401414-4	2008	Overcoming imatinib resistance in LAMA84-r with farnesyltransferase or MEK/ERK inhibitors as well as with cytosine arabinoside led to SphK1 inhibition.	imatinib	11-19	sphingosine kinase 1	Homo sapiens	134-139
18401414-5	2008	Overexpression of SphK1 in LAMA84-s cells impaired apoptosis and inhibited the effects of imatinib on caspase-3 activation, cytochrome c and Smac release from mitochondria through modulation of Bim, Bcl-xL and Mcl-1 expression.	imatinib	90-98	sphingosine kinase 1	Homo sapiens	18-23
18323796-4	2008	Despite outstanding clinical results, imatinib as well as other BCR-ABL1 TKIs have been associated with limited rates of complete molecular response and the development of mutations within the kinase domain of BCR-ABL1 that impairs TKI binding.	imatinib	38-46	BCR activator of RhoGEF and GTPase	Homo sapiens	210-218
18401414-5	2008	Overexpression of SphK1 in LAMA84-s cells impaired apoptosis and inhibited the effects of imatinib on caspase-3 activation, cytochrome c and Smac release from mitochondria through modulation of Bim, Bcl-xL and Mcl-1 expression.	imatinib	90-98	caspase 3	Homo sapiens	102-111
18401414-5	2008	Overexpression of SphK1 in LAMA84-s cells impaired apoptosis and inhibited the effects of imatinib on caspase-3 activation, cytochrome c and Smac release from mitochondria through modulation of Bim, Bcl-xL and Mcl-1 expression.	imatinib	90-98	cytochrome c, somatic	Homo sapiens	124-136
18401414-6	2008	Pharmacological inhibition of SphK1 with F-12509a or its silencing by siRNA induced apoptosis of both imatinib-sensitive and -resistant cells, suggesting that SphK1 inhibition was critical for apoptosis signaling.	imatinib	102-110	sphingosine kinase 1	Homo sapiens	30-35
18401414-8	2008	These results uncover the involvement of SphK1 in regulating imatinib-induced apoptosis and establish that SphK1 is a downstream effector of the Bcr-Abl/Ras/ERK pathway inhibited by imatinib but upstream regulator of Bcl-2 family members.	imatinib	61-69	sphingosine kinase 1	Homo sapiens	41-46
18401414-8	2008	These results uncover the involvement of SphK1 in regulating imatinib-induced apoptosis and establish that SphK1 is a downstream effector of the Bcr-Abl/Ras/ERK pathway inhibited by imatinib but upstream regulator of Bcl-2 family members.	imatinib	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-152
18353972-3	2008	STI571, a c-Abl kinase inhibitor, only inhibited bFGF- but not VEGF-induced angiogenesis.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-15
18353972-3	2008	STI571, a c-Abl kinase inhibitor, only inhibited bFGF- but not VEGF-induced angiogenesis.	imatinib	0-6	fibroblast growth factor 2	Homo sapiens	49-53
18278867-9	2008	We also show that induced disorder is actually operational in kinase inhibitory action: a comparison of the binding of imatinib and PD173955 to Bcr-Abl kinase reveals that imatinib forms stronger intermolecular nonbonded interactions than PD173955, yet the latter binds with higher affinity by boosting the complex entropy.	imatinib	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
18401414-8	2008	These results uncover the involvement of SphK1 in regulating imatinib-induced apoptosis and establish that SphK1 is a downstream effector of the Bcr-Abl/Ras/ERK pathway inhibited by imatinib but upstream regulator of Bcl-2 family members.	imatinib	61-69	mitogen-activated protein kinase 1	Homo sapiens	157-160
18401414-8	2008	These results uncover the involvement of SphK1 in regulating imatinib-induced apoptosis and establish that SphK1 is a downstream effector of the Bcr-Abl/Ras/ERK pathway inhibited by imatinib but upstream regulator of Bcl-2 family members.	imatinib	182-190	sphingosine kinase 1	Homo sapiens	107-112
18401414-8	2008	These results uncover the involvement of SphK1 in regulating imatinib-induced apoptosis and establish that SphK1 is a downstream effector of the Bcr-Abl/Ras/ERK pathway inhibited by imatinib but upstream regulator of Bcl-2 family members.	imatinib	182-190	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-152
18401414-8	2008	These results uncover the involvement of SphK1 in regulating imatinib-induced apoptosis and establish that SphK1 is a downstream effector of the Bcr-Abl/Ras/ERK pathway inhibited by imatinib but upstream regulator of Bcl-2 family members.	imatinib	182-190	mitogen-activated protein kinase 1	Homo sapiens	157-160
18278867-9	2008	We also show that induced disorder is actually operational in kinase inhibitory action: a comparison of the binding of imatinib and PD173955 to Bcr-Abl kinase reveals that imatinib forms stronger intermolecular nonbonded interactions than PD173955, yet the latter binds with higher affinity by boosting the complex entropy.	imatinib	172-180	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
18413724-1	2008	BCR/ABL kinase-positive chronic myelogenous leukemia (CML) cells display genomic instability leading to point mutations in various genes including bcr/abl and p53, eventually causing resistance to imatinib and malignant progression of the disease.	imatinib	197-205	BCR activator of RhoGEF and GTPase	Homo sapiens	0-3
18268096-0	2008	Simultaneous targeting of Aurora kinases and Bcr-Abl kinase by the small molecule inhibitor PHA-739358 is effective against imatinib-resistant BCR-ABL mutations including T315I.	imatinib	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
18268096-0	2008	Simultaneous targeting of Aurora kinases and Bcr-Abl kinase by the small molecule inhibitor PHA-739358 is effective against imatinib-resistant BCR-ABL mutations including T315I.	imatinib	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-150
18268096-1	2008	The emergence of resistance to imatinib (IM) mediated by mutations in the BCR-ABL domain has become a major challenge in the treatment of chronic myeloid leukemia (CML).	imatinib	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
18406870-3	2008	Based on the mechanism of genesis, it has been suggested that the complexity may affect the occurrence of ABL1 and BCR deletions (either or both), or may be associated with the CML disease course, and thus could determine the response to imatinib therapy.	imatinib	238-246	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-110
18406870-3	2008	Based on the mechanism of genesis, it has been suggested that the complexity may affect the occurrence of ABL1 and BCR deletions (either or both), or may be associated with the CML disease course, and thus could determine the response to imatinib therapy.	imatinib	238-246	BCR activator of RhoGEF and GTPase	Homo sapiens	115-118
18483293-1	2008	Blockade of Bcr-Abl by the inhibitor Imatinib has proven efficacious in the therapy of chronic myelogenous leukemia (CML).	imatinib	37-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
18483293-8	2008	More importantly, its superior potency over Imatinib was more pronounced in Bcr-Abl-positive cells coexpressing wild-type p53.	imatinib	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
18421059-0	2008	Major response to imatinib mesylate in KIT-mutated melanoma.	imatinib	18-35	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	39-42
18338744-0	2008	Molecular basis explanation for imatinib resistance of BCR-ABL due to T315I and P-loop mutations from molecular dynamics simulations.	imatinib	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
18338744-2	2008	To the authors" knowledge to date, the mechanism of imatinib resistance in BCR-ABL has not been clarified at the atomic level, and computational studies are required.	imatinib	52-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
18338744-3	2008	METHODS: Molecular dynamics (MD) simulations on the complex of imatinib with the wild-type, T315I mutant, and 10 other P-loop mutants of the tyrosine kinase BCR-ABL were performed to study the mechanism of imatinib resistance.	imatinib	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-164
18338744-3	2008	METHODS: Molecular dynamics (MD) simulations on the complex of imatinib with the wild-type, T315I mutant, and 10 other P-loop mutants of the tyrosine kinase BCR-ABL were performed to study the mechanism of imatinib resistance.	imatinib	206-214	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-164
18338744-7	2008	CONCLUSIONS: The current results indicated that large-scale simulations may offer insight and information that other simple modeling methods cannot provide regarding the problem of BCR-ABL imatinib resistance, especially in the case of conformational changes because of remote mutations.	imatinib	189-197	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	181-188
18413817-1	2008	PURPOSE: Gastrointestinal stromal tumors (GIST) are frequently associated with gain-of-function mutations of KIT, which can be inhibited by imatinib both in vitro and in vivo.	imatinib	140-148	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	109-112
18413724-1	2008	BCR/ABL kinase-positive chronic myelogenous leukemia (CML) cells display genomic instability leading to point mutations in various genes including bcr/abl and p53, eventually causing resistance to imatinib and malignant progression of the disease.	imatinib	197-205	BCR activator of RhoGEF and GTPase	Homo sapiens	147-150
18413724-1	2008	BCR/ABL kinase-positive chronic myelogenous leukemia (CML) cells display genomic instability leading to point mutations in various genes including bcr/abl and p53, eventually causing resistance to imatinib and malignant progression of the disease.	imatinib	197-205	tumor protein p53	Homo sapiens	159-162
18367669-1	2008	Imatinib inhibits Bcr-Abl, the oncogenic tyrosine kinase that causes chronic myeloid leukemia.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
18413817-7	2008	Imatinib-induced inhibition of the phosphorylation of immature and mature mutant KIT proteins resulted in the restoration of KIT expression at the cell surface.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	81-84
18413817-7	2008	Imatinib-induced inhibition of the phosphorylation of immature and mature mutant KIT proteins resulted in the restoration of KIT expression at the cell surface.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	125-128
18367669-2	2008	The second-line inhibitors nilotinib and dasatinib are effective in patients with imatinib resistance resulting from Bcr-Abl kinase domain mutations.	imatinib	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
18313694-6	2008	This enhanced cell adhesion could be reduced to control levels after specifically inhibiting the activity of the tyrosine kinase BCR/ABL using imatinib mesylate (IM).	imatinib	143-160	BCR activator of RhoGEF and GTPase	Mus musculus	129-136
17957805-2	2008	The success of the tyrosine kinase inhibitor (TKI), imatinib, as the currently recommended first-line treatment of early chronic phase CML has both fueled the need for timely and reproducible molecular testing of the BCR-ABL1 fusion transcript in diagnosis and monitoring as well as necessitated the detection of kinase domain mutations that confer resistance to this agent.	imatinib	52-60	BCR activator of RhoGEF and GTPase	Homo sapiens	217-225
18472616-3	2008	Resistance to imatinib is mediated to a great extent by the emergence of mutations within the tyrosine kinase domain of the BCR-ABL oncogene.	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
18194660-3	2008	The dramatic success of the Bcr-Abl inhibitor imatinib as therapy for CML has inspired interest in other PTKs as targets for cancer drug discovery.	imatinib	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
18343792-3	2008	We report 2 cases of sudden BCR/ABL1+ blast crisis in patients with CML who had achieved complete hematologic remission with imatinib therapy but were obligated to discontinue therapy owing to pancytopenia.	imatinib	125-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-36
18202228-0	2008	RUNX1 DNA-binding mutations and RUNX1-PRDM16 cryptic fusions in BCR-ABL+ leukemias are frequently associated with secondary trisomy 21 and may contribute to clonal evolution and imatinib resistance.	imatinib	178-186	RUNX family transcription factor 1	Homo sapiens	0-5
18184863-5	2008	Enhancement of the inhibitory effects of the tyrosine kinase inhibitors, imatinib and nilotinib, by BAG956 was demonstrated against BCR-ABL expressing cells both in vitro and in vivo.	imatinib	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
18202228-0	2008	RUNX1 DNA-binding mutations and RUNX1-PRDM16 cryptic fusions in BCR-ABL+ leukemias are frequently associated with secondary trisomy 21 and may contribute to clonal evolution and imatinib resistance.	imatinib	178-186	RUNX family transcription factor 1	Homo sapiens	32-37
18235045-0	2008	Lyn regulates BCR-ABL and Gab2 tyrosine phosphorylation and c-Cbl protein stability in imatinib-resistant chronic myelogenous leukemia cells.	imatinib	87-95	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	0-3
18202228-0	2008	RUNX1 DNA-binding mutations and RUNX1-PRDM16 cryptic fusions in BCR-ABL+ leukemias are frequently associated with secondary trisomy 21 and may contribute to clonal evolution and imatinib resistance.	imatinib	178-186	PR/SET domain 16	Homo sapiens	38-44
18235045-0	2008	Lyn regulates BCR-ABL and Gab2 tyrosine phosphorylation and c-Cbl protein stability in imatinib-resistant chronic myelogenous leukemia cells.	imatinib	87-95	GRB2 associated binding protein 2	Homo sapiens	26-30
18235045-0	2008	Lyn regulates BCR-ABL and Gab2 tyrosine phosphorylation and c-Cbl protein stability in imatinib-resistant chronic myelogenous leukemia cells.	imatinib	87-95	Cbl proto-oncogene	Homo sapiens	60-65
18202228-0	2008	RUNX1 DNA-binding mutations and RUNX1-PRDM16 cryptic fusions in BCR-ABL+ leukemias are frequently associated with secondary trisomy 21 and may contribute to clonal evolution and imatinib resistance.	imatinib	178-186	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
18235045-1	2008	Lyn kinase functions as a regulator of imatinib sensitivity in chronic myelogenous leukemia (CML) cells through an unknown mechanism.	imatinib	39-47	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	0-3
18235045-2	2008	In patients who fail imatinib therapy but have no detectable BCR-ABL kinase mutation, we detected persistently activated Lyn kinase.	imatinib	21-29	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	121-124
17549478-0	2008	PDGFRalpha/FIP1L1-positive chronic eosinophilic leukemia presenting with retro-orbital localization: efficacy of imatinib treatment.	imatinib	113-121	platelet derived growth factor receptor alpha	Homo sapiens	0-10
18235045-3	2008	In imatinib-resistant CML cells and patients, Lyn activation is BCR-ABL independent, it is complexed with the Gab2 and c-Cbl adapter/scaffold proteins, and it mediates persistent Gab2 and BCR-ABL tyrosine phosphorylation in the presence or absence of imatinib.	imatinib	3-11	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	46-49
18235045-3	2008	In imatinib-resistant CML cells and patients, Lyn activation is BCR-ABL independent, it is complexed with the Gab2 and c-Cbl adapter/scaffold proteins, and it mediates persistent Gab2 and BCR-ABL tyrosine phosphorylation in the presence or absence of imatinib.	imatinib	3-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
18235045-3	2008	In imatinib-resistant CML cells and patients, Lyn activation is BCR-ABL independent, it is complexed with the Gab2 and c-Cbl adapter/scaffold proteins, and it mediates persistent Gab2 and BCR-ABL tyrosine phosphorylation in the presence or absence of imatinib.	imatinib	3-11	GRB2 associated binding protein 2	Homo sapiens	110-114
18235045-3	2008	In imatinib-resistant CML cells and patients, Lyn activation is BCR-ABL independent, it is complexed with the Gab2 and c-Cbl adapter/scaffold proteins, and it mediates persistent Gab2 and BCR-ABL tyrosine phosphorylation in the presence or absence of imatinib.	imatinib	3-11	Cbl proto-oncogene	Homo sapiens	119-124
18235045-3	2008	In imatinib-resistant CML cells and patients, Lyn activation is BCR-ABL independent, it is complexed with the Gab2 and c-Cbl adapter/scaffold proteins, and it mediates persistent Gab2 and BCR-ABL tyrosine phosphorylation in the presence or absence of imatinib.	imatinib	3-11	GRB2 associated binding protein 2	Homo sapiens	179-183
18235045-3	2008	In imatinib-resistant CML cells and patients, Lyn activation is BCR-ABL independent, it is complexed with the Gab2 and c-Cbl adapter/scaffold proteins, and it mediates persistent Gab2 and BCR-ABL tyrosine phosphorylation in the presence or absence of imatinib.	imatinib	3-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	188-195
18235045-3	2008	In imatinib-resistant CML cells and patients, Lyn activation is BCR-ABL independent, it is complexed with the Gab2 and c-Cbl adapter/scaffold proteins, and it mediates persistent Gab2 and BCR-ABL tyrosine phosphorylation in the presence or absence of imatinib.	imatinib	251-259	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	46-49
18235045-4	2008	Lyn silencing or inhibition is necessary to suppress Gab2 and BCR-ABL phosphorylation and to recover imatinib activity.	imatinib	101-109	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	0-3
18307562-0	2008	A single weekly dose of imatinib is sufficient to induce and maintain remission of chronic eosinophilic leukaemia in FIP1L1-PDGFRA-expressing patients.	imatinib	24-32	factor interacting with PAPOLA and CPSF1	Homo sapiens	117-123
18307562-0	2008	A single weekly dose of imatinib is sufficient to induce and maintain remission of chronic eosinophilic leukaemia in FIP1L1-PDGFRA-expressing patients.	imatinib	24-32	platelet derived growth factor receptor alpha	Homo sapiens	124-130
18307562-2	2008	A subset of HES patients presents an interstitial deletion in chromosome 4q12, which leads to the expression of an imatinib-responsive fusion gene, FIP1L1-PDGFRA.	imatinib	115-123	factor interacting with PAPOLA and CPSF1	Homo sapiens	148-154
18307562-2	2008	A subset of HES patients presents an interstitial deletion in chromosome 4q12, which leads to the expression of an imatinib-responsive fusion gene, FIP1L1-PDGFRA.	imatinib	115-123	platelet derived growth factor receptor alpha	Homo sapiens	155-161
18307562-10	2008	These data suggest that a single weekly dose of imatinib is sufficient to maintain remission in FIP1L1-PDGFRA- positive CEL patients.	imatinib	48-56	factor interacting with PAPOLA and CPSF1	Homo sapiens	96-102
18307562-10	2008	These data suggest that a single weekly dose of imatinib is sufficient to maintain remission in FIP1L1-PDGFRA- positive CEL patients.	imatinib	48-56	platelet derived growth factor receptor alpha	Homo sapiens	103-109
18181176-3	2008	To identify novel BCR/ABL1-regulated genes we used global gene expression profiling of several Ph-positive and Ph-negative cell lines treated with imatinib.	imatinib	147-155	BCR activator of RhoGEF and GTPase	Homo sapiens	18-21
18294292-0	2008	Secondary mutations in the kinase domain of the KIT gene are predominant in imatinib-resistant gastrointestinal stromal tumor.	imatinib	76-84	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	48-51
18294292-5	2008	All pre-imatinib samples have KIT mutations either in exon 9 (n = 3) or exon 11 (n = 22), identified in the KIT gene of corresponding resistant tumors.	imatinib	8-16	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	30-33
20425449-2	2008	Given the high rates of complete cytogenetic remission achieved with imatinib therapy, molecular monitoring of BCR-ABL transcript levels by real-time quantitative polymerase chain reaction has become the method of choice to assess the amount of residual disease below the cytogenetic threshold.	imatinib	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
20425449-5	2008	Rising levels of BCR-ABL transcripts indicate the need for an analysis of kinase mutations, the major mechanism of imatinib resistance.	imatinib	115-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
20425450-2	2008	However, about 20% of patients treated in early chronic-phase CML are off therapy after 6 years because of resistance or intolerance, and most patients taking imatinib remain BCR-ABL-positive at the molecular level, indicating primary refractoriness of a leukemic subpopulation.	imatinib	159-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-182
18181176-3	2008	To identify novel BCR/ABL1-regulated genes we used global gene expression profiling of several Ph-positive and Ph-negative cell lines treated with imatinib.	imatinib	147-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-26
18181176-4	2008	Following imatinib treatment, the Ph-positive cells showed decreased growth, viability, and reduced phosphorylation of BCR/ABL1 and STAT5.	imatinib	10-18	BCR activator of RhoGEF and GTPase	Homo sapiens	119-122
18181176-4	2008	Following imatinib treatment, the Ph-positive cells showed decreased growth, viability, and reduced phosphorylation of BCR/ABL1 and STAT5.	imatinib	10-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-127
18181176-4	2008	Following imatinib treatment, the Ph-positive cells showed decreased growth, viability, and reduced phosphorylation of BCR/ABL1 and STAT5.	imatinib	10-18	signal transducer and activator of transcription 5A	Homo sapiens	132-137
18398719-5	2008	This function leads to resistance to ABL kinase small molecular inhibitors (SMIs) imatinib (IM), dasatinib and nilotinib, and contributes to malignant progression of the disease.	imatinib	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-40
17900686-5	2008	These observations suggest that imatinib- resistance is not necessarily dependent on higher activity in BCR-ABL-dependent pathways, but is likely due to the activation of other pathways.	imatinib	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
18322257-5	2008	We sequenced NOTCH1 in T-cell acute lymphoblastic leukemia cases with ABL1 fusions and tested combinations of gamma-secretase inhibitors and the ABL1 inhibitor imatinib in a T-cell acute lymphoblastic leukemia cell line.	imatinib	160-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-149
17851552-0	2008	A new case with rare e6a2 BCR-ABL fusion transcript developing two new resistance mutations during imatinib mesylate, which were replaced by T315I after subsequent dasatinib treatment.	imatinib	99-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
17900686-0	2008	Phosphorylation levels of BCR-ABL, CrkL, AKT and STAT5 in imatinib-resistant chronic myeloid leukemia cells implicate alternative pathway usage as a survival strategy.	imatinib	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
18398721-1	2008	Imatinib was a major breakthrough in the treatment of Bcr/abl-positive leukemias.	imatinib	0-8	BCR activator of RhoGEF and GTPase	Mus musculus	54-57
17900686-0	2008	Phosphorylation levels of BCR-ABL, CrkL, AKT and STAT5 in imatinib-resistant chronic myeloid leukemia cells implicate alternative pathway usage as a survival strategy.	imatinib	58-66	CRK like proto-oncogene, adaptor protein	Homo sapiens	35-39
17920117-0	2008	Restoration of insulin sensitivity following treatment with imatinib mesylate (Gleevec) in non-diabetic patients with chronic myelogenic leukemia (CML).	imatinib	60-77	insulin	Homo sapiens	15-22
17900686-0	2008	Phosphorylation levels of BCR-ABL, CrkL, AKT and STAT5 in imatinib-resistant chronic myeloid leukemia cells implicate alternative pathway usage as a survival strategy.	imatinib	58-66	AKT serine/threonine kinase 1	Homo sapiens	41-44
18398722-3	2008	The most common mechanisms of resistance to imatinib include BCR-ABL kinase domain mutations, BCR-ABL amplification and overexpression, and clonal evolution with activation of additional transformation pathways.	imatinib	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
17900686-0	2008	Phosphorylation levels of BCR-ABL, CrkL, AKT and STAT5 in imatinib-resistant chronic myeloid leukemia cells implicate alternative pathway usage as a survival strategy.	imatinib	58-66	signal transducer and activator of transcription 5A	Homo sapiens	49-54
18398722-3	2008	The most common mechanisms of resistance to imatinib include BCR-ABL kinase domain mutations, BCR-ABL amplification and overexpression, and clonal evolution with activation of additional transformation pathways.	imatinib	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
18398725-2	2008	Imatinib is transported out of cells by the efflux transporter ABCB1 (MDR1, whose product is p-glycoprotein).	imatinib	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	63-68
18398725-2	2008	Imatinib is transported out of cells by the efflux transporter ABCB1 (MDR1, whose product is p-glycoprotein).	imatinib	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	70-74
18398725-2	2008	Imatinib is transported out of cells by the efflux transporter ABCB1 (MDR1, whose product is p-glycoprotein).	imatinib	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	93-107
18398725-3	2008	By contrast, the influx transporter, human organic cation transporter 1 (hOCT1) (also known as SLC22A1), transports imatinib into cells.	imatinib	116-124	solute carrier family 22 member 1	Homo sapiens	43-71
18398725-3	2008	By contrast, the influx transporter, human organic cation transporter 1 (hOCT1) (also known as SLC22A1), transports imatinib into cells.	imatinib	116-124	solute carrier family 22 member 1	Homo sapiens	73-78
19145825-2	2008	The reduction of CD34+ granulocytes number, normalization of CD95 cells, negative correlation between the number of CD95 and p53, Bcl-2 granulocytes in Imatinib treated patients in comparison with a control group was determined.	imatinib	152-160	Fas cell surface death receptor	Homo sapiens	116-120
18398725-3	2008	By contrast, the influx transporter, human organic cation transporter 1 (hOCT1) (also known as SLC22A1), transports imatinib into cells.	imatinib	116-124	solute carrier family 22 member 1	Homo sapiens	95-102
18448557-2	2008	The development of the Bcr-Abl-targeted imatinib represents a paradigm shift in the treatment of CML, because treatment with imatinib resulted in significantly better patient outcome, response rates, and overall survival compared with previous standards.	imatinib	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
19145825-2	2008	The reduction of CD34+ granulocytes number, normalization of CD95 cells, negative correlation between the number of CD95 and p53, Bcl-2 granulocytes in Imatinib treated patients in comparison with a control group was determined.	imatinib	152-160	BCL2 apoptosis regulator	Homo sapiens	130-135
18516991-7	2008	The patient was treated with imatinib, a KIT tyrosine kinase inhibitor; however, the tumors progressed.	imatinib	29-37	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	41-44
18448557-2	2008	The development of the Bcr-Abl-targeted imatinib represents a paradigm shift in the treatment of CML, because treatment with imatinib resulted in significantly better patient outcome, response rates, and overall survival compared with previous standards.	imatinib	125-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
17934801-0	2008	Constitutive overexpression of P-glycoprotein, rather than breast cancer resistance protein or organic cation transporter 1, contributes to acquisition of imatinib-resistance in K562 cells.	imatinib	155-163	ATP binding cassette subfamily B member 1	Homo sapiens	31-45
17934801-12	2008	CONCLUSIONS: P-gp, rather than BCRP or OCT1, is partially responsible for the development of imatinib-resistance due to constitutive and functional overexpression, leading to reduced intracellular accumulation of imatinib in K562/IM.	imatinib	93-101	ATP binding cassette subfamily B member 1	Homo sapiens	13-17
18448557-4	2008	Resistance to imatinib can develop from a number of mechanisms that can be defined as Bcr-Abl-dependent (e.g., most commonly resulting from point mutations in the Abl kinase domain) and Bcr-Abl-independent mechanisms (including the constitutive activation of downstream signaling molecules, e.g., Src family kinases), which could result in the activation of the pathway regardless of Bcr-Abl inhibition.	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
17934801-12	2008	CONCLUSIONS: P-gp, rather than BCRP or OCT1, is partially responsible for the development of imatinib-resistance due to constitutive and functional overexpression, leading to reduced intracellular accumulation of imatinib in K562/IM.	imatinib	93-101	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	31-35
17934801-12	2008	CONCLUSIONS: P-gp, rather than BCRP or OCT1, is partially responsible for the development of imatinib-resistance due to constitutive and functional overexpression, leading to reduced intracellular accumulation of imatinib in K562/IM.	imatinib	93-101	solute carrier family 22 member 1	Homo sapiens	39-43
18428043-9	2008	Point mutations in the kinase domain of BCR-ABL are the most common cause of acquired resistance to imatinib treatment.	imatinib	100-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
18448557-4	2008	Resistance to imatinib can develop from a number of mechanisms that can be defined as Bcr-Abl-dependent (e.g., most commonly resulting from point mutations in the Abl kinase domain) and Bcr-Abl-independent mechanisms (including the constitutive activation of downstream signaling molecules, e.g., Src family kinases), which could result in the activation of the pathway regardless of Bcr-Abl inhibition.	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-193
17934801-12	2008	CONCLUSIONS: P-gp, rather than BCRP or OCT1, is partially responsible for the development of imatinib-resistance due to constitutive and functional overexpression, leading to reduced intracellular accumulation of imatinib in K562/IM.	imatinib	213-221	ATP binding cassette subfamily B member 1	Homo sapiens	13-17
18448557-4	2008	Resistance to imatinib can develop from a number of mechanisms that can be defined as Bcr-Abl-dependent (e.g., most commonly resulting from point mutations in the Abl kinase domain) and Bcr-Abl-independent mechanisms (including the constitutive activation of downstream signaling molecules, e.g., Src family kinases), which could result in the activation of the pathway regardless of Bcr-Abl inhibition.	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-193
18448557-8	2008	Dasatinib, a dual Bcr-Abl/Src kinase inhibitor, has shown efficacy against all imatinib-resistant Bcr-Abl mutations except for T315I.	imatinib	79-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
18448557-8	2008	Dasatinib, a dual Bcr-Abl/Src kinase inhibitor, has shown efficacy against all imatinib-resistant Bcr-Abl mutations except for T315I.	imatinib	79-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
18180382-6	2008	Knockdown of Fyn with shRNA slows leukemia cell growth, inhibits clonogenicity, and leads to increased sensitivity to imatinib, indicating that Fyn mediates CML cell proliferation.	imatinib	118-126	Fyn proto-oncogene	Mus musculus	13-16
18843975-0	2008	[Imatinib induces c-kit positive myeloma cells apoptosis].	imatinib	1-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	18-23
18843975-1	2008	OBJECTIVE: To explore the influence of Imatinib on multiple myeloma cells expressing c-kit in vitro and its mechanism.	imatinib	39-47	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	85-90
18843975-5	2008	Annexin V/PI staining and DNA ladder indicated that Imatinib had a substantial effect on inducing apoptosis of KM3 cells in a dose-dependent manner and induced pro-caspase-3 and poly ADP-ribose polymerase (PARP) cleaved.	imatinib	52-60	annexin A5	Homo sapiens	0-9
18843975-5	2008	Annexin V/PI staining and DNA ladder indicated that Imatinib had a substantial effect on inducing apoptosis of KM3 cells in a dose-dependent manner and induced pro-caspase-3 and poly ADP-ribose polymerase (PARP) cleaved.	imatinib	52-60	caspase 3	Homo sapiens	160-173
18843975-5	2008	Annexin V/PI staining and DNA ladder indicated that Imatinib had a substantial effect on inducing apoptosis of KM3 cells in a dose-dependent manner and induced pro-caspase-3 and poly ADP-ribose polymerase (PARP) cleaved.	imatinib	52-60	poly(ADP-ribose) polymerase 1	Homo sapiens	178-204
18843975-5	2008	Annexin V/PI staining and DNA ladder indicated that Imatinib had a substantial effect on inducing apoptosis of KM3 cells in a dose-dependent manner and induced pro-caspase-3 and poly ADP-ribose polymerase (PARP) cleaved.	imatinib	52-60	poly(ADP-ribose) polymerase 1	Homo sapiens	206-210
18843975-6	2008	Imatinib inhibited expression of c-kit and provoked a decrease of IL-6 induced c-kit phosphorylation in vitro.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	33-38
18843975-6	2008	Imatinib inhibited expression of c-kit and provoked a decrease of IL-6 induced c-kit phosphorylation in vitro.	imatinib	0-8	interleukin 6	Homo sapiens	66-70
18843975-6	2008	Imatinib inhibited expression of c-kit and provoked a decrease of IL-6 induced c-kit phosphorylation in vitro.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	79-84
18843975-7	2008	CONCLUSION: Imatinib inhibits KM3 cells proliferation and induces the cells apoptosis by inhibiting c-kit signalling transduction.	imatinib	12-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	100-105
17960378-5	2008	In marked contrast, deletion of p21 promoted apoptosis induction by imatinib and taxol in BCR-ABL-transformed BM cells.	imatinib	68-76	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	32-35
18188833-6	2008	CYP3A4 isozyme showed the broadest metabolic capacity, whereas CYP1A1, CYP1B1 and FMO3 isozymes biotransformed imatinib with a high intrinsic clearance.	imatinib	111-119	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	82-86
18188833-8	2008	These findings indicate that CYP1A1 and CYP1B1, which are known to be overexpressed in a wide range of tumors, are involved in the biotransformation of imatinib.	imatinib	152-160	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	29-35
18188833-8	2008	These findings indicate that CYP1A1 and CYP1B1, which are known to be overexpressed in a wide range of tumors, are involved in the biotransformation of imatinib.	imatinib	152-160	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	40-46
18223253-2	2008	We have previously shown that the mTOR/p70 S6 kinase (p70 S6K) pathway is constitutively activated in BCR-ABL transformed cells and that inhibition of BCR-ABL kinase activity by imatinib mesylate abrogates such activation.	imatinib	178-195	mechanistic target of rapamycin kinase	Homo sapiens	34-38
18223253-2	2008	We have previously shown that the mTOR/p70 S6 kinase (p70 S6K) pathway is constitutively activated in BCR-ABL transformed cells and that inhibition of BCR-ABL kinase activity by imatinib mesylate abrogates such activation.	imatinib	178-195	ribosomal protein S6 kinase B1	Homo sapiens	54-61
18223253-2	2008	We have previously shown that the mTOR/p70 S6 kinase (p70 S6K) pathway is constitutively activated in BCR-ABL transformed cells and that inhibition of BCR-ABL kinase activity by imatinib mesylate abrogates such activation.	imatinib	178-195	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
18223253-2	2008	We have previously shown that the mTOR/p70 S6 kinase (p70 S6K) pathway is constitutively activated in BCR-ABL transformed cells and that inhibition of BCR-ABL kinase activity by imatinib mesylate abrogates such activation.	imatinib	178-195	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-158
18223253-6	2008	Knockdown of PDCD4 expression results in reversal of the suppressive effects of nilotinib and imatinib mesylate on leukemic progenitor colony formation, suggesting an important role for this protein in the generation of antileukemic responses.	imatinib	94-102	programmed cell death 4	Homo sapiens	13-18
17876770-0	2008	Sustained remissions and low rate of BCR-ABL resistance mutations with imatinib treatment chronic myelogenous leukemia in patients treated in late chronic phase: a 5-year follow up.	imatinib	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
18042796-1	2008	Imatinib inhibits tyrosine kinases important in osteoclast (c-Fms) and osteoblast (platelet-derived growth factor receptor [PDGF-R], c-Abl) function, suggesting that long-term therapy may alter bone homeostasis.	imatinib	0-8	colony stimulating factor 1 receptor	Homo sapiens	60-65
18042796-1	2008	Imatinib inhibits tyrosine kinases important in osteoclast (c-Fms) and osteoblast (platelet-derived growth factor receptor [PDGF-R], c-Abl) function, suggesting that long-term therapy may alter bone homeostasis.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	124-131
18042796-1	2008	Imatinib inhibits tyrosine kinases important in osteoclast (c-Fms) and osteoblast (platelet-derived growth factor receptor [PDGF-R], c-Abl) function, suggesting that long-term therapy may alter bone homeostasis.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-138
18042796-6	2008	In PDGF-stimulated cultures, imatinib dose-dependently inhibited activation of Akt and Crk-L.	imatinib	29-37	AKT serine/threonine kinase 1	Homo sapiens	79-82
18042796-6	2008	In PDGF-stimulated cultures, imatinib dose-dependently inhibited activation of Akt and Crk-L.	imatinib	29-37	CRK like proto-oncogene, adaptor protein	Homo sapiens	87-92
18042796-7	2008	Using pharmacologic inhibitors, inhibition of PI3-kinase/Akt activation promoted mineral formation, suggesting a possible molecular mechanism for the imatinib-mediated increase in TBV in vivo.	imatinib	150-158	AKT serine/threonine kinase 1	Homo sapiens	57-60
18188833-6	2008	CYP3A4 isozyme showed the broadest metabolic capacity, whereas CYP1A1, CYP1B1 and FMO3 isozymes biotransformed imatinib with a high intrinsic clearance.	imatinib	111-119	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	71-77
18188833-0	2008	In vitro biotransformation of imatinib by the tumor expressed CYP1A1 and CYP1B1.	imatinib	30-38	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	62-68
18188833-0	2008	In vitro biotransformation of imatinib by the tumor expressed CYP1A1 and CYP1B1.	imatinib	30-38	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	73-79
18188833-6	2008	CYP3A4 isozyme showed the broadest metabolic capacity, whereas CYP1A1, CYP1B1 and FMO3 isozymes biotransformed imatinib with a high intrinsic clearance.	imatinib	111-119	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
18188833-6	2008	CYP3A4 isozyme showed the broadest metabolic capacity, whereas CYP1A1, CYP1B1 and FMO3 isozymes biotransformed imatinib with a high intrinsic clearance.	imatinib	111-119	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	63-69
18094612-1	2008	PURPOSE: Chronic imatinib exposure has been shown to result in upregulation of the ABCB1 (P-glycoprotein) and ABCG2 (BCRP) transporters in vitro, for which imatinib is a substrate.	imatinib	17-25	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	83-88
18094612-1	2008	PURPOSE: Chronic imatinib exposure has been shown to result in upregulation of the ABCB1 (P-glycoprotein) and ABCG2 (BCRP) transporters in vitro, for which imatinib is a substrate.	imatinib	17-25	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	110-115
18094612-1	2008	PURPOSE: Chronic imatinib exposure has been shown to result in upregulation of the ABCB1 (P-glycoprotein) and ABCG2 (BCRP) transporters in vitro, for which imatinib is a substrate.	imatinib	17-25	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	117-121
18094612-1	2008	PURPOSE: Chronic imatinib exposure has been shown to result in upregulation of the ABCB1 (P-glycoprotein) and ABCG2 (BCRP) transporters in vitro, for which imatinib is a substrate.	imatinib	156-164	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	83-88
18094612-1	2008	PURPOSE: Chronic imatinib exposure has been shown to result in upregulation of the ABCB1 (P-glycoprotein) and ABCG2 (BCRP) transporters in vitro, for which imatinib is a substrate.	imatinib	156-164	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	110-115
19688062-4	2008	STI-571 may constitute a promising therapeutic agent against neuroblastoma, particularly in cases in which c-Kit is expressed preferentially in MYCN-amplified neuroblastoma.	imatinib	0-7	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	107-112
18094612-1	2008	PURPOSE: Chronic imatinib exposure has been shown to result in upregulation of the ABCB1 (P-glycoprotein) and ABCG2 (BCRP) transporters in vitro, for which imatinib is a substrate.	imatinib	156-164	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	117-121
19688062-4	2008	STI-571 may constitute a promising therapeutic agent against neuroblastoma, particularly in cases in which c-Kit is expressed preferentially in MYCN-amplified neuroblastoma.	imatinib	0-7	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	144-148
18190601-2	2008	Because imatinib, a selective inhibitor of the ABL, ARG, PDGFR and c-KIT tyrosine kinases, inhibits T cell activation, this study was conducted to evaluate the potential use of imatinib for the treatment AAV patients refractory to conventional therapy.	imatinib	8-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
19688062-6	2008	RESULTS: MYCN siRNA-treated SK-N-BE(2) cells did not affect apoptosis and cells were arrested in G0/G1 phase after STI-571 treatment.	imatinib	115-122	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	9-13
18190601-2	2008	Because imatinib, a selective inhibitor of the ABL, ARG, PDGFR and c-KIT tyrosine kinases, inhibits T cell activation, this study was conducted to evaluate the potential use of imatinib for the treatment AAV patients refractory to conventional therapy.	imatinib	8-16	platelet derived growth factor receptor beta	Homo sapiens	57-62
18190601-10	2008	The expression of CD25 in naive and memory T cells was decreased significantly by imatinib in activated T cells.	imatinib	82-90	interleukin 2 receptor subunit alpha	Homo sapiens	18-22
18214408-6	2008	Patients with hypereosinophilic syndrome should be tested for the presence of the FIP1L1-PDGRFA-mutatition in order to identify patients that could benefit from a treatment with a tyrosine kinase inhibitor such as Imatinib.	imatinib	214-222	factor interacting with PAPOLA and CPSF1	Homo sapiens	82-88
18190601-12	2008	Imatinib did not influence interleukin-2 and tumour necrosis factor-alpha production but increased interferon-gamma production.	imatinib	0-8	interferon gamma	Homo sapiens	99-115
18234488-4	2008	However, two groups benefited from the treatment with 800 mg/d of imatinib: patients with disease progression on standard-dose therapy, and patients whose tumour harbours an exon 9 mutation in KIT.	imatinib	66-74	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	193-196
18234488-5	2008	Initial treatment with 800 mg/d of imatinib (400mg BID) should be considered for patients with KIT exon 9-mutant GIST.	imatinib	35-43	BH3 interacting domain death agonist	Homo sapiens	51-54
18234488-5	2008	Initial treatment with 800 mg/d of imatinib (400mg BID) should be considered for patients with KIT exon 9-mutant GIST.	imatinib	35-43	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	95-98
19254881-2	2008	However, point mutations in the kinase domain of Bcr-Abl can lead to imatinib resistance and reactivation of kinase activity.	imatinib	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
19254884-2	2008	The first oral inhibitor of Brc-Abl was imatinib, which also targets KIT and platelet-derived growth factor receptor kinase and has demonstrated improved outcomes when compared with interferon, the previous standard of care.	imatinib	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-35
19254884-2	2008	The first oral inhibitor of Brc-Abl was imatinib, which also targets KIT and platelet-derived growth factor receptor kinase and has demonstrated improved outcomes when compared with interferon, the previous standard of care.	imatinib	40-48	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	69-72
19254885-2	2008	The success of imatinib relies on its potent inhibitory activity against the Bcr-Abl kinase that drives the pathogenesis of this disorder.	imatinib	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
18276770-1	2008	Although targeted inhibition of BCR-ABL with imatinib is an effective therapy for patients with chronic myeloid leukemia (CML), a minority of patients acquire mutations in the BCR-ABL kinase domain, resulting in imatinib resistance.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
17661356-2	2008	This is important since the TyrK inhibitor STI571 (Glivec) inhibits proliferation and induces apoptosis in HMC-1(560).	imatinib	43-49	TXK tyrosine kinase	Homo sapiens	28-32
17661356-4	2008	The TyrK inhibitors STI571, lavendustin A and genistein decrease spontaneous histamine release in 24-h pre-incubated cells.	imatinib	20-26	TXK tyrosine kinase	Homo sapiens	4-8
18276770-1	2008	Although targeted inhibition of BCR-ABL with imatinib is an effective therapy for patients with chronic myeloid leukemia (CML), a minority of patients acquire mutations in the BCR-ABL kinase domain, resulting in imatinib resistance.	imatinib	212-220	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
18276770-1	2008	Although targeted inhibition of BCR-ABL with imatinib is an effective therapy for patients with chronic myeloid leukemia (CML), a minority of patients acquire mutations in the BCR-ABL kinase domain, resulting in imatinib resistance.	imatinib	212-220	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	176-183
17822760-0	2008	Imatinib mesylate (IM)-induced growth inhibition is associated with production of spliced osteocalcin-mRNA in cell lines.	imatinib	0-17	bone gamma-carboxyglutamate protein	Homo sapiens	90-101
17570524-0	2008	A recurrent splicing variant without c-ABL Exon 7 in Imatinib-resistant patients.	imatinib	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-42
17822760-0	2008	Imatinib mesylate (IM)-induced growth inhibition is associated with production of spliced osteocalcin-mRNA in cell lines.	imatinib	19-21	bone gamma-carboxyglutamate protein	Homo sapiens	90-101
18059481-9	2008	Imatinib promoted nuclear transport of p210(BCR-ABL)-positive foci.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
17910071-0	2008	Classifying protein kinase structures guides use of ligand-selectivity profiles to predict inactive conformations: structure of lck/imatinib complex.	imatinib	132-140	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	128-131
18079735-1	2008	Small molecule tyrosine kinase inhibitors, such as imatinib, are effective therapies for BCR-ABL-mediated human leukemias.	imatinib	51-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
18079735-7	2008	Furthermore, R18-induced apoptotic cell death in cells expressing diverse imatinib-resistant BCR-ABL mutants, including T315I.	imatinib	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
18337118-3	2008	Imatinib is transported by human and rodent ATP-binding cassette (ABC) transporters like P-glycoprotein (Pgp) and the breast cancer resistance protein (BCRP).	imatinib	0-8	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	44-64
18337118-3	2008	Imatinib is transported by human and rodent ATP-binding cassette (ABC) transporters like P-glycoprotein (Pgp) and the breast cancer resistance protein (BCRP).	imatinib	0-8	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	66-69
18337118-3	2008	Imatinib is transported by human and rodent ATP-binding cassette (ABC) transporters like P-glycoprotein (Pgp) and the breast cancer resistance protein (BCRP).	imatinib	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	89-103
18337118-3	2008	Imatinib is transported by human and rodent ATP-binding cassette (ABC) transporters like P-glycoprotein (Pgp) and the breast cancer resistance protein (BCRP).	imatinib	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	105-108
18337118-3	2008	Imatinib is transported by human and rodent ATP-binding cassette (ABC) transporters like P-glycoprotein (Pgp) and the breast cancer resistance protein (BCRP).	imatinib	0-8	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	118-150
18337118-3	2008	Imatinib is transported by human and rodent ATP-binding cassette (ABC) transporters like P-glycoprotein (Pgp) and the breast cancer resistance protein (BCRP).	imatinib	0-8	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	152-156
18337118-4	2008	We have investigated whether ABC transporters determine the pharmacokinetics of imatinib and its pharmacological active metabolite CGP74588 in rat C6 glioma cells.	imatinib	80-88	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	29-32
18243733-6	2008	Furthermore, the PDGFR kinase inhibitor STI571 blocked the effects of bFGF in control neurosphere cultures.	imatinib	40-46	fibroblast growth factor 2	Mus musculus	70-74
18194138-9	2008	Recently, the resulting FIP1L1-PDGFRalpha fusion gene was characterized as a marker of response to imatinib.	imatinib	99-107	factor interacting with PAPOLA and CPSF1	Homo sapiens	24-30
18337118-8	2008	The accumulation of imatinib into C6 cells increased linearly with the extracellular concentration of imatinib (0.5-50microM) and was not increased by zosuquidar (selective Pgp inhibitor) or elacridar (inhibitor of both Pgp and Bcrp).	imatinib	20-28	phosphoglycolate phosphatase	Rattus norvegicus	173-176
17910071-7	2008	For example, selective inhibition of lck among src-family kinases by imatinib (Gleevec) suggests that the relative stabilities of inactive conformations of lck are different from other src-family kinases.	imatinib	69-77	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	37-40
18337118-8	2008	The accumulation of imatinib into C6 cells increased linearly with the extracellular concentration of imatinib (0.5-50microM) and was not increased by zosuquidar (selective Pgp inhibitor) or elacridar (inhibitor of both Pgp and Bcrp).	imatinib	20-28	phosphoglycolate phosphatase	Rattus norvegicus	220-223
18337118-8	2008	The accumulation of imatinib into C6 cells increased linearly with the extracellular concentration of imatinib (0.5-50microM) and was not increased by zosuquidar (selective Pgp inhibitor) or elacridar (inhibitor of both Pgp and Bcrp).	imatinib	20-28	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	228-232
17910071-7	2008	For example, selective inhibition of lck among src-family kinases by imatinib (Gleevec) suggests that the relative stabilities of inactive conformations of lck are different from other src-family kinases.	imatinib	69-77	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	156-159
17910071-8	2008	We report the X-ray structure of the lck/imatinib complex, confirming that the conformation adopted by lck is distinct from other structurally-characterized src-family kinases and instead resembles kinases abl1 and kit in complex with imatinib.	imatinib	41-49	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	37-40
17910071-8	2008	We report the X-ray structure of the lck/imatinib complex, confirming that the conformation adopted by lck is distinct from other structurally-characterized src-family kinases and instead resembles kinases abl1 and kit in complex with imatinib.	imatinib	41-49	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	103-106
17910071-8	2008	We report the X-ray structure of the lck/imatinib complex, confirming that the conformation adopted by lck is distinct from other structurally-characterized src-family kinases and instead resembles kinases abl1 and kit in complex with imatinib.	imatinib	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	206-210
17910071-8	2008	We report the X-ray structure of the lck/imatinib complex, confirming that the conformation adopted by lck is distinct from other structurally-characterized src-family kinases and instead resembles kinases abl1 and kit in complex with imatinib.	imatinib	235-243	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	37-40
17910071-8	2008	We report the X-ray structure of the lck/imatinib complex, confirming that the conformation adopted by lck is distinct from other structurally-characterized src-family kinases and instead resembles kinases abl1 and kit in complex with imatinib.	imatinib	235-243	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	103-106
17910071-8	2008	We report the X-ray structure of the lck/imatinib complex, confirming that the conformation adopted by lck is distinct from other structurally-characterized src-family kinases and instead resembles kinases abl1 and kit in complex with imatinib.	imatinib	235-243	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	206-210
18086564-4	2008	The FIP1L1-PDGFRalpha inhibitor imatinib inhibited the proliferation of EoL-1 cells and decreased the level of the oncoprotein c-Myc as well as the phosphorylation of extracellular signal-regulated kinase and c-Jun N-terminal kinase (JNK).	imatinib	32-40	factor interacting with PAPOLA and CPSF1	Homo sapiens	4-10
18086564-4	2008	The FIP1L1-PDGFRalpha inhibitor imatinib inhibited the proliferation of EoL-1 cells and decreased the level of the oncoprotein c-Myc as well as the phosphorylation of extracellular signal-regulated kinase and c-Jun N-terminal kinase (JNK).	imatinib	32-40	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	127-132
18086564-4	2008	The FIP1L1-PDGFRalpha inhibitor imatinib inhibited the proliferation of EoL-1 cells and decreased the level of the oncoprotein c-Myc as well as the phosphorylation of extracellular signal-regulated kinase and c-Jun N-terminal kinase (JNK).	imatinib	32-40	platelet derived growth factor receptor alpha	Homo sapiens	11-21
18086564-4	2008	The FIP1L1-PDGFRalpha inhibitor imatinib inhibited the proliferation of EoL-1 cells and decreased the level of the oncoprotein c-Myc as well as the phosphorylation of extracellular signal-regulated kinase and c-Jun N-terminal kinase (JNK).	imatinib	32-40	mitogen-activated protein kinase 8	Homo sapiens	209-232
18024796-5	2008	The effects of PEG-ZnPP and SMA-ZnPP were demonstrable in Ba/F3 cells carrying various imatinib-resistant mutants of BCR/ABL, including the T315I mutant, which exhibits resistance against all clinically available BCR/ABL tyrosine kinase inhibitors.	imatinib	87-95	BCR activator of RhoGEF and GTPase	Mus musculus	117-124
18086564-4	2008	The FIP1L1-PDGFRalpha inhibitor imatinib inhibited the proliferation of EoL-1 cells and decreased the level of the oncoprotein c-Myc as well as the phosphorylation of extracellular signal-regulated kinase and c-Jun N-terminal kinase (JNK).	imatinib	32-40	mitogen-activated protein kinase 8	Homo sapiens	234-237
17615556-7	2008	Strangely, STI571 pre-incubated cells with PKC inhibited by rottlerin show the same effects.	imatinib	11-17	proline rich transmembrane protein 2	Homo sapiens	43-46
18024796-0	2008	Targeting of heat shock protein 32 (Hsp32)/heme oxygenase-1 (HO-1) in leukemic cells in chronic myeloid leukemia: a novel approach to overcome resistance against imatinib.	imatinib	162-170	heme oxygenase 1	Homo sapiens	13-34
18024796-0	2008	Targeting of heat shock protein 32 (Hsp32)/heme oxygenase-1 (HO-1) in leukemic cells in chronic myeloid leukemia: a novel approach to overcome resistance against imatinib.	imatinib	162-170	heme oxygenase 1	Homo sapiens	36-41
18024796-0	2008	Targeting of heat shock protein 32 (Hsp32)/heme oxygenase-1 (HO-1) in leukemic cells in chronic myeloid leukemia: a novel approach to overcome resistance against imatinib.	imatinib	162-170	heme oxygenase 1	Homo sapiens	43-59
18024796-0	2008	Targeting of heat shock protein 32 (Hsp32)/heme oxygenase-1 (HO-1) in leukemic cells in chronic myeloid leukemia: a novel approach to overcome resistance against imatinib.	imatinib	162-170	heme oxygenase 1	Homo sapiens	61-65
18024796-7	2008	Finally, Hsp32/HO-1-targeting compounds were found to synergize with either imatinib or nilotinib in producing growth inhibition in imatinib-resistant K562 cells and in Ba/F3 cells harboring the T315I mutant of BCR/ABL.	imatinib	76-84	heme oxygenase 1	Homo sapiens	9-14
18024796-7	2008	Finally, Hsp32/HO-1-targeting compounds were found to synergize with either imatinib or nilotinib in producing growth inhibition in imatinib-resistant K562 cells and in Ba/F3 cells harboring the T315I mutant of BCR/ABL.	imatinib	76-84	heme oxygenase 1	Homo sapiens	15-19
18024796-7	2008	Finally, Hsp32/HO-1-targeting compounds were found to synergize with either imatinib or nilotinib in producing growth inhibition in imatinib-resistant K562 cells and in Ba/F3 cells harboring the T315I mutant of BCR/ABL.	imatinib	132-140	heme oxygenase 1	Homo sapiens	9-14
18024796-7	2008	Finally, Hsp32/HO-1-targeting compounds were found to synergize with either imatinib or nilotinib in producing growth inhibition in imatinib-resistant K562 cells and in Ba/F3 cells harboring the T315I mutant of BCR/ABL.	imatinib	132-140	heme oxygenase 1	Homo sapiens	15-19
18024796-7	2008	Finally, Hsp32/HO-1-targeting compounds were found to synergize with either imatinib or nilotinib in producing growth inhibition in imatinib-resistant K562 cells and in Ba/F3 cells harboring the T315I mutant of BCR/ABL.	imatinib	132-140	BCR activator of RhoGEF and GTPase	Mus musculus	211-218
18024796-8	2008	In summary, these data show that HO-1 is a promising novel target in imatinib-resistant CML.	imatinib	69-77	heme oxygenase 1	Homo sapiens	33-37
18376233-3	2008	Imatinib, a potent inhibitor of BCR-ABL and c-kit, also inhibits the platelet-derived growth factor receptor tyrosine kinase.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
18376233-3	2008	Imatinib, a potent inhibitor of BCR-ABL and c-kit, also inhibits the platelet-derived growth factor receptor tyrosine kinase.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	44-49
17932248-11	2008	Imatinib continues to be an effective and safe therapy for patients with CP CML after failure of IFN.	imatinib	0-8	interferon alpha 1	Homo sapiens	97-100
18078752-3	2008	The most active compound identified from the enzymatic screening (6a) showed interesting inhibitory activity on Imatinib-sensitive murine myeloid 3B clone and Bcr-Abl-independent Imatinib-resistant leukemia cells.	imatinib	179-187	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	163-166
18240216-8	2008	Blocking platelet-derived growth factor receptor with Gleevec (imatinib mesylate) reduced overall contractile ability and the elevated syndecan 4 expression and ERK activation in SSc fibroblasts.	imatinib	63-80	syndecan 4	Homo sapiens	135-145
18240216-8	2008	Blocking platelet-derived growth factor receptor with Gleevec (imatinib mesylate) reduced overall contractile ability and the elevated syndecan 4 expression and ERK activation in SSc fibroblasts.	imatinib	63-80	mitogen-activated protein kinase 1	Homo sapiens	161-164
17992189-8	2008	Treatment of cells with the c-Abl1 tyrosine kinase inhibitor STI571 decreased STAT1 activation by genotoxic drugs.	imatinib	61-67	signal transducer and activator of transcription 1	Mus musculus	78-83
17953711-8	2008	Imatinib, an inhibitor of the c-Abl kinase, has been investigated as a sensitizer in DNA-damaging therapy, because c-Abl activates Rad51, which plays a key role in HR.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-35
18262053-0	2008	Fusion of PRKG2 and SPTBN1 to the platelet-derived growth factor receptor beta gene (PDGFRB) in imatinib-responsive atypical myeloproliferative disorders.	imatinib	96-104	protein kinase cGMP-dependent 2	Homo sapiens	10-15
17953711-8	2008	Imatinib, an inhibitor of the c-Abl kinase, has been investigated as a sensitizer in DNA-damaging therapy, because c-Abl activates Rad51, which plays a key role in HR.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-120
17953711-8	2008	Imatinib, an inhibitor of the c-Abl kinase, has been investigated as a sensitizer in DNA-damaging therapy, because c-Abl activates Rad51, which plays a key role in HR.	imatinib	0-8	RAD51 recombinase	Homo sapiens	131-136
18262053-0	2008	Fusion of PRKG2 and SPTBN1 to the platelet-derived growth factor receptor beta gene (PDGFRB) in imatinib-responsive atypical myeloproliferative disorders.	imatinib	96-104	spectrin beta, non-erythrocytic 1	Homo sapiens	20-26
18262053-0	2008	Fusion of PRKG2 and SPTBN1 to the platelet-derived growth factor receptor beta gene (PDGFRB) in imatinib-responsive atypical myeloproliferative disorders.	imatinib	96-104	platelet derived growth factor receptor beta	Homo sapiens	34-78
18262053-0	2008	Fusion of PRKG2 and SPTBN1 to the platelet-derived growth factor receptor beta gene (PDGFRB) in imatinib-responsive atypical myeloproliferative disorders.	imatinib	96-104	platelet derived growth factor receptor beta	Homo sapiens	85-91
17568400-0	2008	Expression of the uptake drug transporter hOCT1 is an important clinical determinant of the response to imatinib in chronic myeloid leukemia.	imatinib	104-112	solute carrier family 22 member 1	Homo sapiens	42-47
17568400-6	2008	Imatinib uptake into a CML cell line with high hOCT1 expression was greater than into those with modest or low expression (P=0.002).	imatinib	0-8	solute carrier family 22 member 1	Homo sapiens	47-52
17568400-7	2008	The expression of hOCT1, but not efflux transporters, is important in determining the clinical response to imatinib.	imatinib	107-115	solute carrier family 22 member 1	Homo sapiens	18-23
18223278-0	2008	Dynamics of BCR-ABL mutated clones prior to hematologic or cytogenetic resistance to imatinib.	imatinib	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
18223278-8	2008	In patients harboring mutations, hematologic relapse occurred after a median of 12.9 months (range, 0.9-44.2), and BCR-ABL mutations first became detectable at a median of 5.8 months (range, 0-30.5) after starting imatinib therapy (p<0.0001).	imatinib	214-222	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
18223278-10	2008	CONCLUSIONS: We conclude that: (i) D-HPLC is a sensitive method for screening for BCR-ABL mutations before and during therapy with tyrosine kinase inhibitors; (ii) the occurrence of BCR-ABL mutations during imatinib therapy is predictive of relapse; (iii) mutations may be detectable several months before relapse, and (iv) the sensitive detection of small numbers of mutated clones could provide clinical benefit by triggering early therapeutic interventions.	imatinib	207-215	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
18223278-10	2008	CONCLUSIONS: We conclude that: (i) D-HPLC is a sensitive method for screening for BCR-ABL mutations before and during therapy with tyrosine kinase inhibitors; (ii) the occurrence of BCR-ABL mutations during imatinib therapy is predictive of relapse; (iii) mutations may be detectable several months before relapse, and (iv) the sensitive detection of small numbers of mutated clones could provide clinical benefit by triggering early therapeutic interventions.	imatinib	207-215	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-189
17614352-4	2008	Interestingly, phosphorylated-PDGFRalpha expression was significantly downregulated by imatinib.	imatinib	87-95	platelet derived growth factor receptor alpha	Homo sapiens	30-40
17943734-13	2008	Germ-line deletion of KIT codon 579 in GIST is associated with clinical benefit from imatinib, limited utility of mitoses to predict malignant potential, and a novel homozygous deletion of this codon in one individual.	imatinib	85-93	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	22-25
17614352-11	2008	Furthermore, incubation with progesterone seems to prompt cells to the inhibitory action of imatinib, probably by sustaining PDGFRalpha activity.	imatinib	92-100	platelet derived growth factor receptor alpha	Homo sapiens	125-135
18190445-0	2008	Platelet-derived growth factor receptor alpha mutational status and immunohistochemical expression in Merkel cell carcinoma: implications for treatment with imatinib mesylate.	imatinib	157-174	platelet derived growth factor receptor alpha	Homo sapiens	0-45
17827398-10	2008	The great majority of mutations were located in KIT exon 11, statistically associated with worse prognosis and indicative of favourable response to imatinib-based therapy in this Portuguese series of GISTs.	imatinib	148-156	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	48-51
18245668-5	2008	Here, we show that a highly specific inhibitor of IkappaB kinase beta, a key upstream regulator of the NF-kappaB pathway, induces growth suppression and death in cells expressing wild-type, Imatinib-resistant, or the T315I Imatinib/Dasatinib-resistant forms of BCR-ABL.	imatinib	223-231	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	50-69
18235121-0	2008	Long-term results from a randomized phase II trial of standard- versus higher-dose imatinib mesylate for patients with unresectable or metastatic gastrointestinal stromal tumors expressing KIT.	imatinib	83-100	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	189-192
18245668-0	2008	IkappaB kinase beta inhibition induces cell death in Imatinib-resistant and T315I Dasatinib-resistant BCR-ABL+ cells.	imatinib	53-61	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	0-19
18192285-5	2008	Exposure of chick embryos to the PDGFR inhibitor imatinib mesylate resulted in spina bifida in the absence of NTDs.	imatinib	49-66	platelet-derived growth factor receptor, alpha polypeptide	Gallus gallus	33-38
17690695-0	2008	Evidence for the interaction of imatinib at the transport-substrate site(s) of the multidrug-resistance-linked ABC drug transporters ABCB1 (P-glycoprotein) and ABCG2.	imatinib	32-40	ATP binding cassette subfamily B member 1	Homo sapiens	133-138
17690695-0	2008	Evidence for the interaction of imatinib at the transport-substrate site(s) of the multidrug-resistance-linked ABC drug transporters ABCB1 (P-glycoprotein) and ABCG2.	imatinib	32-40	ATP binding cassette subfamily B member 1	Homo sapiens	140-154
17690695-0	2008	Evidence for the interaction of imatinib at the transport-substrate site(s) of the multidrug-resistance-linked ABC drug transporters ABCB1 (P-glycoprotein) and ABCG2.	imatinib	32-40	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	160-165
17690698-0	2008	CD34+/Ph+ cells are still detectable in chronic myeloid leukemia patients with sustained and prolonged complete cytogenetic remission during treatment with imatinib mesylate.	imatinib	156-173	CD34 molecule	Homo sapiens	0-4
17692911-4	2008	Imatinib treatment resulted in a progressive and consistent decline of the residual disease as measured by quantitative PCR (RQ-PCR) in all but one of the 26 patients; at the end of follow-up, after a median of 32 months (range 21-49) of treatment, a major molecular response (BCR/ABL levels <0.1) was reached in 20 patients (77%), and BCR/ABL transcripts were undetectable in 13 (50%).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	277-284
17692911-4	2008	Imatinib treatment resulted in a progressive and consistent decline of the residual disease as measured by quantitative PCR (RQ-PCR) in all but one of the 26 patients; at the end of follow-up, after a median of 32 months (range 21-49) of treatment, a major molecular response (BCR/ABL levels <0.1) was reached in 20 patients (77%), and BCR/ABL transcripts were undetectable in 13 (50%).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	339-346
17692911-6	2008	These results indicate that patients induced into CCR by IFN treatment represent a subset with very favourable prognosis, which can significantly improve molecular response with imatinib and further support investigative treatment schedules combining these two drugs.	imatinib	178-186	interferon alpha 1	Homo sapiens	57-60
17915318-1	2008	Imatinib and retinoids induce apoptosis in FIP1L1/PDGFRalpha-positive EoL-1 leukemia cells.	imatinib	0-8	factor interacting with PAPOLA and CPSF1	Homo sapiens	43-49
17915318-1	2008	Imatinib and retinoids induce apoptosis in FIP1L1/PDGFRalpha-positive EoL-1 leukemia cells.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	50-60
17915318-2	2008	Although imatinib induces complete remission in most FIP1L1/PDGFRalpha-positive patients, response to imatinib is sometimes suboptimal.	imatinib	9-17	factor interacting with PAPOLA and CPSF1	Homo sapiens	53-59
17915318-2	2008	Although imatinib induces complete remission in most FIP1L1/PDGFRalpha-positive patients, response to imatinib is sometimes suboptimal.	imatinib	9-17	platelet derived growth factor receptor alpha	Homo sapiens	60-70
18281522-1	2008	Altered radiation responses by STI571 (Imatinib, Glivec), a specific inhibitor of the tyrosine kinase activity of Bcr-Abl, was assessed in K562 chronic myelogenous leukemia cells using growth inhibition and colony formation assays.	imatinib	31-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
18281522-1	2008	Altered radiation responses by STI571 (Imatinib, Glivec), a specific inhibitor of the tyrosine kinase activity of Bcr-Abl, was assessed in K562 chronic myelogenous leukemia cells using growth inhibition and colony formation assays.	imatinib	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
18281522-1	2008	Altered radiation responses by STI571 (Imatinib, Glivec), a specific inhibitor of the tyrosine kinase activity of Bcr-Abl, was assessed in K562 chronic myelogenous leukemia cells using growth inhibition and colony formation assays.	imatinib	49-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
18281522-4	2008	STI571 brought about the inhibitory dephosphorylation of Bcr-Abl and STAT5, but the expression of DNA-PKcs and Rad51 was unaffected and the interaction between radiation and STI571 was strictly additive with regard to induction of apoptosis.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
18245668-5	2008	Here, we show that a highly specific inhibitor of IkappaB kinase beta, a key upstream regulator of the NF-kappaB pathway, induces growth suppression and death in cells expressing wild-type, Imatinib-resistant, or the T315I Imatinib/Dasatinib-resistant forms of BCR-ABL.	imatinib	190-198	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	50-69
18245668-5	2008	Here, we show that a highly specific inhibitor of IkappaB kinase beta, a key upstream regulator of the NF-kappaB pathway, induces growth suppression and death in cells expressing wild-type, Imatinib-resistant, or the T315I Imatinib/Dasatinib-resistant forms of BCR-ABL.	imatinib	190-198	nuclear factor kappa B subunit 1	Homo sapiens	103-112
18281522-4	2008	STI571 brought about the inhibitory dephosphorylation of Bcr-Abl and STAT5, but the expression of DNA-PKcs and Rad51 was unaffected and the interaction between radiation and STI571 was strictly additive with regard to induction of apoptosis.	imatinib	0-6	signal transducer and activator of transcription 5A	Homo sapiens	69-74
18245668-5	2008	Here, we show that a highly specific inhibitor of IkappaB kinase beta, a key upstream regulator of the NF-kappaB pathway, induces growth suppression and death in cells expressing wild-type, Imatinib-resistant, or the T315I Imatinib/Dasatinib-resistant forms of BCR-ABL.	imatinib	223-231	nuclear factor kappa B subunit 1	Homo sapiens	103-112
18245668-7	2008	These data indicate that blockage of BCR-ABL-induced NF-kappaB activation via IkappaB kinase beta inhibition represents a potential new approach for treatment of Imatinib- or Dasatinib-resistant forms of chronic myelogenous leukemia.	imatinib	162-170	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
18245668-7	2008	These data indicate that blockage of BCR-ABL-induced NF-kappaB activation via IkappaB kinase beta inhibition represents a potential new approach for treatment of Imatinib- or Dasatinib-resistant forms of chronic myelogenous leukemia.	imatinib	162-170	nuclear factor kappa B subunit 1	Homo sapiens	53-62
18245668-7	2008	These data indicate that blockage of BCR-ABL-induced NF-kappaB activation via IkappaB kinase beta inhibition represents a potential new approach for treatment of Imatinib- or Dasatinib-resistant forms of chronic myelogenous leukemia.	imatinib	162-170	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	78-97
17262795-1	2008	BACKGROUND: Imatinib mesylate is a small molecule inhibitor of certain tyrosine kinases, most notably the chimeric bcr-abl fusion protein found in CML.	imatinib	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
18346528-6	2008	Imatinib resistance has, in part, been addressed with the introduction of the new BCR-ABL inhibitors, namely dasatinib and nilotinib.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
18346528-7	2008	These drugs have shown efficacy in CML patients with wild-type BCR-ABL and some BCR-ABL mutants that are imatinib-resistant.	imatinib	105-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
18346528-8	2008	Unfortunately, some BCR-ABL mutations remain resistant to these therapies and will require the development of alternative treatments, and other mechanisms of imatinib resistance besides BCR-ABL mutation exist.	imatinib	158-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
18346528-8	2008	Unfortunately, some BCR-ABL mutations remain resistant to these therapies and will require the development of alternative treatments, and other mechanisms of imatinib resistance besides BCR-ABL mutation exist.	imatinib	158-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-193
17893873-6	2008	These findings may explain why a clinically used c-Abl inhibitor, imatinib mesylate, fails to inhibit the p38 MAPK pathway alone or in combination with cisplatin, and provide evidence of a novel signaling mechanism in which these antitumor agents act.	imatinib	66-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-54
18728706-3	2008	With the advent of the small molecule inhibitor imatinib mesylate (Glivec((R)), Gleevectrade mark) targeting the causative Bcr-Abl oncoprotein, the era of molecular cancer therapy began with remarkable success especially in chronic phase patients.	imatinib	48-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-130
18315935-5	2008	With the application of imatinib, a ABL-specific tyrosine kinase inhibitor, its remarkable therapeutic effects suggest that blast crisis transition will be postponed in most patients with CML.	imatinib	24-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-39
18223230-2	2008	Imatinib mesylate (STI571; Glivec) is a selective inhibitor of tyrosine kinases as bcr-abl, c-kit, c-fms, and PDGFRbeta and enhances tumor drug uptake by reducing the interstitial fluid pressure.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
18223230-2	2008	Imatinib mesylate (STI571; Glivec) is a selective inhibitor of tyrosine kinases as bcr-abl, c-kit, c-fms, and PDGFRbeta and enhances tumor drug uptake by reducing the interstitial fluid pressure.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	92-97
18223230-2	2008	Imatinib mesylate (STI571; Glivec) is a selective inhibitor of tyrosine kinases as bcr-abl, c-kit, c-fms, and PDGFRbeta and enhances tumor drug uptake by reducing the interstitial fluid pressure.	imatinib	0-17	colony stimulating factor 1 receptor	Homo sapiens	99-104
18223230-2	2008	Imatinib mesylate (STI571; Glivec) is a selective inhibitor of tyrosine kinases as bcr-abl, c-kit, c-fms, and PDGFRbeta and enhances tumor drug uptake by reducing the interstitial fluid pressure.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	110-119
18223230-2	2008	Imatinib mesylate (STI571; Glivec) is a selective inhibitor of tyrosine kinases as bcr-abl, c-kit, c-fms, and PDGFRbeta and enhances tumor drug uptake by reducing the interstitial fluid pressure.	imatinib	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
18223230-2	2008	Imatinib mesylate (STI571; Glivec) is a selective inhibitor of tyrosine kinases as bcr-abl, c-kit, c-fms, and PDGFRbeta and enhances tumor drug uptake by reducing the interstitial fluid pressure.	imatinib	19-25	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	92-97
18223230-2	2008	Imatinib mesylate (STI571; Glivec) is a selective inhibitor of tyrosine kinases as bcr-abl, c-kit, c-fms, and PDGFRbeta and enhances tumor drug uptake by reducing the interstitial fluid pressure.	imatinib	19-25	colony stimulating factor 1 receptor	Homo sapiens	99-104
18223230-2	2008	Imatinib mesylate (STI571; Glivec) is a selective inhibitor of tyrosine kinases as bcr-abl, c-kit, c-fms, and PDGFRbeta and enhances tumor drug uptake by reducing the interstitial fluid pressure.	imatinib	19-25	platelet derived growth factor receptor beta	Homo sapiens	110-119
18223230-3	2008	We previously showed that imatinib mesylate synergizes with gemcitabine and pemetrexed in PDGFRbeta-positive mesothelioma cells.	imatinib	26-43	platelet derived growth factor receptor beta	Homo sapiens	90-99
18566537-4	2008	The vast majority of patients with PDGFRA or PDGFRB fusions achieve rapid and durable complete haematological and molecular responses to sustained imatinib therapy.	imatinib	147-155	platelet derived growth factor receptor alpha	Homo sapiens	35-41
18268406-0	2008	Sustained response to low-dose imatinib mesylate in a patient with chronic myelomonocytic leukemia with t(5;12)(q33;p13).	imatinib	31-48	H3 histone pseudogene 6	Homo sapiens	116-119
19039205-0	2008	Imatinib mesylate resistance in a chronic myeloid leukemia patient with a novel e8a2 BCR-ABL transcript variant.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
19039205-9	2008	CONCLUSION: ABL point mutation is also a mechanism of imatinib resistance for CML patients with the BCR-ABL transcript variant.	imatinib	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-15
19039205-9	2008	CONCLUSION: ABL point mutation is also a mechanism of imatinib resistance for CML patients with the BCR-ABL transcript variant.	imatinib	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
18566537-4	2008	The vast majority of patients with PDGFRA or PDGFRB fusions achieve rapid and durable complete haematological and molecular responses to sustained imatinib therapy.	imatinib	147-155	platelet derived growth factor receptor beta	Homo sapiens	45-51
18294126-0	2008	Role of P-glycoprotein in evolution of populations of chronic myeloid leukemia cells treated with imatinib.	imatinib	98-106	ATP binding cassette subfamily B member 1	Homo sapiens	8-22
17980712-2	2008	Central to this has been the determination that the tyrosine kinase function of BCR-ABL is mainly responsible for its transforming potential, and can be targeted with small molecule inhibitors, such as imatinib mesylate (Gleevec, STI-571).	imatinib	202-219	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
18294126-2	2008	Imatinib inhibits the activity of chimeric kinase BCR-ABL, which is responsible for the development of CML.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
18294126-3	2008	The goal of this study was to investigate the role of a multidrug resistance protein, P-glycoprotein (Pgp), in the evolution of CML treated with imatinib.	imatinib	145-153	ATP binding cassette subfamily B member 1	Homo sapiens	86-100
18294126-3	2008	The goal of this study was to investigate the role of a multidrug resistance protein, P-glycoprotein (Pgp), in the evolution of CML treated with imatinib.	imatinib	145-153	ATP binding cassette subfamily B member 1	Homo sapiens	102-105
18294126-4	2008	We demonstrate here that although imatinib is a substrate for Pgp, cultured CML cells (strain K562/i-S9), overexpressing active Pgp, do not exhibit imatinib resistance.	imatinib	34-42	ATP binding cassette subfamily B member 1	Homo sapiens	62-65
18294126-5	2008	Studies of CML patients in the accelerated phase have shown variations in the number of Pgp-positive cells (Pgp+) among individual patients treated with imatinib.	imatinib	153-161	ATP binding cassette subfamily B member 1	Homo sapiens	88-91
18294126-5	2008	Studies of CML patients in the accelerated phase have shown variations in the number of Pgp-positive cells (Pgp+) among individual patients treated with imatinib.	imatinib	153-161	ATP binding cassette subfamily B member 1	Homo sapiens	108-111
18294126-6	2008	During treatment of patients with imatinib for 6-12 months, the number of Pgp-positive cells significantly increased in most patients.	imatinib	34-42	ATP binding cassette subfamily B member 1	Homo sapiens	74-77
18294126-12	2008	Our data suggest that treatment with imatinib causes selection of leukemic stem cells characterized by expression of Pgp and other ABC transporters.	imatinib	37-45	ATP binding cassette subfamily B member 1	Homo sapiens	117-120
18028486-5	2008	ABT-737 augmented the cell killing effect of imatinib in Bcr-Abl(+) cells with diverse drug-resistance mechanisms unless leukaemic cells harboured imatinib-insensitive Abl kinase domain mutations, such as T315I.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
19850986-2	2008	As resistance against Imatinib a Bcr-abl inhibitor used in CML, was described, Heat shock protein (Hsp90) became an alternative target as inhibition of Bcr-Abl-Hsp90 complex leads to proliferation arrest.	imatinib	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
19850986-2	2008	As resistance against Imatinib a Bcr-abl inhibitor used in CML, was described, Heat shock protein (Hsp90) became an alternative target as inhibition of Bcr-Abl-Hsp90 complex leads to proliferation arrest.	imatinib	22-30	heat shock protein 90 alpha family class A member 1	Homo sapiens	99-104
19850986-2	2008	As resistance against Imatinib a Bcr-abl inhibitor used in CML, was described, Heat shock protein (Hsp90) became an alternative target as inhibition of Bcr-Abl-Hsp90 complex leads to proliferation arrest.	imatinib	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-159
19850986-2	2008	As resistance against Imatinib a Bcr-abl inhibitor used in CML, was described, Heat shock protein (Hsp90) became an alternative target as inhibition of Bcr-Abl-Hsp90 complex leads to proliferation arrest.	imatinib	22-30	heat shock protein 90 alpha family class A member 1	Homo sapiens	160-165
18230576-3	2008	Several studies have shown that response to imatinib in GIST patients mainly depends on the mutational status of KIT or PDGFR alpha.	imatinib	44-52	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	113-116
18190691-14	2008	Zr75.1 cells with NHERF1 knockdown were more resistant to STI-571-induced apoptosis than parental cells.	imatinib	58-65	SLC9A3 regulator 1	Homo sapiens	18-24
18230576-3	2008	Several studies have shown that response to imatinib in GIST patients mainly depends on the mutational status of KIT or PDGFR alpha.	imatinib	44-52	platelet derived growth factor receptor alpha	Homo sapiens	120-131
18190691-15	2008	Similarly, over-expression of NHERF1 rendered MCF10A cells more sensitive to STI-571.	imatinib	77-84	SLC9A3 regulator 1	Homo sapiens	30-36
19079792-0	2008	Disruption of Survivin in K562 cells elevates telomerase activity and protects cells against apoptosis induced by the Bcr-abl kinase inhibitor STI571.	imatinib	143-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
18230575-1	2008	Imatinib mesylate (Gleevec, Glivec, Novartis, Basel, Switzerland) is a small molecule inhibitor of the tyrosine kinase c-abl, c-kit and the platelet derived growth factor receptor (PDGFR).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-124
18230575-1	2008	Imatinib mesylate (Gleevec, Glivec, Novartis, Basel, Switzerland) is a small molecule inhibitor of the tyrosine kinase c-abl, c-kit and the platelet derived growth factor receptor (PDGFR).	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	126-131
18230575-1	2008	Imatinib mesylate (Gleevec, Glivec, Novartis, Basel, Switzerland) is a small molecule inhibitor of the tyrosine kinase c-abl, c-kit and the platelet derived growth factor receptor (PDGFR).	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	140-179
18230575-1	2008	Imatinib mesylate (Gleevec, Glivec, Novartis, Basel, Switzerland) is a small molecule inhibitor of the tyrosine kinase c-abl, c-kit and the platelet derived growth factor receptor (PDGFR).	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	181-186
18230575-3	2008	Given its activity against both c-kit and PDGFR kinases and its remarkable safety profile, imatinib has been "tried" in several solid tumors; results however have often been deceiving.	imatinib	91-99	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	32-37
18230575-3	2008	Given its activity against both c-kit and PDGFR kinases and its remarkable safety profile, imatinib has been "tried" in several solid tumors; results however have often been deceiving.	imatinib	91-99	platelet derived growth factor receptor beta	Homo sapiens	42-47
18230576-1	2008	Approximately 90 % of gastrointestinal tumors (GISTs) harbor an activating mutation in KIT or PDGFR alpha oncogene known to confer imatinib sensitivity.	imatinib	131-139	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	87-90
18230576-1	2008	Approximately 90 % of gastrointestinal tumors (GISTs) harbor an activating mutation in KIT or PDGFR alpha oncogene known to confer imatinib sensitivity.	imatinib	131-139	platelet derived growth factor receptor alpha	Homo sapiens	94-105
18230576-2	2008	Imatinib is a tyrosine kinase inhibitor of KIT and PDGFRs that yields a 6-months progression-free survival (PFS) rate of 80 % in patients with advanced GISTs.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	43-46
18068536-9	2008	Our study indicated that the progenitor of CML was BCR-ABL dependent through the amplification of Ph chromosome as a mechanism of resistance to imatinib therapy.	imatinib	144-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
19079792-1	2008	The Bcr-abl kinase inhibitor STI571 produces clinical responses in most patients with Chronic Myeloid Leukemia (CML); however, development of resistance limits utility.	imatinib	29-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
19079792-3	2008	We reported that disruption of the anti-apoptotic protein Survivin promoted STI571-induced apoptosis in Bcr-abl(+) K562 cells, through caspase-dependent Bcr-abl degradation.	imatinib	76-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
19079792-3	2008	We reported that disruption of the anti-apoptotic protein Survivin promoted STI571-induced apoptosis in Bcr-abl(+) K562 cells, through caspase-dependent Bcr-abl degradation.	imatinib	76-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
19075651-5	2008	The first tyrosine kinase inhibitor (TKI), introduced into clinical practice in 1998, was imatinib mesylate.	imatinib	90-107	TXK tyrosine kinase	Homo sapiens	10-25
18303243-3	2008	Different drug therapies are available, most notably imatinib, which inhibits the oncogenic BCR-ABL1 tyrosine kinase.	imatinib	53-61	BCR activator of RhoGEF and GTPase	Homo sapiens	92-100
18215092-2	2008	In vitro, dasatinib is 325-fold more potent than imatinib against cells expressing wild-type BCR-ABL.	imatinib	49-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
18288997-5	2008	The era of targeted therapy began with the approval of Trastuzumab, a monoclonal antibody against HER2, for treatment of metastatic breast cancer, and Imatinib, a small tyrosine kinase inhibitor targeting BCR-Abl, in Chronic Myeloid Leukemia.	imatinib	151-159	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	205-212
19075651-7	2008	However, approximately 20-25% of patients initially treated with imatinib will need alternative therapy, due to drug resistance, which is often caused by the appearance of clones expressing mutant forms of BCR-ABL.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	206-213
18043265-5	2008	Strategies to overcome the restoration of BCR-ABL signalling and subsequent resistance to therapy include imatinib dose escalation, a more potent tyrosine kinase inhibitor, as well as non-BCR-ABL-dependent approaches and agents in clinical development.	imatinib	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
20425445-5	2008	This is an important distinction because PDGFR-mutated but not other eosinophilic neoplasms are effectively treated with imatinib.	imatinib	121-129	platelet derived growth factor receptor beta	Homo sapiens	41-46
18836918-2	2008	One such example is the new group of tyrosine kinase inhibitors, exemplified by the Bcr-Abl inhibitor imatinib (Glivec).	imatinib	102-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
18673174-5	2008	An ABL inhibitor, imatinib, was approved by the FDA for the treatment of CML, and is currently used as first line therapy.	imatinib	18-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	3-6
18673174-8	2008	In order to address the resistance of mutated BCR-ABL to imatinib, 2(nd) generation inhibitors such as dasatinib, and nilotinib were developed.	imatinib	57-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
18836918-2	2008	One such example is the new group of tyrosine kinase inhibitors, exemplified by the Bcr-Abl inhibitor imatinib (Glivec).	imatinib	112-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
18318563-1	2008	Nilotinib is an orally administered BCR-ABL tyrosine kinase inhibitor that has shown good clinical efficacy in imatinib-resistant or -intolerant, Philadelphia chromosome-positive, chronic myeloid leukaemia (CML) in a phase I/II trial.	imatinib	111-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
18216472-3	2008	OBJECTIVE: Imatinib being an inhibitor of tyrosine kinase receptors such as PDGFR, its effect on scleroderma fibroblasts was evaluated in vitro as a preclinical therapeutic step.	imatinib	11-19	platelet derived growth factor receptor beta	Homo sapiens	76-81
18216472-6	2008	RESULTS: In vitro, imatinib inhibited the proliferation of normal dermal and scleroderma fibroblasts at least partly via the inhibition of the phosphorylation of PDGFR.	imatinib	19-27	platelet derived growth factor receptor beta	Homo sapiens	162-167
17667967-1	2008	Gastrointestinal stromal tumors (GISTs) may be caused by germline mutations of the KIT and platelet-derived growth factor receptor-alpha (PDGFRA) genes and treated by Imatinib mesylate (STI571) or other protein tyrosine kinase inhibitors.	imatinib	167-175	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	83-86
18173550-8	2008	Moreover, rapamycin inhibited the growth of Ba/F3 cells exhibiting various imatinib-resistant mutants of BCR/ABL, including the T315I variant that exhibits resistance against most currently available BCR/ABL kinase inhibitors.	imatinib	75-83	BCR activator of RhoGEF and GTPase	Mus musculus	105-112
18173550-8	2008	Moreover, rapamycin inhibited the growth of Ba/F3 cells exhibiting various imatinib-resistant mutants of BCR/ABL, including the T315I variant that exhibits resistance against most currently available BCR/ABL kinase inhibitors.	imatinib	75-83	BCR activator of RhoGEF and GTPase	Mus musculus	105-108
18173550-8	2008	Moreover, rapamycin inhibited the growth of Ba/F3 cells exhibiting various imatinib-resistant mutants of BCR/ABL, including the T315I variant that exhibits resistance against most currently available BCR/ABL kinase inhibitors.	imatinib	75-83	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	109-112
17667967-1	2008	Gastrointestinal stromal tumors (GISTs) may be caused by germline mutations of the KIT and platelet-derived growth factor receptor-alpha (PDGFRA) genes and treated by Imatinib mesylate (STI571) or other protein tyrosine kinase inhibitors.	imatinib	167-175	platelet derived growth factor receptor alpha	Homo sapiens	91-136
17667967-1	2008	Gastrointestinal stromal tumors (GISTs) may be caused by germline mutations of the KIT and platelet-derived growth factor receptor-alpha (PDGFRA) genes and treated by Imatinib mesylate (STI571) or other protein tyrosine kinase inhibitors.	imatinib	167-175	platelet derived growth factor receptor alpha	Homo sapiens	138-144
18095887-4	2008	However, patients may develop imatinib resistance, which is often due to BCR-ABL mutations.	imatinib	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
18592792-3	2008	Imatinib mesylate acts against a tyrosine kinase encoded by the KIT gene in GISTs, and is more effective in tumors expressing this protein.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	64-67
17912002-0	2008	Effect of prolonged c-kit receptor inhibition by imatinib mesylate on the uterine contractility of pregnant rabbits.	imatinib	49-66	mast/stem cell growth factor receptor Kit	Oryctolagus cuniculus	20-25
18405654-3	2008	Due to their expression of c-kit protein, a positive diagnosis as well as a specific targeted treatment by molecular biology (imatinib) are available.	imatinib	126-134	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	27-32
18028988-5	2008	METHODS: The expression of the imatinib-sensitive tyrosine kinases, c-kit, c-Abl, PDGFR-alpha and PDGFR-beta, was determined using RT-PCR in a panel of GCT.	imatinib	31-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	68-73
17912002-3	2008	METHODS: Imatinib mesylate, a specific c-kit receptor antagonist, was administered to pregnant New Zealand white rabbits (term = 31 days, n = 35) from day 27 gestation by intramuscular injection twice daily at high (50 microg/kg) or medium (10 microg/kg) dose and compared with a control group injected with vehicle only.	imatinib	9-26	mast/stem cell growth factor receptor Kit	Oryctolagus cuniculus	39-44
18166785-0	2008	Activity of imatinib in systemic mastocytosis with chronic basophilic leukemia and a PRKG2-PDGFRB fusion.	imatinib	12-20	protein kinase cGMP-dependent 2	Homo sapiens	85-90
18166785-0	2008	Activity of imatinib in systemic mastocytosis with chronic basophilic leukemia and a PRKG2-PDGFRB fusion.	imatinib	12-20	platelet derived growth factor receptor beta	Homo sapiens	91-97
18166785-7	2008	Molecular analyses revealed that PDGFRB, encoding an imatinib-sensitive tyrosine kinase, was fused to PRKG2.	imatinib	53-61	platelet derived growth factor receptor beta	Homo sapiens	33-39
18421200-3	2008	Although there has been one report of CMPD-U patient with chromosomal abnormalities of the PDGFR gene having complete hematologic responses upon treatment with imatinib, there have not been similar reports of patients without chromosomal abnormalities.	imatinib	160-168	platelet derived growth factor receptor beta	Homo sapiens	91-96
18166785-7	2008	Molecular analyses revealed that PDGFRB, encoding an imatinib-sensitive tyrosine kinase, was fused to PRKG2.	imatinib	53-61	protein kinase cGMP-dependent 2	Homo sapiens	102-107
18401881-1	2008	Imatinib is a small-molecule inhibitor of BCR-ABL tyrosine kinase activity, with proven efficacy and tolerability.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
18401881-3	2008	BCR-ABL-dependent resistance is commonly a result of mutations in the BCR-ABL gene, which can induce a structural predisposition towards the active conformation of the protein, resulting in a shift in the equilibrium of BCR-ABL from inactive, which imatinib binds, to active, which imatinib is unable to bind.	imatinib	249-257	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
18401881-3	2008	BCR-ABL-dependent resistance is commonly a result of mutations in the BCR-ABL gene, which can induce a structural predisposition towards the active conformation of the protein, resulting in a shift in the equilibrium of BCR-ABL from inactive, which imatinib binds, to active, which imatinib is unable to bind.	imatinib	249-257	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
18401881-3	2008	BCR-ABL-dependent resistance is commonly a result of mutations in the BCR-ABL gene, which can induce a structural predisposition towards the active conformation of the protein, resulting in a shift in the equilibrium of BCR-ABL from inactive, which imatinib binds, to active, which imatinib is unable to bind.	imatinib	249-257	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
18401881-3	2008	BCR-ABL-dependent resistance is commonly a result of mutations in the BCR-ABL gene, which can induce a structural predisposition towards the active conformation of the protein, resulting in a shift in the equilibrium of BCR-ABL from inactive, which imatinib binds, to active, which imatinib is unable to bind.	imatinib	282-290	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
18401881-3	2008	BCR-ABL-dependent resistance is commonly a result of mutations in the BCR-ABL gene, which can induce a structural predisposition towards the active conformation of the protein, resulting in a shift in the equilibrium of BCR-ABL from inactive, which imatinib binds, to active, which imatinib is unable to bind.	imatinib	282-290	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
18401881-3	2008	BCR-ABL-dependent resistance is commonly a result of mutations in the BCR-ABL gene, which can induce a structural predisposition towards the active conformation of the protein, resulting in a shift in the equilibrium of BCR-ABL from inactive, which imatinib binds, to active, which imatinib is unable to bind.	imatinib	282-290	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
18401881-4	2008	BCR-ABL gene amplification may play a role in the development of imatinib resistance in patients with CML.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
18401881-5	2008	There are a number of BCR-ABL-independent mechanisms of imatinib resistance, including the efflux protein multidrug resistance protein-1, of which imatinib is a substrate.	imatinib	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
18401881-5	2008	There are a number of BCR-ABL-independent mechanisms of imatinib resistance, including the efflux protein multidrug resistance protein-1, of which imatinib is a substrate.	imatinib	56-64	ATP binding cassette subfamily B member 1	Homo sapiens	106-136
18401881-5	2008	There are a number of BCR-ABL-independent mechanisms of imatinib resistance, including the efflux protein multidrug resistance protein-1, of which imatinib is a substrate.	imatinib	147-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
18401881-5	2008	There are a number of BCR-ABL-independent mechanisms of imatinib resistance, including the efflux protein multidrug resistance protein-1, of which imatinib is a substrate.	imatinib	147-155	ATP binding cassette subfamily B member 1	Homo sapiens	106-136
18401881-8	2008	Dasatinib, with increased binding potency (325-fold greater potency than imatinib for wild-type BCR-ABL), inhibition of both the active and inactive formation of BCR-ABL, and targeting of SRC family kinases, is the only agent approved for the treatment of patients with imatinib-resistant or -intolerant CML and Ph+ ALL.	imatinib	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
18648736-5	2008	Imatinib mesylate was initially developed as an inhibitor of PDGFR.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	61-66
18436994-1	2008	Point mutations of bcr-abl tyrosine kinase are the most frequent causes of imatinib resistance in chronic myeloid leukaemia (CML) patients.	imatinib	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
18436994-2	2008	In most CML cases with BCR-ABL mutations leading to imatinib resistance the second generation of tyrosine kinase inhibitors (TKI- e.g. nilotinib or dasatinib) may be effective.	imatinib	52-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
18648736-8	2008	When we reported gain-of-function mutations of the Kit gene in GISTs, the inhibitory effect of imatinib on KIT was already known.	imatinib	95-103	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	51-54
18648736-10	2008	The interrelationship between the type of Kit gain-of-function mutation and the therapeutic effect of imatinib has been well characterized in GISTs.	imatinib	102-110	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	42-45
18648736-12	2008	After long-term administration of imatinib, however, new imatinib-resistant clones develop a secondary mutation of the Kit or Pdgfr-alpha gene.	imatinib	34-42	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	119-122
18648736-8	2008	When we reported gain-of-function mutations of the Kit gene in GISTs, the inhibitory effect of imatinib on KIT was already known.	imatinib	95-103	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	107-110
18648736-12	2008	After long-term administration of imatinib, however, new imatinib-resistant clones develop a secondary mutation of the Kit or Pdgfr-alpha gene.	imatinib	34-42	platelet derived growth factor receptor alpha	Homo sapiens	126-137
17544504-1	2008	Patients with primary hypereosinophilic disorders who are positive for the FIP1L1-PDGFRA fusion gene mutation are highly responsive to therapy with imatinib mesylate.	imatinib	148-165	factor interacting with PAPOLA and CPSF1	Homo sapiens	75-81
18648736-12	2008	After long-term administration of imatinib, however, new imatinib-resistant clones develop a secondary mutation of the Kit or Pdgfr-alpha gene.	imatinib	57-65	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	119-122
18648736-12	2008	After long-term administration of imatinib, however, new imatinib-resistant clones develop a secondary mutation of the Kit or Pdgfr-alpha gene.	imatinib	57-65	platelet derived growth factor receptor alpha	Homo sapiens	126-137
17882283-7	2008	In 1996, Brian Druker discovered imatinib-a small molecule ABL inhibitor with exceptional therapeutic activity in CML.	imatinib	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-62
18203007-1	2008	The BCR-ABL kinase inhibitor imatinib has shown significant efficacy in chronic myeloid leukemia (CML) and is the standard front-line therapy for patients in chronic phase.	imatinib	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
18203007-6	2008	The dual SFK/BCR-ABL inhibitor dasatinib is now clinically available and has markedly greater potency compared with imatinib against native BCR-ABL and the majority of imatinib-resistant BCR-ABL mutants.	imatinib	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
18203007-6	2008	The dual SFK/BCR-ABL inhibitor dasatinib is now clinically available and has markedly greater potency compared with imatinib against native BCR-ABL and the majority of imatinib-resistant BCR-ABL mutants.	imatinib	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
17544504-1	2008	Patients with primary hypereosinophilic disorders who are positive for the FIP1L1-PDGFRA fusion gene mutation are highly responsive to therapy with imatinib mesylate.	imatinib	148-165	platelet derived growth factor receptor alpha	Homo sapiens	82-88
17544504-2	2008	A 35-year-old man with FIP1L1-PDGFRA positive hypereosinophilic syndrome and cardiac involvement, was treated with imatinib 100 mg daily.	imatinib	115-123	factor interacting with PAPOLA and CPSF1	Homo sapiens	23-29
17544504-2	2008	A 35-year-old man with FIP1L1-PDGFRA positive hypereosinophilic syndrome and cardiac involvement, was treated with imatinib 100 mg daily.	imatinib	115-123	platelet derived growth factor receptor alpha	Homo sapiens	30-36
19116712-2	2008	The ABL kinase inhibitor imatinib is effective in most patients and considered standard first-line therapy.	imatinib	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
18488160-1	2008	Most gastrointestinal stromal tumors (GISTs) are associated with activating kinase mutation in KIT or platelet-derived growth factor receptor alpha (PDGFRA) gene, and imatinib has revolutionized the care of advanced GISTs.	imatinib	167-175	platelet derived growth factor receptor alpha	Homo sapiens	149-155
18792672-2	2008	The discovery of KIT proto-oncogene mutations in the pathogenesis of this tumor, and the development of imatinib mesylate, a specific inhibitor of KIT tyrosine kinase function have revolutionized the treatment of GIST.	imatinib	104-121	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	147-150
18239881-9	2008	To preserve the anus, a rectal GIST expressing the c-kit gene is best treated with Imatinib as neoadjuvant therapy.	imatinib	83-91	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	51-56
19166098-3	2008	NUP214-ABL1 and EML1-ABL1 display constitutive kinase activity and are sensitive to the kinase inhibitor imatinib.	imatinib	105-113	nucleoporin 214	Homo sapiens	0-6
19166098-3	2008	NUP214-ABL1 and EML1-ABL1 display constitutive kinase activity and are sensitive to the kinase inhibitor imatinib.	imatinib	105-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	7-11
19166098-3	2008	NUP214-ABL1 and EML1-ABL1 display constitutive kinase activity and are sensitive to the kinase inhibitor imatinib.	imatinib	105-113	EMAP like 1	Homo sapiens	16-20
19166098-3	2008	NUP214-ABL1 and EML1-ABL1 display constitutive kinase activity and are sensitive to the kinase inhibitor imatinib.	imatinib	105-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-25
18476538-1	2007	OBJECTIVE: To investigate the effects of uroacitide (CDA-2), a cell differentiation agent, on the growth inhibition and differentiation of imatinib-(IM) resistant chronic myeloid leukemia (CML) cells.	imatinib	139-147	activation induced cytidine deaminase	Homo sapiens	53-58
18056927-4	2007	Imatinib, a BCR-ABL inhibitor, has significantly decreased CML mortality by stopping disease progression in CP.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
18056927-7	2007	Mechanisms of imatinib resistance include plasma protein binding, drug efflux, mutation of BCR-ABL, gene amplification of BCR-ABL, and activation of BCR-ABL independent proliferative pathways.	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
18056927-7	2007	Mechanisms of imatinib resistance include plasma protein binding, drug efflux, mutation of BCR-ABL, gene amplification of BCR-ABL, and activation of BCR-ABL independent proliferative pathways.	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
18056927-7	2007	Mechanisms of imatinib resistance include plasma protein binding, drug efflux, mutation of BCR-ABL, gene amplification of BCR-ABL, and activation of BCR-ABL independent proliferative pathways.	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
18056927-15	2007	It binds with a 350-fold greater affinity to BCR-ABL and shows efficacy against a number of imatinib-resistant mutations.	imatinib	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
18056932-7	2007	Imatinib, the first approved tyrosine kinase inhibitor, functions by blocking the ATP binding site on the BCR-ABL kinase.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
18056932-15	2007	Resistance may develop to imatinib most often caused by the evolution of mutations blocking imatinib interactions with the BCR-ABL adenosine triphosphate (ATP) binding site.	imatinib	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-130
18056932-15	2007	Resistance may develop to imatinib most often caused by the evolution of mutations blocking imatinib interactions with the BCR-ABL adenosine triphosphate (ATP) binding site.	imatinib	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-130
18089786-7	2007	The results further show that silencing MUC1 increases sensitivity of CML cells to imatinib-induced apoptosis.	imatinib	83-91	mucin 1, cell surface associated	Homo sapiens	40-44
18089786-8	2007	Analysis of primary CML blasts confirmed that, as found with the CML cell lines, MUC1 blocks differentiation and the apoptotic response to imatinib treatment.	imatinib	139-147	mucin 1, cell surface associated	Homo sapiens	81-85
18203417-0	2007	[Identification of clonal proliferation of T cell and FIP1L1-PDGFRalpha fusion gene in hypereosinophilic syndrome associated with lymphomatoid papulosis which showed rapid and complete response to the treatment with imatinib].	imatinib	216-224	factor interacting with PAPOLA and CPSF1	Homo sapiens	54-60
18203417-0	2007	[Identification of clonal proliferation of T cell and FIP1L1-PDGFRalpha fusion gene in hypereosinophilic syndrome associated with lymphomatoid papulosis which showed rapid and complete response to the treatment with imatinib].	imatinib	216-224	platelet derived growth factor receptor alpha	Homo sapiens	61-71
18202009-0	2008	CXCR4 up-regulation by imatinib induces chronic myelogenous leukemia (CML) cell migration to bone marrow stroma and promotes survival of quiescent CML cells.	imatinib	23-31	C-X-C motif chemokine receptor 4	Homo sapiens	0-5
18202009-3	2008	We proposed that tyrosine kinase inhibitors, imatinib or INNO-406, may restore CXCR4 expression and cause the migration of CML cells to bone marrow microenvironment niches, which in turn results in acquisition of stroma-mediated chemoresistance of CML progenitor cells.	imatinib	45-53	C-X-C motif chemokine receptor 4	Homo sapiens	79-84
18202009-4	2008	In KBM5 and K562 cells, imatinib, INNO-406, or IFN-alpha increased CXCR4 expression and migration.	imatinib	24-32	C-X-C motif chemokine receptor 4	Homo sapiens	67-72
18202009-5	2008	This increase in CXCR4 levels on CML progenitor cells was likewise found in samples from CML patients treated with imatinib or IFN-alpha.	imatinib	115-123	C-X-C motif chemokine receptor 4	Homo sapiens	17-22
18202009-9	2008	Altogether, these findings suggest that the up-regulation of CXCR4 by imatinib promotes migration of CML cells to bone marrow stroma, causing the G0-G1 cell cycle arrest and hence ensuring the survival of quiescent CML progenitor cells.	imatinib	70-78	C-X-C motif chemokine receptor 4	Homo sapiens	61-66
18974832-2	2008	Imatinib, a selective inhibitor of the Bcr-Abl tyrosine kinase, has significantly improved the clinical outcome of patients with CML.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
18036706-0	2008	[Efficacy of imatinib in FIP1L1-PDGFRA positive hypereosinophilic syndrome].	imatinib	13-21	factor interacting with PAPOLA and CPSF1	Homo sapiens	25-31
18036706-0	2008	[Efficacy of imatinib in FIP1L1-PDGFRA positive hypereosinophilic syndrome].	imatinib	13-21	platelet derived growth factor receptor alpha	Homo sapiens	32-38
18085368-0	2008	Secondary c-kit mutation in a recurrent gastrointestinal stromal tumor under long-term treatment with imatinib mesylate: report of a case.	imatinib	102-119	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	10-15
18085368-1	2008	Gastrointestinal stromal tumors (GISTs) commonly harbor oncogenic mutations of the c-kit receptor gene, which are targets for imatinib mesylate.	imatinib	126-143	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	83-88
18053813-3	2007	Imatinib increased the expression of alpha-smooth muscle actin in both SMC populations and that of smoothelin in S-SMCs.	imatinib	0-8	smoothelin	Homo sapiens	99-109
18061581-3	2007	In particular, imatinib inhibits Bcr-Abl kinase activity, c-kit and the phosphorylation of platelet-derived growth factor (PDGF) receptors.	imatinib	15-23	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	58-63
17691110-4	2007	Combination therapy using 25 mg/kg/day of the VEGFR inhibitor PTK787 and 100 mg/kg/day of the PDGFR inhibitor STI571 decreased the tumor growth rate of both tumor types, but the inhibition was only significant in the B16/PDGF-BB tumors.	imatinib	110-116	platelet derived growth factor receptor, beta polypeptide	Mus musculus	94-99
17721919-0	2007	Imatinib inhibits colorectal cancer cell growth and suppresses stromal-induced growth stimulation, MT1-MMP expression and pro-MMP2 activation.	imatinib	0-8	matrix metallopeptidase 14	Homo sapiens	99-106
17721919-0	2007	Imatinib inhibits colorectal cancer cell growth and suppresses stromal-induced growth stimulation, MT1-MMP expression and pro-MMP2 activation.	imatinib	0-8	matrix metallopeptidase 2	Homo sapiens	126-130
17721919-4	2007	The effects of imatinib on gene expression of MMPs and TIMPs were also studied.	imatinib	15-23	matrix metallopeptidase 2	Homo sapiens	46-50
17721919-9	2007	CM stimulated MT1-MMP protein expression by HT-29; this stimulatory effect was suppressed in the presence of imatinib.	imatinib	109-117	matrix metallopeptidase 14	Homo sapiens	14-21
17721919-10	2007	Activation of pro-MMP2 to MMP2 in culture medium of HT-29 treated with CM was increased and this activity was inhibited in presence of imatinib.	imatinib	135-143	matrix metallopeptidase 2	Homo sapiens	18-22
17721919-10	2007	Activation of pro-MMP2 to MMP2 in culture medium of HT-29 treated with CM was increased and this activity was inhibited in presence of imatinib.	imatinib	135-143	matrix metallopeptidase 2	Homo sapiens	26-30
18094422-0	2007	Influence of CYP3A4 inhibition on the steady-state pharmacokinetics of imatinib.	imatinib	71-79	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	13-19
18094422-1	2007	PURPOSE: To evaluate the effects of ritonavir, a potent inhibitor of CYP3A4, on the steady-state pharmacokinetics of imatinib.	imatinib	117-125	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	69-75
18094422-7	2007	In vitro, imatinib was metabolized to the active metabolite CGP74588 by CYP3A4 and CYP3A5 and, to a lesser extent, by CYP2D6.	imatinib	10-18	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	72-78
18094422-7	2007	In vitro, imatinib was metabolized to the active metabolite CGP74588 by CYP3A4 and CYP3A5 and, to a lesser extent, by CYP2D6.	imatinib	10-18	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	83-89
18094422-7	2007	In vitro, imatinib was metabolized to the active metabolite CGP74588 by CYP3A4 and CYP3A5 and, to a lesser extent, by CYP2D6.	imatinib	10-18	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	118-124
18094422-8	2007	Ritonavir (1 micromol/L) completely inhibited CYP3A4-mediated metabolism of imatinib to CGP74588 but inhibited metabolism in microsomes by only 50%.	imatinib	76-84	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	46-52
18094422-9	2007	Imatinib significantly inhibited CYP3A4 activity in vitro.	imatinib	0-8	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	33-39
17599053-7	2007	SPK1 silencing enhances the STI571-induced apoptosis of CML cell lines.	imatinib	28-34	sphingosine kinase 1	Homo sapiens	0-4
17761829-0	2007	Most CML patients who have a suboptimal response to imatinib have low OCT-1 activity: higher doses of imatinib may overcome the negative impact of low OCT-1 activity.	imatinib	102-110	solute carrier family 22 member 1	Homo sapiens	151-156
17761829-1	2007	Interpatient variability in intracellular uptake and retention (IUR) of imatinib may be due to variable function of the OCT-1 influx pump.	imatinib	72-80	solute carrier family 22 member 1	Homo sapiens	120-125
17720881-0	2007	Chemical proteomic profiles of the BCR-ABL inhibitors imatinib, nilotinib, and dasatinib reveal novel kinase and nonkinase targets.	imatinib	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
17761829-2	2007	OCT-1 activity was measured in pretherapy blood from chronic myeloid leukemia (CML) patients by calculating the difference in IUR of [(14)C]-imatinib with and without OCT-1 inhibition.	imatinib	141-149	solute carrier family 22 member 1	Homo sapiens	0-5
17720881-1	2007	The BCR-ABL tyrosine kinase inhibitor imatinib represents the current frontline therapy in chronic myeloid leukemia.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
17761829-6	2007	OCT-1 activity is an important determinant of molecular response to imatinib, with predictive value closely linked to dose.	imatinib	68-76	solute carrier family 22 member 1	Homo sapiens	0-5
17720881-2	2007	Because many patients develop imatinib resistance, 2 second-generation drugs, nilotinib and dasatinib, displaying increased potency against BCR-ABL were developed.	imatinib	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
17720881-7	2007	(4) The oxidoreductase NQO2 was bound and inhibited by imatinib and nilotinib at physiologically relevant drug concentrations, representing the first nonkinase target of these drugs.	imatinib	55-63	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	23-27
17900262-4	2007	To this end, we generated a 4-hydroxytamoxifen-inducible active FKHRL1 (FKHRL1-TM; a triple mutant of FKHRL1 in which all three Akt phosphorylation sites have been mutated)-estrogen receptor fusion protein expression system in CML-derived imatinib-resistant cell lines.	imatinib	239-247	forkhead box O3	Homo sapiens	72-78
19707313-2	2007	During the past 10 years, the BCR/ABL tyrosine kinase inhibitor imatinib (STI571) has successfully been introduced in the treatment of the disease.	imatinib	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
19707313-2	2007	During the past 10 years, the BCR/ABL tyrosine kinase inhibitor imatinib (STI571) has successfully been introduced in the treatment of the disease.	imatinib	74-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
19707313-4	2007	Most of the respective concepts focus on imatinib-resistant mutants of BCR/ABL that are detectable in a high proportion of cases.	imatinib	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
17900262-0	2007	Active FKHRL1 overcomes imatinib resistance in chronic myelogenous leukemia-derived cell lines via the production of tumor necrosis factor-related apoptosis-inducing ligand.	imatinib	24-32	forkhead box O3	Homo sapiens	7-13
17900262-0	2007	Active FKHRL1 overcomes imatinib resistance in chronic myelogenous leukemia-derived cell lines via the production of tumor necrosis factor-related apoptosis-inducing ligand.	imatinib	24-32	TNF superfamily member 10	Homo sapiens	117-172
17900262-2	2007	The Bcr-Abl tyrosine kinase inhibitor imatinib induces cell cycle arrest and subsequent apoptosis via the conversion of FKHRL1 from the phosphorylated inactive form to the dephosphorylated active form in CML-derived cell lines.	imatinib	38-46	forkhead box O3	Homo sapiens	120-126
17900262-3	2007	In the present study, we examined whether active FKHRL1 can overcome resistance to imatinib.	imatinib	83-91	forkhead box O3	Homo sapiens	49-55
17900262-4	2007	To this end, we generated a 4-hydroxytamoxifen-inducible active FKHRL1 (FKHRL1-TM; a triple mutant of FKHRL1 in which all three Akt phosphorylation sites have been mutated)-estrogen receptor fusion protein expression system in CML-derived imatinib-resistant cell lines.	imatinib	239-247	forkhead box O3	Homo sapiens	64-70
19707305-6	2007	Imatinib mesylate is a tyrosine kinase inhibitor with activity against activated PDGFR, and has significant activity against DFSP.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	81-86
17900262-4	2007	To this end, we generated a 4-hydroxytamoxifen-inducible active FKHRL1 (FKHRL1-TM; a triple mutant of FKHRL1 in which all three Akt phosphorylation sites have been mutated)-estrogen receptor fusion protein expression system in CML-derived imatinib-resistant cell lines.	imatinib	239-247	forkhead box O3	Homo sapiens	72-78
17900262-7	2007	In addition, imatinib-resistant cells underwent apoptosis after transfection with full-length TRAIL cDNA.	imatinib	13-21	TNF superfamily member 10	Homo sapiens	94-99
17900262-8	2007	Collectively, our results suggest that active FKHRL1 can overcome imatinib resistance in CML cells, in part via TRAIL production.	imatinib	66-74	forkhead box O3	Homo sapiens	46-52
17900262-8	2007	Collectively, our results suggest that active FKHRL1 can overcome imatinib resistance in CML cells, in part via TRAIL production.	imatinib	66-74	TNF superfamily member 10	Homo sapiens	112-117
18075302-7	2007	In PDGFR expressing immortalized ovarian cancer cells, PDGF potently induced VEGF secretion, while imatinib mesylate (Gleevec), a partially selective PDGFR inhibitor, reduced PDGF stimulated VEGF production to basal state.	imatinib	99-116	platelet derived growth factor receptor beta	Homo sapiens	3-8
18272024-8	2007	Inhibition of the PDGF receptor (PDGFR) with imatinib did not appear to improve efficacy compared retrospectively with the results of treatment with bevacizumab/erlotinib.	imatinib	45-53	platelet derived growth factor receptor beta	Homo sapiens	18-31
18075302-7	2007	In PDGFR expressing immortalized ovarian cancer cells, PDGF potently induced VEGF secretion, while imatinib mesylate (Gleevec), a partially selective PDGFR inhibitor, reduced PDGF stimulated VEGF production to basal state.	imatinib	99-116	platelet derived growth factor receptor beta	Homo sapiens	150-155
18075302-7	2007	In PDGFR expressing immortalized ovarian cancer cells, PDGF potently induced VEGF secretion, while imatinib mesylate (Gleevec), a partially selective PDGFR inhibitor, reduced PDGF stimulated VEGF production to basal state.	imatinib	99-116	vascular endothelial growth factor A	Homo sapiens	191-195
18075302-8	2007	In ovarian cancer cells overexpressing constitutively active Akt, imatinib inhibited partially VEGF secretion, suggesting that the PI3K/Akt pathway is implicated in PDGF-stimulated VEGF secretion.	imatinib	66-74	AKT serine/threonine kinase 1	Homo sapiens	61-64
18075302-8	2007	In ovarian cancer cells overexpressing constitutively active Akt, imatinib inhibited partially VEGF secretion, suggesting that the PI3K/Akt pathway is implicated in PDGF-stimulated VEGF secretion.	imatinib	66-74	vascular endothelial growth factor A	Homo sapiens	95-99
18075302-8	2007	In ovarian cancer cells overexpressing constitutively active Akt, imatinib inhibited partially VEGF secretion, suggesting that the PI3K/Akt pathway is implicated in PDGF-stimulated VEGF secretion.	imatinib	66-74	AKT serine/threonine kinase 1	Homo sapiens	136-139
18075302-8	2007	In ovarian cancer cells overexpressing constitutively active Akt, imatinib inhibited partially VEGF secretion, suggesting that the PI3K/Akt pathway is implicated in PDGF-stimulated VEGF secretion.	imatinib	66-74	vascular endothelial growth factor A	Homo sapiens	181-185
18075302-10	2007	The effects of imatinib on VEGF secretion in tumor cells may affect the tumor microenvironment in a manner detrimental to tumor progression.	imatinib	15-23	vascular endothelial growth factor A	Homo sapiens	27-31
18056186-0	2007	BCR-ABL messenger RNA levels continue to decline in patients with chronic phase chronic myeloid leukemia treated with imatinib for more than 5 years and approximately half of all first-line treated patients have stable undetectable BCR-ABL using strict sensitivity criteria.	imatinib	118-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
18056186-1	2007	PURPOSE: In the first years of imatinib treatment, BCR-ABL remained detectable in all but a small minority of patients with chronic myeloid leukemia.	imatinib	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
18056186-3	2007	EXPERIMENTAL DESIGN: BCR-ABL levels were measured in a subset of 53 imatinib-treated IRIS trial patients for up to 7 years (29 first-line, 24 second-line).	imatinib	68-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
18056186-7	2007	The probability of undetectable BCR-ABL increased considerably from 36 to 81 months of first-line imatinib {7% [95% confidence interval (95% CI), 0-17%] versus 52% (95% CI, 32-72%)}.	imatinib	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
18272024-8	2007	Inhibition of the PDGF receptor (PDGFR) with imatinib did not appear to improve efficacy compared retrospectively with the results of treatment with bevacizumab/erlotinib.	imatinib	45-53	platelet derived growth factor receptor beta	Homo sapiens	33-38
18159130-5	2007	When ABCG2 was inhibited by imatinib or novobiocin, however, those cells became sensitive to light.	imatinib	28-36	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	5-10
18035968-2	2007	In an in vitro study, dasatinib had 325-fold greater potency than imatinib for inhibiting unmutated BCR-ABL.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
18060025-3	2007	describe a novel method by which the ABL-inhibitory activity of imatinib was deleted by modifying its chemical structure (see the related article beginning on page 4044).	imatinib	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-40
17852433-6	2007	In this study, mechanisms of resistance to imatinib-induced apoptosis in human Meg-01 CML cells were examined.	imatinib	43-51	protein tyrosine phosphatase non-receptor type 4	Homo sapiens	79-82
17852433-7	2007	Continuous exposure of cells to step-wise increasing concentrations of imatinib resulted in the selection of 200- and 1000 nM imatinib-resistant sub-lines referred to as Meg-01/IMA-0,2 and Meg-01/IMA-1, respectively.	imatinib	71-79	protein tyrosine phosphatase non-receptor type 4	Homo sapiens	170-173
17852433-7	2007	Continuous exposure of cells to step-wise increasing concentrations of imatinib resulted in the selection of 200- and 1000 nM imatinib-resistant sub-lines referred to as Meg-01/IMA-0,2 and Meg-01/IMA-1, respectively.	imatinib	71-79	protein tyrosine phosphatase non-receptor type 4	Homo sapiens	189-192
17852433-7	2007	Continuous exposure of cells to step-wise increasing concentrations of imatinib resulted in the selection of 200- and 1000 nM imatinib-resistant sub-lines referred to as Meg-01/IMA-0,2 and Meg-01/IMA-1, respectively.	imatinib	71-79	transmembrane protein 201	Homo sapiens	196-201
17852433-7	2007	Continuous exposure of cells to step-wise increasing concentrations of imatinib resulted in the selection of 200- and 1000 nM imatinib-resistant sub-lines referred to as Meg-01/IMA-0,2 and Meg-01/IMA-1, respectively.	imatinib	126-134	protein tyrosine phosphatase non-receptor type 4	Homo sapiens	170-173
17852433-7	2007	Continuous exposure of cells to step-wise increasing concentrations of imatinib resulted in the selection of 200- and 1000 nM imatinib-resistant sub-lines referred to as Meg-01/IMA-0,2 and Meg-01/IMA-1, respectively.	imatinib	126-134	transmembrane protein 201	Homo sapiens	196-201
17852433-8	2007	MTT cell proliferation, cell cycle analyses and trypan blue dye exclusion analyses showed that Meg-01/IMA-1 cells were resistant to imatinib-induced apoptosis as compared to parental sensitive cells.	imatinib	132-140	protein tyrosine phosphatase non-receptor type 4	Homo sapiens	95-98
17852433-8	2007	MTT cell proliferation, cell cycle analyses and trypan blue dye exclusion analyses showed that Meg-01/IMA-1 cells were resistant to imatinib-induced apoptosis as compared to parental sensitive cells.	imatinib	132-140	transmembrane protein 201	Homo sapiens	102-107
17852433-12	2007	In this study, it has been shown that the degree of BCR/ABL expression appears to be directly proportional to the levels of imatinib resistance.	imatinib	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
17852433-13	2007	In addition, there have been BCR/ABL-independent mechanisms reported for deriving resistance against imatinib.	imatinib	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
18056005-0	2007	Imatinib mesylate in the treatment of newly diagnosed or refractory/resistant c-KIT positive acute myeloid leukemia.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	78-83
18265633-9	2007	In view of the result that c-kit protein expression was found in 8% of IDC of the pancreas, a clinical trial for STI-571 (Glivec) against pancreatic cancer may be warranted for selected pancreatic cancer patients with c-kit protein expression.	imatinib	113-120	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	27-32
18265633-9	2007	In view of the result that c-kit protein expression was found in 8% of IDC of the pancreas, a clinical trial for STI-571 (Glivec) against pancreatic cancer may be warranted for selected pancreatic cancer patients with c-kit protein expression.	imatinib	113-120	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	218-223
18060038-3	2007	The lack of specificity of the anticancer drug imatinib enables it to be used to treat chronic myeloid leukemia, where its target is the Bcr-Abl kinase, as well as a proportion of gastrointestinal stromal tumors (GISTs), where its target is the C-Kit kinase.	imatinib	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-144
18060038-3	2007	The lack of specificity of the anticancer drug imatinib enables it to be used to treat chronic myeloid leukemia, where its target is the Bcr-Abl kinase, as well as a proportion of gastrointestinal stromal tumors (GISTs), where its target is the C-Kit kinase.	imatinib	47-55	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	245-250
18060038-5	2007	Motivated by this finding, we made a modification to imatinib that hampers Bcr-Abl inhibition; refocuses the impact on the C-Kit kinase; and promotes inhibition of an additional target, JNK, a change that is required to reinforce prevention of cardiotoxicity.	imatinib	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
18060038-5	2007	Motivated by this finding, we made a modification to imatinib that hampers Bcr-Abl inhibition; refocuses the impact on the C-Kit kinase; and promotes inhibition of an additional target, JNK, a change that is required to reinforce prevention of cardiotoxicity.	imatinib	53-61	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	123-128
18060038-5	2007	Motivated by this finding, we made a modification to imatinib that hampers Bcr-Abl inhibition; refocuses the impact on the C-Kit kinase; and promotes inhibition of an additional target, JNK, a change that is required to reinforce prevention of cardiotoxicity.	imatinib	53-61	mitogen-activated protein kinase 8	Homo sapiens	186-189
18088462-0	2007	[STI571 induces apoptosis of K562 cells through down-regulation of anti-apoptotic protein Mcl-1 and Bcl-xl expression].	imatinib	1-7	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	90-95
17728783-0	2007	Deregulation of the Wilms" tumour gene 1 protein (WT1) by BCR/ABL1 mediates resistance to imatinib in human leukaemia cells.	imatinib	90-98	WT1 transcription factor	Homo sapiens	20-40
17728783-0	2007	Deregulation of the Wilms" tumour gene 1 protein (WT1) by BCR/ABL1 mediates resistance to imatinib in human leukaemia cells.	imatinib	90-98	WT1 transcription factor	Homo sapiens	50-53
17728783-0	2007	Deregulation of the Wilms" tumour gene 1 protein (WT1) by BCR/ABL1 mediates resistance to imatinib in human leukaemia cells.	imatinib	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-66
17728783-9	2007	Our data demonstrate that WT1 expression is induced by oncogenic signalling from BCR/ABL1 and that WT1 contributes to resistance against apoptosis induced by imatinib.	imatinib	158-166	WT1 transcription factor	Homo sapiens	99-102
17715395-8	2007	All three PDGFRA isoforms are fully constitutively activated, insensitive to the growth factor PDGF-BB, but show differential sensitivity of their constitutive activity to be inhibited by the inhibitor imatinib (Gleevec).	imatinib	202-210	platelet derived growth factor receptor alpha	Homo sapiens	10-16
17715395-8	2007	All three PDGFRA isoforms are fully constitutively activated, insensitive to the growth factor PDGF-BB, but show differential sensitivity of their constitutive activity to be inhibited by the inhibitor imatinib (Gleevec).	imatinib	212-219	platelet derived growth factor receptor alpha	Homo sapiens	10-16
17604596-0	2007	Docosahexaenoic acid enhances the toxic effect of imatinib on Bcr-Abl expressing HL-60 cells.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
17604596-1	2007	The effect of docosahexaenoic acid (DHA) on the killing efficacy of imatinib on HL-60 cells expressing the Bcr-Abl protein was investigated.	imatinib	68-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
17604596-5	2007	These results indicate that long-term pre-treatment with DHA makes Bcr-Abl HL-60 cells more susceptible to the toxic effect of imatinib.	imatinib	127-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
18054881-1	2007	Updated findings from a randomised comparison of imatinib versus previous standard treatment in the treatment of newly diagnosed chronic myeloid leukaemia suggest that this first-generation tyrosine-kinase inhibitor can induce excellent long-term responses in most patients.	imatinib	49-57	TXK tyrosine kinase	Homo sapiens	190-205
18067005-1	2007	Imatinib was the first treatment for chronic myeloid leukemia (CML) that specifically targeted the causative BCR-ABL oncoprotein, and represented a major therapeutic advance in this disease; however, some patients develop resistance or intolerance.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
18088462-0	2007	[STI571 induces apoptosis of K562 cells through down-regulation of anti-apoptotic protein Mcl-1 and Bcl-xl expression].	imatinib	1-7	BCL2 like 1	Homo sapiens	100-106
17546049-0	2007	KIT oncogenic signaling mechanisms in imatinib-resistant gastrointestinal stromal tumor: PI3-kinase/AKT is a crucial survival pathway.	imatinib	38-46	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
17546049-0	2007	KIT oncogenic signaling mechanisms in imatinib-resistant gastrointestinal stromal tumor: PI3-kinase/AKT is a crucial survival pathway.	imatinib	38-46	AKT serine/threonine kinase 1	Homo sapiens	100-103
18088462-8	2007	It is concluded that STI571 induces the apoptosis of CML cells by down-regulating the expressions of Mcl-1 and Bcl-xl, which suggests that Mcl-1 and Bcl-xl may play an important role in anti-apoptotic process of CML cells.	imatinib	21-27	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	101-106
17546049-1	2007	Most gastrointestinal stromal tumor (GIST) patients respond to KIT inhibition with imatinib, yet will eventually exhibit resistance.	imatinib	83-91	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	63-66
18088462-8	2007	It is concluded that STI571 induces the apoptosis of CML cells by down-regulating the expressions of Mcl-1 and Bcl-xl, which suggests that Mcl-1 and Bcl-xl may play an important role in anti-apoptotic process of CML cells.	imatinib	21-27	BCL2 like 1	Homo sapiens	111-117
17546049-2	2007	Imatinib-resistance mechanisms are heterogeneous, and little is known about KIT functional roles in imatinib-resistant GIST.	imatinib	100-108	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	76-79
17546049-6	2007	After treatment with 1 muM imatinib, residual KIT activation was 6- and 2.8-fold higher in GIST430 and GIST48, respectively, compared to GIST882.	imatinib	27-35	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	46-49
18478917-1	2007	OBJECTIVE: To analyze and evaluate the clinical efficacy and safety of imatinib mesylate (IM) as a tyrosine kinase inhibitor on Ph-positive or BCR/ABL positive chronic myelogenous leukemia (CML).	imatinib	71-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-150
18088462-8	2007	It is concluded that STI571 induces the apoptosis of CML cells by down-regulating the expressions of Mcl-1 and Bcl-xl, which suggests that Mcl-1 and Bcl-xl may play an important role in anti-apoptotic process of CML cells.	imatinib	21-27	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	139-144
17546049-10	2007	We conclude that GIST secondary KIT mutations can be associated with KIT hyperactivation and imatinib resistance.	imatinib	93-101	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	32-35
18088462-8	2007	It is concluded that STI571 induces the apoptosis of CML cells by down-regulating the expressions of Mcl-1 and Bcl-xl, which suggests that Mcl-1 and Bcl-xl may play an important role in anti-apoptotic process of CML cells.	imatinib	21-27	BCL2 like 1	Homo sapiens	149-155
17709602-0	2007	Relapse following discontinuation of imatinib mesylate therapy for FIP1L1/PDGFRA-positive chronic eosinophilic leukemia: implications for optimal dosing.	imatinib	37-54	factor interacting with PAPOLA and CPSF1	Homo sapiens	67-73
17990362-11	2007	Given the resistance of this tumor to conventional chemotherapy and radiation, the incidence of the c-kit alteration may represent a novel approach to a gene-directed treatment using a c-kit inhibitor (STI571) similar to that which has been proposed in GISTs.	imatinib	202-208	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	100-105
17990362-11	2007	Given the resistance of this tumor to conventional chemotherapy and radiation, the incidence of the c-kit alteration may represent a novel approach to a gene-directed treatment using a c-kit inhibitor (STI571) similar to that which has been proposed in GISTs.	imatinib	202-208	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	185-190
17709602-0	2007	Relapse following discontinuation of imatinib mesylate therapy for FIP1L1/PDGFRA-positive chronic eosinophilic leukemia: implications for optimal dosing.	imatinib	37-54	platelet derived growth factor receptor alpha	Homo sapiens	74-80
17709602-1	2007	Although imatinib is clearly the treatment of choice for FIP1L1/PDGFRA-positive chronic eosinophilic leukemia (CEL), little is known about optimal dosing, duration of treatment, and the possibility of cure in this disorder.	imatinib	9-17	factor interacting with PAPOLA and CPSF1	Homo sapiens	57-63
17709602-1	2007	Although imatinib is clearly the treatment of choice for FIP1L1/PDGFRA-positive chronic eosinophilic leukemia (CEL), little is known about optimal dosing, duration of treatment, and the possibility of cure in this disorder.	imatinib	9-17	platelet derived growth factor receptor alpha	Homo sapiens	64-70
17715389-6	2007	Nilotinib was effective in patients harboring BCR-ABL mutations associated with imatinib resistance (except T315I), and also in patients with a resistance mechanism independent of BCR-ABL mutations.	imatinib	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
18006774-0	2007	Association of intratumoral vascular endothelial growth factor expression and clinical outcome for patients with gastrointestinal stromal tumors treated with imatinib mesylate.	imatinib	158-175	vascular endothelial growth factor A	Homo sapiens	28-62
18006774-10	2007	Imatinib resulted in decreased production of VEGF in only a subset of GIST patients (2 of 12) and both cell lines.	imatinib	0-8	vascular endothelial growth factor A	Homo sapiens	45-49
17591671-2	2007	With the development of the compound imatinib mesylate, which specifically inhibits tyrosine kinase receptors, C-kit has emerged as a potential therapeutic target.	imatinib	37-54	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	111-116
19662183-3	2007	A good example is the recent success with the Bcr-Abl tyrosine kinase inhibitor imatinib mesylate (Gleevec) in the treatment of chronic myeloid leukemia.	imatinib	80-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
19662183-3	2007	A good example is the recent success with the Bcr-Abl tyrosine kinase inhibitor imatinib mesylate (Gleevec) in the treatment of chronic myeloid leukemia.	imatinib	99-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
19662183-4	2007	Though imatinib has dramatically improved the treatment of Bcr-Abl-positive chronic myeloid leukemia, resistance is often found in patients with advanced-stage disease.	imatinib	7-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
17986854-0	2007	PDGFRbeta and HIF-1alpha inhibition with imatinib and radioimmunotherapy of experimental prostate cancer.	imatinib	41-49	platelet derived growth factor receptor, beta polypeptide	Mus musculus	0-9
17986854-0	2007	PDGFRbeta and HIF-1alpha inhibition with imatinib and radioimmunotherapy of experimental prostate cancer.	imatinib	41-49	hypoxia inducible factor 1, alpha subunit	Mus musculus	14-24
17986854-2	2007	The purpose of reported here studies was to develop a multimodality approach to RIT of prostate cancer that includes imatinib, a potent PDGFRbeta inhibitor, and in the course of these studies to define the mechanism of imatinib effects on RIT.	imatinib	219-227	platelet derived growth factor receptor, beta polypeptide	Mus musculus	136-145
17986854-4	2007	Levels of HIF-1alpha, IGF-1, PDGF-BB, phospho-PDGFRbeta and VEGF in response to imatinib were examined in PC-3 human prostate adenocarcinoma cells in vitro and in xenografts.	imatinib	80-88	hypoxia inducible factor 1 subunit alpha	Homo sapiens	10-20
17986854-4	2007	Levels of HIF-1alpha, IGF-1, PDGF-BB, phospho-PDGFRbeta and VEGF in response to imatinib were examined in PC-3 human prostate adenocarcinoma cells in vitro and in xenografts.	imatinib	80-88	platelet derived growth factor receptor beta	Homo sapiens	46-55
17986854-4	2007	Levels of HIF-1alpha, IGF-1, PDGF-BB, phospho-PDGFRbeta and VEGF in response to imatinib were examined in PC-3 human prostate adenocarcinoma cells in vitro and in xenografts.	imatinib	80-88	vascular endothelial growth factor A	Homo sapiens	60-64
17986854-4	2007	Levels of HIF-1alpha, IGF-1, PDGF-BB, phospho-PDGFRbeta and VEGF in response to imatinib were examined in PC-3 human prostate adenocarcinoma cells in vitro and in xenografts.	imatinib	80-88	chromobox 8	Mus musculus	106-110
17986854-7	2007	PC-3 cells and PC-3 xenografts express constitutive HIF-1alpha, which was significantly inhibited by imatinib.	imatinib	101-109	chromobox 8	Mus musculus	0-4
17986854-7	2007	PC-3 cells and PC-3 xenografts express constitutive HIF-1alpha, which was significantly inhibited by imatinib.	imatinib	101-109	chromobox 8	Mus musculus	15-19
17986854-7	2007	PC-3 cells and PC-3 xenografts express constitutive HIF-1alpha, which was significantly inhibited by imatinib.	imatinib	101-109	hypoxia inducible factor 1, alpha subunit	Mus musculus	52-62
17986854-10	2007	Improved PC-3 responses to RIT+imatinib treatment were significant and lasted approximately two weeks.	imatinib	31-39	chromobox 8	Mus musculus	9-13
17986854-13	2007	In conclusion, imatinib inhibits HIF-1alpha expression in PC-3 tumors and improves RIT, but it has no effect on VEGF indicating absence of anti-angiogenic effects.	imatinib	15-23	hypoxia inducible factor 1, alpha subunit	Mus musculus	33-43
17986854-13	2007	In conclusion, imatinib inhibits HIF-1alpha expression in PC-3 tumors and improves RIT, but it has no effect on VEGF indicating absence of anti-angiogenic effects.	imatinib	15-23	chromobox 8	Mus musculus	58-62
17986854-14	2007	There is a significant time- and dose-dependent reduction in the expression of IGF-1 suggesting an alternative pathway of imatinib-regulated HIF-1alpha expression leading to the improved PC-3 responses to RIT.	imatinib	122-130	insulin-like growth factor 1	Mus musculus	79-84
17986854-14	2007	There is a significant time- and dose-dependent reduction in the expression of IGF-1 suggesting an alternative pathway of imatinib-regulated HIF-1alpha expression leading to the improved PC-3 responses to RIT.	imatinib	122-130	hypoxia inducible factor 1, alpha subunit	Mus musculus	141-151
17986854-14	2007	There is a significant time- and dose-dependent reduction in the expression of IGF-1 suggesting an alternative pathway of imatinib-regulated HIF-1alpha expression leading to the improved PC-3 responses to RIT.	imatinib	122-130	chromobox 8	Mus musculus	187-191
17996650-4	2007	We utilize NSC23766, a small molecule antagonist of Rac activation, to validate biochemically and functionally Rac as a molecular target in both a relevant animal model and in primary human CML cells in vitro and in a xenograft model in vivo, including in Imatinib-resistant p210-BCR-ABL disease.	imatinib	256-264	AKT serine/threonine kinase 1	Homo sapiens	111-114
17999742-5	2007	The protein tyrosine kinase inhibitor, imatinib (Gleevec), decreases the proliferation of non-parenchymal cells (NPC) in vitro and in vivo, with concomitant inhibition of Akt.	imatinib	39-47	thymoma viral proto-oncogene 1	Mus musculus	171-174
17999742-6	2007	In vivo treatment with imatinib also blocks the expression of CD34 in PDGF-C Tg mice.	imatinib	23-31	CD34 antigen	Mus musculus	62-66
17999742-6	2007	In vivo treatment with imatinib also blocks the expression of CD34 in PDGF-C Tg mice.	imatinib	23-31	platelet-derived growth factor, C polypeptide	Mus musculus	70-76
17999742-8	2007	In summary, the small molecule inhibitor imatinib attenuates stromal cell proliferation in PDGF-C-induced HCC, which coincides with decreased expression of both CD34 and PDGFRalpha, and activated Akt.	imatinib	41-49	platelet-derived growth factor, C polypeptide	Mus musculus	91-97
17999742-8	2007	In summary, the small molecule inhibitor imatinib attenuates stromal cell proliferation in PDGF-C-induced HCC, which coincides with decreased expression of both CD34 and PDGFRalpha, and activated Akt.	imatinib	41-49	CD34 antigen	Mus musculus	161-165
17999742-8	2007	In summary, the small molecule inhibitor imatinib attenuates stromal cell proliferation in PDGF-C-induced HCC, which coincides with decreased expression of both CD34 and PDGFRalpha, and activated Akt.	imatinib	41-49	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	170-180
17999742-8	2007	In summary, the small molecule inhibitor imatinib attenuates stromal cell proliferation in PDGF-C-induced HCC, which coincides with decreased expression of both CD34 and PDGFRalpha, and activated Akt.	imatinib	41-49	thymoma viral proto-oncogene 1	Mus musculus	196-199
17663639-2	2007	We show that inhibition by imatinib of PDGFR signaling in osteoblasts activates osteoblast differentiation and inhibits osteoblast proliferation and that imatinib inhibits osteoclastogenesis by both stromal cell-dependent and direct effects on osteoclast precursors.	imatinib	27-35	platelet derived growth factor receptor, beta polypeptide	Mus musculus	39-44
17663639-0	2007	Imatinib promotes osteoblast differentiation by inhibiting PDGFR signaling and inhibits osteoclastogenesis by both direct and stromal cell-dependent mechanisms.	imatinib	0-8	platelet derived growth factor receptor, beta polypeptide	Mus musculus	59-64
17912440-0	2007	Imatinib impairs the proliferation and function of CD4+CD25+ regulatory T cells in a dose-dependent manner.	imatinib	0-8	CD4 molecule	Homo sapiens	51-54
17912440-0	2007	Imatinib impairs the proliferation and function of CD4+CD25+ regulatory T cells in a dose-dependent manner.	imatinib	0-8	interleukin 2 receptor subunit alpha	Homo sapiens	55-59
17912440-1	2007	The tyrosine kinase inhibitor imatinib has been reported to inhibit CD8+ T lymphocytes.	imatinib	30-38	CD8a molecule	Homo sapiens	68-71
17912440-4	2007	Here, we demonstrate that the proliferation of CD4+CD25+ T(reg) cells and their production of IL-10, TGF-beta1 and granzyme B as markers of activation were significantly down-regulated by imatinib in a dose-dependent manner.	imatinib	188-196	CD4 molecule	Homo sapiens	47-50
17912440-4	2007	Here, we demonstrate that the proliferation of CD4+CD25+ T(reg) cells and their production of IL-10, TGF-beta1 and granzyme B as markers of activation were significantly down-regulated by imatinib in a dose-dependent manner.	imatinib	188-196	interleukin 2 receptor subunit alpha	Homo sapiens	51-55
17912440-4	2007	Here, we demonstrate that the proliferation of CD4+CD25+ T(reg) cells and their production of IL-10, TGF-beta1 and granzyme B as markers of activation were significantly down-regulated by imatinib in a dose-dependent manner.	imatinib	188-196	interleukin 10	Homo sapiens	94-99
17912440-4	2007	Here, we demonstrate that the proliferation of CD4+CD25+ T(reg) cells and their production of IL-10, TGF-beta1 and granzyme B as markers of activation were significantly down-regulated by imatinib in a dose-dependent manner.	imatinib	188-196	transforming growth factor beta 1	Homo sapiens	101-110
17912440-4	2007	Here, we demonstrate that the proliferation of CD4+CD25+ T(reg) cells and their production of IL-10, TGF-beta1 and granzyme B as markers of activation were significantly down-regulated by imatinib in a dose-dependent manner.	imatinib	188-196	granzyme B	Homo sapiens	115-125
17912440-5	2007	In addition, the expression of surface CD69, both surface and intracellular GITR, FoxP3, CD152 (CTLA) of activated CD4+CD25+ T(reg) cells were inhibited by imatinib in a dose-dependent manner.	imatinib	156-164	CD69 molecule	Homo sapiens	39-43
17912440-5	2007	In addition, the expression of surface CD69, both surface and intracellular GITR, FoxP3, CD152 (CTLA) of activated CD4+CD25+ T(reg) cells were inhibited by imatinib in a dose-dependent manner.	imatinib	156-164	TNF receptor superfamily member 18	Homo sapiens	76-80
17912440-5	2007	In addition, the expression of surface CD69, both surface and intracellular GITR, FoxP3, CD152 (CTLA) of activated CD4+CD25+ T(reg) cells were inhibited by imatinib in a dose-dependent manner.	imatinib	156-164	forkhead box P3	Homo sapiens	82-87
17912440-5	2007	In addition, the expression of surface CD69, both surface and intracellular GITR, FoxP3, CD152 (CTLA) of activated CD4+CD25+ T(reg) cells were inhibited by imatinib in a dose-dependent manner.	imatinib	156-164	cytotoxic T-lymphocyte associated protein 4	Homo sapiens	89-94
17912440-5	2007	In addition, the expression of surface CD69, both surface and intracellular GITR, FoxP3, CD152 (CTLA) of activated CD4+CD25+ T(reg) cells were inhibited by imatinib in a dose-dependent manner.	imatinib	156-164	CD4 molecule	Homo sapiens	115-118
17912440-5	2007	In addition, the expression of surface CD69, both surface and intracellular GITR, FoxP3, CD152 (CTLA) of activated CD4+CD25+ T(reg) cells were inhibited by imatinib in a dose-dependent manner.	imatinib	156-164	interleukin 2 receptor subunit alpha	Homo sapiens	119-123
17663639-3	2007	INTRODUCTION: Imatinib mesylate, an orally active inhibitor of the c-abl, c-kit, and platelet-derived growth factor receptor (PDGFR) tyrosine kinases, is in clinical use for the treatment of chronic myeloid leukemia (CML) and gastrointestinal stromal cell tumors.	imatinib	14-31	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	67-72
17663639-3	2007	INTRODUCTION: Imatinib mesylate, an orally active inhibitor of the c-abl, c-kit, and platelet-derived growth factor receptor (PDGFR) tyrosine kinases, is in clinical use for the treatment of chronic myeloid leukemia (CML) and gastrointestinal stromal cell tumors.	imatinib	14-31	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	74-79
17663639-3	2007	INTRODUCTION: Imatinib mesylate, an orally active inhibitor of the c-abl, c-kit, and platelet-derived growth factor receptor (PDGFR) tyrosine kinases, is in clinical use for the treatment of chronic myeloid leukemia (CML) and gastrointestinal stromal cell tumors.	imatinib	14-31	platelet derived growth factor receptor, beta polypeptide	Mus musculus	85-124
17663639-3	2007	INTRODUCTION: Imatinib mesylate, an orally active inhibitor of the c-abl, c-kit, and platelet-derived growth factor receptor (PDGFR) tyrosine kinases, is in clinical use for the treatment of chronic myeloid leukemia (CML) and gastrointestinal stromal cell tumors.	imatinib	14-31	platelet derived growth factor receptor, beta polypeptide	Mus musculus	126-131
17663639-4	2007	Interruption of both c-kit and c-abl signaling in mice induces osteopenia, suggesting that imatinib might have adverse effects on the skeleton.	imatinib	91-99	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	21-26
17663639-4	2007	Interruption of both c-kit and c-abl signaling in mice induces osteopenia, suggesting that imatinib might have adverse effects on the skeleton.	imatinib	91-99	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	31-36
17663639-14	2007	In murine bone marrow cultures, imatinib inhibits osteoclastogenesis stimulated by 1,25-dihydroxyvitamin D(3) and partially inhibits osteoclastogenesis induced by RANKL and macrophage-colony stimulating factor.	imatinib	32-40	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	163-168
18205699-1	2007	BCR-ABL tyrosine kinase inhibitors, such as imatinib (Gleevec) are highly effective in treating human Philadelphia chromosome-positive (Ph+) chronic myeloid leukaemia (CML) in chronic phase but not in terminal acute phase; acquired drug resistance caused mainly by the development of BCR-ABL kinase domain mutations prevents cure of the leukaemia.	imatinib	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
18205699-1	2007	BCR-ABL tyrosine kinase inhibitors, such as imatinib (Gleevec) are highly effective in treating human Philadelphia chromosome-positive (Ph+) chronic myeloid leukaemia (CML) in chronic phase but not in terminal acute phase; acquired drug resistance caused mainly by the development of BCR-ABL kinase domain mutations prevents cure of the leukaemia.	imatinib	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	284-291
18205699-1	2007	BCR-ABL tyrosine kinase inhibitors, such as imatinib (Gleevec) are highly effective in treating human Philadelphia chromosome-positive (Ph+) chronic myeloid leukaemia (CML) in chronic phase but not in terminal acute phase; acquired drug resistance caused mainly by the development of BCR-ABL kinase domain mutations prevents cure of the leukaemia.	imatinib	54-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
17663639-15	2007	Imatinib partially inhibited osteoclastogenesis in RANKL-stimulated RAW-264.7 cells.	imatinib	0-8	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	51-56
18205699-1	2007	BCR-ABL tyrosine kinase inhibitors, such as imatinib (Gleevec) are highly effective in treating human Philadelphia chromosome-positive (Ph+) chronic myeloid leukaemia (CML) in chronic phase but not in terminal acute phase; acquired drug resistance caused mainly by the development of BCR-ABL kinase domain mutations prevents cure of the leukaemia.	imatinib	54-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	284-291
17663639-16	2007	Treatment with imatinib increases the expression of osteoprotegerin in bone marrow from patients with CML and osteoblastic cells.	imatinib	15-23	TNF receptor superfamily member 11b	Homo sapiens	52-67
18205699-3	2007	This type of drug resistance that is unrelated to BCR-ABL kinase domain mutations is caused by the insensitivity of leukaemic stem cells to kinase inhibitors such as imatinib and dasatinib, and by activation of a newly-identified signalling pathway involving SRC kinases that are independent of BCR-ABL kinase activity for activation.	imatinib	166-174	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	295-302
17663639-17	2007	CONCLUSIONS: Taken together with recent in vivo data, these results suggest a role for the molecular targets of imatinib in bone cell function, that inhibition by imatinib of PDGFR signaling in osteoblasts activates bone formation, and that the antiresorptive actions of imatinib are mediated by both stromal cell-dependent and direct effects on osteoclast precursors.	imatinib	112-120	platelet derived growth factor receptor, beta polypeptide	Mus musculus	175-180
17663639-17	2007	CONCLUSIONS: Taken together with recent in vivo data, these results suggest a role for the molecular targets of imatinib in bone cell function, that inhibition by imatinib of PDGFR signaling in osteoblasts activates bone formation, and that the antiresorptive actions of imatinib are mediated by both stromal cell-dependent and direct effects on osteoclast precursors.	imatinib	163-171	platelet derived growth factor receptor, beta polypeptide	Mus musculus	175-180
17663639-17	2007	CONCLUSIONS: Taken together with recent in vivo data, these results suggest a role for the molecular targets of imatinib in bone cell function, that inhibition by imatinib of PDGFR signaling in osteoblasts activates bone formation, and that the antiresorptive actions of imatinib are mediated by both stromal cell-dependent and direct effects on osteoclast precursors.	imatinib	163-171	platelet derived growth factor receptor, beta polypeptide	Mus musculus	175-180
17976614-0	2007	Complete response after treatment with imatinib in pretreated disseminated testicular seminoma with overexpression of c-KIT.	imatinib	39-47	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	118-123
17926190-7	2007	Enhanced apoptosis, cytochrome C release, and caspase 3 cleavage as well as noticeable decrease of Mcl-1 and Bcl-XL were observed in K562 cells treated with both (-)gossypol and imatinib.	imatinib	178-186	cytochrome c, somatic	Homo sapiens	20-32
17637811-2	2007	Here, 19 imatinib treated CML patients in first chronic phase were vaccinated with BCR-ABL peptides spanning the e14a2 fusion junction, some of which were linked to the pan DR epitope PADRE to augment CD4+ T cell help.	imatinib	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
17637811-10	2007	Vaccination may improve the fall in BCR-ABL transcripts in patients who have received imatinib for more than 12 months.	imatinib	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
18024285-0	2007	[STI571 enhances the effect of arsenic trioxide and Velcade on bcr/abl+-CD34+ cell proliferation and apoptosis].	imatinib	1-7	CD34 molecule	Homo sapiens	72-76
17637811-11	2007	BCR-ABL peptide vaccination may improve control of CML, especially in patients responding well to imatinib.	imatinib	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
17690707-0	2007	Extramedullary BCR-ABL1-negative myeloid leukemia in a patient with chronic myeloid leukemia and synchronous cytogenetic abnormalities in Philadelphia-positive and -negative clones during imatinib therapy.	imatinib	188-196	BCR activator of RhoGEF and GTPase	Homo sapiens	15-23
17926190-7	2007	Enhanced apoptosis, cytochrome C release, and caspase 3 cleavage as well as noticeable decrease of Mcl-1 and Bcl-XL were observed in K562 cells treated with both (-)gossypol and imatinib.	imatinib	178-186	caspase 3	Homo sapiens	46-55
17926190-7	2007	Enhanced apoptosis, cytochrome C release, and caspase 3 cleavage as well as noticeable decrease of Mcl-1 and Bcl-XL were observed in K562 cells treated with both (-)gossypol and imatinib.	imatinib	178-186	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	99-104
17926190-7	2007	Enhanced apoptosis, cytochrome C release, and caspase 3 cleavage as well as noticeable decrease of Mcl-1 and Bcl-XL were observed in K562 cells treated with both (-)gossypol and imatinib.	imatinib	178-186	BCL2 like 1	Homo sapiens	109-115
18024285-2	2007	METHODS: bcr/abl+-CD34+ cells isolated from the bone marrow of patients with chronic myeloid leukemia (CML) were treated for 96 h with STI571, As2O3 and Velcade either alone and in combination, and the cell proliferation and apoptosis were analyzed by CCK-8 assay and flow cytometry.	imatinib	135-141	CD34 molecule	Homo sapiens	18-22
18024285-5	2007	RESULTS: Low-concentration STI571, As2O3 or Velcade all dose-dependently inhibited bcr/abl+-CD34+ cell proliferation without obvious apoptosis-inducing effects.	imatinib	27-33	CD34 molecule	Homo sapiens	92-96
18024285-6	2007	STI571 at 0.25-2 micromol/L combined with As2O3 at 2.5 micromol/L and with Velcade at 15 nmol/L both significantly increased the cell inhibition and apoptosis rates, showing obvious additive or synergistic effects of the drugs without further enhancement of normal CD34+ cell inhibition.	imatinib	0-6	CD34 molecule	Homo sapiens	265-269
18024285-7	2007	CONCLUSION: Combination with STI571 enhances the effects of As2O3 and Velcade on bcr/abl+-CD34+ cells, suggesting the potential clinical value of this regimen.	imatinib	29-35	CD34 molecule	Homo sapiens	90-94
17958915-2	2007	Nilotinib is a selective Bcr/Abl tyrosine kinase inhibitor related to imatinib, which is widely used to treat chronic myelogenous leukemia.	imatinib	70-78	BCR activator of RhoGEF and GTPase	Mus musculus	25-28
17647063-8	2007	Recently, imatinib, a potent, selective inhibitor of the PDGFR alpha and PDGFR beta protein-tyrosine kinases, has been reported to induce complete or partial remissions in most patients treated for advanced DFSP.	imatinib	10-18	platelet derived growth factor receptor alpha	Homo sapiens	57-68
17947479-0	2007	A half-log increase in BCR-ABL RNA predicts a higher risk of relapse in patients with chronic myeloid leukemia with an imatinib-induced complete cytogenetic response.	imatinib	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
17947479-10	2007	CONCLUSIONS: In chronic myeloid leukemia patients with an imatinib-induced CCR, a minimal half-log increase in BCR-ABL RNA (including loss of MMR) is a significant risk factor for future relapse.	imatinib	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
17647063-8	2007	Recently, imatinib, a potent, selective inhibitor of the PDGFR alpha and PDGFR beta protein-tyrosine kinases, has been reported to induce complete or partial remissions in most patients treated for advanced DFSP.	imatinib	10-18	platelet derived growth factor receptor beta	Homo sapiens	73-83
17704653-6	2007	Using alymphoid Rag2/gammac-/- mice, we showed that the effect of STI571 was not dependent on the presence of natural killer cells.	imatinib	66-72	recombination activating gene 2	Mus musculus	16-20
17601986-5	2007	Treatment of animals with the ABL kinase inhibitor imatinib mesylate induced specific modulation of blasts and progenitor cells but not stem- cell populations, thereby recapitulating events inferred to occur in human chronic myelogenous leukemia (CML) patients.	imatinib	51-68	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	30-33
17704653-6	2007	Using alymphoid Rag2/gammac-/- mice, we showed that the effect of STI571 was not dependent on the presence of natural killer cells.	imatinib	66-72	interleukin 2 receptor, gamma chain	Mus musculus	21-27
17704653-8	2007	Finally, using nonimmunodeficient mice, we observed an in-vivo decrease of CD4-positive T-cells and mature B-cell lymphocytes after imatinib administration.	imatinib	132-140	CD4 antigen	Mus musculus	75-78
17496200-1	2007	Mutations in the kinase domain (KD) of BCR-ABL are the most prevalent mechanism of acquired imatinib resistance in patients with chronic myeloid leukemia (CML).	imatinib	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
17496200-3	2007	We also provide a perspective on how the second-line Abl inhibitors dasatinib and nilotinib are faring in the treatment of imatinib-resistant CML, especially in relation to specific KD mutations.	imatinib	123-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
17496201-7	2007	The presence of BCR-ABL mutations conferring imatinib resistance did not preclude a response to dasatinib.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
17579186-4	2007	The T-cell repertoire of a patient with CML in major molecular remission due to imatinib mesylate was also dominated by T cells directed against Bcr-Abl-regulated antigens.	imatinib	80-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-152
17964980-4	2007	However, despite these remarkable improvements, new problems arise as sub-optimal responses, imatinib-resistances with recently identified BCR-ABL protein point mutations, responsible for a variety of therapeutic consequences : imatinib dose increase, alternative treatments with second generation tyrosine kinase inhibitors (TKIs : dastinib, nilotinib) or allogeneic stem cell transplantation.	imatinib	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-146
17964980-4	2007	However, despite these remarkable improvements, new problems arise as sub-optimal responses, imatinib-resistances with recently identified BCR-ABL protein point mutations, responsible for a variety of therapeutic consequences : imatinib dose increase, alternative treatments with second generation tyrosine kinase inhibitors (TKIs : dastinib, nilotinib) or allogeneic stem cell transplantation.	imatinib	228-236	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-146
17964981-2	2007	In Philadelphia chromosome-positive ALL, the optimal treatment requires the addition of BCR-ABL tyrosine kinase inhibitors, as imatinib.	imatinib	127-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
17964981-4	2007	The emergence of resistance to the Bcr-Abl inhibitor imatinib mesylate in patients with Philadelphia chromosome-positive (Ph+) ALL has prompted the development of second-generation compounds active against mutant forms, including dasatinib and nilotinib.	imatinib	53-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
17703986-4	2007	Following the discovery of the leukemic oncogene BCR/ABL and its causal association with CML, the potent BCR/ABL tyrosine kinase inhibitor imatinib mesylate was developed.	imatinib	139-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-56
17851575-2	2007	Genetic technology has led to some very important therapeutic innovations, including the use of imatinib mesylate (Gleevec) in BCR-ABL chronic myeloid leukemia and of trastuzumab (Herceptin) in Her2-positive breast cancer, but the much anticipated explosion of new effective treatments has been more modest than expected.	imatinib	96-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
17908974-1	2007	PURPOSE: To further assess preclinical and early clinical evidence that imatinib mesylate, a platelet-derived growth factor receptor (PDGFR) inhibitor, modulates taxane activity in prostate cancer and bone metastases, a randomized study was conducted.	imatinib	72-89	platelet derived growth factor receptor beta	Homo sapiens	134-139
17908974-9	2007	In peripheral blood leukocytes, p-PDGFR reduction was more likely in docetaxel + imatinib-treated patients compared with docetaxel + placebo (P < 0.0001), as were reductions in urine N-telopeptides (P = 0.004) but not serum bone-specific alkaline phosphatase (P = 0.099).	imatinib	81-89	platelet derived growth factor receptor beta	Homo sapiens	32-39
17703986-4	2007	Following the discovery of the leukemic oncogene BCR/ABL and its causal association with CML, the potent BCR/ABL tyrosine kinase inhibitor imatinib mesylate was developed.	imatinib	139-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
17196360-6	2007	However, their molecular genetics, i.e. the mutations of the genes coding for KIT or platelet-derived growth factor receptor alpha, two receptor tyrosine kinases, have been targeted for therapeutic intervention by imatinib mesylate -- a tyrosine kinase inhibitor.	imatinib	214-231	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	78-81
17987222-1	2007	Imatinib mesylate (Gleevec; Novartis, Basel, Switzerland) is a highly effective inhibitor of the deregulated kinase activity of BCR-ABL in chronic myelogenous leukemia (CML) and represents the current standard of care for patients with this disease.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
17987222-1	2007	Imatinib mesylate (Gleevec; Novartis, Basel, Switzerland) is a highly effective inhibitor of the deregulated kinase activity of BCR-ABL in chronic myelogenous leukemia (CML) and represents the current standard of care for patients with this disease.	imatinib	19-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
17196360-6	2007	However, their molecular genetics, i.e. the mutations of the genes coding for KIT or platelet-derived growth factor receptor alpha, two receptor tyrosine kinases, have been targeted for therapeutic intervention by imatinib mesylate -- a tyrosine kinase inhibitor.	imatinib	214-231	platelet derived growth factor receptor alpha	Homo sapiens	85-130
17922620-1	2007	The outcome of patients with gastrointestinal stromal tumors has been dramatically improved by therapy with imatinib mesilate (imatinib mesylate), a KIT and platelet-derived growth factor (PDGFR) tyrosine kinase inhibitor.	imatinib	108-125	platelet derived growth factor receptor beta	Homo sapiens	157-187
17727673-2	2007	The BCR/ABL tyrosine kinase inhibitor imatinib is highly effective in patients with CML, but hardly crosses the blood-brain barrier.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
17922620-1	2007	The outcome of patients with gastrointestinal stromal tumors has been dramatically improved by therapy with imatinib mesilate (imatinib mesylate), a KIT and platelet-derived growth factor (PDGFR) tyrosine kinase inhibitor.	imatinib	127-144	platelet derived growth factor receptor beta	Homo sapiens	157-187
17922620-3	2007	Recent elucidation of the mechanisms of resistance to imatinib, particularly the acquisition of secondary mutations of the KIT and PDGF receptors, has provided significant insight and potential for the development of novel therapies.	imatinib	54-62	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	123-126
17906206-0	2007	Measurement of in vivo BCR-ABL kinase inhibition to monitor imatinib-induced target blockade and predict response in chronic myeloid leukemia.	imatinib	60-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
17929114-0	2007	The Bcr-Abl tyrosine kinase inhibitor imatinib and promising new agents against Philadelphia chromosome-positive leukemias.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
17929114-3	2007	Imatinib mesylate (IM, Gleevec, Novartis Pharmaceuticals, Basel, Switzerland), which specifically inhibits the autophosphorylation of the Abl TK, has improved the treatment of CML.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-141
17988989-0	2007	Successful imatinib treatment of cardiac involvement of FIP1L1-PDGFRA-positive chronic eosinophilic leukemia followed by severe hepatotoxicity.	imatinib	11-19	factor interacting with PAPOLA and CPSF1	Homo sapiens	56-62
17988989-0	2007	Successful imatinib treatment of cardiac involvement of FIP1L1-PDGFRA-positive chronic eosinophilic leukemia followed by severe hepatotoxicity.	imatinib	11-19	platelet derived growth factor receptor alpha	Homo sapiens	63-69
17988989-1	2007	Imatinib is highly effective for the treatment of chronic eosinophilic leukemia (CEL) caused by the FIP1L1-PDGFRA fusion gene.	imatinib	0-8	factor interacting with PAPOLA and CPSF1	Homo sapiens	100-106
17988989-1	2007	Imatinib is highly effective for the treatment of chronic eosinophilic leukemia (CEL) caused by the FIP1L1-PDGFRA fusion gene.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	107-113
17988989-13	2007	Thus, imatinib may be very effective for treating the early cardiac involvement of FIP1L1-PDGFRA-positive CEL, but it needs to be used cautiously.	imatinib	6-14	factor interacting with PAPOLA and CPSF1	Homo sapiens	83-89
17988989-13	2007	Thus, imatinib may be very effective for treating the early cardiac involvement of FIP1L1-PDGFRA-positive CEL, but it needs to be used cautiously.	imatinib	6-14	platelet derived growth factor receptor alpha	Homo sapiens	90-96
17906206-9	2007	CONCLUSION: In vivo BCR-ABL kinase inhibition can be assessed in the first month of imatinib therapy and may provide a valuable guide to optimization of dosage.	imatinib	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
17686996-4	2007	The Abl kinase inhibitor, imatinib, also stimulates cell spreading and its effect is overridden by the imatinib-resistant AblT315I.	imatinib	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
17970609-10	2007	BCR-ABL inhibitors, such as imatinib, are proof that targeting specific genetic mutations associated with cancer yields a high degree of efficacy with minimal toxicity.	imatinib	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
17970609-20	2007	Imatinib functions by competing with adenosine triphosphate (ATP) for binding to the BCr-ABL tyrosine kinase.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
17970609-22	2007	The International randomized Interferon versus STI571 clinical trial was the first to document the efficacy of imatinib as a first-line therapy for patients in CP.	imatinib	111-119	interferon alpha 1	Homo sapiens	29-39
17970609-31	2007	resistance is usually caused by mutations within BCr-ABL, decreasing the affinity of imatinib binding.	imatinib	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
17970610-3	2007	Imatinib is a small molecule that binds to BCR-ABL at the site in which adenosine triphosphate (ATP) binds and blocks BCR-ABL function by blocking its ability to use ATP.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
17970610-3	2007	Imatinib is a small molecule that binds to BCR-ABL at the site in which adenosine triphosphate (ATP) binds and blocks BCR-ABL function by blocking its ability to use ATP.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
17970610-10	2007	resistance can manifest through 1 of several mechanisms, including increased plasma protein binding, increased drug efflux, the appearance of BCR-ABL mutants that have low affinity for imatinib, the appearance of BCR-ABL independent proliferation signals, and the amplification of the BCR-ABL gene.	imatinib	185-193	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
17970610-17	2007	It is capable of blocking several BCR-ABL mutants that are resistant to imatinib.	imatinib	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
17686996-8	2007	Ectopic expression of a dynamin-2 mutant, previously shown to induce Rac-GTP localization to the dorsal membrane, abolishes the stimulatory effect of imatinib on cell spreading.	imatinib	150-158	dynamin 2	Homo sapiens	24-33
17686996-4	2007	The Abl kinase inhibitor, imatinib, also stimulates cell spreading and its effect is overridden by the imatinib-resistant AblT315I.	imatinib	103-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
17701051-13	2007	Secondary resistance to imatinib treatment is increasing, at least partly due to secondary mutations in the tyrosine kinase domain of the KIT receptor.	imatinib	24-32	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	138-141
17853901-1	2007	The introduction of the BCR-ABL kinase inhibitor imatinib mesylate (Gleevec; Novartis) revolutionized the treatment of chronic myeloid leukaemia (CML).	imatinib	49-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
17853901-1	2007	The introduction of the BCR-ABL kinase inhibitor imatinib mesylate (Gleevec; Novartis) revolutionized the treatment of chronic myeloid leukaemia (CML).	imatinib	68-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
17853901-3	2007	The second-generation BCR-ABL inhibitors nilotinib (Tasigna; Novartis) and dasatinib (Sprycel; Bristol-Myers Squibb) have shown significant activity after imatinib failure in clinical trials, but still face similar obstacles to imatinib, including negligible activity against the frequent BCR-ABL T315I mutation and modest effects in advanced phases of CML.	imatinib	155-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
17853901-3	2007	The second-generation BCR-ABL inhibitors nilotinib (Tasigna; Novartis) and dasatinib (Sprycel; Bristol-Myers Squibb) have shown significant activity after imatinib failure in clinical trials, but still face similar obstacles to imatinib, including negligible activity against the frequent BCR-ABL T315I mutation and modest effects in advanced phases of CML.	imatinib	228-236	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
17853901-4	2007	Various medicinal chemistry efforts, in part aided by structural studies of the ABL kinase-imatinib complex have resulted in the synthesis of a new generation of BCR-ABL inhibitors, some of which have shown encouraging preliminary activity in clinical trials, including against T315I mutants.	imatinib	91-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-169
17536018-1	2007	Mutation in the target oncoprotein is a common mechanism of resistance to tyrosine kinase inhibitors, as exemplified by the many BCR/ABL mutations that thwart imatinib activity in patients with chronic myelogenous leukemia.	imatinib	159-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
17452978-3	2007	Tyrosine-phosphorylated KIT oncoproteins interacted with PDGFRA, PDGFRB, phosphatidylinositol 3-kinase (PI3-K) and PKCtheta in GIST cells, and these interactions were abolished by KIT inhibition with imatinib or PKC412 or KIT RNAi.	imatinib	200-208	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	24-27
17712313-1	2007	Imatinib, an inhibitor of PDGF-Rbeta and other tyrosine kinase receptors, has been shown to decrease microvessel density and interstitial fluid pressure in solid tumours, thereby improving subsequent delivery of small molecules.	imatinib	0-8	platelet derived growth factor receptor, beta polypeptide	Mus musculus	26-36
17620332-4	2007	Inhibition of c-Abl tyrosine kinase by STI571 attenuates the effect of insulin on Akt/GSK-3beta phosphorylation and glycogen synthesis, and at the same time, it enhances the effect of insulin on ERK activation, cell proliferation, and migration.	imatinib	39-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
17701954-6	2007	Imatinib is an oral competitive inhibitor of ABL with demonstrated phase 2 efficacy in patients with treatment-naive and pretreated ALL.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-48
17701954-7	2007	Despite its efficacy, imatinib may induce specific resistance in a large proportion of patients, mainly because of the occurrence of ABL1 mutations.	imatinib	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-137
17701954-12	2007	Nilotinib is another BCR-ABL targeted agent that is similar in structure to imatinib but has significantly greater binding affinity.	imatinib	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
17623672-4	2007	WAVE3-Abl interaction promotes the tyrosine phosphorylation of WAVE3 by Abl, and STI-571, a specific inhibitor of Abl kinase activity, abrogates the Abl-mediated phosphorylation of WAVE3.	imatinib	81-88	WASP family member 3	Homo sapiens	0-5
17554062-5	2007	Cholesterol depletion by methyl-beta-cyclodextrin prevented Kit-mediated activation of the PI3-K downstream target Akt and inhibited cellular proliferation by KL-activated or oncogenic Kit, including mutants resistant to the Kit inhibitor imatinib-mesylate.	imatinib	239-256	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	60-63
17554062-5	2007	Cholesterol depletion by methyl-beta-cyclodextrin prevented Kit-mediated activation of the PI3-K downstream target Akt and inhibited cellular proliferation by KL-activated or oncogenic Kit, including mutants resistant to the Kit inhibitor imatinib-mesylate.	imatinib	239-256	AKT serine/threonine kinase 1	Homo sapiens	115-118
17620332-4	2007	Inhibition of c-Abl tyrosine kinase by STI571 attenuates the effect of insulin on Akt/GSK-3beta phosphorylation and glycogen synthesis, and at the same time, it enhances the effect of insulin on ERK activation, cell proliferation, and migration.	imatinib	39-45	insulin	Homo sapiens	71-78
17623672-4	2007	WAVE3-Abl interaction promotes the tyrosine phosphorylation of WAVE3 by Abl, and STI-571, a specific inhibitor of Abl kinase activity, abrogates the Abl-mediated phosphorylation of WAVE3.	imatinib	81-88	WASP family member 3	Homo sapiens	63-68
17623672-4	2007	WAVE3-Abl interaction promotes the tyrosine phosphorylation of WAVE3 by Abl, and STI-571, a specific inhibitor of Abl kinase activity, abrogates the Abl-mediated phosphorylation of WAVE3.	imatinib	81-88	WASP family member 3	Homo sapiens	63-68
17620332-4	2007	Inhibition of c-Abl tyrosine kinase by STI571 attenuates the effect of insulin on Akt/GSK-3beta phosphorylation and glycogen synthesis, and at the same time, it enhances the effect of insulin on ERK activation, cell proliferation, and migration.	imatinib	39-45	AKT serine/threonine kinase 1	Homo sapiens	82-85
17620332-4	2007	Inhibition of c-Abl tyrosine kinase by STI571 attenuates the effect of insulin on Akt/GSK-3beta phosphorylation and glycogen synthesis, and at the same time, it enhances the effect of insulin on ERK activation, cell proliferation, and migration.	imatinib	39-45	glycogen synthase kinase 3 beta	Homo sapiens	86-95
17620332-4	2007	Inhibition of c-Abl tyrosine kinase by STI571 attenuates the effect of insulin on Akt/GSK-3beta phosphorylation and glycogen synthesis, and at the same time, it enhances the effect of insulin on ERK activation, cell proliferation, and migration.	imatinib	39-45	insulin	Homo sapiens	184-191
17620332-5	2007	This effect of STI571 is specific to c-Abl inhibition, because it does not occur in Abl-null cells and is restored in c-Abl-reconstituted cells.	imatinib	15-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-42
17620332-5	2007	This effect of STI571 is specific to c-Abl inhibition, because it does not occur in Abl-null cells and is restored in c-Abl-reconstituted cells.	imatinib	15-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-123
17723177-6	2007	Imatinib mesylate/ Gleevec/STI571, which inhibits the tyrosine kinase activity of BCR-ABL oncoprotein, has now become the new gold standard for the treatment of chronic myeloid leukemia.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
17907802-6	2007	The anti-cancer agent Imatinib inhibited M-CSF receptor activation and restored the apoptotic sensitivity of HIV-1-infected macrophages, suggesting a novel strategy to curtail viral persistence in the macrophage reservoir.	imatinib	22-30	colony stimulating factor 1	Homo sapiens	41-46
17723177-6	2007	Imatinib mesylate/ Gleevec/STI571, which inhibits the tyrosine kinase activity of BCR-ABL oncoprotein, has now become the new gold standard for the treatment of chronic myeloid leukemia.	imatinib	27-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
17824795-0	2007	Imatinib in the management of multiple gastrointestinal stromal tumors associated with a germline KIT K642E mutation.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	98-101
17435997-5	2007	CONCLUSION: The results suggest that TCS not only by itself involves but also synergizes activities of imatinib to induce K562 cell growth arrest, down-regulation of p210(Bcr-Abl) and its downstream signals and to stimulate the effect of the tyrosine kinase inhibition.	imatinib	103-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-178
17940488-4	2007	Karyotypically occult FIP1L1- platelet-derived growth factor receptor alpha and beta rearranged eosinophilic disorders respond to imatinib mesylate with almost 100% efficacy.	imatinib	130-147	factor interacting with PAPOLA and CPSF1	Homo sapiens	22-28
17510658-1	2007	Bcr-Abl is the cause of Philadelphia-positive (Ph(+)) leukemias and also constitutes their principal therapeutic target, as exemplified by dramatic effects of imatinib mesylate.	imatinib	159-176	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
17510658-3	2007	Here we demonstrate that INNO-406, a much more active Bcr-Abl tyrosine kinase inhibitor than imatinib, augments the activities of several proapoptotic Bcl-2 homology (BH)3-only proteins (Bim, Bad, Bmf and Bik) and induces apoptosis in Ph(+) leukemia cells via Bcl-2 family-regulated intrinsic apoptosis pathway.	imatinib	93-101	BCL2 apoptosis regulator	Homo sapiens	151-156
17804707-1	2007	Mutations in the kinase domain of Bcr-Abl are the most common cause of resistance to therapy with imatinib in patients with chronic myelogenous leukemia (CML).	imatinib	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
17804707-2	2007	Second-generation Bcr-Abl inhibitors are able to overcome most imatinib-resistant mutants, with the exception of the frequent T315I substitution, which is emerging as a major cause of resistance to these drugs in CML patients.	imatinib	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
17940488-5	2007	If standard therapies fail, the FIP1L1- platelet-derived growth factor receptor-negative cases of hypereosinophilic syndrome should also be considered for treatment with imatinib.	imatinib	170-178	factor interacting with PAPOLA and CPSF1	Homo sapiens	32-38
17940488-10	2007	The FIP1L1- platelet-derived growth factor receptor alpha-negative responders to imatinib pose a question as to the existence of subentities with unrecognized tyrosine kinases-based mutation.	imatinib	81-89	factor interacting with PAPOLA and CPSF1	Homo sapiens	4-10
17849262-2	2007	Imatinib mesylate, a tyrosine kinase inhibitor specific for Abl, platelet-derived growth factor receptor (PDGFR) and c-Kit tyrosine kinases, has been shown to inhibit fibrosis and profibrotic signaling in mouse models of inflammation-mediated lung reactions.	imatinib	0-17	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	60-63
17849262-2	2007	Imatinib mesylate, a tyrosine kinase inhibitor specific for Abl, platelet-derived growth factor receptor (PDGFR) and c-Kit tyrosine kinases, has been shown to inhibit fibrosis and profibrotic signaling in mouse models of inflammation-mediated lung reactions.	imatinib	0-17	platelet derived growth factor receptor, beta polypeptide	Mus musculus	65-104
17849262-2	2007	Imatinib mesylate, a tyrosine kinase inhibitor specific for Abl, platelet-derived growth factor receptor (PDGFR) and c-Kit tyrosine kinases, has been shown to inhibit fibrosis and profibrotic signaling in mouse models of inflammation-mediated lung reactions.	imatinib	0-17	platelet derived growth factor receptor, beta polypeptide	Mus musculus	106-111
17849262-2	2007	Imatinib mesylate, a tyrosine kinase inhibitor specific for Abl, platelet-derived growth factor receptor (PDGFR) and c-Kit tyrosine kinases, has been shown to inhibit fibrosis and profibrotic signaling in mouse models of inflammation-mediated lung reactions.	imatinib	0-17	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	117-122
17666373-0	2007	The efficacy of imatinib mesylate in patients with FIP1L1-PDGFRalpha-positive hypereosinophilic syndrome.	imatinib	16-33	factor interacting with PAPOLA and CPSF1	Homo sapiens	51-57
17504974-4	2007	Inhibition of PDGFR kinase with imatinib or AG1296 blocks 5-HT-stimulated PDGFRbeta phosphorylation.	imatinib	32-40	platelet derived growth factor receptor, beta polypeptide	Mus musculus	14-19
17504974-4	2007	Inhibition of PDGFR kinase with imatinib or AG1296 blocks 5-HT-stimulated PDGFRbeta phosphorylation.	imatinib	32-40	platelet derived growth factor receptor, beta polypeptide	Mus musculus	74-83
17504974-9	2007	Inhibition of PDGFR kinase with imatinib or AG1296 significantly inhibits SMC proliferation and migration induced by 5-HT in vitro.	imatinib	32-40	platelet derived growth factor receptor, beta polypeptide	Mus musculus	14-19
17666373-0	2007	The efficacy of imatinib mesylate in patients with FIP1L1-PDGFRalpha-positive hypereosinophilic syndrome.	imatinib	16-33	platelet derived growth factor receptor alpha	Homo sapiens	58-68
17530620-0	2007	First and second line imatinib treatment in chronic myelogenous leukemia patients expressing rare e1a2 or e19a2 BCR-ABL transcripts.	imatinib	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
17666373-3	2007	These cases with FIP1L1-PDGFRalpha rearrangement have been reported to be very sensitive to the tyrosine kinase inhibitor imatinib mesylate.	imatinib	122-139	factor interacting with PAPOLA and CPSF1	Homo sapiens	17-23
17666373-3	2007	These cases with FIP1L1-PDGFRalpha rearrangement have been reported to be very sensitive to the tyrosine kinase inhibitor imatinib mesylate.	imatinib	122-139	platelet derived growth factor receptor alpha	Homo sapiens	24-34
17768119-0	2007	Clinical outcome of 27 imatinib mesylate-resistant chronic myelogenous leukemia patients harboring a T315I BCR-ABL mutation.	imatinib	23-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
17458563-0	2007	Predictive factors for long-term effects of imatinib therapy in patients with inoperable/metastatic CD117(+) gastrointestinal stromal tumors (GISTs).	imatinib	44-52	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	100-105
17458563-1	2007	THE PURPOSE: To analyze the outcomes of treatment and factors predicting effects of imatinib (IM) therapy in inoperable/metastatic gastrointestinal stromal tumors (GIST) CD117(+) patients.	imatinib	84-92	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	170-175
17717597-4	2007	Our data indicate that FTY720 induces apoptosis and impairs clonogenicity of imatinib/dasatinib-sensitive and -resistant p210/p190(BCR/ABL) myeloid and lymphoid cell lines and CML-BC(CD34+) and Ph1 ALL(CD34+/CD19+) progenitors but not of normal CD34+ and CD34+/CD19+ bone marrow cells.	imatinib	77-85	CD34 molecule	Homo sapiens	183-187
17710227-3	2007	Analysis of BCR-ABL genotypes in CML patients who relapsed after sequential treatment with the ABL inhibitors imatinib and dasatinib revealed evolving resistant BCR-ABL kinase domain mutations in all cases.	imatinib	110-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
17717597-4	2007	Our data indicate that FTY720 induces apoptosis and impairs clonogenicity of imatinib/dasatinib-sensitive and -resistant p210/p190(BCR/ABL) myeloid and lymphoid cell lines and CML-BC(CD34+) and Ph1 ALL(CD34+/CD19+) progenitors but not of normal CD34+ and CD34+/CD19+ bone marrow cells.	imatinib	77-85	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	194-197
17710227-4	2007	Twelve patients relapsed with the pan-resistant T315I mutation, whereas 6 patients developed novel BCR-ABL mutations predicted to retain sensitivity to imatinib based on in vitro studies.	imatinib	152-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
17717597-4	2007	Our data indicate that FTY720 induces apoptosis and impairs clonogenicity of imatinib/dasatinib-sensitive and -resistant p210/p190(BCR/ABL) myeloid and lymphoid cell lines and CML-BC(CD34+) and Ph1 ALL(CD34+/CD19+) progenitors but not of normal CD34+ and CD34+/CD19+ bone marrow cells.	imatinib	77-85	CD34 molecule	Homo sapiens	202-206
17717597-4	2007	Our data indicate that FTY720 induces apoptosis and impairs clonogenicity of imatinib/dasatinib-sensitive and -resistant p210/p190(BCR/ABL) myeloid and lymphoid cell lines and CML-BC(CD34+) and Ph1 ALL(CD34+/CD19+) progenitors but not of normal CD34+ and CD34+/CD19+ bone marrow cells.	imatinib	77-85	CD19 molecule	Homo sapiens	208-212
17717597-4	2007	Our data indicate that FTY720 induces apoptosis and impairs clonogenicity of imatinib/dasatinib-sensitive and -resistant p210/p190(BCR/ABL) myeloid and lymphoid cell lines and CML-BC(CD34+) and Ph1 ALL(CD34+/CD19+) progenitors but not of normal CD34+ and CD34+/CD19+ bone marrow cells.	imatinib	77-85	CD34 molecule	Homo sapiens	202-206
17717597-4	2007	Our data indicate that FTY720 induces apoptosis and impairs clonogenicity of imatinib/dasatinib-sensitive and -resistant p210/p190(BCR/ABL) myeloid and lymphoid cell lines and CML-BC(CD34+) and Ph1 ALL(CD34+/CD19+) progenitors but not of normal CD34+ and CD34+/CD19+ bone marrow cells.	imatinib	77-85	CD34 molecule	Homo sapiens	202-206
17717597-4	2007	Our data indicate that FTY720 induces apoptosis and impairs clonogenicity of imatinib/dasatinib-sensitive and -resistant p210/p190(BCR/ABL) myeloid and lymphoid cell lines and CML-BC(CD34+) and Ph1 ALL(CD34+/CD19+) progenitors but not of normal CD34+ and CD34+/CD19+ bone marrow cells.	imatinib	77-85	CD19 molecule	Homo sapiens	261-265
17721511-5	2007	Quantitative profiling of the drugs imatinib (Gleevec), dasatinib (Sprycel) and bosutinib in K562 cells confirms known targets including ABL and SRC family kinases and identifies the receptor tyrosine kinase DDR1 and the oxidoreductase NQO2 as novel targets of imatinib.	imatinib	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-140
17923802-1	2007	Imatinib mesylate is a selective competitive inhibitor of the bcr-abl tyrosine kinase and c-KIT.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	90-95
17923802-2	2007	Other kinases, such as phosphatidylinositol- 3"-kinase (PI-3K) involved in insulin signaling, have also been shown to be indirectly affected by imatinib.	imatinib	144-152	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	23-54
17569822-0	2007	Bcr-Abl-independent imatinib-resistant K562 cells show aberrant protein acetylation and increased sensitivity to histone deacetylase inhibitors.	imatinib	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
17569822-1	2007	Bcr-Abl-independent signaling pathways are known to be involved in imatinib resistance in some patients with chronic myelogenous leukemia (CML).	imatinib	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
17569822-2	2007	In this study, to find new targets for imatinib-resistant CML displaying loss of Bcr-Abl kinase target dependence, we isolated imatinib-resistant variants, K562/R1, K562/R2, and K562/R3, which showed profound declines of Bcr-Abl levels and its tyrosine kinase activity, from K562 cells.	imatinib	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
17569822-2	2007	In this study, to find new targets for imatinib-resistant CML displaying loss of Bcr-Abl kinase target dependence, we isolated imatinib-resistant variants, K562/R1, K562/R2, and K562/R3, which showed profound declines of Bcr-Abl levels and its tyrosine kinase activity, from K562 cells.	imatinib	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	221-228
17569822-2	2007	In this study, to find new targets for imatinib-resistant CML displaying loss of Bcr-Abl kinase target dependence, we isolated imatinib-resistant variants, K562/R1, K562/R2, and K562/R3, which showed profound declines of Bcr-Abl levels and its tyrosine kinase activity, from K562 cells.	imatinib	127-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	221-228
17569822-3	2007	Importantly, the imatinib resistance mechanism in these variants also included aberrant acetylation of nonhistone proteins such as p53, Ku70, and Hsp90 that was due to upregulation of histone deacetylases (HDACs) and down-regulation of histone acetyltransferase (HAT).	imatinib	17-25	tumor protein p53	Homo sapiens	131-134
17569822-3	2007	Importantly, the imatinib resistance mechanism in these variants also included aberrant acetylation of nonhistone proteins such as p53, Ku70, and Hsp90 that was due to upregulation of histone deacetylases (HDACs) and down-regulation of histone acetyltransferase (HAT).	imatinib	17-25	X-ray repair cross complementing 6	Homo sapiens	136-140
17569822-3	2007	Importantly, the imatinib resistance mechanism in these variants also included aberrant acetylation of nonhistone proteins such as p53, Ku70, and Hsp90 that was due to upregulation of histone deacetylases (HDACs) and down-regulation of histone acetyltransferase (HAT).	imatinib	17-25	heat shock protein 90 alpha family class A member 1	Homo sapiens	146-151
17569822-4	2007	In comparison with K562 cells, the imatinib-resistant variants showed up-regulation of HDAC1, -2, and -3 (class I HDACs) and class III SIRT1 and down-regulation of CBP/p300 and PCAF with HAT activity, and thereby p53 and cytoplasmic Ku70 were aberrantly acetylated.	imatinib	35-43	histone deacetylase 1	Homo sapiens	87-104
17569822-4	2007	In comparison with K562 cells, the imatinib-resistant variants showed up-regulation of HDAC1, -2, and -3 (class I HDACs) and class III SIRT1 and down-regulation of CBP/p300 and PCAF with HAT activity, and thereby p53 and cytoplasmic Ku70 were aberrantly acetylated.	imatinib	35-43	sirtuin 1	Homo sapiens	135-140
17569822-4	2007	In comparison with K562 cells, the imatinib-resistant variants showed up-regulation of HDAC1, -2, and -3 (class I HDACs) and class III SIRT1 and down-regulation of CBP/p300 and PCAF with HAT activity, and thereby p53 and cytoplasmic Ku70 were aberrantly acetylated.	imatinib	35-43	CREB binding protein	Homo sapiens	164-172
17569822-4	2007	In comparison with K562 cells, the imatinib-resistant variants showed up-regulation of HDAC1, -2, and -3 (class I HDACs) and class III SIRT1 and down-regulation of CBP/p300 and PCAF with HAT activity, and thereby p53 and cytoplasmic Ku70 were aberrantly acetylated.	imatinib	35-43	lysine acetyltransferase 2B	Homo sapiens	177-181
17569822-4	2007	In comparison with K562 cells, the imatinib-resistant variants showed up-regulation of HDAC1, -2, and -3 (class I HDACs) and class III SIRT1 and down-regulation of CBP/p300 and PCAF with HAT activity, and thereby p53 and cytoplasmic Ku70 were aberrantly acetylated.	imatinib	35-43	tumor protein p53	Homo sapiens	213-216
17569822-4	2007	In comparison with K562 cells, the imatinib-resistant variants showed up-regulation of HDAC1, -2, and -3 (class I HDACs) and class III SIRT1 and down-regulation of CBP/p300 and PCAF with HAT activity, and thereby p53 and cytoplasmic Ku70 were aberrantly acetylated.	imatinib	35-43	X-ray repair cross complementing 6	Homo sapiens	233-237
17569822-6	2007	In contrast, the class II HDAC6 level was significantly decreased, and this was accompanied by an increase of Hsp90 acetylation in the imatinib-resistant variants, which was closely associated with loss of Bcr-Abl.	imatinib	135-143	histone deacetylase 6	Homo sapiens	26-31
17569822-6	2007	In contrast, the class II HDAC6 level was significantly decreased, and this was accompanied by an increase of Hsp90 acetylation in the imatinib-resistant variants, which was closely associated with loss of Bcr-Abl.	imatinib	135-143	heat shock protein 90 alpha family class A member 1	Homo sapiens	110-115
17569822-6	2007	In contrast, the class II HDAC6 level was significantly decreased, and this was accompanied by an increase of Hsp90 acetylation in the imatinib-resistant variants, which was closely associated with loss of Bcr-Abl.	imatinib	135-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	206-213
17569822-7	2007	These results indicate that alteration of the normal balance of HATs and HDACs leads to deregulated acetylation of Hsp90, p53, and Ku70 and thereby leads to imatinib resistance, suggesting the importance of the acetylation status of apoptosis-related nonhistone proteins in Bcr-Abl-independent imatinib resistance.	imatinib	157-165	heat shock protein 90 alpha family class A member 1	Homo sapiens	115-120
17569822-7	2007	These results indicate that alteration of the normal balance of HATs and HDACs leads to deregulated acetylation of Hsp90, p53, and Ku70 and thereby leads to imatinib resistance, suggesting the importance of the acetylation status of apoptosis-related nonhistone proteins in Bcr-Abl-independent imatinib resistance.	imatinib	157-165	tumor protein p53	Homo sapiens	122-125
17569822-7	2007	These results indicate that alteration of the normal balance of HATs and HDACs leads to deregulated acetylation of Hsp90, p53, and Ku70 and thereby leads to imatinib resistance, suggesting the importance of the acetylation status of apoptosis-related nonhistone proteins in Bcr-Abl-independent imatinib resistance.	imatinib	157-165	X-ray repair cross complementing 6	Homo sapiens	131-135
17569822-7	2007	These results indicate that alteration of the normal balance of HATs and HDACs leads to deregulated acetylation of Hsp90, p53, and Ku70 and thereby leads to imatinib resistance, suggesting the importance of the acetylation status of apoptosis-related nonhistone proteins in Bcr-Abl-independent imatinib resistance.	imatinib	157-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	274-281
17569822-7	2007	These results indicate that alteration of the normal balance of HATs and HDACs leads to deregulated acetylation of Hsp90, p53, and Ku70 and thereby leads to imatinib resistance, suggesting the importance of the acetylation status of apoptosis-related nonhistone proteins in Bcr-Abl-independent imatinib resistance.	imatinib	294-302	heat shock protein 90 alpha family class A member 1	Homo sapiens	115-120
17595328-0	2007	The multikinase inhibitor sorafenib induces apoptosis in highly imatinib mesylate-resistant bcr/abl+ human leukemia cells in association with signal transducer and activator of transcription 5 inhibition and myeloid cell leukemia-1 down-regulation.	imatinib	64-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
17595328-0	2007	The multikinase inhibitor sorafenib induces apoptosis in highly imatinib mesylate-resistant bcr/abl+ human leukemia cells in association with signal transducer and activator of transcription 5 inhibition and myeloid cell leukemia-1 down-regulation.	imatinib	64-81	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	208-231
17595328-2	2007	When administered at pharmacologically relevant concentrations (10-15 microM), sorafenib potently induced apoptosis in imatinib mesylate-resistant cells expressing high levels of Bcr/Abl, cells exhibiting a Bcr/Abl-independent, Lyn-dependent form of resistance, and CD34(+) cells obtained from imatinib-resistant patients.	imatinib	119-136	BCR activator of RhoGEF and GTPase	Homo sapiens	179-182
17595328-2	2007	When administered at pharmacologically relevant concentrations (10-15 microM), sorafenib potently induced apoptosis in imatinib mesylate-resistant cells expressing high levels of Bcr/Abl, cells exhibiting a Bcr/Abl-independent, Lyn-dependent form of resistance, and CD34(+) cells obtained from imatinib-resistant patients.	imatinib	119-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	179-186
17696988-0	2007	Influence of breast cancer resistance protein (Abcg2) and p-glycoprotein (Abcb1a) on the transport of imatinib mesylate (Gleevec) across the mouse blood-brain barrier.	imatinib	102-119	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	47-52
17696988-0	2007	Influence of breast cancer resistance protein (Abcg2) and p-glycoprotein (Abcb1a) on the transport of imatinib mesylate (Gleevec) across the mouse blood-brain barrier.	imatinib	102-119	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	74-80
17696988-5	2007	The inhibition of p-gp, by valspodar and zosuquidar, increased imatinib uptake (2.5-fold), as did the deficiency of p-gp in Mdr1a/1b(-/-) mice (5.5-fold).	imatinib	63-71	phosphoglycolate phosphatase	Mus musculus	18-22
17696988-6	2007	Perfusing imatinib with the p-gp/Bcrp1 inhibitor, elacridar, enhanced the brain uptake of imatinib in wild-type (4.1-fold) and Mdr1a/1b(-/-) mice (1.2-fold).	imatinib	10-18	phosphoglycolate phosphatase	Mus musculus	28-32
17696988-6	2007	Perfusing imatinib with the p-gp/Bcrp1 inhibitor, elacridar, enhanced the brain uptake of imatinib in wild-type (4.1-fold) and Mdr1a/1b(-/-) mice (1.2-fold).	imatinib	10-18	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	33-38
17696988-6	2007	Perfusing imatinib with the p-gp/Bcrp1 inhibitor, elacridar, enhanced the brain uptake of imatinib in wild-type (4.1-fold) and Mdr1a/1b(-/-) mice (1.2-fold).	imatinib	10-18	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	127-132
17696988-6	2007	Perfusing imatinib with the p-gp/Bcrp1 inhibitor, elacridar, enhanced the brain uptake of imatinib in wild-type (4.1-fold) and Mdr1a/1b(-/-) mice (1.2-fold).	imatinib	90-98	phosphoglycolate phosphatase	Mus musculus	28-32
17696988-6	2007	Perfusing imatinib with the p-gp/Bcrp1 inhibitor, elacridar, enhanced the brain uptake of imatinib in wild-type (4.1-fold) and Mdr1a/1b(-/-) mice (1.2-fold).	imatinib	90-98	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	33-38
17696988-11	2007	These data suggest that imatinib transport at the mouse BBB is limited by p-gp and probably by Bcrp1, and that CGP74588 transport is restricted by Bcrp1.	imatinib	24-32	phosphoglycolate phosphatase	Mus musculus	74-78
17696988-11	2007	These data suggest that imatinib transport at the mouse BBB is limited by p-gp and probably by Bcrp1, and that CGP74588 transport is restricted by Bcrp1.	imatinib	24-32	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	95-100
17805064-2	2007	Imatinib targets KIT expression, providing rationale for studying its role in combination with chemotherapy in SCLC in a multicenter phase II trial.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	17-20
17597804-7	2007	Therapeutic doses of imatinib did not revert the aberrant phenotype, but counteracted the observed reverting effect of bcr-abl gene expression switch off.	imatinib	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-126
17697368-9	2007	Pre-treatment with p38 MAPK (SB203580) or c-Abl (STI-571) inhibitors completely blocked 2-ME-induced apoptosis, implicating these two pathways in the response.	imatinib	49-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-47
17380257-2	2007	P-glycoprotein (P-gp, rodent Mdr1a/1b or Abcb1a/1b) and Breast cancer resistance protein (rodent Bcrp1 or Abcg2) were suggested to restrict the delivery of imatinib to the brain.	imatinib	156-164	phosphoglycolate phosphatase	Mus musculus	0-14
17380257-2	2007	P-glycoprotein (P-gp, rodent Mdr1a/1b or Abcb1a/1b) and Breast cancer resistance protein (rodent Bcrp1 or Abcg2) were suggested to restrict the delivery of imatinib to the brain.	imatinib	156-164	phosphoglycolate phosphatase	Mus musculus	16-20
17380257-2	2007	P-glycoprotein (P-gp, rodent Mdr1a/1b or Abcb1a/1b) and Breast cancer resistance protein (rodent Bcrp1 or Abcg2) were suggested to restrict the delivery of imatinib to the brain.	imatinib	156-164	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	29-34
17380257-2	2007	P-glycoprotein (P-gp, rodent Mdr1a/1b or Abcb1a/1b) and Breast cancer resistance protein (rodent Bcrp1 or Abcg2) were suggested to restrict the delivery of imatinib to the brain.	imatinib	156-164	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	97-102
17380257-2	2007	P-glycoprotein (P-gp, rodent Mdr1a/1b or Abcb1a/1b) and Breast cancer resistance protein (rodent Bcrp1 or Abcg2) were suggested to restrict the delivery of imatinib to the brain.	imatinib	156-164	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	106-111
17380257-6	2007	RESULTS: The blockade of P-gp by valspodar or zosuquidar (>3 mg/kg) enhanced the brain uptake of imatinib ( approximately 4-fold) in wild-type mice, but not that of its metabolites.	imatinib	100-108	phosphoglycolate phosphatase	Mus musculus	25-29
17380257-7	2007	Blockade of both P-gp and Bcrp1 by elacridar (>3 mg/kg) produced significantly greater brain penetration of imatinib (9.3-fold) and its metabolites (2.8-fold).	imatinib	111-119	phosphoglycolate phosphatase	Mus musculus	17-21
17380257-7	2007	Blockade of both P-gp and Bcrp1 by elacridar (>3 mg/kg) produced significantly greater brain penetration of imatinib (9.3-fold) and its metabolites (2.8-fold).	imatinib	111-119	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	26-31
17380257-8	2007	In contrast, only the lack of P-gp enhanced imatinib brain penetration (6.4-fold) in knockout mice.	imatinib	44-52	phosphoglycolate phosphatase	Mus musculus	30-34
17380257-10	2007	CONCLUSIONS: Imatinib and its metabolites penetrate into the brain poorly and their penetration is limited by P-gp and (probably) Bcrp1.	imatinib	13-21	phosphoglycolate phosphatase	Mus musculus	110-114
17380257-10	2007	CONCLUSIONS: Imatinib and its metabolites penetrate into the brain poorly and their penetration is limited by P-gp and (probably) Bcrp1.	imatinib	13-21	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	130-135
17380257-11	2007	Administering imatinib together with P-gp (and Bcrp1) transporter inhibitors such as elacridar may improve the delivery of imatinib to the brain, making it potentially more effective against malignant gliomas.	imatinib	123-131	phosphoglycolate phosphatase	Mus musculus	37-41
17380257-11	2007	Administering imatinib together with P-gp (and Bcrp1) transporter inhibitors such as elacridar may improve the delivery of imatinib to the brain, making it potentially more effective against malignant gliomas.	imatinib	123-131	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	47-52
17607681-2	2007	The question of whether IFN-alpha-responsive patients can experience further improvements with imatinib has not been answered.	imatinib	95-103	interferon alpha 1	Homo sapiens	24-33
17607681-6	2007	The primary objective was to determine whether ceasing therapy with IFN-alpha and switching to 12 months of imatinib treatment at a dose of 400 mg/day could improve the molecular response as assessed by real-time quantitative polymerase chain reaction of BCR-ABL transcript levels.	imatinib	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	255-262
17607681-10	2007	Every patient who had already achieved an MMR while receiving IFN-alpha (n = 7 patients) maintained an MMR while receiving imatinib.	imatinib	123-131	interferon alpha 1	Homo sapiens	62-71
17607681-12	2007	CONCLUSIONS: These data suggest that switching IFN-alpha-responsive patients to imatinib leads to a rapid improvement in achieving an MMR, a response with established prognostic value, and is well tolerated.	imatinib	80-88	interferon alpha 1	Homo sapiens	47-56
17399949-7	2007	As a corollary, we found that Abl inhibitors, such as the STI571 compound, significantly enhanced Met-induced cell motility, but failed to do so in cells that expressed the CrkII-Y221F mutant protein.	imatinib	58-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-33
17301975-0	2007	Inv (11)(p15q21) in donor-derived Ph-negative cells in a patient with chronic myeloid leukemia in relapse successfully treated with imatinib mesylate post allogeneic stem cell transplantation.	imatinib	132-149	inversin	Homo sapiens	0-3
17400722-8	2007	ML-9 and imatinib actually enhanced the NPY-induced proliferation of cells.	imatinib	9-17	neuropeptide Y	Rattus norvegicus	40-43
17699867-1	2007	PURPOSE: Resistance is commonly acquired in patients with metastatic gastrointestinal stromal tumor who are treated with imatinib mesylate, often due to the development of secondary mutations in the KIT kinase domain.	imatinib	121-138	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	199-202
17699867-2	2007	We sought to investigate the efficacy of second-line tyrosine kinase inhibitors, such as sorafenib, dasatinib, and nilotinib, against the commonly observed imatinib-resistant KIT mutations (KIT(V654A), KIT(T670I), KIT(D820Y), and KIT(N822K)) expressed in the Ba/F3 cellular system.	imatinib	156-164	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	175-178
17699867-2	2007	We sought to investigate the efficacy of second-line tyrosine kinase inhibitors, such as sorafenib, dasatinib, and nilotinib, against the commonly observed imatinib-resistant KIT mutations (KIT(V654A), KIT(T670I), KIT(D820Y), and KIT(N822K)) expressed in the Ba/F3 cellular system.	imatinib	156-164	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	190-193
17699867-2	2007	We sought to investigate the efficacy of second-line tyrosine kinase inhibitors, such as sorafenib, dasatinib, and nilotinib, against the commonly observed imatinib-resistant KIT mutations (KIT(V654A), KIT(T670I), KIT(D820Y), and KIT(N822K)) expressed in the Ba/F3 cellular system.	imatinib	156-164	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	190-193
17699867-3	2007	EXPERIMENTAL DESIGN: In vitro drug screening of stable Ba/F3 KIT mutants recapitulating the genotype of imatinib-resistant patients harboring primary and secondary KIT mutations was investigated.	imatinib	104-112	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	61-64
17699867-4	2007	Comparison was made to imatinib-sensitive Ba/F3 KIT mutant cells as well as Ba/F3 cells expressing only secondary KIT mutations.	imatinib	23-31	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	48-51
17699867-9	2007	The Ba/F3 KIT(WK557-8del/T670I) cells were sensitive only to sorafenib inhibition, whereas nilotinib was more potent on imatinib-resistant KIT(V560del/V654A) and KIT(V559D/D820Y) mutant cells than dasatinib and sorafenib.	imatinib	120-128	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	139-142
17699867-9	2007	The Ba/F3 KIT(WK557-8del/T670I) cells were sensitive only to sorafenib inhibition, whereas nilotinib was more potent on imatinib-resistant KIT(V560del/V654A) and KIT(V559D/D820Y) mutant cells than dasatinib and sorafenib.	imatinib	120-128	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	139-142
17560008-3	2007	The aim of this study was to clarify the effect of imatinib on CD8+ and CD4+ T-cell effector functions.	imatinib	51-59	CD8a molecule	Homo sapiens	63-66
17661208-2	2007	Most GISTs have an activating mutation in KIT or PDGFR-alpha and respond to treatment with imatinib mesylate (Gleevec, Novartis), a small molecule tyrosine kinase inhibitor that blocks downstream signaling of the mutated kinase.	imatinib	91-108	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	42-45
17661208-2	2007	Most GISTs have an activating mutation in KIT or PDGFR-alpha and respond to treatment with imatinib mesylate (Gleevec, Novartis), a small molecule tyrosine kinase inhibitor that blocks downstream signaling of the mutated kinase.	imatinib	91-108	platelet derived growth factor receptor alpha	Homo sapiens	49-60
17671155-2	2007	Imatinib mesylate is one such agent inhibiting the tyrosine kinase that results from the Bcr-Abl translocation.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
17683977-2	2007	Blocking BCR-ABL by the ABL tyrosine kinase inhibitor imatinib mesylate (IM, Gleevec) is clinically highly efficient.	imatinib	54-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
17560008-3	2007	The aim of this study was to clarify the effect of imatinib on CD8+ and CD4+ T-cell effector functions.	imatinib	51-59	CD4 molecule	Homo sapiens	72-75
17560008-6	2007	RESULTS: It was demonstrated that imatinib inhibits antigen-specific IFN-gamma secretion of both CD4+ and CD8+ T-effector cells at therapeutically relevant concentrations, while T cells remain responsive.	imatinib	34-42	interferon gamma	Homo sapiens	69-78
17694440-3	2007	Imatinib modified the inflammatory responses and expression patterns of PDGF-A and PDGF receptors.	imatinib	0-8	platelet derived growth factor subunit A	Homo sapiens	72-78
17560008-6	2007	RESULTS: It was demonstrated that imatinib inhibits antigen-specific IFN-gamma secretion of both CD4+ and CD8+ T-effector cells at therapeutically relevant concentrations, while T cells remain responsive.	imatinib	34-42	CD4 molecule	Homo sapiens	97-100
17560008-6	2007	RESULTS: It was demonstrated that imatinib inhibits antigen-specific IFN-gamma secretion of both CD4+ and CD8+ T-effector cells at therapeutically relevant concentrations, while T cells remain responsive.	imatinib	34-42	CD8a molecule	Homo sapiens	106-109
17562354-5	2007	Imatinib (Gleevec) and ACK2 were used to block, and stem cell factor was used to stimulate, c-kit activity.	imatinib	0-8	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	92-97
17671641-2	2007	This in turn led to the development of imatinib mesylate, a clinically successful inhibitor of the BCR-ABL kinase.	imatinib	39-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
17705809-0	2007	Inhibition of tyrosine kinases PDGFR and C-Kit by imatinib mesylate interferes with postnatal testicular development in the rat.	imatinib	50-67	platelet derived growth factor receptor beta	Homo sapiens	31-36
17705809-0	2007	Inhibition of tyrosine kinases PDGFR and C-Kit by imatinib mesylate interferes with postnatal testicular development in the rat.	imatinib	50-67	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	41-46
17687201-2	2007	Imatinib mesilate, which efficiently inhibits BCR-ABL,and KIT as well as platelet-derived growth factor receptor (PDGF-R) kinases, is highly effective for clinical treatment of CML, Ph+ALL, and advanced GIST with good tolerability, respectively.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
17687201-2	2007	Imatinib mesilate, which efficiently inhibits BCR-ABL,and KIT as well as platelet-derived growth factor receptor (PDGF-R) kinases, is highly effective for clinical treatment of CML, Ph+ALL, and advanced GIST with good tolerability, respectively.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	58-61
17453242-5	2007	On the other hand, the number of kinases blocked by imatinib mesylate is notching up, for instance the tyrosine kinase, which is associated with macrophage-colony stimulating factor receptor (M-CSFR).	imatinib	52-69	colony stimulating factor 1 receptor	Homo sapiens	194-198
17453242-15	2007	There have been established four kinases (p210(bcr/abl), c-kit, PDGFR-alfa, PDGFR-beta) suggested as the target for imatinib mesylate.	imatinib	116-124	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	57-62
17453242-15	2007	There have been established four kinases (p210(bcr/abl), c-kit, PDGFR-alfa, PDGFR-beta) suggested as the target for imatinib mesylate.	imatinib	116-124	platelet derived growth factor receptor beta	Homo sapiens	64-69
17453242-15	2007	There have been established four kinases (p210(bcr/abl), c-kit, PDGFR-alfa, PDGFR-beta) suggested as the target for imatinib mesylate.	imatinib	116-124	platelet derived growth factor receptor beta	Homo sapiens	76-86
17453242-16	2007	Other potential targets will be discovered as it has lately been determined that M-CSFR kinase activity was blocked by imatinib mesylate.	imatinib	119-136	colony stimulating factor 1 receptor	Homo sapiens	83-87
17641778-5	2007	Treatment of PDGF-BB-overexpressing tumors with imatinib mesylate (PDGFR inhibitor) resulted in increased growth and decreased total pericyte content compared with those in untreated PDGF-BB-overexpressing tumors.	imatinib	48-65	platelet derived growth factor receptor beta	Homo sapiens	67-72
17671641-3	2007	Incorporating the use of markers of BCR-ABL kinase inhibition into clinical trials led to the realization that imatinib-resistant kinase domain mutations are the major cause of relapse during imatinib therapy and the subsequent development of new inhibitors to treat CML patients.	imatinib	111-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
17671641-3	2007	Incorporating the use of markers of BCR-ABL kinase inhibition into clinical trials led to the realization that imatinib-resistant kinase domain mutations are the major cause of relapse during imatinib therapy and the subsequent development of new inhibitors to treat CML patients.	imatinib	192-200	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
17187856-2	2007	Currently, the most effective treatment of CML is the inhibition of Bcr-Abl activity by imatinib mesylate (Gleevec).	imatinib	88-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
17503411-11	2007	Also, the decrease in Shp1 and subsequently its inhibitory effect on Bcr-Abl could provide an explanation for imatinib resistance seen in advanced stage CML patients.	imatinib	110-118	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	22-26
17503411-11	2007	Also, the decrease in Shp1 and subsequently its inhibitory effect on Bcr-Abl could provide an explanation for imatinib resistance seen in advanced stage CML patients.	imatinib	110-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
17721040-3	2007	However, there is no therapeutic agents that can selectively modulate the Wnt/beta-catenin signaling pathway, although some existing drugs (e.g., non-steroidal anti-inflammatory drugs, vitamins, and imatinib mesylate) have been suggested to inhibit this pathway.	imatinib	199-216	catenin beta 1	Homo sapiens	78-90
17508004-0	2007	A novel ETV6-PDGFRB fusion transcript missed by standard screening in a patient with an imatinib responsive chronic myeloproliferative disease.	imatinib	88-96	ETS variant transcription factor 6	Homo sapiens	8-12
17508004-0	2007	A novel ETV6-PDGFRB fusion transcript missed by standard screening in a patient with an imatinib responsive chronic myeloproliferative disease.	imatinib	88-96	platelet derived growth factor receptor beta	Homo sapiens	13-19
17187856-3	2007	Imatinib efficacy is limited by development of resistance through either expression of Bcr-Abl variants that bind imatinib less avidly, increased expression of Bcr-Abl, or expression of multidrug transport proteins.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
17554385-0	2007	The rho-kinase inhibitors Y-27632 and fasudil act synergistically with imatinib to inhibit the expansion of ex vivo CD34(+) CML progenitor cells.	imatinib	71-79	CD34 molecule	Homo sapiens	116-120
17554385-3	2007	We compared the effects of rho-kinase inhibition in those cells with the effects of direct inhibition of BCR/ABL using the specific inhibitor imatinib.	imatinib	142-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-112
17187856-3	2007	Imatinib efficacy is limited by development of resistance through either expression of Bcr-Abl variants that bind imatinib less avidly, increased expression of Bcr-Abl, or expression of multidrug transport proteins.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-167
17187856-3	2007	Imatinib efficacy is limited by development of resistance through either expression of Bcr-Abl variants that bind imatinib less avidly, increased expression of Bcr-Abl, or expression of multidrug transport proteins.	imatinib	114-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
17921955-2	2007	Approximately 80% of c-Kit mutations occur in exon 11, being a response factor to imatinib (Gleevec) therapy.	imatinib	82-90	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	21-26
17558420-9	2007	Inhibition of PDGFR-beta phosphorylation by pretreatment with herbimycin A and imatinib mesylate effectively suppressed basement membrane invasion and cell growth in vitro.	imatinib	79-96	platelet derived growth factor receptor beta	Homo sapiens	14-24
17921955-2	2007	Approximately 80% of c-Kit mutations occur in exon 11, being a response factor to imatinib (Gleevec) therapy.	imatinib	92-99	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	21-26
17372901-11	2007	In vitro drug testing of stable transformant Ba/F3 KIT(L576P) mutant cells showed sensitivity for dasatinib (previously known as BMS-354825), a dual SRC/ABL kinase inhibitor, and imatinib.	imatinib	179-187	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	51-56
17311837-2	2007	Imatinib mesylate is a selective inhibitor of tyrosine kinases such as bcr-abl, c-Kit, c-Fms and platelet derived growth factor receptor beta (PDGFRbeta).	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	80-85
17311837-2	2007	Imatinib mesylate is a selective inhibitor of tyrosine kinases such as bcr-abl, c-Kit, c-Fms and platelet derived growth factor receptor beta (PDGFRbeta).	imatinib	0-17	colony stimulating factor 1 receptor	Homo sapiens	87-92
17311837-2	2007	Imatinib mesylate is a selective inhibitor of tyrosine kinases such as bcr-abl, c-Kit, c-Fms and platelet derived growth factor receptor beta (PDGFRbeta).	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	97-141
17311837-2	2007	Imatinib mesylate is a selective inhibitor of tyrosine kinases such as bcr-abl, c-Kit, c-Fms and platelet derived growth factor receptor beta (PDGFRbeta).	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	143-152
17311837-3	2007	PDGFRbeta is often overexpressed in mesothelioma cells and is a therapeutic target for imatinib in some solid tumours.	imatinib	87-95	platelet derived growth factor receptor beta	Homo sapiens	0-9
17311837-6	2007	RESULTS: Imatinib induced cytotoxicity and apoptosis selectively on PDGFRbeta positive mesothelioma cells via blockade of receptor phosphorylation and interference with the Akt pathway.	imatinib	9-17	platelet derived growth factor receptor beta	Homo sapiens	68-77
17311837-6	2007	RESULTS: Imatinib induced cytotoxicity and apoptosis selectively on PDGFRbeta positive mesothelioma cells via blockade of receptor phosphorylation and interference with the Akt pathway.	imatinib	9-17	AKT serine/threonine kinase 1	Homo sapiens	173-176
17395781-7	2007	These results provide a rationale for use of an Hsp90 inhibitor as a first-line treatment in CML by inhibiting leukemia stem cells and preventing the emergence of imatinib-resistant clones in patients.	imatinib	163-171	heat shock protein 90 alpha family class A member 1	Homo sapiens	48-53
17405907-0	2007	Kinase domain mutations of BCR-ABL frequently precede imatinib-based therapy and give rise to relapse in patients with de novo Philadelphia-positive acute lymphoblastic leukemia (Ph+ ALL).	imatinib	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
17849316-3	2007	The authors recently have shown that a tyrosine kinase inhibitor, imatinib mesylate, induces clearance of PrP(Sc) via specific inhibition of c-Abl in prion-infected cell culture models.	imatinib	66-83	prion protein	Mus musculus	106-109
17849316-5	2007	The authors found that imatinib mesylate abolished prion infectivity to almost undetectable level in ScN2a cells and the level of PrP(Sc) was significantly decreased by the drug in scrapie-infected mouse spleens as well as in ScN2a cells.	imatinib	23-40	sodium channel, voltage-gated, type II, alpha	Mus musculus	101-106
17849316-5	2007	The authors found that imatinib mesylate abolished prion infectivity to almost undetectable level in ScN2a cells and the level of PrP(Sc) was significantly decreased by the drug in scrapie-infected mouse spleens as well as in ScN2a cells.	imatinib	23-40	sodium channel, voltage-gated, type II, alpha	Mus musculus	226-231
17431132-0	2007	Enhanced phosphorylation of Nbs1, a member of DNA repair/checkpoint complex Mre11-RAD50-Nbs1, can be targeted to increase the efficacy of imatinib mesylate against BCR/ABL-positive leukemia cells.	imatinib	138-155	nibrin	Homo sapiens	28-32
17431132-0	2007	Enhanced phosphorylation of Nbs1, a member of DNA repair/checkpoint complex Mre11-RAD50-Nbs1, can be targeted to increase the efficacy of imatinib mesylate against BCR/ABL-positive leukemia cells.	imatinib	138-155	MRE11 homolog, double strand break repair nuclease	Homo sapiens	76-81
17405907-1	2007	Acquired imatinib resistance in advanced Philadelphia-positive acute lymphoblastic leukemia (Ph(+) ALL) has been associated with mutations in the kinase domain (KD) of BCR-ABL.	imatinib	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	168-175
17405907-7	2007	BCR-ABL mutations conferring high-level imatinib resistance are present in a substantial proportion of patients with de novo Ph(+) ALL and eventually give rise to relapse.	imatinib	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
17431132-0	2007	Enhanced phosphorylation of Nbs1, a member of DNA repair/checkpoint complex Mre11-RAD50-Nbs1, can be targeted to increase the efficacy of imatinib mesylate against BCR/ABL-positive leukemia cells.	imatinib	138-155	RAD50 double strand break repair protein	Homo sapiens	82-87
17431132-0	2007	Enhanced phosphorylation of Nbs1, a member of DNA repair/checkpoint complex Mre11-RAD50-Nbs1, can be targeted to increase the efficacy of imatinib mesylate against BCR/ABL-positive leukemia cells.	imatinib	138-155	nibrin	Homo sapiens	88-92
17431132-0	2007	Enhanced phosphorylation of Nbs1, a member of DNA repair/checkpoint complex Mre11-RAD50-Nbs1, can be targeted to increase the efficacy of imatinib mesylate against BCR/ABL-positive leukemia cells.	imatinib	138-155	BCR activator of RhoGEF and GTPase	Homo sapiens	164-167
17372901-12	2007	However, compared to an imatinib-sensitive KIT mutant, dasatinib was potent at lower doses than imatinib in the KIT(L576P) mutant.	imatinib	24-32	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	43-46
17372901-12	2007	However, compared to an imatinib-sensitive KIT mutant, dasatinib was potent at lower doses than imatinib in the KIT(L576P) mutant.	imatinib	96-104	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	112-117
17634558-5	2007	Similar results were obtained in imatinib mesylate-resistant cells expressing activated Lyn as well as in primary CD34(+) bone marrow cells obtained from CML patients.	imatinib	33-50	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	88-91
17431132-6	2007	Interestingly, inhibition of Nbs1 phosphorylation by S343A mutant enhanced the antileukemia effect of the combination of imatinib and genotoxic agent.	imatinib	121-129	nibrin	Homo sapiens	29-33
17559139-0	2007	A prospective analysis of imatinib-induced c-KIT modulation in ovarian cancer: a phase II clinical study with proteomic profiling.	imatinib	26-34	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	43-48
17223257-1	2007	In this study, we have tried to find new targets and effective drugs for imatinib-resistant chronic myelogenous leukemia (CML) cells displaying loss of Bcr-Abl kinase target dependence.	imatinib	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-159
17638918-7	2007	Blocking BCR/ABL-Y177-mediated signaling enhances targeting of CML progenitors by imatinib mesylate.	imatinib	82-99	BCR activator of RhoGEF and GTPase	Homo sapiens	9-12
17638918-7	2007	Blocking BCR/ABL-Y177-mediated signaling enhances targeting of CML progenitors by imatinib mesylate.	imatinib	82-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
17656262-0	2007	A report of early cytogenetic response to imatinib in two patients with chronic myeloid leukemia at accelerated phase and carrying the e19a2 BCR-ABL transcript.	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-148
17656262-1	2007	The development of imatinib is a milestone in the treatment of chronic myeloid leukemia (CML), and its therapeutic effect has been extensively investigated in CML patients carrying M-bcr and m-bcr BCR/ABL fusion transcripts.	imatinib	19-27	BCR activator of RhoGEF and GTPase	Homo sapiens	183-186
17656262-1	2007	The development of imatinib is a milestone in the treatment of chronic myeloid leukemia (CML), and its therapeutic effect has been extensively investigated in CML patients carrying M-bcr and m-bcr BCR/ABL fusion transcripts.	imatinib	19-27	BCR activator of RhoGEF and GTPase	Homo sapiens	193-196
17656262-1	2007	The development of imatinib is a milestone in the treatment of chronic myeloid leukemia (CML), and its therapeutic effect has been extensively investigated in CML patients carrying M-bcr and m-bcr BCR/ABL fusion transcripts.	imatinib	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	197-204
17223257-2	2007	The imatinib-resistant K562/R1, -R2 and -R3 cells showed profound declines of Bcr-Abl level and concurrently exhibited up-regulation of Bcl-2 and Ku70/80, and down-regulation of Bax, DNA-PKcs and BRCA1, suggesting that loss of Bcr-Abl after exposure to imatinib might be accompanied by other cell survival mechanism.	imatinib	4-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
17223257-2	2007	The imatinib-resistant K562/R1, -R2 and -R3 cells showed profound declines of Bcr-Abl level and concurrently exhibited up-regulation of Bcl-2 and Ku70/80, and down-regulation of Bax, DNA-PKcs and BRCA1, suggesting that loss of Bcr-Abl after exposure to imatinib might be accompanied by other cell survival mechanism.	imatinib	4-12	BCL2 apoptosis regulator	Homo sapiens	136-141
17223257-2	2007	The imatinib-resistant K562/R1, -R2 and -R3 cells showed profound declines of Bcr-Abl level and concurrently exhibited up-regulation of Bcl-2 and Ku70/80, and down-regulation of Bax, DNA-PKcs and BRCA1, suggesting that loss of Bcr-Abl after exposure to imatinib might be accompanied by other cell survival mechanism.	imatinib	4-12	X-ray repair cross complementing 6	Homo sapiens	146-150
17223257-2	2007	The imatinib-resistant K562/R1, -R2 and -R3 cells showed profound declines of Bcr-Abl level and concurrently exhibited up-regulation of Bcl-2 and Ku70/80, and down-regulation of Bax, DNA-PKcs and BRCA1, suggesting that loss of Bcr-Abl after exposure to imatinib might be accompanied by other cell survival mechanism.	imatinib	4-12	BCL2 associated X, apoptosis regulator	Homo sapiens	178-181
17223257-2	2007	The imatinib-resistant K562/R1, -R2 and -R3 cells showed profound declines of Bcr-Abl level and concurrently exhibited up-regulation of Bcl-2 and Ku70/80, and down-regulation of Bax, DNA-PKcs and BRCA1, suggesting that loss of Bcr-Abl after exposure to imatinib might be accompanied by other cell survival mechanism.	imatinib	4-12	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	183-191
17223257-2	2007	The imatinib-resistant K562/R1, -R2 and -R3 cells showed profound declines of Bcr-Abl level and concurrently exhibited up-regulation of Bcl-2 and Ku70/80, and down-regulation of Bax, DNA-PKcs and BRCA1, suggesting that loss of Bcr-Abl after exposure to imatinib might be accompanied by other cell survival mechanism.	imatinib	4-12	BRCA1 DNA repair associated	Homo sapiens	196-201
17223257-2	2007	The imatinib-resistant K562/R1, -R2 and -R3 cells showed profound declines of Bcr-Abl level and concurrently exhibited up-regulation of Bcl-2 and Ku70/80, and down-regulation of Bax, DNA-PKcs and BRCA1, suggesting that loss of Bcr-Abl after exposure to imatinib might be accompanied by other cell survival mechanism.	imatinib	4-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	227-234
17223257-4	2007	Moreover, when K562 cells were treated with the combination of imatinib with CPT, the level of Bax and the cleavage of PARP-1 and DNA-PK were significantly increased in comparison with the effects of each drug.	imatinib	63-71	BCL2 associated X, apoptosis regulator	Homo sapiens	95-98
17223257-4	2007	Moreover, when K562 cells were treated with the combination of imatinib with CPT, the level of Bax and the cleavage of PARP-1 and DNA-PK were significantly increased in comparison with the effects of each drug.	imatinib	63-71	poly(ADP-ribose) polymerase 1	Homo sapiens	119-125
17223257-4	2007	Moreover, when K562 cells were treated with the combination of imatinib with CPT, the level of Bax and the cleavage of PARP-1 and DNA-PK were significantly increased in comparison with the effects of each drug.	imatinib	63-71	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	130-136
18159983-0	2007	Study of the interaction surface for the c-Src-imatinib complex by a molecular dicing technique.	imatinib	47-55	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	41-46
18159983-2	2007	Imatinib is a clinically well-tolerated small molecule that exerts selective, dual inhibition of the transforming growth factor beta (TGFbeta) and platelet-derived growth factor (PDGF) pathways.	imatinib	0-8	transforming growth factor beta 1	Homo sapiens	101-132
18159983-2	2007	Imatinib is a clinically well-tolerated small molecule that exerts selective, dual inhibition of the transforming growth factor beta (TGFbeta) and platelet-derived growth factor (PDGF) pathways.	imatinib	0-8	transforming growth factor beta 1	Homo sapiens	134-141
18159983-4	2007	An interesting point to be clarified regarding the mechanism of imatinib is its interaction with c-Src.	imatinib	64-72	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	97-102
18159983-5	2007	Fortunately, complexing of c-Src and imatinib has recently reported, which provides a basis for further study of the interactions between the two molecules.	imatinib	37-45	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	27-32
17547845-4	2007	In vitro experiments, however, showed that mast cells carrying the D816V c-kit mutation were resistant to the prototypical tyrosine kinase inhibitor imatinib.	imatinib	149-157	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-78
17555450-0	2007	Two novel imatinib-responsive PDGFRA fusion genes in chronic eosinophilic leukaemia.	imatinib	10-18	platelet derived growth factor receptor alpha	Homo sapiens	30-36
17581316-0	2007	Induction of urokinase-type plasminogen activator, interleukin-8 and early growth response-1 by STI571 through activating mitogen activated protein kinase in human small cell lung cancer cells.	imatinib	96-102	plasminogen activator, urokinase	Homo sapiens	13-49
17581316-0	2007	Induction of urokinase-type plasminogen activator, interleukin-8 and early growth response-1 by STI571 through activating mitogen activated protein kinase in human small cell lung cancer cells.	imatinib	96-102	C-X-C motif chemokine ligand 8	Homo sapiens	51-64
17581316-2	2007	NCI-H69 cells expressed one of the receptor tyrosine kinases, c-Kit, and STI571 inhibited the cell growth and stem cell factor-induced phosphorylation of c-Kit.	imatinib	73-79	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	154-159
17581316-3	2007	We therefore investigated the effects of STI571 on the expression of urokinase-type plasminogen activator and interleukin-8 in NCI-H69 cells.	imatinib	41-47	plasminogen activator, urokinase	Homo sapiens	69-105
17581316-3	2007	We therefore investigated the effects of STI571 on the expression of urokinase-type plasminogen activator and interleukin-8 in NCI-H69 cells.	imatinib	41-47	C-X-C motif chemokine ligand 8	Homo sapiens	110-123
17581316-5	2007	Treatment with STI571 resulted in the induction of phosphorylation of all three mitogen-activated protein kinases, such as extracellular signal-regulated kinase 1/2, p38 mitogen-activated protein kinase and stress-activated protein kinase/c-jun N-terminal protein kinase.	imatinib	15-21	mitogen-activated protein kinase 3	Homo sapiens	123-164
17581316-5	2007	Treatment with STI571 resulted in the induction of phosphorylation of all three mitogen-activated protein kinases, such as extracellular signal-regulated kinase 1/2, p38 mitogen-activated protein kinase and stress-activated protein kinase/c-jun N-terminal protein kinase.	imatinib	15-21	mitogen-activated protein kinase 14	Homo sapiens	166-169
17581316-6	2007	U0126, an inhibitor against extracellular signal-regulated kinase 1/2, however, only inhibited the STI571-induced interleukin-8 accumulation.	imatinib	99-105	mitogen-activated protein kinase 3	Homo sapiens	28-78
17581316-6	2007	U0126, an inhibitor against extracellular signal-regulated kinase 1/2, however, only inhibited the STI571-induced interleukin-8 accumulation.	imatinib	99-105	C-X-C motif chemokine ligand 8	Homo sapiens	114-127
17495881-7	2007	ABCB1 genotype was associated with steady-state CL/F due to an apparent genotype-specific influence of imatinib on elimination.	imatinib	103-111	ATP binding cassette subfamily B member 1	Homo sapiens	0-5
17495975-6	2007	Moreover, EXEL-0862 induced apoptotic death in EOL-1 cells and imatinib-resistant T674I FIP1L1-PDGFR-alpha-expressing cells, and resulted in significant downregulation of the antiapoptotic protein Mcl-1 through a caspase-dependent mechanism.	imatinib	63-71	factor interacting with PAPOLA and CPSF1	Homo sapiens	88-94
17546507-0	2007	Effect of imatinib mesylate in a patient with a metastatic gastrointestinal stromal tumor with a c-kit mutation in exon 11.	imatinib	10-27	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	97-102
17642017-4	2007	However, imatinib resistance occurs in a significant proportion of patients, mainly through the development of mutations in the Bcr-Abl tyrosine kinase domain that impair imatinib binding.	imatinib	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
17642017-4	2007	However, imatinib resistance occurs in a significant proportion of patients, mainly through the development of mutations in the Bcr-Abl tyrosine kinase domain that impair imatinib binding.	imatinib	171-179	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
17495975-2	2007	Imatinib mesylate is a potent inhibitor of ABL but also of PDGFR-alpha, and has been associated with durable hematologic responses in patients with HES.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-46
20425368-4	2007	Novel tyrosine kinase inhibitors with enhanced inhibitory potency against ABL and other kinases may further improve on the results observed with imatinib.	imatinib	145-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-77
17708241-0	2007	Lack of activity of imatinib in two cases of KIT+ retroperitoneal liposarcoma.	imatinib	20-28	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	45-48
17549412-1	2007	Approximately 30% of chronic myeloid leukemia patients show initially no response to Imatinib, a potent inhibitor of BCR-ABL.	imatinib	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
17429432-0	2007	Resistance reversal by RNAi silencing of MDR1 in CML cells associated with increase in imatinib intracellular levels.	imatinib	87-95	ATP binding cassette subfamily B member 1	Homo sapiens	41-45
17495975-6	2007	Moreover, EXEL-0862 induced apoptotic death in EOL-1 cells and imatinib-resistant T674I FIP1L1-PDGFR-alpha-expressing cells, and resulted in significant downregulation of the antiapoptotic protein Mcl-1 through a caspase-dependent mechanism.	imatinib	63-71	platelet derived growth factor receptor alpha	Homo sapiens	95-106
17495975-2	2007	Imatinib mesylate is a potent inhibitor of ABL but also of PDGFR-alpha, and has been associated with durable hematologic responses in patients with HES.	imatinib	0-17	platelet derived growth factor receptor alpha	Homo sapiens	59-70
17495975-5	2007	EXEL-0862 inhibited the proliferation of EOL-1 and imatinib-resistant T674I FIP1L1-PDGFR-alpha-expressing cells and resulted in potent inhibition of the phosphorylation of PDGFR-alpha and downstream proteins STAT3 and Erk1/2, both in vitro and ex vivo.	imatinib	51-59	factor interacting with PAPOLA and CPSF1	Homo sapiens	76-82
17347407-0	2007	Role of BCR/ABL gene-expression levels in determining the phenotype and imatinib sensitivity of transformed human hematopoietic cells.	imatinib	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-15
17495975-5	2007	EXEL-0862 inhibited the proliferation of EOL-1 and imatinib-resistant T674I FIP1L1-PDGFR-alpha-expressing cells and resulted in potent inhibition of the phosphorylation of PDGFR-alpha and downstream proteins STAT3 and Erk1/2, both in vitro and ex vivo.	imatinib	51-59	platelet derived growth factor receptor alpha	Homo sapiens	83-94
17495975-5	2007	EXEL-0862 inhibited the proliferation of EOL-1 and imatinib-resistant T674I FIP1L1-PDGFR-alpha-expressing cells and resulted in potent inhibition of the phosphorylation of PDGFR-alpha and downstream proteins STAT3 and Erk1/2, both in vitro and ex vivo.	imatinib	51-59	platelet derived growth factor receptor alpha	Homo sapiens	172-183
17495975-5	2007	EXEL-0862 inhibited the proliferation of EOL-1 and imatinib-resistant T674I FIP1L1-PDGFR-alpha-expressing cells and resulted in potent inhibition of the phosphorylation of PDGFR-alpha and downstream proteins STAT3 and Erk1/2, both in vitro and ex vivo.	imatinib	51-59	signal transducer and activator of transcription 3	Homo sapiens	208-213
17495975-5	2007	EXEL-0862 inhibited the proliferation of EOL-1 and imatinib-resistant T674I FIP1L1-PDGFR-alpha-expressing cells and resulted in potent inhibition of the phosphorylation of PDGFR-alpha and downstream proteins STAT3 and Erk1/2, both in vitro and ex vivo.	imatinib	51-59	mitogen-activated protein kinase 3	Homo sapiens	218-224
17549375-5	2007	We analyzed 14 chordoma samples for the expression of the Imatinib mesylate targets by means of RT-PCR and immunohistochemistry and found that PDGFR alpha and PDGFR beta are in some cases expressed in neoplastic cells, while the stromal counterpart of the same tumor shows the above receptors.	imatinib	58-66	platelet derived growth factor receptor alpha	Homo sapiens	143-154
17549375-5	2007	We analyzed 14 chordoma samples for the expression of the Imatinib mesylate targets by means of RT-PCR and immunohistochemistry and found that PDGFR alpha and PDGFR beta are in some cases expressed in neoplastic cells, while the stromal counterpart of the same tumor shows the above receptors.	imatinib	58-66	platelet derived growth factor receptor beta	Homo sapiens	159-169
17347407-1	2007	Increased levels of Bcr-Abl expression in chronic myelogenous leukemia (CML) cells are associated with disease progression and imatinib (IM) resistance.	imatinib	127-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
18542042-4	2007	Imatinib (STI571), used in the treatment of unresectable GIST, selectively inhibits the enzymatic activity of the tyrosine kinase c-KIT.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	130-135
17213809-3	2007	The fact because the combination of imatinib and dasatinib shows the additive/synergistic growth inhibition on wild-type p210 BCR-ABL-expressing cells, we reasoned that these ABL kinase inhibitors might induce the different molecular pathways.	imatinib	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
17213809-9	2007	K562 and TF-1BCR-ABL cells, pretreated with CDK2 or CDK8 small interfering RNA, showed additive growth inhibition with imatinib, but not with dasatinib.	imatinib	119-127	cyclin dependent kinase 2	Homo sapiens	44-48
17213809-9	2007	K562 and TF-1BCR-ABL cells, pretreated with CDK2 or CDK8 small interfering RNA, showed additive growth inhibition with imatinib, but not with dasatinib.	imatinib	119-127	cyclin dependent kinase 8	Homo sapiens	52-56
17213809-10	2007	These findings demonstrate that the additive/synergistic growth inhibition by imatinib and dasatinib may be mediated in part by CDK2 and CDK8.	imatinib	78-86	cyclin dependent kinase 2	Homo sapiens	128-132
17213809-10	2007	These findings demonstrate that the additive/synergistic growth inhibition by imatinib and dasatinib may be mediated in part by CDK2 and CDK8.	imatinib	78-86	cyclin dependent kinase 8	Homo sapiens	137-141
17141949-5	2007	Interestingly, imatinib mesylate (10 microM) strikingly induced the expression of the pro-inflammatory and pro-angiogenic cytokines interleukin (IL)-6 and IL-8, and mildly stimulated the release of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF).	imatinib	15-32	C-X-C motif chemokine ligand 8	Homo sapiens	155-159
17141949-5	2007	Interestingly, imatinib mesylate (10 microM) strikingly induced the expression of the pro-inflammatory and pro-angiogenic cytokines interleukin (IL)-6 and IL-8, and mildly stimulated the release of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF).	imatinib	15-32	vascular endothelial growth factor A	Homo sapiens	198-232
17141949-5	2007	Interestingly, imatinib mesylate (10 microM) strikingly induced the expression of the pro-inflammatory and pro-angiogenic cytokines interleukin (IL)-6 and IL-8, and mildly stimulated the release of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF).	imatinib	15-32	vascular endothelial growth factor A	Homo sapiens	234-238
17141949-5	2007	Interestingly, imatinib mesylate (10 microM) strikingly induced the expression of the pro-inflammatory and pro-angiogenic cytokines interleukin (IL)-6 and IL-8, and mildly stimulated the release of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF).	imatinib	15-32	fibroblast growth factor 2	Homo sapiens	244-274
17141949-5	2007	Interestingly, imatinib mesylate (10 microM) strikingly induced the expression of the pro-inflammatory and pro-angiogenic cytokines interleukin (IL)-6 and IL-8, and mildly stimulated the release of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF).	imatinib	15-32	fibroblast growth factor 2	Homo sapiens	276-280
18542042-4	2007	Imatinib (STI571), used in the treatment of unresectable GIST, selectively inhibits the enzymatic activity of the tyrosine kinase c-KIT.	imatinib	10-16	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	130-135
18542042-5	2007	However, it is known that some mutations in the c-kit gene lead to resistance to imatinib.	imatinib	81-89	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	48-53
17591808-6	2007	Most GISTs express constitutively activated mutant isoforms of KIT or kinase platelet-derived growth factor receptor alpha (PDGFRA) that are potential therapeutic targets for imatinib mesylate.	imatinib	175-183	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	63-66
17533389-1	2007	Palliative imatinib treatment has dramatically improved survival in patients with malignant gastrointestinal stromal tumours, particularly in patients with tumours harbouring activating KIT mutations.	imatinib	11-19	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	186-189
17442779-3	2007	FLT3, as a member of the type III RTK subfamily, is closely related to c-kit, c-FMS, and PDGFalpha/beta and is an unspecific target of tyrosine kinase inhibitors, such as imatinib.	imatinib	171-179	fms related receptor tyrosine kinase 3	Homo sapiens	0-4
17591808-6	2007	Most GISTs express constitutively activated mutant isoforms of KIT or kinase platelet-derived growth factor receptor alpha (PDGFRA) that are potential therapeutic targets for imatinib mesylate.	imatinib	175-183	platelet derived growth factor receptor alpha	Homo sapiens	124-130
17591830-2	2007	Imatinib, an inhibitor of the BCR-ABL tyrosine kinase, significantly improves the outcome of patients with CML.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
17591830-4	2007	The understanding of mechanisms of imatinib resistance has led to the development of novel BCR-ABL inhibitors; among these, dasatinib emerged as the most promising, being approximately 300-fold more potent than imatinib; it also inhibits SRC family kinases.	imatinib	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
17550324-9	2007	Eleven of 14 patients with known CML on imatinib treatment tested positive for the BCR-ABL transcript, whereas 10 normal controls tested negative.	imatinib	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
17591830-4	2007	The understanding of mechanisms of imatinib resistance has led to the development of novel BCR-ABL inhibitors; among these, dasatinib emerged as the most promising, being approximately 300-fold more potent than imatinib; it also inhibits SRC family kinases.	imatinib	211-219	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
17591830-6	2007	Recently, dasatinib emerged as a potent inhibitor of imatinib-resistant protein tyrosine kinase (KIT) activation loop mutants and it is able to induce apoptosis in mast cell and leukemic cell lines expressing these mutations.	imatinib	53-61	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	97-100
17299092-0	2007	Low-dose imatinib mesylate leads to rapid induction of major molecular responses and achievement of complete molecular remission in FIP1L1-PDGFRA-positive chronic eosinophilic leukemia.	imatinib	9-26	factor interacting with PAPOLA and CPSF1	Homo sapiens	132-138
17299092-0	2007	Low-dose imatinib mesylate leads to rapid induction of major molecular responses and achievement of complete molecular remission in FIP1L1-PDGFRA-positive chronic eosinophilic leukemia.	imatinib	9-26	platelet derived growth factor receptor alpha	Homo sapiens	139-145
17299092-1	2007	The FIP1L1-PDGFRA fusion gene is a recurrent molecular lesion in eosinophilia-associated myeloproliferative disorders, predicting a favorable response to imatinib mesylate.	imatinib	154-171	factor interacting with PAPOLA and CPSF1	Homo sapiens	4-10
17299092-1	2007	The FIP1L1-PDGFRA fusion gene is a recurrent molecular lesion in eosinophilia-associated myeloproliferative disorders, predicting a favorable response to imatinib mesylate.	imatinib	154-171	platelet derived growth factor receptor alpha	Homo sapiens	11-17
17299092-5	2007	Normalized FIP1L1-PDGFRA transcript levels in patient samples prior to imatinib varied by almost 3 logs.	imatinib	71-79	factor interacting with PAPOLA and CPSF1	Homo sapiens	11-17
17299092-5	2007	Normalized FIP1L1-PDGFRA transcript levels in patient samples prior to imatinib varied by almost 3 logs.	imatinib	71-79	platelet derived growth factor receptor alpha	Homo sapiens	18-24
17299092-8	2007	In 2 patients, withdrawal of imatinib was followed by a rapid rise in FIP1L1-PDGFRA transcript levels.	imatinib	29-37	factor interacting with PAPOLA and CPSF1	Homo sapiens	70-76
17299092-8	2007	In 2 patients, withdrawal of imatinib was followed by a rapid rise in FIP1L1-PDGFRA transcript levels.	imatinib	29-37	platelet derived growth factor receptor alpha	Homo sapiens	77-83
19707322-6	2007	Preliminary studies demonstrated that nilotinib has more efficacy than imatinib in inhibiting proliferation of BCR-ABL-dependent cells, a relatively safety profile and clinical efficacy in all phases of CML.	imatinib	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
17299092-9	2007	Overall, these data are consistent with the exquisite sensitivity of the FIP1L1-PDGFRalpha fusion to imatinib, as compared with BCR-ABL, and underline the importance of RQ-PCR monitoring to guide management using molecularly targeted therapies.	imatinib	101-109	factor interacting with PAPOLA and CPSF1	Homo sapiens	73-79
19707322-2	2007	The most frequent clinically relevant mechanisms that change imatinib sensitivity in BCR-ABL-transformed cells are mutations within the Abl kinase domain, affecting several of its properties.	imatinib	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
19707322-3	2007	Crystal structure analysis of the Abl-imatinib complex has proven helpful in identifying potential critical residues that hinder interactions of imatinib with mutated Abl.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-37
19707322-2	2007	The most frequent clinically relevant mechanisms that change imatinib sensitivity in BCR-ABL-transformed cells are mutations within the Abl kinase domain, affecting several of its properties.	imatinib	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-139
17303698-1	2007	Patients with advanced stages of chronic myeloid leukemia (CML) often manifest imatinib mesylate resistance associated with point mutations in BCR-ABL.	imatinib	79-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-150
19707322-3	2007	Crystal structure analysis of the Abl-imatinib complex has proven helpful in identifying potential critical residues that hinder interactions of imatinib with mutated Abl.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-170
19707322-3	2007	Crystal structure analysis of the Abl-imatinib complex has proven helpful in identifying potential critical residues that hinder interactions of imatinib with mutated Abl.	imatinib	145-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-37
19707322-3	2007	Crystal structure analysis of the Abl-imatinib complex has proven helpful in identifying potential critical residues that hinder interactions of imatinib with mutated Abl.	imatinib	145-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-170
19707323-0	2007	Imatinib and tyrosine kinase inhibition, in the management of BCR-ABL negative myeloproliferative disorders.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
17914187-8	2007	DEAD-box protein 3, heat shock protein 105 kDa, and peroxiredoxin-3 were identified as potential protein markers for response to imatinib.	imatinib	129-137	peroxiredoxin 3	Homo sapiens	52-67
17009043-0	2007	Imatinib impairs CD8+ T lymphocytes specifically directed against the leukemia-associated antigen RHAMM/CD168 in vitro.	imatinib	0-8	CD8a molecule	Homo sapiens	17-20
17009043-0	2007	Imatinib impairs CD8+ T lymphocytes specifically directed against the leukemia-associated antigen RHAMM/CD168 in vitro.	imatinib	0-8	hyaluronan mediated motility receptor	Homo sapiens	98-103
17009043-0	2007	Imatinib impairs CD8+ T lymphocytes specifically directed against the leukemia-associated antigen RHAMM/CD168 in vitro.	imatinib	0-8	hyaluronan mediated motility receptor	Homo sapiens	104-109
17009043-4	2007	The release of IFN-gamma and granzyme B by CD8+ T-lymphocytes specific for R3, a recently described T-cell epitope peptide derived from a leukemia-associated antigen designated RHAMM/CD168 (receptor for hyaluronic acid mediated motility), was inhibited by imatinib in a dose-dependent fashion (range: 1-25 microM).	imatinib	256-264	interferon gamma	Homo sapiens	15-24
17009043-4	2007	The release of IFN-gamma and granzyme B by CD8+ T-lymphocytes specific for R3, a recently described T-cell epitope peptide derived from a leukemia-associated antigen designated RHAMM/CD168 (receptor for hyaluronic acid mediated motility), was inhibited by imatinib in a dose-dependent fashion (range: 1-25 microM).	imatinib	256-264	CD8a molecule	Homo sapiens	43-46
17431887-2	2007	The development of imatinib, a tyrosine kinase inhibitor (TKI) targeted against the causative Bcr-Abl oncoprotein in CML, has resulted in hematologic and cytogenetic remissions in all phases of CML.	imatinib	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
17431887-4	2007	This is often a result of mutated forms of the Bcr-Abl oncoprotein to which imatinib is unable to bind.	imatinib	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
17545631-4	2007	In our study, we found that inhibition of BCR-ABL leads to a down-regulation of immunogenic antigens on the CML cells in response to imatinib treatment, which results in the inhibition of CML-directed immune responses.	imatinib	133-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
17545631-5	2007	By treating CML cells with imatinib, we could show that the resulting inhibition of BCR-ABL leads to a decreased expression of tumor antigens, including survivin, adipophilin, hTERT, WT-1, Bcl-x(L), and Bcl-2 in correlation to a decreased development of CML-specific CTLs.	imatinib	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
17545631-5	2007	By treating CML cells with imatinib, we could show that the resulting inhibition of BCR-ABL leads to a decreased expression of tumor antigens, including survivin, adipophilin, hTERT, WT-1, Bcl-x(L), and Bcl-2 in correlation to a decreased development of CML-specific CTLs.	imatinib	27-35	perilipin 2	Homo sapiens	163-174
17545631-5	2007	By treating CML cells with imatinib, we could show that the resulting inhibition of BCR-ABL leads to a decreased expression of tumor antigens, including survivin, adipophilin, hTERT, WT-1, Bcl-x(L), and Bcl-2 in correlation to a decreased development of CML-specific CTLs.	imatinib	27-35	telomerase reverse transcriptase	Homo sapiens	176-181
17545631-5	2007	By treating CML cells with imatinib, we could show that the resulting inhibition of BCR-ABL leads to a decreased expression of tumor antigens, including survivin, adipophilin, hTERT, WT-1, Bcl-x(L), and Bcl-2 in correlation to a decreased development of CML-specific CTLs.	imatinib	27-35	WT1 transcription factor	Homo sapiens	183-187
17545631-5	2007	By treating CML cells with imatinib, we could show that the resulting inhibition of BCR-ABL leads to a decreased expression of tumor antigens, including survivin, adipophilin, hTERT, WT-1, Bcl-x(L), and Bcl-2 in correlation to a decreased development of CML-specific CTLs.	imatinib	27-35	BCL2 like 1	Homo sapiens	189-194
17545631-5	2007	By treating CML cells with imatinib, we could show that the resulting inhibition of BCR-ABL leads to a decreased expression of tumor antigens, including survivin, adipophilin, hTERT, WT-1, Bcl-x(L), and Bcl-2 in correlation to a decreased development of CML-specific CTLs.	imatinib	27-35	BCL2 apoptosis regulator	Homo sapiens	203-208
17609876-0	2007	Therapeutic application of small interfering RNA directed against bcr-abl transcripts to a patient with imatinib-resistant chronic myeloid leukaemia.	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
17609876-2	2007	We herein present a first report on the in vivo application of targeted non-virally delivered synthetic bcr-abl siRNA in a female patient with recurrent Philadelphia chromosome-positive chronic myeloid leukaemia (CML) resistant to imatinib (Y253F mutation) and chemotherapy after allogeneic haematopoietic stem cell transplantation.	imatinib	231-239	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
17533047-6	2007	RESULTS: Imatinib showed a specific time- and dose-dependent growth inhibitory effect on FDCP cells expressing JAK2(V617F), wherein we observed imatinib"s inactivation of JAK2, STAT5 and cKIT proteins.	imatinib	9-17	Janus kinase 2	Homo sapiens	111-115
17533047-6	2007	RESULTS: Imatinib showed a specific time- and dose-dependent growth inhibitory effect on FDCP cells expressing JAK2(V617F), wherein we observed imatinib"s inactivation of JAK2, STAT5 and cKIT proteins.	imatinib	9-17	Janus kinase 2	Homo sapiens	171-175
17533047-6	2007	RESULTS: Imatinib showed a specific time- and dose-dependent growth inhibitory effect on FDCP cells expressing JAK2(V617F), wherein we observed imatinib"s inactivation of JAK2, STAT5 and cKIT proteins.	imatinib	9-17	signal transducer and activator of transcription 5A	Homo sapiens	177-182
17533047-6	2007	RESULTS: Imatinib showed a specific time- and dose-dependent growth inhibitory effect on FDCP cells expressing JAK2(V617F), wherein we observed imatinib"s inactivation of JAK2, STAT5 and cKIT proteins.	imatinib	9-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	187-191
17533047-6	2007	RESULTS: Imatinib showed a specific time- and dose-dependent growth inhibitory effect on FDCP cells expressing JAK2(V617F), wherein we observed imatinib"s inactivation of JAK2, STAT5 and cKIT proteins.	imatinib	144-152	Janus kinase 2	Homo sapiens	171-175
17533047-6	2007	RESULTS: Imatinib showed a specific time- and dose-dependent growth inhibitory effect on FDCP cells expressing JAK2(V617F), wherein we observed imatinib"s inactivation of JAK2, STAT5 and cKIT proteins.	imatinib	144-152	signal transducer and activator of transcription 5A	Homo sapiens	177-182
17533047-6	2007	RESULTS: Imatinib showed a specific time- and dose-dependent growth inhibitory effect on FDCP cells expressing JAK2(V617F), wherein we observed imatinib"s inactivation of JAK2, STAT5 and cKIT proteins.	imatinib	144-152	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	187-191
17533047-8	2007	In an ongoing clinical study, a PV patient showed strong correlation between the percent JAK2 T-allele and his responsiveness to imatinib therapy.	imatinib	129-137	Janus kinase 2	Homo sapiens	89-93
17541129-2	2007	We hypothesized that imatinib mesylate (Gleevec, Glivec, formerly known as STI571), a relatively selective inhibitor of protein tyrosine kinases including platelet-derived growth factor receptor (PDGFR), would inhibit hCASMC proliferation and migration in vitro with little effect on endothelial cell proliferation and prevent restenosis in a swine balloon injury model.	imatinib	21-38	platelet derived growth factor receptor beta	Homo sapiens	196-201
17541129-5	2007	RESULTS: Increasing doses of imatinib-inhibited autophosphorylation of the PDGFR and its downstream effects of proliferation and migration of human CASMC in a dose-responsive manner, yet had no effect on stimulated human aortic endothelial cells.	imatinib	29-37	platelet derived growth factor receptor beta	Homo sapiens	75-80
17513418-0	2007	c-Abl tyrosine kinase and inhibition by the cancer drug imatinib (Gleevec/STI-571).	imatinib	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
17513418-2	2007	The small-molecule inhibitor imatinib (Gleevec/STI-571) can specifically inactivate the tyrosine kinase c-Abl, whose normal mechanism of autoinhibition is disrupted in chronic myelogenous leukemia.	imatinib	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-109
17513418-2	2007	The small-molecule inhibitor imatinib (Gleevec/STI-571) can specifically inactivate the tyrosine kinase c-Abl, whose normal mechanism of autoinhibition is disrupted in chronic myelogenous leukemia.	imatinib	47-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-109
17513418-3	2007	Crystallographic analysis of c-Abl reveals that imatinib recognizes a distinct inactive conformation of the Abl kinase domain that relies on the mechanism of autoinhibition achieved in the context of a larger fragment of the protein.	imatinib	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-34
17513418-3	2007	Crystallographic analysis of c-Abl reveals that imatinib recognizes a distinct inactive conformation of the Abl kinase domain that relies on the mechanism of autoinhibition achieved in the context of a larger fragment of the protein.	imatinib	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-34
17513418-7	2007	These differences help explain the ability of imatinib to preferentially inhibit Abl over Src.	imatinib	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-84
17513418-7	2007	These differences help explain the ability of imatinib to preferentially inhibit Abl over Src.	imatinib	46-54	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	90-93
17428238-1	2007	Zoledronic acid inhibits the prenylation of ras-related proteins downstream of bcr-abl and preclinical studies have shown augmentation of the inhibitory effects of imatinib in BCR-ABL expressing cells.	imatinib	164-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
17428238-1	2007	Zoledronic acid inhibits the prenylation of ras-related proteins downstream of bcr-abl and preclinical studies have shown augmentation of the inhibitory effects of imatinib in BCR-ABL expressing cells.	imatinib	164-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	176-183
17538248-0	2007	Imatinib and nilotinib induce apoptosis of chronic myeloid leukemia cells through a Bim-dependant pathway modulated by cytokines.	imatinib	0-8	BCL2 like 11	Homo sapiens	84-87
17538248-3	2007	Apoptosis induced by imatinib and nilotinib was determined in BCR-ABL expressing cell lines and primary CML CD34+ cells.	imatinib	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
17538248-3	2007	Apoptosis induced by imatinib and nilotinib was determined in BCR-ABL expressing cell lines and primary CML CD34+ cells.	imatinib	21-29	CD34 molecule	Homo sapiens	108-112
17538248-6	2007	In K562, 80% inhibition of the BCR-ABL auto-phosphorylation by either imatinib or nilotinib induced a two fold increase in Bim-EL expression and induction of apoptosis in 48 h. Bim accumulation preceded apoptosis induction which was completely abolished by depletion in Bim using shRNA.	imatinib	70-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
17538248-6	2007	In K562, 80% inhibition of the BCR-ABL auto-phosphorylation by either imatinib or nilotinib induced a two fold increase in Bim-EL expression and induction of apoptosis in 48 h. Bim accumulation preceded apoptosis induction which was completely abolished by depletion in Bim using shRNA.	imatinib	70-78	BCL2 like 11	Homo sapiens	123-126
17538248-6	2007	In K562, 80% inhibition of the BCR-ABL auto-phosphorylation by either imatinib or nilotinib induced a two fold increase in Bim-EL expression and induction of apoptosis in 48 h. Bim accumulation preceded apoptosis induction which was completely abolished by depletion in Bim using shRNA.	imatinib	70-78	BCL2 like 11	Homo sapiens	177-180
17538248-6	2007	In K562, 80% inhibition of the BCR-ABL auto-phosphorylation by either imatinib or nilotinib induced a two fold increase in Bim-EL expression and induction of apoptosis in 48 h. Bim accumulation preceded apoptosis induction which was completely abolished by depletion in Bim using shRNA.	imatinib	70-78	BCL2 like 11	Homo sapiens	177-180
17538248-7	2007	However, the anti-proliferative effect of imatinib was preserved in Bim-depleted cells.	imatinib	42-50	BCL2 like 11	Homo sapiens	68-71
17538248-10	2007	In conclusion, both nilotinib and imatinib induce apoptosis through Bim accumulation independently of cell cycle arrest.	imatinib	34-42	BCL2 like 11	Homo sapiens	68-71
17545544-0	2007	Sorafenib inhibits imatinib-resistant KIT and platelet-derived growth factor receptor beta gatekeeper mutants.	imatinib	19-27	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	38-41
17545544-1	2007	PURPOSE: Targeting of KIT and platelet-derived growth factor receptor (PDGFR) tyrosine kinases by imatinib is an effective anticancer strategy.	imatinib	98-106	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	22-25
17545544-2	2007	However, mutations of the gatekeeper residue (T670 in KIT and T681 in PDGFRbeta) render the two kinases resistant to imatinib.	imatinib	117-125	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	54-57
17545544-2	2007	However, mutations of the gatekeeper residue (T670 in KIT and T681 in PDGFRbeta) render the two kinases resistant to imatinib.	imatinib	117-125	platelet derived growth factor receptor beta	Homo sapiens	70-79
17545544-3	2007	The aim of this study was to evaluate whether sorafenib (BAY 43-9006), a multitargeted ATP-competitive inhibitor of KIT and PDGFR, was active against imatinib-resistant KIT and PDGFRbeta kinases.	imatinib	150-158	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	169-172
17704745-7	2007	RESULTS: Exposure of SKNMC cells to STI-571 resulted in a dose-dependent antiproliferative effect and a decrease in phosphorylated AKT expression.	imatinib	36-43	AKT serine/threonine kinase 1	Homo sapiens	131-134
17550858-0	2007	Enhanced Bcr-Abl-specific antileukemic activity of arsenic trioxide (Trisenox) through glutathione-depletion in imatinib-resistant cells.	imatinib	112-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
17550858-1	2007	The development of resistance to imatinib mesylate may partly depend on high Bcr-Abl-expression levels.	imatinib	33-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
17498050-6	2007	Inhibition of the most important growth factor receptor of human MCs, c-Kit, by the selective tyrosine kinase inhibitor imatinib mesylate, induces apoptosis of synovial tissue MCs.	imatinib	120-137	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	70-75
17519960-0	2007	Imatinib mesylate and nilotinib (AMN107) exhibit high-affinity interaction with ABCG2 on primitive hematopoietic stem cells.	imatinib	0-17	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	80-85
17519960-5	2007	Herein we demonstrate a dose-dependent, reversible inhibition of ABCG2-mediated Hoechst 33342 dye efflux in primary human and murine HSC by both imatinib and nilotinib (AMN107), a novel aminopyrimidine inhibitor of BCR-ABL.	imatinib	145-153	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	65-70
17519960-6	2007	ABCG2-transduced K562 cells were protected from imatinib and nilotinib-mediated cell death and from downregulation of P-CRKL.	imatinib	48-56	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
17420275-9	2007	Furthermore, we show that the inhibition of Bcr-Abl kinase by treatment with imatinib caused the up-regulation of Gfi-1B in K562 cells, where Gfi-1B also cooperated with GATA-1 to repress Bcl-x(L) transcription.	imatinib	77-85	growth factor independent 1B transcriptional repressor	Homo sapiens	114-120
17420275-9	2007	Furthermore, we show that the inhibition of Bcr-Abl kinase by treatment with imatinib caused the up-regulation of Gfi-1B in K562 cells, where Gfi-1B also cooperated with GATA-1 to repress Bcl-x(L) transcription.	imatinib	77-85	growth factor independent 1B transcriptional repressor	Homo sapiens	142-148
17420275-9	2007	Furthermore, we show that the inhibition of Bcr-Abl kinase by treatment with imatinib caused the up-regulation of Gfi-1B in K562 cells, where Gfi-1B also cooperated with GATA-1 to repress Bcl-x(L) transcription.	imatinib	77-85	BCL2 like 1	Homo sapiens	188-193
17420275-10	2007	Gfi-1B knockdown by RNA interference diminished imatinib-induced apoptosis, while the overexpression of Gfi-1B sensitized K562 cells to arsenic-induced death.	imatinib	48-56	growth factor independent 1B transcriptional repressor	Homo sapiens	0-6
17603257-4	2007	Imatinib also inhibits the activation of c-Abl, which is a key downstream molecule of transforming growth factor-beta signaling, and PDGF receptors.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-46
17130834-2	2007	Here, we demonstrate that rottlerin, a putative protein kinase C-delta (PKCdelta)-specific inhibitor, acts synergistically with imatinib to induce apoptosis of BCR/ABL-expressing K562 and Ton.B210 cells.	imatinib	128-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-167
17173066-0	2007	Semaxinib (SU5416) as a therapeutic agent targeting oncogenic Kit mutants resistant to imatinib mesylate.	imatinib	87-104	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	62-65
17264298-2	2007	Dasatinib is a novel, potent, oral, multitargeted kinase inhibitor of BCR-ABL and SRC-family kinases that showed marked efficacy in a phase 1 trial of patients with imatinib-resistant CML.	imatinib	165-173	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
17130834-0	2007	Rottlerin synergistically enhances imatinib-induced apoptosis of BCR/ABL-expressing cells through its mitochondrial uncoupling effect independent of protein kinase C-delta.	imatinib	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
17130834-1	2007	Although the BCR/ABL tyrosine kinase inhibitor imatinib is highly effective for treatment of chronic myeloid leukemia (CML) and Philadelphia-chromosome positive acute lymphoblastic leukemia (ALL), relapse with emerging imatinib-resistance mutations in the BCR/ABL kinase domain poses a significant problem.	imatinib	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
17130834-1	2007	Although the BCR/ABL tyrosine kinase inhibitor imatinib is highly effective for treatment of chronic myeloid leukemia (CML) and Philadelphia-chromosome positive acute lymphoblastic leukemia (ALL), relapse with emerging imatinib-resistance mutations in the BCR/ABL kinase domain poses a significant problem.	imatinib	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	256-263
17130834-1	2007	Although the BCR/ABL tyrosine kinase inhibitor imatinib is highly effective for treatment of chronic myeloid leukemia (CML) and Philadelphia-chromosome positive acute lymphoblastic leukemia (ALL), relapse with emerging imatinib-resistance mutations in the BCR/ABL kinase domain poses a significant problem.	imatinib	219-227	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
17575668-16	2007	Imatinib (anti c-Kit) can now be offered to patients presenting with recurrent GIST, if further surgery is deemed inappropriate.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	15-20
17702135-9	2007	This was replaced by a new golden standard--interferon alpha, which was, in turn, replaced by the specific blocker of bcr-abl thyrosine kinase-imatinib.	imatinib	143-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
17160016-2	2007	By oligonucleotide microarray hybridization of polysomal RNA of untreated and STI571-treated 32D-BCR/ABL cells, we identified the beta-chemokine CCL9 as a gene regulated by BCR/ABL in a tyrosine kinase-dependent manner.	imatinib	78-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
17160016-2	2007	By oligonucleotide microarray hybridization of polysomal RNA of untreated and STI571-treated 32D-BCR/ABL cells, we identified the beta-chemokine CCL9 as a gene regulated by BCR/ABL in a tyrosine kinase-dependent manner.	imatinib	78-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	173-180
17284533-3	2007	In 3 bcr-abl-positive cell lines, expression of miRNAs encoded within the polycistronic miR-17-92 cluster is specifically down-regulated (2- to 5-fold) by both imatinib treatment and anti-BCR-ABL RNA interference (RNAi).	imatinib	160-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	5-12
17284533-3	2007	In 3 bcr-abl-positive cell lines, expression of miRNAs encoded within the polycistronic miR-17-92 cluster is specifically down-regulated (2- to 5-fold) by both imatinib treatment and anti-BCR-ABL RNA interference (RNAi).	imatinib	160-168	miR-17-92a-1 cluster host gene	Homo sapiens	88-97
17289809-3	2007	Depletion of endogenous c-Kit or inhibition of c-Kit enzymatic activity by imatinib mesylate prevented adhesion of EPCs to activated ECs both in vitro and in vivo, indicating that a functional c-Kit on EPCs is essential.	imatinib	75-92	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	47-52
17289809-3	2007	Depletion of endogenous c-Kit or inhibition of c-Kit enzymatic activity by imatinib mesylate prevented adhesion of EPCs to activated ECs both in vitro and in vivo, indicating that a functional c-Kit on EPCs is essential.	imatinib	75-92	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	47-52
17130834-5	2007	Moreover, two other mitochondrial uncouplers, FCCP and DNP, very similarly induced apoptosis of BCR/ABL-expressing cells in a synergistic manner with imatinib.	imatinib	150-158	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
17130834-7	2007	Rottlerin also enhanced the cytotoxic effect of imatinib in leukemic cells from patients with CML blast crisis and Ph-positive ALL or a cell line expressing the imatinib-resistant E255K BCR/ABL mutant.	imatinib	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-193
17130834-7	2007	Rottlerin also enhanced the cytotoxic effect of imatinib in leukemic cells from patients with CML blast crisis and Ph-positive ALL or a cell line expressing the imatinib-resistant E255K BCR/ABL mutant.	imatinib	161-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-193
17130834-8	2007	The present study indicates that rottlerin synergistically enhances imatinib-induced apoptosis through its mitochondrial uncoupling effect independent of PKCdelta and may contribute to the development of new treatment strategy to overcome the imatinib resistance and to cure the BCR/ABL expressing leukemias.	imatinib	68-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	279-286
17449802-0	2007	Myelofibrosis evolving during imatinib treatment of a chronic myeloproliferative disease with coexisting BCR-ABL translocation and JAK2V617F mutation.	imatinib	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-112
17218385-9	2007	Together, these findings suggest that strategies combining dasatanib with MEK1/2 inhibitors warrant further investigation in Bcr/Abl(+) malignancies, particularly in the setting of imatinib mesylate-resistant disease.	imatinib	181-198	mitogen-activated protein kinase kinase 1	Homo sapiens	74-80
17470736-2	2007	We hypothesized that imatinib-resistant leukemic cells emerge from CML stem cells that acquire BCR-ABL gene mutations even before exposure to BCR-ABL-targeted agents such as imatinib.	imatinib	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
17470736-2	2007	We hypothesized that imatinib-resistant leukemic cells emerge from CML stem cells that acquire BCR-ABL gene mutations even before exposure to BCR-ABL-targeted agents such as imatinib.	imatinib	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
17211520-0	2007	Fusion of H4/D10S170 to PDGFRbeta in a patient with chronic myelomonocytic leukemia and long-term responsiveness to imatinib.	imatinib	116-124	coiled-coil domain containing 6	Homo sapiens	10-20
17211520-0	2007	Fusion of H4/D10S170 to PDGFRbeta in a patient with chronic myelomonocytic leukemia and long-term responsiveness to imatinib.	imatinib	116-124	platelet derived growth factor receptor beta	Homo sapiens	24-33
17488167-10	2007	In contrast, patients carrying the FIP1L1-PDGFRA mutation achieve complete responses with low-dose imatinib therapy.	imatinib	99-107	factor interacting with PAPOLA and CPSF1	Homo sapiens	35-41
17488167-10	2007	In contrast, patients carrying the FIP1L1-PDGFRA mutation achieve complete responses with low-dose imatinib therapy.	imatinib	99-107	platelet derived growth factor receptor alpha	Homo sapiens	42-48
17461740-3	2007	Imatinib (a BCR-ABL tyrosine kinase inhibitor) produces haematological and cytogenetic remissions across all phases of CML and is the present standard of care.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
17180388-3	2007	The purpose of this study was to investigate in vitro, whether hydroxyurea could enhance the central nervous system penetration of imatinib, by inhibition of the ATP-dependent transporter proteins P-glycoprotein (ABCB1; MDR1; Pgp) and Breast Cancer Resistance Protein (ABCG2; BCRP), or by inhibition of cytochrome P450 3A (CYP3A) metabolism of imatinib.	imatinib	131-139	ATP binding cassette subfamily B member 1	Homo sapiens	197-211
17180388-3	2007	The purpose of this study was to investigate in vitro, whether hydroxyurea could enhance the central nervous system penetration of imatinib, by inhibition of the ATP-dependent transporter proteins P-glycoprotein (ABCB1; MDR1; Pgp) and Breast Cancer Resistance Protein (ABCG2; BCRP), or by inhibition of cytochrome P450 3A (CYP3A) metabolism of imatinib.	imatinib	131-139	ATP binding cassette subfamily B member 1	Homo sapiens	213-218
17180388-3	2007	The purpose of this study was to investigate in vitro, whether hydroxyurea could enhance the central nervous system penetration of imatinib, by inhibition of the ATP-dependent transporter proteins P-glycoprotein (ABCB1; MDR1; Pgp) and Breast Cancer Resistance Protein (ABCG2; BCRP), or by inhibition of cytochrome P450 3A (CYP3A) metabolism of imatinib.	imatinib	131-139	ATP binding cassette subfamily B member 1	Homo sapiens	220-224
17180388-3	2007	The purpose of this study was to investigate in vitro, whether hydroxyurea could enhance the central nervous system penetration of imatinib, by inhibition of the ATP-dependent transporter proteins P-glycoprotein (ABCB1; MDR1; Pgp) and Breast Cancer Resistance Protein (ABCG2; BCRP), or by inhibition of cytochrome P450 3A (CYP3A) metabolism of imatinib.	imatinib	131-139	phosphoglycolate phosphatase	Homo sapiens	226-229
17180388-3	2007	The purpose of this study was to investigate in vitro, whether hydroxyurea could enhance the central nervous system penetration of imatinib, by inhibition of the ATP-dependent transporter proteins P-glycoprotein (ABCB1; MDR1; Pgp) and Breast Cancer Resistance Protein (ABCG2; BCRP), or by inhibition of cytochrome P450 3A (CYP3A) metabolism of imatinib.	imatinib	131-139	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	235-267
17180388-3	2007	The purpose of this study was to investigate in vitro, whether hydroxyurea could enhance the central nervous system penetration of imatinib, by inhibition of the ATP-dependent transporter proteins P-glycoprotein (ABCB1; MDR1; Pgp) and Breast Cancer Resistance Protein (ABCG2; BCRP), or by inhibition of cytochrome P450 3A (CYP3A) metabolism of imatinib.	imatinib	131-139	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	269-274
17180388-3	2007	The purpose of this study was to investigate in vitro, whether hydroxyurea could enhance the central nervous system penetration of imatinib, by inhibition of the ATP-dependent transporter proteins P-glycoprotein (ABCB1; MDR1; Pgp) and Breast Cancer Resistance Protein (ABCG2; BCRP), or by inhibition of cytochrome P450 3A (CYP3A) metabolism of imatinib.	imatinib	131-139	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	276-280
17180388-3	2007	The purpose of this study was to investigate in vitro, whether hydroxyurea could enhance the central nervous system penetration of imatinib, by inhibition of the ATP-dependent transporter proteins P-glycoprotein (ABCB1; MDR1; Pgp) and Breast Cancer Resistance Protein (ABCG2; BCRP), or by inhibition of cytochrome P450 3A (CYP3A) metabolism of imatinib.	imatinib	131-139	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	303-321
17180388-3	2007	The purpose of this study was to investigate in vitro, whether hydroxyurea could enhance the central nervous system penetration of imatinib, by inhibition of the ATP-dependent transporter proteins P-glycoprotein (ABCB1; MDR1; Pgp) and Breast Cancer Resistance Protein (ABCG2; BCRP), or by inhibition of cytochrome P450 3A (CYP3A) metabolism of imatinib.	imatinib	131-139	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	323-328
17180388-3	2007	The purpose of this study was to investigate in vitro, whether hydroxyurea could enhance the central nervous system penetration of imatinib, by inhibition of the ATP-dependent transporter proteins P-glycoprotein (ABCB1; MDR1; Pgp) and Breast Cancer Resistance Protein (ABCG2; BCRP), or by inhibition of cytochrome P450 3A (CYP3A) metabolism of imatinib.	imatinib	344-352	ATP binding cassette subfamily B member 1	Homo sapiens	197-211
17180388-3	2007	The purpose of this study was to investigate in vitro, whether hydroxyurea could enhance the central nervous system penetration of imatinib, by inhibition of the ATP-dependent transporter proteins P-glycoprotein (ABCB1; MDR1; Pgp) and Breast Cancer Resistance Protein (ABCG2; BCRP), or by inhibition of cytochrome P450 3A (CYP3A) metabolism of imatinib.	imatinib	344-352	ATP binding cassette subfamily B member 1	Homo sapiens	213-218
17180388-3	2007	The purpose of this study was to investigate in vitro, whether hydroxyurea could enhance the central nervous system penetration of imatinib, by inhibition of the ATP-dependent transporter proteins P-glycoprotein (ABCB1; MDR1; Pgp) and Breast Cancer Resistance Protein (ABCG2; BCRP), or by inhibition of cytochrome P450 3A (CYP3A) metabolism of imatinib.	imatinib	344-352	ATP binding cassette subfamily B member 1	Homo sapiens	220-224
17180388-4	2007	METHODS: The effect of hydroxyurea on the Pgp and BCRP mediated transport of imatinib was investigated by the sulforhodamine-B (SRB) drug cytotoxicity assay and transepithelial transport assay.	imatinib	77-85	phosphoglycolate phosphatase	Homo sapiens	42-45
17180388-4	2007	METHODS: The effect of hydroxyurea on the Pgp and BCRP mediated transport of imatinib was investigated by the sulforhodamine-B (SRB) drug cytotoxicity assay and transepithelial transport assay.	imatinib	77-85	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	50-54
17180388-4	2007	METHODS: The effect of hydroxyurea on the Pgp and BCRP mediated transport of imatinib was investigated by the sulforhodamine-B (SRB) drug cytotoxicity assay and transepithelial transport assay.	imatinib	77-85	chaperonin containing TCP1 subunit 4	Homo sapiens	110-126
17180388-4	2007	METHODS: The effect of hydroxyurea on the Pgp and BCRP mediated transport of imatinib was investigated by the sulforhodamine-B (SRB) drug cytotoxicity assay and transepithelial transport assay.	imatinib	77-85	chaperonin containing TCP1 subunit 4	Homo sapiens	128-131
17504122-1	2007	The phenylaminopyrimidine-derivate Imatinib mesylate has been developed for targeted inhibition of the Abelson kinase (c-ABL), which is constitutively activated when translocated to the genetic locus of the breakpoint cluster region (leading to the BCR/ABL fusion gene), thereby forming the causative pathogenetic event for the development of chronic myeloid leukemia (CML).	imatinib	35-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-124
17504122-6	2007	The latter mediate Imatinib/IL-2-induced regression of tumors in pre-clinical animal models via production of high amounts of IFN-gamma and the death receptor ligand TRAIL.	imatinib	19-27	interleukin 2	Homo sapiens	28-32
17504122-6	2007	The latter mediate Imatinib/IL-2-induced regression of tumors in pre-clinical animal models via production of high amounts of IFN-gamma and the death receptor ligand TRAIL.	imatinib	19-27	interferon gamma	Homo sapiens	126-135
17504122-6	2007	The latter mediate Imatinib/IL-2-induced regression of tumors in pre-clinical animal models via production of high amounts of IFN-gamma and the death receptor ligand TRAIL.	imatinib	19-27	TNF superfamily member 10	Homo sapiens	166-171
17180388-0	2007	The effect of hydroxyurea on P-glycoprotein/BCRP-mediated transport and CYP3A metabolism of imatinib mesylate.	imatinib	92-109	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	44-48
17180388-0	2007	The effect of hydroxyurea on P-glycoprotein/BCRP-mediated transport and CYP3A metabolism of imatinib mesylate.	imatinib	92-109	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	72-77
17483365-0	2007	Dormant tumor cells develop cross-resistance to apoptosis induced by CTLs or imatinib mesylate via methylation of suppressor of cytokine signaling 1.	imatinib	77-94	suppressor of cytokine signaling 1	Mus musculus	114-148
20425353-5	2007	Unfortunately, BCR/ABL kinase compromises the fidelity of DNA repair mechanisms, thus contributing to the accumulation of additional genetic abnormalities that lead to resistance to inhibitors such as imatinib mesylate and to malignant progression of the disease.	imatinib	201-209	BCR activator of RhoGEF and GTPase	Homo sapiens	15-18
20425353-5	2007	Unfortunately, BCR/ABL kinase compromises the fidelity of DNA repair mechanisms, thus contributing to the accumulation of additional genetic abnormalities that lead to resistance to inhibitors such as imatinib mesylate and to malignant progression of the disease.	imatinib	201-209	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-22
17432976-2	2007	TRAIL could be one of the reagents for therapeutic use in combination with imatinib in chronic myeloid leukemia (CML).	imatinib	75-83	TNF superfamily member 10	Homo sapiens	0-5
17432976-3	2007	Here we examined serum-soluble TRAIL (sTRAIL) levels in CML patients either before or during therapies with IFNalpha or imatinib.	imatinib	120-128	TNF superfamily member 10	Homo sapiens	31-36
17432977-0	2007	Establishment and characterization of a novel imatinib-sensitive chronic myeloid leukemia cell line MYL, and an imatinib-resistant subline MYL-R showing overexpression of Lyn.	imatinib	112-120	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	171-174
17432977-4	2007	Treatment with imatinib inhibited phosphorylation of BCR-ABL and CrkL in both MYL and MYL-R, even though imatinib-induced apoptosis was preferentially observed in MYL than MYL-R, indicating that the resistance is based on a BCR-ABL-independent mechanism.	imatinib	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
17432977-4	2007	Treatment with imatinib inhibited phosphorylation of BCR-ABL and CrkL in both MYL and MYL-R, even though imatinib-induced apoptosis was preferentially observed in MYL than MYL-R, indicating that the resistance is based on a BCR-ABL-independent mechanism.	imatinib	15-23	CRK like proto-oncogene, adaptor protein	Homo sapiens	65-69
17432977-4	2007	Treatment with imatinib inhibited phosphorylation of BCR-ABL and CrkL in both MYL and MYL-R, even though imatinib-induced apoptosis was preferentially observed in MYL than MYL-R, indicating that the resistance is based on a BCR-ABL-independent mechanism.	imatinib	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	224-231
17432977-4	2007	Treatment with imatinib inhibited phosphorylation of BCR-ABL and CrkL in both MYL and MYL-R, even though imatinib-induced apoptosis was preferentially observed in MYL than MYL-R, indicating that the resistance is based on a BCR-ABL-independent mechanism.	imatinib	105-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	224-231
17432977-6	2007	Silencing of Lyn by short-interfering RNA (siRNA) in MYL-R, but not in MYL, induced significant growth-inhibition, increased caspase-3 activity, and induced partial recovery from imatinib-resistance.	imatinib	179-187	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	13-16
17432977-8	2007	Expression of Bim, which plays an important role in imatinib-induced cell-killing, was not suppressed in MYL-R.	imatinib	52-60	BCL2 like 11	Homo sapiens	14-17
17432977-12	2007	Taken together, Lyn may play an important role in imatinib-resistance in MYL-R.	imatinib	50-58	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	16-19
17461740-4	2007	Imatinib resistance occurs in a significant proportion of patients and mechanisms of resistance include BCR-ABL mutations and activation of alternate oncogenic pathways.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
17564324-2	2007	The development of imatinib mesylate (Gleevec), a tyrosine kinase inhibitor targeted against the causative Bcr-Abl protein in chronic myeloid leukemia (CML), has resulted in hematologic and cytogenetic remissions in all phases of CML.	imatinib	19-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
17437861-2	2007	Approximately 80% of patients with metastatic GIST show at least some clinical response to the targeted small molecule KIT inhibitor imatinib.	imatinib	133-141	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	119-122
17437861-3	2007	The response to imatinib is closely correlated with the presence and type of KIT mutation.	imatinib	16-24	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	77-80
17437861-4	2007	GISTs with the most common KIT exon 11 mutations have the highest response rate by far, whereas GISTs lacking mutations in KIT or the alternative receptor tyrosine kinase PDGFRA show much lower rates of response to imatinib.	imatinib	215-223	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	123-126
17437861-4	2007	GISTs with the most common KIT exon 11 mutations have the highest response rate by far, whereas GISTs lacking mutations in KIT or the alternative receptor tyrosine kinase PDGFRA show much lower rates of response to imatinib.	imatinib	215-223	platelet derived growth factor receptor alpha	Homo sapiens	171-177
17437861-5	2007	Less than 5% of GISTs are KIT-immunonegative; and many of these tumors have activating mutations of PDGFRA, some of which are also inhibited by imatinib.	imatinib	144-152	platelet derived growth factor receptor alpha	Homo sapiens	100-106
17437861-6	2007	Most patients who initially respond to imatinib become resistant and eventually progress, which coincides with the selection of imatinib-resistant secondary KIT mutations in the kinase domain.	imatinib	39-47	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	157-160
17437861-6	2007	Most patients who initially respond to imatinib become resistant and eventually progress, which coincides with the selection of imatinib-resistant secondary KIT mutations in the kinase domain.	imatinib	128-136	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	157-160
17390013-9	2007	Imatinib inhibited the functional activation of R3-specific CD8+ T lymphocytes.	imatinib	0-8	CD8a molecule	Homo sapiens	60-63
17390013-10	2007	In summary, we demonstrated R3-specific CD8+ effector T lymphocytes after allo-SCT in CML patients which might have been augumented by R3 peptide vaccination and hampered at least partially by imatinib in this particular patient cohort.	imatinib	193-201	CD8a molecule	Homo sapiens	40-43
17509258-4	2007	Data have recently shown that inhibiting platelet-derived growth factor receptors (PDGFR) with imatinib can induce high rates of clinical response in patients with unresectable or metastatic DFSP.	imatinib	95-103	platelet derived growth factor receptor beta	Homo sapiens	41-81
17509258-4	2007	Data have recently shown that inhibiting platelet-derived growth factor receptors (PDGFR) with imatinib can induce high rates of clinical response in patients with unresectable or metastatic DFSP.	imatinib	95-103	platelet derived growth factor receptor beta	Homo sapiens	83-88
17509258-6	2007	Although wide surgical excision remains standard care, patients with locally advanced disease not suitable for surgical excision can be treated with the PDGFR-inhibitor imatinib, which sometimes allows residual DFSP to be surgically excised.	imatinib	169-177	platelet derived growth factor receptor beta	Homo sapiens	153-158
17315025-3	2007	Clonal culture of purified CD41(+)CD42(-) cells, a population highly enriched in MK progenitors, combined with the conditional expression of p210(BCR-ABL) tyrosine kinase activity by imatinib identified a true lineage reprogramming.	imatinib	183-191	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	146-153
17330101-2	2007	Here we show that the lesser effect of imatinib mesylate (IM) on the 3-week output of cells produced in vitro from lin(-)CD34(+)CD38(-) CML (stem) cells compared with cultures initiated with the CD38(+) subset of lin(-)CD34(+) cells is markedly enhanced (>10-fold) when conditions of reduced growth factor stimulation are used.	imatinib	39-56	CD38 molecule	Homo sapiens	128-132
17483434-3	2007	For example, because they can distinguish cancer cells from their normal counterparts, agents such as imatinib mesylate, a Bcr-Abl and Kit kinase inhibitor, can result in remarkable responses with minimal host toxicity in patients suffering from diseases characterized by abnormalities in the targeted kinases.	imatinib	102-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-130
17483434-4	2007	Indeed, studies of imatinib mesylate in early-stage chronic myelogenous leukemia, whose hallmark is the aberrant Bcr-Abl, show response rates of more than 90%.	imatinib	19-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
17457302-0	2007	Second generation inhibitors of BCR-ABL for the treatment of imatinib-resistant chronic myeloid leukaemia.	imatinib	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
17457302-1	2007	Imatinib, a small-molecule ABL kinase inhibitor, is a highly effective therapy for early-phase chronic myeloid leukaemia (CML), which has constitutively active ABL kinase activity owing to the expression of the BCR-ABL fusion protein.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	211-218
17376172-0	2007	Total CD34+ cells per 10 HPF in bone marrow trephines of patients with chronic myeloid leukaemia correlates with probability of complete cytogenetic response following imatinib treatment.	imatinib	168-176	CD34 molecule	Homo sapiens	6-10
17396139-2	2007	A compelling example is the use of small molecule drugs, such as imatinib (Gleevec), which inhibit the KIT tyrosine kinase in gastrointestinal stromal tumors (GIST).	imatinib	65-73	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	103-106
17396139-2	2007	A compelling example is the use of small molecule drugs, such as imatinib (Gleevec), which inhibit the KIT tyrosine kinase in gastrointestinal stromal tumors (GIST).	imatinib	75-82	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	103-106
17396139-6	2007	KIT was inhibited with imatinib, and mTOR with RAD001.	imatinib	23-31	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
17390033-2	2007	Gefitinib and imatinib are tyrosine kinase inhibitors which have clinical activities in several malignancies and they are also potent inhibitors of breast cancer resistance protein (BCRP) transporter, which confers the resistance of topoisomerase I inhibitors including SN-38 and topotecan.	imatinib	14-22	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	148-180
17390033-2	2007	Gefitinib and imatinib are tyrosine kinase inhibitors which have clinical activities in several malignancies and they are also potent inhibitors of breast cancer resistance protein (BCRP) transporter, which confers the resistance of topoisomerase I inhibitors including SN-38 and topotecan.	imatinib	14-22	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	182-186
17390033-10	2007	BCRP was equally overexpressed in the SBC-3/SN-38 with and without gefitinib or imatinib.	imatinib	80-88	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-4
17564324-2	2007	The development of imatinib mesylate (Gleevec), a tyrosine kinase inhibitor targeted against the causative Bcr-Abl protein in chronic myeloid leukemia (CML), has resulted in hematologic and cytogenetic remissions in all phases of CML.	imatinib	38-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
17523053-0	2007	Plasma pharmacokinetics and CYP3A12-dependent metabolism of c-kit inhibitor imatinib in dogs.	imatinib	76-84	cytochrome P450 3A12	Canis lupus familiaris	28-35
17523053-0	2007	Plasma pharmacokinetics and CYP3A12-dependent metabolism of c-kit inhibitor imatinib in dogs.	imatinib	76-84	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	60-65
17523053-6	2007	Recombinant system of dog CYP3A12 and CYP2C21 showed that CYP3A12 contributed to the metabolism of imatinib.	imatinib	99-107	cytochrome P450 3A12	Canis lupus familiaris	26-33
17523053-6	2007	Recombinant system of dog CYP3A12 and CYP2C21 showed that CYP3A12 contributed to the metabolism of imatinib.	imatinib	99-107	cytochrome P450 2C21	Canis lupus familiaris	38-45
17523053-6	2007	Recombinant system of dog CYP3A12 and CYP2C21 showed that CYP3A12 contributed to the metabolism of imatinib.	imatinib	99-107	cytochrome P450 3A12	Canis lupus familiaris	58-65
17523053-7	2007	The inhibition of CYP3A-dependent activity using a rat anti-CYP3A antibody or ketoconazole revealed that CYP3A12 plays a major role in the metabolism of imatinib in dog liver microsomes.	imatinib	153-161	cytochrome P450 3A12	Canis lupus familiaris	105-112
17440089-1	2007	An interstitial deletion on chromosome 4q12 resulting in the formation of the FIP1L1-PDGFRA fusion protein is involved in the pathogenesis of imatinib-sensitive chronic eosinophilic leukemia.	imatinib	142-150	factor interacting with PAPOLA and CPSF1	Homo sapiens	78-84
17202319-2	2007	Bcr/Abl point mutations and other alterations reduce the kinase inhibitory activity of imatinib mesylate; thus, agents that target Bcr/Abl through unique mechanisms may be needed.	imatinib	87-104	BCR activator of RhoGEF and GTPase	Mus musculus	0-3
17202319-2	2007	Bcr/Abl point mutations and other alterations reduce the kinase inhibitory activity of imatinib mesylate; thus, agents that target Bcr/Abl through unique mechanisms may be needed.	imatinib	87-104	BCR activator of RhoGEF and GTPase	Mus musculus	131-134
17185463-8	2007	Response rates were similar in patients with and without BCR-ABL mutations known to confer resistance to imatinib.	imatinib	105-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
17438095-0	2007	c-Kit/PDGFRA gene status alterations possibly related to primary imatinib resistance in gastrointestinal stromal tumors.	imatinib	65-73	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-5
17438095-0	2007	c-Kit/PDGFRA gene status alterations possibly related to primary imatinib resistance in gastrointestinal stromal tumors.	imatinib	65-73	platelet derived growth factor receptor alpha	Homo sapiens	6-12
17438106-0	2007	The tyrosine kinase inhibitor imatinib mesylate enhances the efficacy of photodynamic therapy by inhibiting ABCG2.	imatinib	30-47	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	108-113
17438106-7	2007	Imatinib mesylate increased accumulation of HPPH, PpIX, and BPD-MA from 1.3- to 6-fold in ABCG2+ cells, but not in ABCG2- cells, and enhanced PDT efficacy both in vitro and in vivo.	imatinib	0-17	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	90-95
17438106-8	2007	CONCLUSIONS: Second-generation clinical photosensitizers are transported out of cells by ABCG2, and this effect can be abrogated by coadministration of imatinib mesylate.	imatinib	152-169	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	89-94
17438106-9	2007	By increasing intracellular photosensitizer levels in ABCG2+ tumors, imatinib mesylate or other ABCG2 transport inhibitors may enhance efficacy and selectivity of clinical PDT.	imatinib	69-86	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	54-59
17452251-0	2007	Complete cytogenetic and molecular response after imatinib treatment for chronic myeloid leukemia in a patient with atypical karyotype and BCR-ABL b2a3 transcript.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-146
17452251-2	2007	The amplification of the BCR-ABL hybrid gene resulting from additional copies of the Ph chromosome has been identified as a mechanism for imatinib (IM) resistance.	imatinib	138-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
17440089-1	2007	An interstitial deletion on chromosome 4q12 resulting in the formation of the FIP1L1-PDGFRA fusion protein is involved in the pathogenesis of imatinib-sensitive chronic eosinophilic leukemia.	imatinib	142-150	platelet derived growth factor receptor alpha	Homo sapiens	85-91
17452255-1	2007	Amplification/duplication of the BCR-ABL gene has been found to be one of the key factors leading to drug resistance to imatinib mesylate (IM).	imatinib	120-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
17440089-4	2007	FIP1L1-PDGFRA induced both proliferation and differentiation of eosinophils, neutrophils, and erythrocytes in the absence of cytokines, which could be inhibited by imatinib.	imatinib	164-172	factor interacting with PAPOLA and CPSF1	Homo sapiens	0-6
17440089-4	2007	FIP1L1-PDGFRA induced both proliferation and differentiation of eosinophils, neutrophils, and erythrocytes in the absence of cytokines, which could be inhibited by imatinib.	imatinib	164-172	platelet derived growth factor receptor alpha	Homo sapiens	7-13
17110460-8	2007	Moreover, MCL-1 ASOs were found to cooperate with various tyrosine kinase inhibitors in producing growth inhibition in neoplastic MCs, with synergistic effects observed with PKC412, AMN107, and imatinib in HMC-1.1 cells and with PKC412 in HMC-1.2 cells.	imatinib	194-202	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	10-15
17043649-1	2007	Imatinib targets the Bcr-Abl oncogene that causes chronic myelogenous leukemia (CML) in humans.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
17043649-7	2007	Furthermore, imatinib and PD166326, another Bcr-Abl inhibitory molecule, triggered erythroid differentiation of K562 cell clones, nevertheless resistant to Bcr-Abl inhibitor-induced apoptosis.	imatinib	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
17043649-7	2007	Furthermore, imatinib and PD166326, another Bcr-Abl inhibitory molecule, triggered erythroid differentiation of K562 cell clones, nevertheless resistant to Bcr-Abl inhibitor-induced apoptosis.	imatinib	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
17043649-8	2007	Finally, short hairpin RNA inhibitor (shRNAi) silencing of caspase 3 efficiently inhibited caspase activity but had no effect on erythroid differentiation, whereas silencing of Bcr-Abl mimicked imatinib or PD166326 treatment, leading to increased apoptosis and erythroid differentiation of K562 cells.	imatinib	194-202	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	177-184
17348685-5	2007	Cell treatment with Src or Abl inhibitors PP2 or STI571, prior to receptor stimulation, affects caveolin-1 phosphorylation without affecting receptor autophosphorylation, suggesting that both Src and Abl are involved in VEGFR-3-dependent caveolin-1 phosphorylation.	imatinib	49-55	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	20-23
17348685-5	2007	Cell treatment with Src or Abl inhibitors PP2 or STI571, prior to receptor stimulation, affects caveolin-1 phosphorylation without affecting receptor autophosphorylation, suggesting that both Src and Abl are involved in VEGFR-3-dependent caveolin-1 phosphorylation.	imatinib	49-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-30
17348685-5	2007	Cell treatment with Src or Abl inhibitors PP2 or STI571, prior to receptor stimulation, affects caveolin-1 phosphorylation without affecting receptor autophosphorylation, suggesting that both Src and Abl are involved in VEGFR-3-dependent caveolin-1 phosphorylation.	imatinib	49-55	caveolin 1	Homo sapiens	96-106
17348685-5	2007	Cell treatment with Src or Abl inhibitors PP2 or STI571, prior to receptor stimulation, affects caveolin-1 phosphorylation without affecting receptor autophosphorylation, suggesting that both Src and Abl are involved in VEGFR-3-dependent caveolin-1 phosphorylation.	imatinib	49-55	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	192-195
17348685-5	2007	Cell treatment with Src or Abl inhibitors PP2 or STI571, prior to receptor stimulation, affects caveolin-1 phosphorylation without affecting receptor autophosphorylation, suggesting that both Src and Abl are involved in VEGFR-3-dependent caveolin-1 phosphorylation.	imatinib	49-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	200-203
17348685-5	2007	Cell treatment with Src or Abl inhibitors PP2 or STI571, prior to receptor stimulation, affects caveolin-1 phosphorylation without affecting receptor autophosphorylation, suggesting that both Src and Abl are involved in VEGFR-3-dependent caveolin-1 phosphorylation.	imatinib	49-55	fms related receptor tyrosine kinase 4	Homo sapiens	220-227
17348685-5	2007	Cell treatment with Src or Abl inhibitors PP2 or STI571, prior to receptor stimulation, affects caveolin-1 phosphorylation without affecting receptor autophosphorylation, suggesting that both Src and Abl are involved in VEGFR-3-dependent caveolin-1 phosphorylation.	imatinib	49-55	caveolin 1	Homo sapiens	238-248
17303574-3	2007	Measurement of endogenous ceramides by high performance liquid chromatography/mass spectroscopy showed that treatment with imatinib increased the generation of ceramide, mainly C18-ceramide, which is generated by the human longevity assurance gene 1 (hLASS1), in sensitive, but not in resistant cells.	imatinib	123-131	ceramide synthase 1	Homo sapiens	251-257
17303574-4	2007	Inhibition of hLASS1 by small interfering RNA partially prevented imatinib-induced cell death in sensitive cells.	imatinib	66-74	ceramide synthase 1	Homo sapiens	14-20
17303574-5	2007	In reciprocal experiments, overexpression of hLASS1, and not hLASS6, in drug-resistant cells caused a marked increase in imatinib-induced C18-ceramide generation, and enhanced apoptosis.	imatinib	121-129	ceramide synthase 1	Homo sapiens	45-51
17303574-8	2007	The partial inhibition of SK1 expression by small interference RNA modulated S1P levels and increased sensitivity to imatinib-induced apoptosis in resistant cells.	imatinib	117-125	sphingosine kinase 1	Homo sapiens	26-29
17303574-9	2007	On the other hand, forced expression of SK1 in K562 cells increased the ratio between total S1P/C18-ceramide levels approximately 6-fold and prevented apoptosis significantly in response to imatinib.	imatinib	190-198	sphingosine kinase 1	Homo sapiens	40-43
17303574-10	2007	Additional data indicated a role for SK1/S1P signaling in the up-regulation of the Bcr-Abl expression at the post-transcriptional level, which suggested a possible mechanism for resistance to imatinib-mediated apoptosis.	imatinib	192-200	sphingosine kinase 1	Homo sapiens	37-44
17303574-10	2007	Additional data indicated a role for SK1/S1P signaling in the up-regulation of the Bcr-Abl expression at the post-transcriptional level, which suggested a possible mechanism for resistance to imatinib-mediated apoptosis.	imatinib	192-200	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
17303574-11	2007	In conclusion, these data suggest a role for endogenous C18-ceramide synthesis mainly via hLASS1 in imatinib-induced apoptosis in sensitive cells, whereas in resistant cells, alterations of the balance between the levels of ceramide and S1P by overexpression of SK1 result in resistance to imatinib-induced apoptosis.	imatinib	100-108	ceramide synthase 1	Homo sapiens	90-96
17303574-11	2007	In conclusion, these data suggest a role for endogenous C18-ceramide synthesis mainly via hLASS1 in imatinib-induced apoptosis in sensitive cells, whereas in resistant cells, alterations of the balance between the levels of ceramide and S1P by overexpression of SK1 result in resistance to imatinib-induced apoptosis.	imatinib	100-108	sphingosine kinase 1	Homo sapiens	262-265
17349636-5	2007	Additionally, growth of Bcr-Abl-expressing CD34+ cells from chronic phase CML patients is inhibited by TGFbeta and, interestingly, treatment of a non-proliferating CD34+ CML cell sub-population with the TGFbeta kinase inhibitor SB431542 enhanced cell death mediated by the Bcr-Abl inhibitor imatinib.	imatinib	291-299	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
17349636-5	2007	Additionally, growth of Bcr-Abl-expressing CD34+ cells from chronic phase CML patients is inhibited by TGFbeta and, interestingly, treatment of a non-proliferating CD34+ CML cell sub-population with the TGFbeta kinase inhibitor SB431542 enhanced cell death mediated by the Bcr-Abl inhibitor imatinib.	imatinib	291-299	CD34 molecule	Homo sapiens	43-47
17349636-5	2007	Additionally, growth of Bcr-Abl-expressing CD34+ cells from chronic phase CML patients is inhibited by TGFbeta and, interestingly, treatment of a non-proliferating CD34+ CML cell sub-population with the TGFbeta kinase inhibitor SB431542 enhanced cell death mediated by the Bcr-Abl inhibitor imatinib.	imatinib	291-299	transforming growth factor beta 1	Homo sapiens	203-210
17268837-15	2007	C-kit positive tumors respond extremely well to chemotherapy with Imatinib (Glivec, Gleevec) [10-12].	imatinib	66-74	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-5
17883045-13	2007	CD117 positive cases are ideal candidates for treatment with molecularly targeted specific chemotherapeutic agents, e.g., imatinib as these tumours are non-responsive to conventional chemotherapy.	imatinib	122-130	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-5
17379100-2	2007	Imatinib (Glivec, Gleevec), a specific small molecule inhibitor of Bcr-Abl, has become the standard drug therapy for CML, and has dramatically diminished the use of allogeneic stem cell transplantation.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
17169414-0	2007	AKT mediates the pro-survival effects of KIT in ovarian cancer cells and is a determinant of sensitivity to imatinib mesylate.	imatinib	108-125	AKT serine/threonine kinase 1	Homo sapiens	0-3
17169414-12	2007	CONCLUSIONS: This study demonstrates that KIT transduces anti-apoptotic signals and its inhibition with imatinib may represent a valuable therapeutic strategy for sensitizing chemoresistant ovarian cancer.	imatinib	104-112	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	42-45
17202400-0	2007	STI-571 (imatinib mesylate) enhances the apoptotic efficacy of pyrrolo-1,5-benzoxazepine-6, a novel microtubule-targeting agent, in both STI-571-sensitive and -resistant Bcr-Abl-positive human chronic myeloid leukemia cells.	imatinib	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-177
17624250-3	2007	Moreover, MPD5 elicited IgG antibody responses in a subset of PV patients who had benefited from a variety of therapies--including IFN-alpha, Hydroxyurea, Imatinib mesylate, Anagrelide, and phlebotomy--but not in untreated PV patients or healthy donors, suggesting that MPD5 is a PV-associated, therapy-related antigen.	imatinib	155-172	adenylosuccinate synthase 1	Homo sapiens	10-14
17384206-1	2007	Gastrointestinal stromal tumors (GISTs) frequently harbor mutations in the KIT and PDGFRA genes, the presence and type of which correlate with the response to the kinase inhibitor imatinib mesylate.	imatinib	180-197	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	75-78
17384206-1	2007	Gastrointestinal stromal tumors (GISTs) frequently harbor mutations in the KIT and PDGFRA genes, the presence and type of which correlate with the response to the kinase inhibitor imatinib mesylate.	imatinib	180-197	platelet derived growth factor receptor alpha	Homo sapiens	83-89
17381803-0	2007	Merkel cell carcinoma: evaluation of KIT (CD117) expression and failure to demonstrate activating mutations in the C-KIT proto-oncogene - implications for treatment with imatinib mesylate.	imatinib	170-187	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	115-120
17381803-2	2007	However, it is not known if MCCs have activating mutations in KIT that would make them responsive to treatment with imatinib mesylate.	imatinib	116-133	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	62-65
17381803-9	2007	Imatinib mesylate is unlikely to provide effective therapy in MCC unless activating mutations in other areas of KIT or activating mutations in other related genes can be detected.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	112-115
17202400-0	2007	STI-571 (imatinib mesylate) enhances the apoptotic efficacy of pyrrolo-1,5-benzoxazepine-6, a novel microtubule-targeting agent, in both STI-571-sensitive and -resistant Bcr-Abl-positive human chronic myeloid leukemia cells.	imatinib	9-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-177
17202400-1	2007	Interactions between the Bcr-Abl kinase inhibitor STI-571 (imatinib mesylate) and a novel microtubule-targeting agent (MTA), pyrrolo-1,5-benzoxazepine (PBOX)-6, were investigated in STI-571-sensitive and -resistant human chronic myeloid leukemia (CML) cells.	imatinib	50-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
17202400-1	2007	Interactions between the Bcr-Abl kinase inhibitor STI-571 (imatinib mesylate) and a novel microtubule-targeting agent (MTA), pyrrolo-1,5-benzoxazepine (PBOX)-6, were investigated in STI-571-sensitive and -resistant human chronic myeloid leukemia (CML) cells.	imatinib	59-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
17202400-2	2007	Cotreatment of PBOX-6 with STI-571 induced significantly more apoptosis in Bcr-Abl-positive CML cell lines (K562 and LAMA-84) than either drug alone (P < 0.01).	imatinib	27-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
17259998-0	2007	Juxtamembrane-type c-kit gene mutation found in aggressive systemic mastocytosis induces imatinib-resistant constitutive KIT activation.	imatinib	89-97	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	19-24
16916543-0	2007	Long-term remission in BCR/ABL-positive AML-M6 patient treated with Imatinib Mesylate.	imatinib	68-85	BCR activator of RhoGEF and GTPase	Homo sapiens	23-26
17259998-0	2007	Juxtamembrane-type c-kit gene mutation found in aggressive systemic mastocytosis induces imatinib-resistant constitutive KIT activation.	imatinib	89-97	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	121-124
16916543-0	2007	Long-term remission in BCR/ABL-positive AML-M6 patient treated with Imatinib Mesylate.	imatinib	68-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-30
17259998-7	2007	Imatinib, at a concentration of 10 microM, inhibited autophosphorylation of the mutant KIT with Val559Asp, but not that with the Val559Ile.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	87-90
16916543-2	2007	Here we report a case of BCR/ABL-positive AML-M6 who, after relapse, was treated with Imatinib Mesylate (600 mg/die) and within 4 months achieved a cytogenetic and molecular complete response.	imatinib	86-103	BCR activator of RhoGEF and GTPase	Homo sapiens	25-28
16916543-2	2007	Here we report a case of BCR/ABL-positive AML-M6 who, after relapse, was treated with Imatinib Mesylate (600 mg/die) and within 4 months achieved a cytogenetic and molecular complete response.	imatinib	86-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-32
16916543-3	2007	After more than 4 years of continuous Imatinib therapy, nested RT-PCR for BCR/ABL is persistently negative.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
17259998-8	2007	Phosphorylation of MAPK and STAT5 was also inhibited by imatinib at the same concentration, in cells expressing Val559Asp but not in those expressing Val559Ile.	imatinib	56-64	signal transducer and activator of transcription 5A	Homo sapiens	28-33
16916543-4	2007	The case reported shows that the response obtained with Imatinib Mesylate in BCR/ABL-positive AML may be long lasting, offering a chance of successful treatment for this poor prognosis group of patients.	imatinib	56-73	BCR activator of RhoGEF and GTPase	Homo sapiens	77-80
16916543-4	2007	The case reported shows that the response obtained with Imatinib Mesylate in BCR/ABL-positive AML may be long lasting, offering a chance of successful treatment for this poor prognosis group of patients.	imatinib	56-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-84
17259998-9	2007	These results suggest that different mutations, even at the same codon, in juxtamembrane domain of the c-kit gene show different inhibitory effects of imatinib, and that patients with GISTs or mast cell neoplasms possessing this Val559Ile mutation are resistant to imatinib therapy.	imatinib	151-159	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	103-108
17486696-0	2007	Not all c-kit mutations can be corrected by imatinib.	imatinib	44-52	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	8-13
17259998-9	2007	These results suggest that different mutations, even at the same codon, in juxtamembrane domain of the c-kit gene show different inhibitory effects of imatinib, and that patients with GISTs or mast cell neoplasms possessing this Val559Ile mutation are resistant to imatinib therapy.	imatinib	265-273	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	103-108
17363589-0	2007	Histone H2AX is a mediator of gastrointestinal stromal tumor cell apoptosis following treatment with imatinib mesylate.	imatinib	101-118	H2A.X variant histone	Homo sapiens	0-12
17454792-3	2007	This tyrosine kinase can be semi-selectively inhibited by signal transduction inhibitors such as imatinib mesylate (Glivec), which is a competitive inhibitor of c-kit, c-abl, platelet-derived growth factor receptor-alpha (PDGFR-alpha) and PDGFR-beta, and abl-related gene (arg).	imatinib	97-114	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	161-166
17454792-3	2007	This tyrosine kinase can be semi-selectively inhibited by signal transduction inhibitors such as imatinib mesylate (Glivec), which is a competitive inhibitor of c-kit, c-abl, platelet-derived growth factor receptor-alpha (PDGFR-alpha) and PDGFR-beta, and abl-related gene (arg).	imatinib	97-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	168-173
17454792-3	2007	This tyrosine kinase can be semi-selectively inhibited by signal transduction inhibitors such as imatinib mesylate (Glivec), which is a competitive inhibitor of c-kit, c-abl, platelet-derived growth factor receptor-alpha (PDGFR-alpha) and PDGFR-beta, and abl-related gene (arg).	imatinib	97-114	platelet derived growth factor receptor alpha	Homo sapiens	175-220
17454792-3	2007	This tyrosine kinase can be semi-selectively inhibited by signal transduction inhibitors such as imatinib mesylate (Glivec), which is a competitive inhibitor of c-kit, c-abl, platelet-derived growth factor receptor-alpha (PDGFR-alpha) and PDGFR-beta, and abl-related gene (arg).	imatinib	97-114	platelet derived growth factor receptor alpha	Homo sapiens	222-233
17454792-3	2007	This tyrosine kinase can be semi-selectively inhibited by signal transduction inhibitors such as imatinib mesylate (Glivec), which is a competitive inhibitor of c-kit, c-abl, platelet-derived growth factor receptor-alpha (PDGFR-alpha) and PDGFR-beta, and abl-related gene (arg).	imatinib	97-114	platelet derived growth factor receptor beta	Homo sapiens	239-249
17454792-3	2007	This tyrosine kinase can be semi-selectively inhibited by signal transduction inhibitors such as imatinib mesylate (Glivec), which is a competitive inhibitor of c-kit, c-abl, platelet-derived growth factor receptor-alpha (PDGFR-alpha) and PDGFR-beta, and abl-related gene (arg).	imatinib	116-122	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	161-166
17454792-3	2007	This tyrosine kinase can be semi-selectively inhibited by signal transduction inhibitors such as imatinib mesylate (Glivec), which is a competitive inhibitor of c-kit, c-abl, platelet-derived growth factor receptor-alpha (PDGFR-alpha) and PDGFR-beta, and abl-related gene (arg).	imatinib	116-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	168-173
17454792-3	2007	This tyrosine kinase can be semi-selectively inhibited by signal transduction inhibitors such as imatinib mesylate (Glivec), which is a competitive inhibitor of c-kit, c-abl, platelet-derived growth factor receptor-alpha (PDGFR-alpha) and PDGFR-beta, and abl-related gene (arg).	imatinib	116-122	platelet derived growth factor receptor alpha	Homo sapiens	175-220
17454792-3	2007	This tyrosine kinase can be semi-selectively inhibited by signal transduction inhibitors such as imatinib mesylate (Glivec), which is a competitive inhibitor of c-kit, c-abl, platelet-derived growth factor receptor-alpha (PDGFR-alpha) and PDGFR-beta, and abl-related gene (arg).	imatinib	116-122	platelet derived growth factor receptor alpha	Homo sapiens	222-233
17454792-3	2007	This tyrosine kinase can be semi-selectively inhibited by signal transduction inhibitors such as imatinib mesylate (Glivec), which is a competitive inhibitor of c-kit, c-abl, platelet-derived growth factor receptor-alpha (PDGFR-alpha) and PDGFR-beta, and abl-related gene (arg).	imatinib	116-122	platelet derived growth factor receptor beta	Homo sapiens	239-249
17138817-6	2007	Importantly, comparable responses were achieved by patients carrying BCR-ABL mutations conferring imatinib resistance.	imatinib	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
17461760-1	2007	Accumulating knowledge about the molecular mechanisms causing human diseases can support the development of targeted therapies such as imatinib, a BCR-ABL-specific tyrosine kinase inhibitor to treat chronic myeloid leukemia (CML).	imatinib	135-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-154
17461760-4	2007	We demonstrate that conventional anti-leukemic drugs have small or no differential effects under different cell culture conditions, whereas both imatinib and specific RNAi significantly inhibit proliferation of TonB cells in the presence of BCR-ABL but not IL-3.	imatinib	145-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	241-248
16919303-4	2007	Imatinib is the first member of a new class of agents that act by inhibiting particular tyrosin kinase enzymes, including KIT which is a product of the c-kit.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	122-125
16919303-4	2007	Imatinib is the first member of a new class of agents that act by inhibiting particular tyrosin kinase enzymes, including KIT which is a product of the c-kit.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	152-157
16919303-5	2007	In this study the efficacy of imatinib to reduce or abolish canine MCT [CMC-1] using xenografted MCT in severe combined immunodeficient [SCID] mice was evaluated.	imatinib	30-38	C-X9-C motif containing 1	Canis lupus familiaris	72-77
17493325-4	2007	After treatment with imatinib in mononuclear cell (MNC) of CML patients and K562 in vitro, expression of DNA-PKcs mRNA was detected by RT-PCR and DNA-PKcs protein level, tyrosine phosphorylation of bcr-abl fusion protein were detected by Western blot.	imatinib	21-29	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	105-113
17493325-4	2007	After treatment with imatinib in mononuclear cell (MNC) of CML patients and K562 in vitro, expression of DNA-PKcs mRNA was detected by RT-PCR and DNA-PKcs protein level, tyrosine phosphorylation of bcr-abl fusion protein were detected by Western blot.	imatinib	21-29	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	146-154
17493325-6	2007	In 26 CML patients received allo-PBSCT and 4 CML patients treated with imatinib, the expression of DNA-PKcs protein was enhanced while the expression of bcr-abl mRNA decreased.	imatinib	71-79	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	99-107
17493325-7	2007	After treatment of MNC of CML and K562 with imatinib in vitro, the expression of DNA-PKcs protein was enhanced while tyrosine phosphorylation of bcr-abl fusion protein decreased.	imatinib	44-52	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	81-89
17363589-5	2007	We found that untreated GIST cells down-regulate H2AX in a pathway that involves KIT, phosphoinositide-3-kinase, and the ubiquitin/proteasome machinery, and that the imatinib-mediated H2AX up-regulation correlates with imatinib sensitivity.	imatinib	219-227	H2A.X variant histone	Homo sapiens	184-188
17363589-6	2007	Depletion of H2AX attenuated the apoptotic response of GIST cells to imatinib.	imatinib	69-77	H2A.X variant histone	Homo sapiens	13-17
17363589-8	2007	Our results underscore the importance of H2AX as a human tumor suppressor protein, provide mechanistic insights into imatinib-induced tumor cell apoptosis and establish H2AX as a novel target in cancer therapy.	imatinib	117-125	H2A.X variant histone	Homo sapiens	41-45
17363589-8	2007	Our results underscore the importance of H2AX as a human tumor suppressor protein, provide mechanistic insights into imatinib-induced tumor cell apoptosis and establish H2AX as a novel target in cancer therapy.	imatinib	117-125	H2A.X variant histone	Homo sapiens	169-173
17363589-2	2007	GISTs can be successfully treated with imatinib mesylate, a selective small-molecule protein kinase inhibitor that was first clinically approved to target the oncogenic BCR-ABL fusion protein kinase in chronic myelogenous leukemia, but which also potently inhibits KIT and PDGFR family members.	imatinib	39-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	169-176
17363589-2	2007	GISTs can be successfully treated with imatinib mesylate, a selective small-molecule protein kinase inhibitor that was first clinically approved to target the oncogenic BCR-ABL fusion protein kinase in chronic myelogenous leukemia, but which also potently inhibits KIT and PDGFR family members.	imatinib	39-56	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	265-268
17363589-2	2007	GISTs can be successfully treated with imatinib mesylate, a selective small-molecule protein kinase inhibitor that was first clinically approved to target the oncogenic BCR-ABL fusion protein kinase in chronic myelogenous leukemia, but which also potently inhibits KIT and PDGFR family members.	imatinib	39-56	platelet derived growth factor receptor alpha	Homo sapiens	273-278
17363589-4	2007	We report here that imatinib triggers GIST cell apoptosis in part through the up-regulation of soluble histone H2AX, a core histone H2A variant.	imatinib	20-28	H2A.X variant histone	Homo sapiens	111-115
17363589-5	2007	We found that untreated GIST cells down-regulate H2AX in a pathway that involves KIT, phosphoinositide-3-kinase, and the ubiquitin/proteasome machinery, and that the imatinib-mediated H2AX up-regulation correlates with imatinib sensitivity.	imatinib	166-174	H2A.X variant histone	Homo sapiens	184-188
17363589-5	2007	We found that untreated GIST cells down-regulate H2AX in a pathway that involves KIT, phosphoinositide-3-kinase, and the ubiquitin/proteasome machinery, and that the imatinib-mediated H2AX up-regulation correlates with imatinib sensitivity.	imatinib	219-227	H2A.X variant histone	Homo sapiens	49-53
17360569-1	2007	The kinase inhibitor imatinib mesylate targeting the oncoprotein Bcr-Abl has revolutionized the treatment of chronic myeloid leukemia (CML).	imatinib	21-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
17360569-6	2007	We transplanted mice with bone marrow cells retrovirally infected with the Bcr-Abl oncogene and subsequently treated the animals with imatinib to select for leukemic cells in which the proviral integration had affected genes modulating the imatinib response.	imatinib	240-248	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
17360569-9	2007	Proviral integration near the RUNX3 promoter induced RUNX3 expression, and Bcr-Abl-positive cell lines with stable or inducible expression of RUNX1 or RUNX3 were protected from imatinib-induced apoptosis.	imatinib	177-185	RUNX family transcription factor 3	Homo sapiens	30-35
17360569-9	2007	Proviral integration near the RUNX3 promoter induced RUNX3 expression, and Bcr-Abl-positive cell lines with stable or inducible expression of RUNX1 or RUNX3 were protected from imatinib-induced apoptosis.	imatinib	177-185	RUNX family transcription factor 3	Homo sapiens	53-58
16953222-4	2007	Hck was found strongly phosphorylated in Tel-Abl-expressing Ba/F3 cells and sensitive to imatinib mesylate treatment, providing evidence that Hck is a target of Tel-Abl tyrosine kinase activity.	imatinib	89-106	hemopoietic cell kinase	Mus musculus	0-3
16953222-4	2007	Hck was found strongly phosphorylated in Tel-Abl-expressing Ba/F3 cells and sensitive to imatinib mesylate treatment, providing evidence that Hck is a target of Tel-Abl tyrosine kinase activity.	imatinib	89-106	ets variant 6	Mus musculus	41-44
16953222-4	2007	Hck was found strongly phosphorylated in Tel-Abl-expressing Ba/F3 cells and sensitive to imatinib mesylate treatment, providing evidence that Hck is a target of Tel-Abl tyrosine kinase activity.	imatinib	89-106	hemopoietic cell kinase	Mus musculus	142-145
17360569-9	2007	Proviral integration near the RUNX3 promoter induced RUNX3 expression, and Bcr-Abl-positive cell lines with stable or inducible expression of RUNX1 or RUNX3 were protected from imatinib-induced apoptosis.	imatinib	177-185	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
16953222-4	2007	Hck was found strongly phosphorylated in Tel-Abl-expressing Ba/F3 cells and sensitive to imatinib mesylate treatment, providing evidence that Hck is a target of Tel-Abl tyrosine kinase activity.	imatinib	89-106	ets variant 6	Mus musculus	161-164
17360569-9	2007	Proviral integration near the RUNX3 promoter induced RUNX3 expression, and Bcr-Abl-positive cell lines with stable or inducible expression of RUNX1 or RUNX3 were protected from imatinib-induced apoptosis.	imatinib	177-185	RUNX family transcription factor 1	Homo sapiens	142-147
17360569-9	2007	Proviral integration near the RUNX3 promoter induced RUNX3 expression, and Bcr-Abl-positive cell lines with stable or inducible expression of RUNX1 or RUNX3 were protected from imatinib-induced apoptosis.	imatinib	177-185	RUNX family transcription factor 3	Homo sapiens	53-58
17360569-10	2007	Furthermore, imatinib treatment selected for RUNX1-expressing cells in vitro and in vivo after infection of primary bone marrow cells with Bcr-Abl and RUNX1.	imatinib	13-21	RUNX family transcription factor 1	Homo sapiens	45-50
17360569-10	2007	Furthermore, imatinib treatment selected for RUNX1-expressing cells in vitro and in vivo after infection of primary bone marrow cells with Bcr-Abl and RUNX1.	imatinib	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-146
17360569-10	2007	Furthermore, imatinib treatment selected for RUNX1-expressing cells in vitro and in vivo after infection of primary bone marrow cells with Bcr-Abl and RUNX1.	imatinib	13-21	RUNX family transcription factor 1	Homo sapiens	151-156
17318191-6	2007	Imatinib, a Bcr-Abl antagonist, impairs the beta-catenin/TCF-related transcription causing a rapid cytosolic retention of Y-unphosphorylated beta-catenin, which presents an increased binding affinity for the Axin/GSK3beta complex.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
17318191-6	2007	Imatinib, a Bcr-Abl antagonist, impairs the beta-catenin/TCF-related transcription causing a rapid cytosolic retention of Y-unphosphorylated beta-catenin, which presents an increased binding affinity for the Axin/GSK3beta complex.	imatinib	0-8	catenin beta 1	Homo sapiens	44-56
17318191-6	2007	Imatinib, a Bcr-Abl antagonist, impairs the beta-catenin/TCF-related transcription causing a rapid cytosolic retention of Y-unphosphorylated beta-catenin, which presents an increased binding affinity for the Axin/GSK3beta complex.	imatinib	0-8	hepatocyte nuclear factor 4 alpha	Homo sapiens	57-60
17318191-6	2007	Imatinib, a Bcr-Abl antagonist, impairs the beta-catenin/TCF-related transcription causing a rapid cytosolic retention of Y-unphosphorylated beta-catenin, which presents an increased binding affinity for the Axin/GSK3beta complex.	imatinib	0-8	catenin beta 1	Homo sapiens	141-153
17318191-6	2007	Imatinib, a Bcr-Abl antagonist, impairs the beta-catenin/TCF-related transcription causing a rapid cytosolic retention of Y-unphosphorylated beta-catenin, which presents an increased binding affinity for the Axin/GSK3beta complex.	imatinib	0-8	axin 1	Homo sapiens	208-212
17318191-6	2007	Imatinib, a Bcr-Abl antagonist, impairs the beta-catenin/TCF-related transcription causing a rapid cytosolic retention of Y-unphosphorylated beta-catenin, which presents an increased binding affinity for the Axin/GSK3beta complex.	imatinib	0-8	glycogen synthase kinase 3 beta	Homo sapiens	213-221
17318191-8	2007	Silencing of beta-catenin by small interfering RNA inhibited proliferation and clonogenicity of Bcr-Abl(+) CML cells, in synergism with Imatinib.	imatinib	136-144	catenin beta 1	Homo sapiens	13-25
17068153-2	2007	The BCR-ABL inhibitor, nilotinib (AMN107), is significantly more potent against BCR-ABL than imatinib, and is active against many imatinib-resistant BCR-ABL mutants.	imatinib	130-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
17195905-1	2007	PURPOSE: Most gastrointestinal stromal tumors (GISTs) express constitutively activated mutation of kit or platelet-derived growth factor receptor alpha (PDGFRA), which are therapeutic targets for imatinib.	imatinib	196-204	platelet derived growth factor receptor alpha	Homo sapiens	106-151
17195905-1	2007	PURPOSE: Most gastrointestinal stromal tumors (GISTs) express constitutively activated mutation of kit or platelet-derived growth factor receptor alpha (PDGFRA), which are therapeutic targets for imatinib.	imatinib	196-204	platelet derived growth factor receptor alpha	Homo sapiens	153-159
17068153-1	2007	Drug resistance resulting from emergence of imatinib-resistant BCR-ABL point mutations is a significant problem in advanced-stage chronic myelogenous leukemia (CML).	imatinib	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
17068153-2	2007	The BCR-ABL inhibitor, nilotinib (AMN107), is significantly more potent against BCR-ABL than imatinib, and is active against many imatinib-resistant BCR-ABL mutants.	imatinib	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
17068153-5	2007	Here, we show that exposure of a variety of BCR-ABL+ cell lines to imatinib and nilotinib results in additive or synergistic cytotoxicity, including testing of a large panel of cells expressing BCR-ABL point mutations causing resistance to imatinib in patients.	imatinib	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
17068153-5	2007	Here, we show that exposure of a variety of BCR-ABL+ cell lines to imatinib and nilotinib results in additive or synergistic cytotoxicity, including testing of a large panel of cells expressing BCR-ABL point mutations causing resistance to imatinib in patients.	imatinib	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	194-201
17285599-1	2007	BACKGROUND: Imatinib (IM) is a potent tyrosine kinase inhibitor of c-Kit.	imatinib	12-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	67-72
17068153-5	2007	Here, we show that exposure of a variety of BCR-ABL+ cell lines to imatinib and nilotinib results in additive or synergistic cytotoxicity, including testing of a large panel of cells expressing BCR-ABL point mutations causing resistance to imatinib in patients.	imatinib	240-248	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
17068153-7	2007	These results suggest that despite binding to the same site in the same target kinase, the combination of imatinib and nilotinib is highly efficacious in these models, indicating that clinical testing of combinations of BCR-ABL kinase inhibitors is warranted.	imatinib	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	220-227
17090651-0	2007	Adaptive secretion of granulocyte-macrophage colony-stimulating factor (GM-CSF) mediates imatinib and nilotinib resistance in BCR/ABL+ progenitors via JAK-2/STAT-5 pathway activation.	imatinib	89-97	colony stimulating factor 2	Homo sapiens	22-70
17090651-0	2007	Adaptive secretion of granulocyte-macrophage colony-stimulating factor (GM-CSF) mediates imatinib and nilotinib resistance in BCR/ABL+ progenitors via JAK-2/STAT-5 pathway activation.	imatinib	89-97	colony stimulating factor 2	Homo sapiens	72-78
17382013-4	2007	The Bcr-Abl tyrosine kinase inhibitor imatinib represented a major advance over conventional CML therapy.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
17382021-1	2007	In 2006, most newly diagnosed patients with chronic myeloid leukemia (CML) underwent first-line, molecular-targeted therapy with the Bcr-Abl tyrosine kinase inhibitor, imatinib.	imatinib	168-176	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
17382021-3	2007	Studies of patients with acquired imatinib resistance revealed that Bcr-Abl signaling is reactivated at the time of resistance, predominantly because of mutations that interfere with drug binding in the kinase domain of Bcr-Abl.	imatinib	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
17382021-3	2007	Studies of patients with acquired imatinib resistance revealed that Bcr-Abl signaling is reactivated at the time of resistance, predominantly because of mutations that interfere with drug binding in the kinase domain of Bcr-Abl.	imatinib	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	220-227
17382021-4	2007	The knowledge that Bcr-Abl remains the optimal target for treating imatinib-refractory CML has driven an already highly successful search for alternative approaches to restore target inhibition.	imatinib	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
17382021-5	2007	Here, we review the current state of affairs in the realm of controlling drug resistance in CML, including cutting-edge strategies to reign in Bcr-AblT315I, which is cross resistant to imatinib, as well as the "next generation" Bcr-Abl inhibitors, nilotinib and dasatinib.	imatinib	185-193	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-150
17382023-3	2007	For patients who develop resistance to imatinib, the Bcr-Abl signaling pathway is often re-activated, second generation tyrosine kinase inhibitors, such as dasatinib or nilotinib, might restore the kinase inhibition.	imatinib	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
17339191-1	2007	The emergence of resistance to the Bcr-Abl inhibitor imatinib mesylate in patients with Philadelphia chromosome-positive (Ph+) leukemia has prompted the development of second-generation compounds active against several imatinib-insensitive mutant forms of Bcr-Abl, including dasatinib (BMS-354825; Bristol-Myers Squibb).	imatinib	53-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
17338645-0	2007	Imatinib mesylate, a selective inhibitor of BCR-ABL, in chronic myeloid leukemia.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
17355219-3	2007	One of the most clear examples is the identification of KIT and platelet-derived growth factor receptor-alpha kinase mutations in gastrointestinal stromal tumours, a subset of sarcomas arising from precursors of the interstitial cells of Cajal in the digestive tract, which led to the development of imatinib, sunitinib and other tyrosine kinase inhibitors for the treatment of solid tumours.	imatinib	300-308	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	56-59
17355219-3	2007	One of the most clear examples is the identification of KIT and platelet-derived growth factor receptor-alpha kinase mutations in gastrointestinal stromal tumours, a subset of sarcomas arising from precursors of the interstitial cells of Cajal in the digestive tract, which led to the development of imatinib, sunitinib and other tyrosine kinase inhibitors for the treatment of solid tumours.	imatinib	300-308	platelet derived growth factor receptor alpha	Homo sapiens	64-109
17355221-4	2007	The addition of imatinib in patients with BCR-ABL-positive ALL has improved the prognosis of this subgroup, but their survival is still poor.	imatinib	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
17049587-3	2007	The primary target of imatinib is c-kit, but the drug also inhibits PDGFR-alpha and PDGFR-beta.	imatinib	22-30	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	34-39
17049587-3	2007	The primary target of imatinib is c-kit, but the drug also inhibits PDGFR-alpha and PDGFR-beta.	imatinib	22-30	platelet derived growth factor receptor alpha	Homo sapiens	68-79
17049587-3	2007	The primary target of imatinib is c-kit, but the drug also inhibits PDGFR-alpha and PDGFR-beta.	imatinib	22-30	platelet derived growth factor receptor beta	Homo sapiens	84-94
17339191-1	2007	The emergence of resistance to the Bcr-Abl inhibitor imatinib mesylate in patients with Philadelphia chromosome-positive (Ph+) leukemia has prompted the development of second-generation compounds active against several imatinib-insensitive mutant forms of Bcr-Abl, including dasatinib (BMS-354825; Bristol-Myers Squibb).	imatinib	53-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	256-263
17339191-1	2007	The emergence of resistance to the Bcr-Abl inhibitor imatinib mesylate in patients with Philadelphia chromosome-positive (Ph+) leukemia has prompted the development of second-generation compounds active against several imatinib-insensitive mutant forms of Bcr-Abl, including dasatinib (BMS-354825; Bristol-Myers Squibb).	imatinib	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
17339191-1	2007	The emergence of resistance to the Bcr-Abl inhibitor imatinib mesylate in patients with Philadelphia chromosome-positive (Ph+) leukemia has prompted the development of second-generation compounds active against several imatinib-insensitive mutant forms of Bcr-Abl, including dasatinib (BMS-354825; Bristol-Myers Squibb).	imatinib	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	256-263
17229817-7	2007	Inhibition of c-Abl activity by STI571 in normal BM cultures significantly increased apoptosis in B cell precursors while the survival of immature B cells was not affected.	imatinib	32-38	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	14-19
17131346-2	2007	To date however, there are no reports on the activity of imatinib mesylate, a selective PDGFR inhibitor, in RMS preclinical models.	imatinib	57-74	platelet derived growth factor receptor beta	Homo sapiens	88-93
17131346-3	2007	A panel of 5 RMS cell lines was used to investigate the expression of PDGFRalpha and PDGFRbeta, c-Kit and the multidrug transporter ABCG2 (also inhibited by imatinib).	imatinib	157-165	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	132-137
17131346-8	2007	Significant ABCG2-mediated extrusion of Hoechst 33342 was demonstrated in RH30 but not in RD, and was inhibited by imatinib and the specific ABCG2 inhibitor Ko143.	imatinib	115-123	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	12-17
17131346-8	2007	Significant ABCG2-mediated extrusion of Hoechst 33342 was demonstrated in RH30 but not in RD, and was inhibited by imatinib and the specific ABCG2 inhibitor Ko143.	imatinib	115-123	Rh blood group D antigen	Homo sapiens	74-78
17131346-11	2007	These results suggest that at least 2 different mechanisms--inhibition of ABCG2 and/or PDGFRbeta--are involved in the synergistic interaction between imatinib and TPT, and support the use of this combination for the treatment of high-risk RMS patients.	imatinib	150-158	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	74-79
17131346-11	2007	These results suggest that at least 2 different mechanisms--inhibition of ABCG2 and/or PDGFRbeta--are involved in the synergistic interaction between imatinib and TPT, and support the use of this combination for the treatment of high-risk RMS patients.	imatinib	150-158	platelet derived growth factor receptor beta	Homo sapiens	87-96
17327598-0	2007	Imatinib in melanoma: a selective treatment option based on KIT mutation status?	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	60-63
17551678-8	2007	Novel therapeutic options theoretically devoid of leukaemic risk, such as alpha-interferon and imatinib, affect JAK2 expression in some patients.	imatinib	95-103	Janus kinase 2	Homo sapiens	112-116
17329198-0	2007	Second-line treatment with dasatinib in patients resistant to imatinib can select novel inhibitor-specific BCR-ABL mutants in Ph+ ALL.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
17309464-1	2007	BACKGROUND: Imatinib mesylate (IM), the first-line treatment of chronic myeloid leukaemia (CML), is a tyrosine kinase inhibitor that targets those proteins involved in BCR-ABL signal transduction in CML, c-kit (KIT) and platelet-derived growth-factor (PDGFR) receptor.	imatinib	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	168-175
17309464-1	2007	BACKGROUND: Imatinib mesylate (IM), the first-line treatment of chronic myeloid leukaemia (CML), is a tyrosine kinase inhibitor that targets those proteins involved in BCR-ABL signal transduction in CML, c-kit (KIT) and platelet-derived growth-factor (PDGFR) receptor.	imatinib	12-29	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	204-209
17309464-1	2007	BACKGROUND: Imatinib mesylate (IM), the first-line treatment of chronic myeloid leukaemia (CML), is a tyrosine kinase inhibitor that targets those proteins involved in BCR-ABL signal transduction in CML, c-kit (KIT) and platelet-derived growth-factor (PDGFR) receptor.	imatinib	12-29	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	211-214
17252009-0	2007	Mutations of the BCR-ABL-kinase domain occur in a minority of patients with stable complete cytogenetic response to imatinib.	imatinib	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
17252009-2	2007	In patients who relapse during imatinib therapy, a high rate of mutations in the kinase domain of BCR-ABL have been identified, but the mechanisms underlying disease persistence in patients with a CCR are poorly characterized.	imatinib	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
17252018-1	2007	Imatinib mesylate is a selective inhibitor of the oncogenic tyrosine kinase, Bcr-Abl, and is widely used as a first-line treatment for chronic myeloid leukaemia (CML).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
17373201-6	2007	Dasatinib is a multi-targeted tyrosine kinase inhibitor active in vitro against most cell lines containing BCR-ABL mutations that confer resistance to imatinib.	imatinib	151-159	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
17294421-12	2007	Endothelial cell and tumour cell expression of activated KIT might explain in part the responsiveness of glioblastomas to the combination of imatinib (an inhibitor of KIT) and hydroxyurea.	imatinib	141-149	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	57-60
17294421-12	2007	Endothelial cell and tumour cell expression of activated KIT might explain in part the responsiveness of glioblastomas to the combination of imatinib (an inhibitor of KIT) and hydroxyurea.	imatinib	141-149	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	167-170
17215855-8	2007	This study provided evidence for marked differences in the leukemic masses which are targeted by imatinib in CEL or CML, as harboring FIP1L1-PDGFRA or BCR-ABL1.	imatinib	97-105	factor interacting with PAPOLA and CPSF1	Homo sapiens	134-140
17215855-8	2007	This study provided evidence for marked differences in the leukemic masses which are targeted by imatinib in CEL or CML, as harboring FIP1L1-PDGFRA or BCR-ABL1.	imatinib	97-105	platelet derived growth factor receptor alpha	Homo sapiens	141-147
17215855-8	2007	This study provided evidence for marked differences in the leukemic masses which are targeted by imatinib in CEL or CML, as harboring FIP1L1-PDGFRA or BCR-ABL1.	imatinib	97-105	BCR activator of RhoGEF and GTPase	Homo sapiens	151-159
17363509-3	2007	The kinase inhibitor imatinib potently inhibits c-KIT and is approved for treatment of GIST.	imatinib	21-29	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	48-53
17363509-12	2007	Analysis of the crystal structure of imatinib in complex with the kinase domain of c-KIT predicts that the V654A substitution directly affects the binding of imatinib to the receptor.	imatinib	37-45	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	83-88
17355866-0	2007	c-Src binds to the cancer drug imatinib with an inactive Abl/c-Kit conformation and a distributed thermodynamic penalty.	imatinib	31-39	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	0-5
17363509-12	2007	Analysis of the crystal structure of imatinib in complex with the kinase domain of c-KIT predicts that the V654A substitution directly affects the binding of imatinib to the receptor.	imatinib	158-166	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	83-88
17363509-13	2007	Alternative c-KIT inhibitors, nilotinib (AMN107) and PKC412, were also less active on V560G/V654A c-KIT than on the V560G single mutant; however, nilotinib, like imatinib, potently inhibited the V560G mutant.	imatinib	162-170	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	12-17
17363509-14	2007	PKC412 strongly inhibited imatinib-resistant D816V c-KIT.	imatinib	26-34	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	51-56
17582306-1	2007	Imatinib (Glivec) is a specific inhibitor of tyrosine kinase receptor, in particular of the proto-oncogene c-kit.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	92-112
17582306-1	2007	Imatinib (Glivec) is a specific inhibitor of tyrosine kinase receptor, in particular of the proto-oncogene c-kit.	imatinib	10-16	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	92-112
17355866-2	2007	Imatinib is less effective against c-Src, which is difficult to understand because residues interacting with imatinib in crystal structures of Abl and c-Kit are conserved in c-Src.	imatinib	0-8	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	174-179
17355866-0	2007	c-Src binds to the cancer drug imatinib with an inactive Abl/c-Kit conformation and a distributed thermodynamic penalty.	imatinib	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-60
17355866-2	2007	Imatinib is less effective against c-Src, which is difficult to understand because residues interacting with imatinib in crystal structures of Abl and c-Kit are conserved in c-Src.	imatinib	109-117	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	35-40
17355866-0	2007	c-Src binds to the cancer drug imatinib with an inactive Abl/c-Kit conformation and a distributed thermodynamic penalty.	imatinib	31-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	61-66
17355866-2	2007	Imatinib is less effective against c-Src, which is difficult to understand because residues interacting with imatinib in crystal structures of Abl and c-Kit are conserved in c-Src.	imatinib	109-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-146
17355866-2	2007	Imatinib is less effective against c-Src, which is difficult to understand because residues interacting with imatinib in crystal structures of Abl and c-Kit are conserved in c-Src.	imatinib	109-117	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	151-156
17355866-1	2007	The cancer drug imatinib inhibits the tyrosine kinases c-Abl, c-Kit, and the PDGF receptor.	imatinib	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-60
17355866-3	2007	The crystal structure of the c-Src kinase domain in complex with imatinib closely resembles that of Abl*imatinib and c-Kit*imatinib, and differs significantly from the inactive "Src/CDK" conformation of the Src family kinases.	imatinib	65-73	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	29-34
17355866-1	2007	The cancer drug imatinib inhibits the tyrosine kinases c-Abl, c-Kit, and the PDGF receptor.	imatinib	16-24	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	62-67
17355866-3	2007	The crystal structure of the c-Src kinase domain in complex with imatinib closely resembles that of Abl*imatinib and c-Kit*imatinib, and differs significantly from the inactive "Src/CDK" conformation of the Src family kinases.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-103
17355866-3	2007	The crystal structure of the c-Src kinase domain in complex with imatinib closely resembles that of Abl*imatinib and c-Kit*imatinib, and differs significantly from the inactive "Src/CDK" conformation of the Src family kinases.	imatinib	65-73	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	117-122
17382158-13	2007	CONCLUSIONS: The results of our study have demonstrated that imatinib mesylate delivered at a dose of 400 mg twice daily is associated with a moderate degree of toxicity and a limited PSA response in this patient population.	imatinib	61-78	kallikrein related peptidase 3	Homo sapiens	184-187
17355866-2	2007	Imatinib is less effective against c-Src, which is difficult to understand because residues interacting with imatinib in crystal structures of Abl and c-Kit are conserved in c-Src.	imatinib	0-8	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	35-40
17355866-3	2007	The crystal structure of the c-Src kinase domain in complex with imatinib closely resembles that of Abl*imatinib and c-Kit*imatinib, and differs significantly from the inactive "Src/CDK" conformation of the Src family kinases.	imatinib	65-73	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	31-34
17355866-3	2007	The crystal structure of the c-Src kinase domain in complex with imatinib closely resembles that of Abl*imatinib and c-Kit*imatinib, and differs significantly from the inactive "Src/CDK" conformation of the Src family kinases.	imatinib	65-73	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	178-181
17355866-2	2007	Imatinib is less effective against c-Src, which is difficult to understand because residues interacting with imatinib in crystal structures of Abl and c-Kit are conserved in c-Src.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-146
17355866-3	2007	The crystal structure of the c-Src kinase domain in complex with imatinib closely resembles that of Abl*imatinib and c-Kit*imatinib, and differs significantly from the inactive "Src/CDK" conformation of the Src family kinases.	imatinib	104-112	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	29-34
17355866-2	2007	Imatinib is less effective against c-Src, which is difficult to understand because residues interacting with imatinib in crystal structures of Abl and c-Kit are conserved in c-Src.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	151-156
17355866-3	2007	The crystal structure of the c-Src kinase domain in complex with imatinib closely resembles that of Abl*imatinib and c-Kit*imatinib, and differs significantly from the inactive "Src/CDK" conformation of the Src family kinases.	imatinib	104-112	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	31-34
17355866-3	2007	The crystal structure of the c-Src kinase domain in complex with imatinib closely resembles that of Abl*imatinib and c-Kit*imatinib, and differs significantly from the inactive "Src/CDK" conformation of the Src family kinases.	imatinib	104-112	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	29-34
17355866-3	2007	The crystal structure of the c-Src kinase domain in complex with imatinib closely resembles that of Abl*imatinib and c-Kit*imatinib, and differs significantly from the inactive "Src/CDK" conformation of the Src family kinases.	imatinib	104-112	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	31-34
17355866-4	2007	Attempts to increase the affinity of c-Src for imatinib by swapping residues with the corresponding residues in Abl have not been successful, suggesting that the thermodynamic penalty for adoption of the imatinib-binding conformation by c-Src is distributed over a broad region of the structure.	imatinib	47-55	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	37-42
17355866-4	2007	Attempts to increase the affinity of c-Src for imatinib by swapping residues with the corresponding residues in Abl have not been successful, suggesting that the thermodynamic penalty for adoption of the imatinib-binding conformation by c-Src is distributed over a broad region of the structure.	imatinib	204-212	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	37-42
17355866-5	2007	Two mutations that are expected to destabilize the inactive Src/CDK conformation increase drug sensitivity 15-fold, suggesting that the free-energy balance between different inactive states is a key to imatinib binding.	imatinib	202-210	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	60-63
17008552-1	2007	Inhibition of BCR-ABL tyrosine kinase with imatinib represents a major breakthrough in the treatment of patients with chronic myeloid leukemia (CML).	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
16936779-4	2007	Experiments with rapamycin and the Bcr-Abl inhibitor, imatinib mesylate, in Bcr-Abl-expressing cell lines and primary CML cells indicated that Bcr-Abl and mTORC1 induced formation of the translation initiation complex, eIF4F.	imatinib	54-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
16936779-4	2007	Experiments with rapamycin and the Bcr-Abl inhibitor, imatinib mesylate, in Bcr-Abl-expressing cell lines and primary CML cells indicated that Bcr-Abl and mTORC1 induced formation of the translation initiation complex, eIF4F.	imatinib	54-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
16936779-4	2007	Experiments with rapamycin and the Bcr-Abl inhibitor, imatinib mesylate, in Bcr-Abl-expressing cell lines and primary CML cells indicated that Bcr-Abl and mTORC1 induced formation of the translation initiation complex, eIF4F.	imatinib	54-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
16936779-4	2007	Experiments with rapamycin and the Bcr-Abl inhibitor, imatinib mesylate, in Bcr-Abl-expressing cell lines and primary CML cells indicated that Bcr-Abl and mTORC1 induced formation of the translation initiation complex, eIF4F.	imatinib	54-71	CREB regulated transcription coactivator 1	Mus musculus	155-161
16936779-4	2007	Experiments with rapamycin and the Bcr-Abl inhibitor, imatinib mesylate, in Bcr-Abl-expressing cell lines and primary CML cells indicated that Bcr-Abl and mTORC1 induced formation of the translation initiation complex, eIF4F.	imatinib	54-71	eukaryotic translation initiation factor 4E	Homo sapiens	219-224
16936779-8	2007	These experiments establish a novel mechanism of action for Bcr-Abl, and they provide insights into the modes of action of imatinib mesylate and rapamycin in treatment of CML.	imatinib	123-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
17360660-1	2007	Gastrointestinal stromal tumor (GIST) has emerged as a clinically distinct type of sarcoma with frequent overexpression and mutation of the c-Kit oncogene and a favorable response to imatinib mesylate [also known as STI571 (Gleevec)] therapy.	imatinib	183-200	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	140-145
17008552-3	2007	To identify new cellular BCR-ABL downstream targets, we analyzed differences in global protein expression in BCR-ABL-positive K562 cells treated with or without imatinib in vitro.	imatinib	161-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
17008552-3	2007	To identify new cellular BCR-ABL downstream targets, we analyzed differences in global protein expression in BCR-ABL-positive K562 cells treated with or without imatinib in vitro.	imatinib	161-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
17008552-7	2007	However, the synergistic dose-response relationship found for the combination of imatinib and HI was restricted to Bcr-Abl-positive cells.	imatinib	81-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
17008552-9	2007	Specificity of this effect could be demonstrated by cotreatment of K562 cells with imatinib and siRNA against eIF5.	imatinib	83-91	eukaryotic translation initiation factor 5	Homo sapiens	110-114
17240308-0	2007	KIT-negative undifferentiated endometrial sarcoma with the amplified epidermal growth factor receptor gene showing a temporary response to imatinib mesylate.	imatinib	139-156	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
17277106-0	2007	Imatinib mesylate inhibits antigen-specific memory CD8 T cell responses in vivo.	imatinib	0-17	CD8a molecule	Homo sapiens	51-54
17139461-0	2007	Surgical management after neoadjuvant imatinib therapy in gastrointestinal stromal tumours (GISTs) with respect to imatinib resistance caused by secondary KIT mutations.	imatinib	115-123	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	155-158
17139461-1	2007	BACKGROUND: In metastasized GISTs, resistance to imatinib after initial tumour response has been associated with observation of secondary mutations in the activation loop of KIT.	imatinib	49-57	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	174-177
17139461-2	2007	The aim of the current study was to evaluate the tumour response and observance of secondary KIT mutations in a case of GIST undergoing neoadjuvant imatinib therapy.	imatinib	148-156	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	93-96
17139461-10	2007	Since resistance relevant secondary mutations of the activation loop of KIT may be observed after neoadjuvant imatinib therapy, the time elapse with preoperative imatinib therapy should be chosen as short as curative tumour resection or function sparing surgery can be carried out.	imatinib	110-118	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	72-75
17240308-0	2007	KIT-negative undifferentiated endometrial sarcoma with the amplified epidermal growth factor receptor gene showing a temporary response to imatinib mesylate.	imatinib	139-156	epidermal growth factor receptor	Homo sapiens	69-101
17139461-10	2007	Since resistance relevant secondary mutations of the activation loop of KIT may be observed after neoadjuvant imatinib therapy, the time elapse with preoperative imatinib therapy should be chosen as short as curative tumour resection or function sparing surgery can be carried out.	imatinib	162-170	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	72-75
17240308-5	2007	Multiple regional recurrences around the urinary bladder were noted after 5 months, and treatment with imatinib mesylate was started, based on the provisional interpretation of KIT immunoreactivity on a biopsy specimen of the recurrent tumor.	imatinib	103-120	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	177-180
17240308-12	2007	We speculated that imatinib was temporarily effective on the clone with amplified EGFR, and that it became ineffective after this clone was eradicated.	imatinib	19-27	epidermal growth factor receptor	Homo sapiens	82-86
17305499-6	2007	Imatinib induces high response rates in patients associated with constitutive activation of ABL, PDGFRalpha, PDGFRbeta and some KIT mutants.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-95
17218776-5	2007	Treatment with either PD16839, an EGFr antagonist, or imatinib mesylate (Gleevec), a PDGFr, c-kit and bcr/abl antagonist, enhanced the anti-proliferative effects of rapamycin.	imatinib	54-71	platelet derived growth factor receptor beta	Homo sapiens	85-90
17218776-5	2007	Treatment with either PD16839, an EGFr antagonist, or imatinib mesylate (Gleevec), a PDGFr, c-kit and bcr/abl antagonist, enhanced the anti-proliferative effects of rapamycin.	imatinib	54-71	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	92-97
17208434-2	2007	These rare neoplasms are remarkably sensitive to the KIT and PDGFRA kinase inhibitors imatinib (also known as Gleevec) and sunitinib (Sutent), which have recently been approved as the standard therapeutic courses for patients with inoperable GIST.	imatinib	86-94	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	53-56
17208434-2	2007	These rare neoplasms are remarkably sensitive to the KIT and PDGFRA kinase inhibitors imatinib (also known as Gleevec) and sunitinib (Sutent), which have recently been approved as the standard therapeutic courses for patients with inoperable GIST.	imatinib	86-94	platelet derived growth factor receptor alpha	Homo sapiens	61-67
17208434-4	2007	Imatinib and sunitinib resistance generally result from secondary mutations in the KIT and/or PDGFRA kinase domains.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	83-86
17208434-4	2007	Imatinib and sunitinib resistance generally result from secondary mutations in the KIT and/or PDGFRA kinase domains.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	94-100
17305499-6	2007	Imatinib induces high response rates in patients associated with constitutive activation of ABL, PDGFRalpha, PDGFRbeta and some KIT mutants.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	97-107
17305499-6	2007	Imatinib induces high response rates in patients associated with constitutive activation of ABL, PDGFRalpha, PDGFRbeta and some KIT mutants.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	109-118
17305499-6	2007	Imatinib induces high response rates in patients associated with constitutive activation of ABL, PDGFRalpha, PDGFRbeta and some KIT mutants.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	128-131
17305499-7	2007	Other inhibitors under development are promising candidates for effective treatment of patients with constitutive activation of JAK2, FGFR1 and imatinib-resistant KIT mutants.	imatinib	144-152	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	163-166
17364993-3	2007	Imatinib blocks proliferation and induces apoptosis of BCR-ABL-expression in CML.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
17296563-8	2007	Of note, in CP-CML, extensive HAGE hypomethylation was associated with poorer prognosis in terms of cytogenetic response to interferon (p=0.01) or imatinib (p=0.01), molecular response to imatinib (p=0.003) and progression-free survival (p=0.05).	imatinib	147-155	DEAD-box helicase 43	Homo sapiens	30-34
17296563-8	2007	Of note, in CP-CML, extensive HAGE hypomethylation was associated with poorer prognosis in terms of cytogenetic response to interferon (p=0.01) or imatinib (p=0.01), molecular response to imatinib (p=0.003) and progression-free survival (p=0.05).	imatinib	188-196	DEAD-box helicase 43	Homo sapiens	30-34
17296564-0	2007	Characterization of three new imatinib-responsive fusion genes in chronic myeloproliferative disorders generated by disruption of the platelet-derived growth factor receptor beta gene.	imatinib	30-38	platelet derived growth factor receptor beta	Homo sapiens	134-178
17135364-5	2007	The imatinib effect was mimicked by siRNA-mediated knockdown of c-Abl mRNA.	imatinib	4-12	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	64-69
17301549-0	2007	[Innovation of clinical trials for anti-cancer drugs in Japan--proposals from academia with special reference to the development of novel Bcr-Abl/Lyn tyrosine kinase inhibitor INNO-406 (NS-187) for imatinib-resistant chronic myelogenous leukemia].	imatinib	198-206	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
17301549-0	2007	[Innovation of clinical trials for anti-cancer drugs in Japan--proposals from academia with special reference to the development of novel Bcr-Abl/Lyn tyrosine kinase inhibitor INNO-406 (NS-187) for imatinib-resistant chronic myelogenous leukemia].	imatinib	198-206	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	146-149
17203222-0	2007	STI571 sensitizes nasopharyngeal carcinoma cells to cisplatin: sustained activation of ERK with improved growth inhibition.	imatinib	0-6	mitogen-activated protein kinase 1	Homo sapiens	87-90
17203222-6	2007	The effects of STI571 were shown to be mediated by the sustained activation of ERK but did not involve the inhibition of c-kit signal activity.	imatinib	15-21	mitogen-activated protein kinase 1	Homo sapiens	79-82
17203222-7	2007	When the STI571 (5 microM) and cisplatin (5 microg/ml) treatments were combined, there were further inductions of ERK activation resulting in obviously enhanced growth inhibition and induction of cell apoptosis.	imatinib	9-15	mitogen-activated protein kinase 1	Homo sapiens	114-117
17132628-7	2007	Inhibition of Bcr-Abl by the chemical inhibitor STI571 resulted in activation of FOXO3a and down-regulation of Id1 expression.	imatinib	48-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
17490518-11	2007	The percentage of apoptotic cells greatly increased after transfection with p15-pcDNA3.1-K562 cells combined with imatinib, and cell survival rate notably declined.	imatinib	114-122	cyclin dependent kinase inhibitor 2B	Homo sapiens	76-79
17132628-7	2007	Inhibition of Bcr-Abl by the chemical inhibitor STI571 resulted in activation of FOXO3a and down-regulation of Id1 expression.	imatinib	48-54	forkhead box O3	Homo sapiens	81-87
17957275-1	2007	STI571 (imatinib mesylate; Gleevec) is an inhibitor that targets the tyrosine kinase activity of Bcr-Abl present in chronic myelogenous leukemia (CML) cells.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
17132628-7	2007	Inhibition of Bcr-Abl by the chemical inhibitor STI571 resulted in activation of FOXO3a and down-regulation of Id1 expression.	imatinib	48-54	inhibitor of DNA binding 1, HLH protein	Homo sapiens	111-114
16990603-2	2007	The T315I BCR-ABL mutation mediates resistance to imatinib, nilotinib, and dasatinib.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
17957275-1	2007	STI571 (imatinib mesylate; Gleevec) is an inhibitor that targets the tyrosine kinase activity of Bcr-Abl present in chronic myelogenous leukemia (CML) cells.	imatinib	8-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
17106192-5	2007	It was found that their BCL2 and BAD expression was significantly different compared to the normal controls, and a lower BAD expression was associated with a better molecular response to imatinib treatment at 12 months.	imatinib	187-195	BCL2 apoptosis regulator	Homo sapiens	24-28
17957275-2	2007	Some preclinical studies have demonstrated that the combination of STI571 with chemotherapeutic drugs results in enhanced toxicity in Bcr-Abl-positive leukemias.	imatinib	67-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
17957275-5	2007	Higher concentrations of STI571 used in combinations with doxorubicin caused mainly apoptosis as shown by DNA degradation and nuclear fragmentation visualized by fluorescence microscopy after DAPI staining, changes in cell morphology observed after Giemza-May Grunwald staining and cellular membrane organization estimated by flow cytometry after Annexin V staining.	imatinib	25-31	annexin A5	Homo sapiens	347-356
17633880-3	2007	The developement of a tyrosine kinase inhibitor, STI571/imatinib mesylate/Gleevec, Glivec which inhibits the BCR-ABL, PDGF-R alpha, and C-Kit receptors, has changed the management of unresectable malignant GIST and has improved the survival of patients with metastaic disease.	imatinib	49-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
17633880-3	2007	The developement of a tyrosine kinase inhibitor, STI571/imatinib mesylate/Gleevec, Glivec which inhibits the BCR-ABL, PDGF-R alpha, and C-Kit receptors, has changed the management of unresectable malignant GIST and has improved the survival of patients with metastaic disease.	imatinib	49-55	platelet derived growth factor receptor alpha	Homo sapiens	118-130
17633880-3	2007	The developement of a tyrosine kinase inhibitor, STI571/imatinib mesylate/Gleevec, Glivec which inhibits the BCR-ABL, PDGF-R alpha, and C-Kit receptors, has changed the management of unresectable malignant GIST and has improved the survival of patients with metastaic disease.	imatinib	49-55	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	136-141
17633880-3	2007	The developement of a tyrosine kinase inhibitor, STI571/imatinib mesylate/Gleevec, Glivec which inhibits the BCR-ABL, PDGF-R alpha, and C-Kit receptors, has changed the management of unresectable malignant GIST and has improved the survival of patients with metastaic disease.	imatinib	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
17633880-3	2007	The developement of a tyrosine kinase inhibitor, STI571/imatinib mesylate/Gleevec, Glivec which inhibits the BCR-ABL, PDGF-R alpha, and C-Kit receptors, has changed the management of unresectable malignant GIST and has improved the survival of patients with metastaic disease.	imatinib	56-64	platelet derived growth factor receptor alpha	Homo sapiens	118-130
17164530-4	2007	The crystal structures of wild-type and mutant Abl kinase in complex with imatinib and other small-molecule Abl inhibitors were determined, with the aim of understanding the molecular basis of resistance and to aid in the design and optimization of inhibitors active against the resistance mutants.	imatinib	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
17695724-8	2007	Hence, IL-7 can reduce the sensitivity of Bcr-Abl+ pre-B cells to imatinib.	imatinib	66-74	interleukin 7	Mus musculus	7-11
17170522-4	2007	Clonal evolution with addition of the PML/RAR alpha translocation may have arisen in the early chronic phase of CML, with expansion of this clone during imatinib treatment.	imatinib	153-161	PML nuclear body scaffold	Homo sapiens	38-51
17633880-3	2007	The developement of a tyrosine kinase inhibitor, STI571/imatinib mesylate/Gleevec, Glivec which inhibits the BCR-ABL, PDGF-R alpha, and C-Kit receptors, has changed the management of unresectable malignant GIST and has improved the survival of patients with metastaic disease.	imatinib	56-64	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	136-141
17433911-4	2007	More recently, tyrosine kinase inhibitor STI-571/Imatinib mesylate/Gleevec in the treatment of Breakpoint Cluster Region-Abelson (BCR-ABL) positive leukemia elicits paradigm of mutant PTKs as ideal antileukemia targets.	imatinib	41-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-128
17433911-4	2007	More recently, tyrosine kinase inhibitor STI-571/Imatinib mesylate/Gleevec in the treatment of Breakpoint Cluster Region-Abelson (BCR-ABL) positive leukemia elicits paradigm of mutant PTKs as ideal antileukemia targets.	imatinib	41-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
17876712-8	2007	Furthermore, incubation with recombinant PDGF as well as, with progesterone seems to sustain PDGFR-alpha activity, prompting these cells to the inhibitory action of imatinib.	imatinib	165-173	platelet derived growth factor receptor alpha	Homo sapiens	93-104
17433911-4	2007	More recently, tyrosine kinase inhibitor STI-571/Imatinib mesylate/Gleevec in the treatment of Breakpoint Cluster Region-Abelson (BCR-ABL) positive leukemia elicits paradigm of mutant PTKs as ideal antileukemia targets.	imatinib	49-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-128
17433911-4	2007	More recently, tyrosine kinase inhibitor STI-571/Imatinib mesylate/Gleevec in the treatment of Breakpoint Cluster Region-Abelson (BCR-ABL) positive leukemia elicits paradigm of mutant PTKs as ideal antileukemia targets.	imatinib	49-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
17279309-1	2007	Imatinib, a tyrosine kinase inhibitor directed against the enzymatic domain of KIT protein, was found to produce dramatic clinical responses in metastatic gastrointestinal stromal tumors (GISTs).	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	79-82
17133421-0	2007	Imatinib mesylate responsiveness in aggressive systemic mastocytosis: novel association with a platelet derived growth factor receptor beta mutation.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	95-139
17145623-2	2007	Approximately 80% of c-Kit mutations occur in exon 11, being a response factor to imatinib (Gleevec) therapy.	imatinib	82-90	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	21-26
17145623-2	2007	Approximately 80% of c-Kit mutations occur in exon 11, being a response factor to imatinib (Gleevec) therapy.	imatinib	92-99	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	21-26
16960151-3	2007	Twelve patients with BCR-ABL-negative CMPDs and reciprocal translocations involving PDGFRB received imatinib for a median of 47 months (range, 0.1-60 months).	imatinib	100-108	platelet derived growth factor receptor beta	Homo sapiens	84-90
16912224-2	2007	Whereas KIT juxtamembrane domain mutations seen in most patients with GIST are highly sensitive to imatinib, the kinase activation loop mutant D816V, frequently encountered in SM, hampers the binding ability of imatinib.	imatinib	99-107	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	8-11
17352263-5	2007	Imatinib mesylate inhibited the proliferation of MFH cells that expressed PDGFRs and/or c-Kit.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	88-93
17352263-8	2007	Immunohistochemistry was used to analyze the inhibitory effect of imatinib mesylate on phosphorylation of PDGFRs and c-Kit in vivo.	imatinib	66-74	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	117-122
17352263-11	2007	Imatinib mesylate inhibited PDGFRs and c-Kit phosphorylation in TNMY1 cells affecting the tumorigenicity, in the control group (139 mm3 SD +/- 1.03) and treatment group (126.2 mm3 SD +/- 1.63) but did not affect the tumorigenicity of Nara H cells.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	39-44
17352263-12	2007	CONCLUSION: Imatinib mesylate reduced in vivo tumor growth of MFH that express PDGFRs and c-Kit associated with phosphorylation suppression.	imatinib	12-29	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	90-95
17195235-1	2007	OBJECTIVE: Imatinib mesylate is a clinically well-tolerated small molecule inhibitor that exerts selective, dual inhibition of the transforming growth factor beta (TGFbeta) and platelet-derived growth factor (PDGF) pathways.	imatinib	11-28	transforming growth factor beta 1	Homo sapiens	131-162
17195235-1	2007	OBJECTIVE: Imatinib mesylate is a clinically well-tolerated small molecule inhibitor that exerts selective, dual inhibition of the transforming growth factor beta (TGFbeta) and platelet-derived growth factor (PDGF) pathways.	imatinib	11-28	transforming growth factor beta 1	Homo sapiens	164-171
17195235-7	2007	RESULTS: Imatinib mesylate efficiently reduced basal synthesis of COL1A1, COL1A2, and fibronectin 1 messenger RNA in SSc and normal dermal fibroblasts, in a dose-dependent manner.	imatinib	9-17	collagen type I alpha 1 chain	Homo sapiens	66-72
17195235-7	2007	RESULTS: Imatinib mesylate efficiently reduced basal synthesis of COL1A1, COL1A2, and fibronectin 1 messenger RNA in SSc and normal dermal fibroblasts, in a dose-dependent manner.	imatinib	9-17	collagen type I alpha 2 chain	Homo sapiens	74-80
17195235-7	2007	RESULTS: Imatinib mesylate efficiently reduced basal synthesis of COL1A1, COL1A2, and fibronectin 1 messenger RNA in SSc and normal dermal fibroblasts, in a dose-dependent manner.	imatinib	9-17	fibronectin 1	Homo sapiens	86-99
17195235-8	2007	The induction of ECM proteins after stimulation with TGFbeta and PDGF was also strongly and dose-dependently inhibited by imatinib mesylate.	imatinib	122-139	transforming growth factor beta 1	Homo sapiens	53-60
16954504-3	2007	To overcome imatinib mesylate-resistance mechanisms such as bcr-abl amplification, mutations within the ABL kinase domain, and activation of Lyn, we developed a dual BCR-ABL/Lyn inhibitor, INNO-406 (formerly NS-187), which is 25 to 55 times more potent than imatinib mesylate in vitro and at least 10 times more potent in vivo.	imatinib	12-29	LYN proto-oncogene, Src family tyrosine kinase	Mus musculus	174-177
16954504-3	2007	To overcome imatinib mesylate-resistance mechanisms such as bcr-abl amplification, mutations within the ABL kinase domain, and activation of Lyn, we developed a dual BCR-ABL/Lyn inhibitor, INNO-406 (formerly NS-187), which is 25 to 55 times more potent than imatinib mesylate in vitro and at least 10 times more potent in vivo.	imatinib	258-275	LYN proto-oncogene, Src family tyrosine kinase	Mus musculus	174-177
16960151-0	2007	Durable responses to imatinib in patients with PDGFRB fusion gene-positive and BCR-ABL-negative chronic myeloproliferative disorders.	imatinib	21-29	platelet derived growth factor receptor beta	Homo sapiens	47-53
16960151-0	2007	Durable responses to imatinib in patients with PDGFRB fusion gene-positive and BCR-ABL-negative chronic myeloproliferative disorders.	imatinib	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
16960151-6	2007	Our data show that durable hematologic and cytogenetic responses are achieved with imatinib in patients with PDGFRB fusion-positive, BCR-ABL-negative CMPDs.	imatinib	83-91	platelet derived growth factor receptor beta	Homo sapiens	109-115
16960151-6	2007	Our data show that durable hematologic and cytogenetic responses are achieved with imatinib in patients with PDGFRB fusion-positive, BCR-ABL-negative CMPDs.	imatinib	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
17233818-7	2007	Reducing Bim levels by short hairpin RNA targeting inhibited imatinib and mitoxantrone-induced cell death.	imatinib	61-69	BCL2 like 11	Homo sapiens	9-12
17233818-9	2007	Together our data indicate that disrupting beta1 integrin-mediated regulation of Bim degradation may increase the efficacy of drugs, including imatinib, used to treat haematopoietic malignancies.	imatinib	143-151	integrin subunit beta 1	Homo sapiens	43-57
17233818-9	2007	Together our data indicate that disrupting beta1 integrin-mediated regulation of Bim degradation may increase the efficacy of drugs, including imatinib, used to treat haematopoietic malignancies.	imatinib	143-151	BCL2 like 11	Homo sapiens	81-84
17200369-5	2007	Radioimmunotherapy based on (131)ICC49, a TAG-72-targeting monoclonal antibody, was augmented with imatinib, a potent inhibitor of platelet-derived growth factor receptor-beta.	imatinib	99-107	platelet derived growth factor receptor, beta polypeptide	Mus musculus	131-175
17200352-13	2007	Second-site KIT mutations are rare in imatinib-responsive GISTs compared with imatinib-resistant tumors.	imatinib	38-46	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	12-15
18034597-1	2007	* Imatinib inhibits the breakpoint cluster region-Abelson (BCR-ABL) tyrosine kinase, which is produced by the chromosomal abnormality known as the Philadelphia (Ph) chromosome in patients with Ph chromosome-positive acute lymphoblastic leukaemia (Ph+ ALL).	imatinib	2-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-57
17346159-10	2007	Imatinib (STI571), which is a selective tyrosine kinase inhibitor and particularly of c-Kit and PDGF-R, exhibited encouraging results in respect to its inhibitory effect in cell growth and invasion potential in a panel of human breast cancer cell lines.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	86-91
17346159-10	2007	Imatinib (STI571), which is a selective tyrosine kinase inhibitor and particularly of c-Kit and PDGF-R, exhibited encouraging results in respect to its inhibitory effect in cell growth and invasion potential in a panel of human breast cancer cell lines.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	96-102
17346159-10	2007	Imatinib (STI571), which is a selective tyrosine kinase inhibitor and particularly of c-Kit and PDGF-R, exhibited encouraging results in respect to its inhibitory effect in cell growth and invasion potential in a panel of human breast cancer cell lines.	imatinib	10-16	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	86-91
17346159-10	2007	Imatinib (STI571), which is a selective tyrosine kinase inhibitor and particularly of c-Kit and PDGF-R, exhibited encouraging results in respect to its inhibitory effect in cell growth and invasion potential in a panel of human breast cancer cell lines.	imatinib	10-16	platelet derived growth factor receptor beta	Homo sapiens	96-102
18034597-1	2007	* Imatinib inhibits the breakpoint cluster region-Abelson (BCR-ABL) tyrosine kinase, which is produced by the chromosomal abnormality known as the Philadelphia (Ph) chromosome in patients with Ph chromosome-positive acute lymphoblastic leukaemia (Ph+ ALL).	imatinib	2-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
17315048-2	2007	Preclinical studies have shown dasatinib to be a much more potent inhibitor of BCR-ABL than imatinib is, and to harbor efficacy against nearly all imatinib-resistant BCR-ABL mutants.	imatinib	147-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-173
21901074-8	2007	In addition, drugs like Avastin and Gleevec target the molecular targets such as vascular endothelial cell growth factor receptor, platelet-derived growth factor receptors, and BRC-ABL/Akt.	imatinib	36-43	AKT serine/threonine kinase 1	Homo sapiens	185-188
21901078-3	2007	Imatinib mesylate inhibits the activation of PDGF receptor as well as c-Abl, Bcr-Abl and c-Kit tyrosine kinases.	imatinib	0-17	steroid sulfatase	Homo sapiens	67-71
21901078-3	2007	Imatinib mesylate inhibits the activation of PDGF receptor as well as c-Abl, Bcr-Abl and c-Kit tyrosine kinases.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-75
21901078-3	2007	Imatinib mesylate inhibits the activation of PDGF receptor as well as c-Abl, Bcr-Abl and c-Kit tyrosine kinases.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
18024654-5	2007	For patients treated with imatinib, a rising level of BCR-ABL is a trigger for kinase domain mutation analysis.	imatinib	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
17229632-8	2007	The imatinib-resistant KIT(D816V) mutant, associated with systemic mastocytosis, was found to be resistant to sorafenib.	imatinib	4-12	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	23-28
18024662-5	2007	The development of novel TKIs with enhanced inhibitory potency against ABL and other kinases may further improve on the results observed with imatinib.	imatinib	142-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-74
17109025-0	2007	Overexpression of the heat-shock protein 70 is associated to imatinib resistance in chronic myeloid leukemia.	imatinib	61-69	heat shock protein family A (Hsp70) member 4	Homo sapiens	22-43
17350876-2	2007	Retained activation of Src kinases by the BCR-ABL oncoprotein in leukaemic cells following inhibition of BCR-ABL kinase activity by imatinib indicates that Src activation by BCR-ABL is independent of BCR-ABL kinase activity and provides an explanation for reduced effectiveness of the BCR-ABL kinase activity inhibitors in Philadelphia chromosome-positive acute lymphoblastic leukaemia.	imatinib	132-140	Rous sarcoma oncogene	Mus musculus	23-26
17350876-2	2007	Retained activation of Src kinases by the BCR-ABL oncoprotein in leukaemic cells following inhibition of BCR-ABL kinase activity by imatinib indicates that Src activation by BCR-ABL is independent of BCR-ABL kinase activity and provides an explanation for reduced effectiveness of the BCR-ABL kinase activity inhibitors in Philadelphia chromosome-positive acute lymphoblastic leukaemia.	imatinib	132-140	Rous sarcoma oncogene	Mus musculus	156-159
17044046-2	2007	Expression of BACH2 is induced in BCR-ABL positive lymphoid cell lines including BV173 by imatinib, a molecular targeting agent for the treatment of chronic myeloid leukemia (CML).	imatinib	90-98	BTB domain and CNC homolog 2	Homo sapiens	14-19
17044046-2	2007	Expression of BACH2 is induced in BCR-ABL positive lymphoid cell lines including BV173 by imatinib, a molecular targeting agent for the treatment of chronic myeloid leukemia (CML).	imatinib	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
17044046-6	2007	In BV173 cells, the BACH2-centromere distance increased after imatinib treatment to levels similar to those in NAMALWA cells.	imatinib	62-70	BTB domain and CNC homolog 2	Homo sapiens	20-25
17203980-4	2007	Several heat shock proteins known to complex Bcr-Abl were overexpressed in imatinib resistant cells, showing a possible involvement of these proteins in the mechanism of resistance.	imatinib	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
17109025-1	2007	Imatinib is an effective therapy for chronic myeloid leukemia (CML), a myeloproliferative disorder characterized by the expression of the recombinant oncoprotein Bcr-Abl.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-169
17109025-6	2007	Overexpression of Hsp70 in the imatinib-sensitive K562 line induced resistance to imatinib as detected by a large reduction in cell death in the presence of 1 muM of imatinib.	imatinib	31-39	heat shock protein family A (Hsp70) member 4	Homo sapiens	18-23
17109025-6	2007	Overexpression of Hsp70 in the imatinib-sensitive K562 line induced resistance to imatinib as detected by a large reduction in cell death in the presence of 1 muM of imatinib.	imatinib	82-90	heat shock protein family A (Hsp70) member 4	Homo sapiens	18-23
17109025-6	2007	Overexpression of Hsp70 in the imatinib-sensitive K562 line induced resistance to imatinib as detected by a large reduction in cell death in the presence of 1 muM of imatinib.	imatinib	82-90	heat shock protein family A (Hsp70) member 4	Homo sapiens	18-23
17109025-7	2007	Hsp70 level was also increased in blast cells of CML patients resistant to imatinib, whereas the level remained low in responding patients.	imatinib	75-83	heat shock protein family A (Hsp70) member 4	Homo sapiens	0-5
17109025-8	2007	Taken together, the results demonstrate that overexpression of Hsp70 can lead to both in vitro and in vivo resistance to imatinib in CML cells.	imatinib	121-129	heat shock protein family A (Hsp70) member 4	Homo sapiens	63-68
17109025-9	2007	Moreover, the overexpression of Hsp70 detected in imatinib-resistant CML patients supports this mechanism and identifies potentially a marker and a therapeutic target of CML evolution.	imatinib	50-58	heat shock protein family A (Hsp70) member 4	Homo sapiens	32-37
17122866-0	2007	Chronic idiopathic myelofibrosis expressing a novel type of TEL-PDGFRB chimaera responded to imatinib mesylate therapy.	imatinib	93-110	ETS variant transcription factor 6	Homo sapiens	60-63
17122866-0	2007	Chronic idiopathic myelofibrosis expressing a novel type of TEL-PDGFRB chimaera responded to imatinib mesylate therapy.	imatinib	93-110	platelet derived growth factor receptor beta	Homo sapiens	64-70
17298867-4	2007	Imatinib is a selective inhibitor of KIT, PDGFR, and ABL tyrosine kinase activity and exerts different anti-tumor effects according to the regions of mutations in c-kit and PDGFR genes.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	37-40
17961046-10	2007	Moreover, an increase in the proapoptotic Bax/Bcl-2 protein ratio was demonstrated with the combination of imatinib and nelfinavir.	imatinib	107-115	BCL2 associated X, apoptosis regulator	Homo sapiens	42-45
17961046-10	2007	Moreover, an increase in the proapoptotic Bax/Bcl-2 protein ratio was demonstrated with the combination of imatinib and nelfinavir.	imatinib	107-115	BCL2 apoptosis regulator	Homo sapiens	46-51
16757202-3	2007	Imatinib mesylate (Gleevec) inhibits several protein-tyrosine kinases, including c-kit.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	81-86
16757202-3	2007	Imatinib mesylate (Gleevec) inhibits several protein-tyrosine kinases, including c-kit.	imatinib	19-26	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	81-86
18369825-5	2007	This observation suggests that combined use of telomerase inhibitors and imatinib or other chemotherapeutic agents may be a very useful approach to treatment of BCR-ABL-positive leukemia.	imatinib	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-168
17694264-2	2007	Imatinib mesylate (imatinib) is an inhibitor that specifically targets a set of protein tyrosine kinase, such as abl, c-kit, and platelet-derived growth factor receptor (PDGFR) and it is widely used to treat chronic myeloid leukemia (CML).	imatinib	0-17	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	118-123
17694264-2	2007	Imatinib mesylate (imatinib) is an inhibitor that specifically targets a set of protein tyrosine kinase, such as abl, c-kit, and platelet-derived growth factor receptor (PDGFR) and it is widely used to treat chronic myeloid leukemia (CML).	imatinib	0-17	platelet derived growth factor receptor, beta polypeptide	Mus musculus	129-168
17694264-2	2007	Imatinib mesylate (imatinib) is an inhibitor that specifically targets a set of protein tyrosine kinase, such as abl, c-kit, and platelet-derived growth factor receptor (PDGFR) and it is widely used to treat chronic myeloid leukemia (CML).	imatinib	0-17	platelet derived growth factor receptor, beta polypeptide	Mus musculus	170-175
17694264-2	2007	Imatinib mesylate (imatinib) is an inhibitor that specifically targets a set of protein tyrosine kinase, such as abl, c-kit, and platelet-derived growth factor receptor (PDGFR) and it is widely used to treat chronic myeloid leukemia (CML).	imatinib	19-27	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	118-123
17694264-2	2007	Imatinib mesylate (imatinib) is an inhibitor that specifically targets a set of protein tyrosine kinase, such as abl, c-kit, and platelet-derived growth factor receptor (PDGFR) and it is widely used to treat chronic myeloid leukemia (CML).	imatinib	19-27	platelet derived growth factor receptor, beta polypeptide	Mus musculus	129-168
17694264-2	2007	Imatinib mesylate (imatinib) is an inhibitor that specifically targets a set of protein tyrosine kinase, such as abl, c-kit, and platelet-derived growth factor receptor (PDGFR) and it is widely used to treat chronic myeloid leukemia (CML).	imatinib	19-27	platelet derived growth factor receptor, beta polypeptide	Mus musculus	170-175
17626041-6	2007	c-Abl-dependent phosphorylation of CSB increased in cells treated with hydrogen peroxide and decreased in cells pre-treated with STI-571, a c-Abl-specific protein kinase inhibitor.	imatinib	129-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
17626041-6	2007	c-Abl-dependent phosphorylation of CSB increased in cells treated with hydrogen peroxide and decreased in cells pre-treated with STI-571, a c-Abl-specific protein kinase inhibitor.	imatinib	129-136	ERCC excision repair 6, chromatin remodeling factor	Homo sapiens	35-38
17626041-6	2007	c-Abl-dependent phosphorylation of CSB increased in cells treated with hydrogen peroxide and decreased in cells pre-treated with STI-571, a c-Abl-specific protein kinase inhibitor.	imatinib	129-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-145
17298867-4	2007	Imatinib is a selective inhibitor of KIT, PDGFR, and ABL tyrosine kinase activity and exerts different anti-tumor effects according to the regions of mutations in c-kit and PDGFR genes.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	42-47
17298867-4	2007	Imatinib is a selective inhibitor of KIT, PDGFR, and ABL tyrosine kinase activity and exerts different anti-tumor effects according to the regions of mutations in c-kit and PDGFR genes.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	163-168
17298867-4	2007	Imatinib is a selective inhibitor of KIT, PDGFR, and ABL tyrosine kinase activity and exerts different anti-tumor effects according to the regions of mutations in c-kit and PDGFR genes.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	173-178
17294720-10	2007	By flow cytometry, P-gp was not detected on K562R cell, indicating that low intracellular imatinib concentration may not be due to P-gp mediated efflux.	imatinib	90-98	phosphoglycolate phosphatase	Homo sapiens	19-23
17607922-2	2007	Imatinib can block the activated receptor tyrosine kinase activity of c-kit.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	70-75
17607922-8	2007	Sunitinib, another tyrosine kinase inhibitor, seems to be useful especially in patients with exon 9 mutations of c-kit, who usually have a worse response to imatinib.	imatinib	157-165	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	113-118
17292737-1	2007	The advent of the Bcr-Abl selective tyrosine kinase inhibitor imatinib mesylate (Glivec, Gleevec, Novartis, East Hanover, NJ) has substantially changed the treatment landscape for chronic myelogenous leukemia (CML).	imatinib	62-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
17292737-3	2007	Imatinib resistance or intolerance frequently depends on the re-emergence of Bcr-Abl kinase activity, but can also indicate Bcr-Abl-independent disease progression.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
17292737-3	2007	Imatinib resistance or intolerance frequently depends on the re-emergence of Bcr-Abl kinase activity, but can also indicate Bcr-Abl-independent disease progression.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
17292737-5	2007	To date, more than 40 different point mutations that code for distinct single amino acid substitutions in the Bcr-Abl kinase domain have been isolated from imatinib-resistant patients.	imatinib	156-164	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
17292737-6	2007	These mutations affect amino acids involved in imatinib binding or in regulatory regions of the Bcr-Abl kinase domain, resulting in decreased sensitivity to imatinib while retaining aberrant kinase activity.	imatinib	157-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
17292737-8	2007	To overcome imatinib-resistant disease, novel tyrosine kinase inhibitors with activity against imatinib-resistant mutations and/or with inhibition of alternative pathways, such as Src activation, have recently been developed.	imatinib	12-20	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	180-183
18314612-9	2007	The expression of KIT in neoplastic MC has led to the development of targeted therapies using tyrosine kinase inhibitors (TKI) like STI571 (Imatinib, Gleevec).	imatinib	140-148	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	18-21
17292738-4	2007	In 40% to 50% of cases, this is attributed to the development of mutations that impair the ability of imatinib to bind to and inhibit the constitutively active Bcr-Abl kinase.	imatinib	102-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-167
18314611-2	2007	One very effective tyrosine kinase inhibitor is imatinib mesylate inhibiting the KIT receptor tyrosine kinase in gastrointestinal stromal tumors (GISTs) which often carry activating mutations in the KIT gene.	imatinib	48-65	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	81-84
17179059-4	2006	Imatinib, a selective inhibitor of BCR-ABL, represents a major success in the era of target-directed cancer chemotherapy.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
18314611-2	2007	One very effective tyrosine kinase inhibitor is imatinib mesylate inhibiting the KIT receptor tyrosine kinase in gastrointestinal stromal tumors (GISTs) which often carry activating mutations in the KIT gene.	imatinib	48-65	ret proto-oncogene	Homo sapiens	85-109
18314611-2	2007	One very effective tyrosine kinase inhibitor is imatinib mesylate inhibiting the KIT receptor tyrosine kinase in gastrointestinal stromal tumors (GISTs) which often carry activating mutations in the KIT gene.	imatinib	48-65	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	199-202
18314611-6	2007	RESULTS: The best response to treatment with imatinib is achieved in GISTs with an underlying KIT mutation in exon 11 encoding the juxtamembranous domain.	imatinib	45-53	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	94-97
18314612-9	2007	The expression of KIT in neoplastic MC has led to the development of targeted therapies using tyrosine kinase inhibitors (TKI) like STI571 (Imatinib, Gleevec).	imatinib	132-138	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	18-21
17179059-7	2006	Insight into factors involved in imatinib resistance and disease progression has highlighted a role for such BCR-ABL-dependent factors as amplification and overexpression of the BCR-ABL gene and the emergence of mutant isoforms of BCR-ABL.	imatinib	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
17179059-7	2006	Insight into factors involved in imatinib resistance and disease progression has highlighted a role for such BCR-ABL-dependent factors as amplification and overexpression of the BCR-ABL gene and the emergence of mutant isoforms of BCR-ABL.	imatinib	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185
17179059-7	2006	Insight into factors involved in imatinib resistance and disease progression has highlighted a role for such BCR-ABL-dependent factors as amplification and overexpression of the BCR-ABL gene and the emergence of mutant isoforms of BCR-ABL.	imatinib	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185
16983347-0	2006	Imatinib enhances human melanoma cell susceptibility to TRAIL-induced cell death: Relationship to Bcl-2 family and caspase activation.	imatinib	0-8	TNF superfamily member 10	Homo sapiens	56-61
16823786-6	2006	STI571 10 microM was used to specifically inhibit the activity of Kit, the receptor for stem cell factor, and 10 nM wortmannin as a PI3K inhibitor.	imatinib	0-6	KIT ligand	Homo sapiens	88-104
17189410-1	2006	PURPOSE: ABL kinase domain mutations have been implicated in the resistance to the BCR-ABL inhibitor imatinib mesylate of Philadelphia-positive (Ph+) leukemia patients.	imatinib	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
16817200-2	2006	Recent evidence suggests that the PDGF receptor (PDGFR) tyrosine kinase inhibitor, imatinib, can prevent arterial proliferative diseases.	imatinib	83-91	platelet derived growth factor receptor beta	Homo sapiens	34-47
16817200-2	2006	Recent evidence suggests that the PDGF receptor (PDGFR) tyrosine kinase inhibitor, imatinib, can prevent arterial proliferative diseases.	imatinib	83-91	platelet derived growth factor receptor beta	Homo sapiens	49-54
16817200-8	2006	Imatinib also more effectively inhibited PDGF-induced phosphorylation of PDGFRbeta and Akt in VSMC, compared to ASMC.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	73-82
16817200-8	2006	Imatinib also more effectively inhibited PDGF-induced phosphorylation of PDGFRbeta and Akt in VSMC, compared to ASMC.	imatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	87-90
16983347-8	2006	Surprisingly, imatinib inhibited cell proliferation and TRAIL-mediated apoptosis in melanoma cells.	imatinib	14-22	TNF superfamily member 10	Homo sapiens	56-61
16983347-14	2006	Our results also show that imatinib enhances TRAIL-induced cell death independently of BH3-interacting domain death agonist translocation, in a process involving the Bax:Bcl-X(L) ratio, Bax:Bcl-X(L)/Bcl-2 translocation, cytochrome c release and caspase activation.	imatinib	27-35	TNF superfamily member 10	Homo sapiens	45-50
16983347-15	2006	Our data indicate that imatinib sensitizes T1 cells by directly downregulating c-FLIP(L), with the use of an alternative pathway for antitumor activity, because PDGFRalpha is not activated in T1 cells and these cells do not express c-kit, c-ABL or PDGFRbeta.	imatinib	23-31	CASP8 and FADD like apoptosis regulator	Homo sapiens	79-85
16983347-15	2006	Our data indicate that imatinib sensitizes T1 cells by directly downregulating c-FLIP(L), with the use of an alternative pathway for antitumor activity, because PDGFRalpha is not activated in T1 cells and these cells do not express c-kit, c-ABL or PDGFRbeta.	imatinib	23-31	platelet derived growth factor receptor alpha	Homo sapiens	161-171
16983347-0	2006	Imatinib enhances human melanoma cell susceptibility to TRAIL-induced cell death: Relationship to Bcl-2 family and caspase activation.	imatinib	0-8	BCL2 apoptosis regulator	Homo sapiens	98-103
23662039-3	2006	FIP1L1/PDGFRalpha, the product of the gene FIP1L1/PDGFRA, is a constitutively activated tyrosine kinase and can be inhibited by imatinib mesylate.	imatinib	128-145	factor interacting with PAPOLA and CPSF1	Homo sapiens	0-6
16983347-15	2006	Our data indicate that imatinib sensitizes T1 cells by directly downregulating c-FLIP(L), with the use of an alternative pathway for antitumor activity, because PDGFRalpha is not activated in T1 cells and these cells do not express c-kit, c-ABL or PDGFRbeta.	imatinib	23-31	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	232-237
16983347-15	2006	Our data indicate that imatinib sensitizes T1 cells by directly downregulating c-FLIP(L), with the use of an alternative pathway for antitumor activity, because PDGFRalpha is not activated in T1 cells and these cells do not express c-kit, c-ABL or PDGFRbeta.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	239-244
16983347-15	2006	Our data indicate that imatinib sensitizes T1 cells by directly downregulating c-FLIP(L), with the use of an alternative pathway for antitumor activity, because PDGFRalpha is not activated in T1 cells and these cells do not express c-kit, c-ABL or PDGFRbeta.	imatinib	23-31	platelet derived growth factor receptor beta	Homo sapiens	248-257
16983347-16	2006	Caspase cascade activation and mitochondria also play a key role in the imatinib-mediated sensitization of melanoma cells to the proapoptotic action of TRAIL.	imatinib	72-80	TNF superfamily member 10	Homo sapiens	152-157
23662039-3	2006	FIP1L1/PDGFRalpha, the product of the gene FIP1L1/PDGFRA, is a constitutively activated tyrosine kinase and can be inhibited by imatinib mesylate.	imatinib	128-145	platelet derived growth factor receptor alpha	Homo sapiens	7-17
23662039-3	2006	FIP1L1/PDGFRalpha, the product of the gene FIP1L1/PDGFRA, is a constitutively activated tyrosine kinase and can be inhibited by imatinib mesylate.	imatinib	128-145	factor interacting with PAPOLA and CPSF1	Homo sapiens	43-49
23662039-3	2006	FIP1L1/PDGFRalpha, the product of the gene FIP1L1/PDGFRA, is a constitutively activated tyrosine kinase and can be inhibited by imatinib mesylate.	imatinib	128-145	platelet derived growth factor receptor alpha	Homo sapiens	50-56
17148668-8	2006	Imatinib alone or in combination with irinotecan inhibited phosphorylation of PDGF-Rbeta of tumor-associated stromal cells and pericytes.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	78-88
17217104-2	2006	The reason for this is explanation of the pathogenetic mechanism of tumor growth by activation of c-Kit protein, followed by a rationally designed suppressor, a drug named imatinib.	imatinib	172-180	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	98-103
17106016-4	2006	Dasatinib is 300 times more potent than imatinib at BCR-ABL inhibition, has few side effects, and inhibits the SRC family kinases.	imatinib	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
17106015-7	2006	The recognition of the role for BCR-ABL in CML has led to the development of specific kinase inhibitors such as imatinib.	imatinib	112-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
17106015-11	2006	Although combinations of imatinib with IFN alpha show small improvements compared to imatinib therapy alone, the biggest improvements were seen when imatinib doses were doubled.	imatinib	85-93	interferon alpha 1	Homo sapiens	39-48
17106015-11	2006	Although combinations of imatinib with IFN alpha show small improvements compared to imatinib therapy alone, the biggest improvements were seen when imatinib doses were doubled.	imatinib	85-93	interferon alpha 1	Homo sapiens	39-48
17114238-0	2006	In vitro and in vivo activity of SKI-606, a novel Src-Abl inhibitor, against imatinib-resistant Bcr-Abl+ neoplastic cells.	imatinib	77-85	SKI proto-oncogene	Homo sapiens	33-36
17106015-13	2006	The most common mechanism for imatinib resistance is the presence of a mutated BCR-ABL kinase.	imatinib	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
17106015-15	2006	CONCLUSION: Molecular-targeted BCR-ABL kinase inhibitors, such as imatinib, are now first-line treatment for CML.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
17106015-17	2006	Next generation BCR-ABL kinase inhibitors hold promise for patients with mutated BCR-ABL kinase that confer resistance to imatinib.	imatinib	122-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
17106015-17	2006	Next generation BCR-ABL kinase inhibitors hold promise for patients with mutated BCR-ABL kinase that confer resistance to imatinib.	imatinib	122-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
17106016-2	2006	Mutations of the BCR-ABL kinase domain, a common mechanism of resistance to imatinib in CML, are discussed.	imatinib	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
17006667-0	2006	Not all imatinib resistance in CML are BCR-ABL kinase domain mutations.	imatinib	8-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
17006667-1	2006	Point mutations within the ABL kinase domain of the BCR-ABL gene are associated with clinical resistance to imatinib mesylate in chronic myeloid leukemia (CML).	imatinib	108-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
17006667-2	2006	To obtain more information about the association between BCR-ABL mutations and type of imatinib resistance, we studied 30 early chronic phase (CP) CML patients, commencing imatinib therapy, using a conventional sequencing technique.	imatinib	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
17114238-5	2006	SKI-606 retained activity in cells where resistance to imatinib was caused by BCR-ABL gene amplification and in three of four Bcr-Abl point mutants tested.	imatinib	55-63	SKI proto-oncogene	Homo sapiens	0-3
17114238-5	2006	SKI-606 retained activity in cells where resistance to imatinib was caused by BCR-ABL gene amplification and in three of four Bcr-Abl point mutants tested.	imatinib	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
17114238-7	2006	Modeling considerations attribute the superior activity of SKI-606 to its ability to bind a conformation of Bcr-Abl different from imatinib.	imatinib	131-139	SKI proto-oncogene	Homo sapiens	59-62
17148686-3	2006	Here, we studied the effects of platelet-derived growth factor receptor-beta blockade in vivo using the platelet-derived growth factor receptor (PDGFR)-beta inhibitor imatinib mesylate on tissue repair.	imatinib	167-184	platelet derived growth factor receptor, beta polypeptide	Mus musculus	145-156
17020808-1	2006	The tyrosine kinase inhibitor imatinib mesylate (Gleevec) has been demonstrated to protect various cell types from death by inhibition of Abelson tyrosine kinase (c-Abl).	imatinib	30-47	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	163-168
17020808-1	2006	The tyrosine kinase inhibitor imatinib mesylate (Gleevec) has been demonstrated to protect various cell types from death by inhibition of Abelson tyrosine kinase (c-Abl).	imatinib	49-56	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	163-168
17020808-5	2006	The beneficial effects of imatinib may be related to inhibition of the pro-apoptotic MAP kinase JNK.	imatinib	26-34	mitogen-activated protein kinase 8	Mus musculus	96-99
17114238-0	2006	In vitro and in vivo activity of SKI-606, a novel Src-Abl inhibitor, against imatinib-resistant Bcr-Abl+ neoplastic cells.	imatinib	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
17114238-3	2006	SKI-606 proved to be an active inhibitor of Bcr-Abl in several chronic myelogenous leukemia cell lines and transfectants, with IC(50) values in the low nanomolar range, 1 to 2 logs lower than those obtained with imatinib.	imatinib	212-220	SKI proto-oncogene	Homo sapiens	0-3
22792021-3	2006	The availability of imatinib mesylate, a selective inhibitor of Bcr/Abl approved by Health Canada in 2001, has profoundly altered the clinical and laboratory management of cml.	imatinib	20-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
17145809-1	2006	PURPOSE: We have previously shown the presence of an activated platelet-derived growth factor (PDGF) receptor (PDGFR) B and its ligand PDGFB in a limited number of patients with clinical and radiological responses to imatinib mesylate treatment.	imatinib	217-234	platelet derived growth factor receptor beta	Homo sapiens	111-116
17145809-1	2006	PURPOSE: We have previously shown the presence of an activated platelet-derived growth factor (PDGF) receptor (PDGFR) B and its ligand PDGFB in a limited number of patients with clinical and radiological responses to imatinib mesylate treatment.	imatinib	217-234	platelet derived growth factor subunit B	Homo sapiens	135-140
17040960-1	2006	BACKGROUND: The 2447 A > T pathogenic variation at codon 816 of exon 17 (D816V) in the KIT gene, occurring in systemic mastocytosis (SM), leads to constitutive activation of tyrosine kinase activity and confers resistance to the tyrosine kinase inhibitor imatinib mesylate.	imatinib	258-275	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	90-93
17145844-2	2006	Imatinib mesylate, a selective inhibitor of BCR-ABL, represents current frontline therapy for CML; however, emerging evidence suggests that drug resistance to imatinib may limit its long-term success.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
17155893-1	2006	Mutations within the ABL kinase domain and overexpression of SRC family kinases have been identified among the known mechanisms of resistance to imatinib in chronic myeloid leukemia (CML).	imatinib	145-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-24
17087936-0	2006	Effects of PKC412, nilotinib, and imatinib against GIST-associated PDGFRA mutants with differential imatinib sensitivity.	imatinib	34-42	platelet derived growth factor receptor alpha	Homo sapiens	67-73
17087936-0	2006	Effects of PKC412, nilotinib, and imatinib against GIST-associated PDGFRA mutants with differential imatinib sensitivity.	imatinib	100-108	platelet derived growth factor receptor alpha	Homo sapiens	67-73
17087936-2	2006	The responsiveness of mutant PDGFRA-positive GIST to imatinib depends on the location of the PDGFRA mutation; for example, the V561D juxtamembrane domain mutation is more sensitive to imatinib than the D842V kinase domain mutation.	imatinib	53-61	platelet derived growth factor receptor alpha	Homo sapiens	29-35
17087936-2	2006	The responsiveness of mutant PDGFRA-positive GIST to imatinib depends on the location of the PDGFRA mutation; for example, the V561D juxtamembrane domain mutation is more sensitive to imatinib than the D842V kinase domain mutation.	imatinib	53-61	platelet derived growth factor receptor alpha	Homo sapiens	93-99
17087936-2	2006	The responsiveness of mutant PDGFRA-positive GIST to imatinib depends on the location of the PDGFRA mutation; for example, the V561D juxtamembrane domain mutation is more sensitive to imatinib than the D842V kinase domain mutation.	imatinib	184-192	platelet derived growth factor receptor alpha	Homo sapiens	29-35
17155893-2	2006	The development of agents with dual inhibitory activity against SRC and ABL kinases is one approach to overcome imatinib resistance.	imatinib	112-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-75
17087936-3	2006	In this study, we compare the effects of 3 tyrosine kinase inhibitors, PKC412 and nilotinib, and imatinib, on 2 GIST-related PDGFRA mutants, V561D and D842V, which possess differential sensitivity to imatinib.	imatinib	97-105	platelet derived growth factor receptor alpha	Homo sapiens	125-131
17189224-0	2006	Usefulness of quantitative assessment of JunB gene expression as a marker for monitoring chronic myeloid leukemia patients undergoing imatinib therapy.	imatinib	134-142	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	41-45
17087936-7	2006	Both imatinib and nilotinib displayed potent activity in vitro against the V561D-PDGFRA mutant but were significantly less efficacious against D842V-PDGFRA.	imatinib	5-13	platelet derived growth factor receptor alpha	Homo sapiens	81-87
17087936-7	2006	Both imatinib and nilotinib displayed potent activity in vitro against the V561D-PDGFRA mutant but were significantly less efficacious against D842V-PDGFRA.	imatinib	5-13	platelet derived growth factor receptor alpha	Homo sapiens	149-155
16988930-1	2006	Imatinib mesylate, binding to the inactive conformation of Bcr-Abl tyrosine kinase and suppressing the Ph chromosome positive clone, has revolutionized the treatment of chronic myeloid leukaemia (CML) patients.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
16988930-4	2006	Studies of imatinib-treated patients have determined that the BCR-ABL levels measured early in therapy may predict durable cytogenetic remission and in turn prolonged progression free-survival or acquisition of resistance.	imatinib	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
16988930-5	2006	The major mechanism of imatinib resistance is clonal expansion of leukaemia cells with mutations in the Bcr-Abl fusion tyrosine kinase.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
17189224-4	2006	We used real-time quantitative reverse transcription-polymerase chain reaction analysis to monitor both JunB and BCR-ABL expression during imatinib therapy.	imatinib	139-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
17189224-6	2006	After imatinib therapy, an increase in JunB expression was found in 5 patients, all of whom achieved a complete cytogenetic response (CCR) and molecular response (MR), with a decrease in BCR-ABL expression.	imatinib	6-14	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	39-43
17189224-6	2006	After imatinib therapy, an increase in JunB expression was found in 5 patients, all of whom achieved a complete cytogenetic response (CCR) and molecular response (MR), with a decrease in BCR-ABL expression.	imatinib	6-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	187-194
17189224-10	2006	This study revealed that an increase in JunB expression is a good prognostic marker for predicting clinical response in CML patients treated with imatinib when such data are combined with an evaluation of BCR-ABL expression.	imatinib	146-154	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	40-44
17189224-10	2006	This study revealed that an increase in JunB expression is a good prognostic marker for predicting clinical response in CML patients treated with imatinib when such data are combined with an evaluation of BCR-ABL expression.	imatinib	146-154	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	205-212
17001705-6	2006	As a very tangible example of how translational research has led to a marked improvement in patient outcome, the signal transduction inhibitor imatinib (a tyrosine kinase inhibitor of c-kit and PDGF) was administered to patients with KS whose tumors were serially biopsied.	imatinib	143-151	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	184-189
17178293-3	2006	The dysregulated KIT protein is oncogenic and is an ideal target for imatinib, a KIT-selective inhibitor.	imatinib	69-77	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	17-20
16630657-6	2006	We here report on a Ph(+) CML case in long lasting CCR following interferon-alpha treatment (IFN) which reached CMR with imatinib but soon relapsed at molecular level after this latter drug discontinuation; we considered the present observation also in the light of previously reported data.	imatinib	121-129	interferon alpha 1	Homo sapiens	93-96
16682077-3	2006	Cumulative evidence indicates that the Bcr-Abl tyrosine kinase inhibitor imatinib mesylate (Gleevec) is active for the treatment of patients with HES, particularly those expressing the FIP1L1-PDGFR-alpha oncoprotein.	imatinib	73-90	factor interacting with PAPOLA and CPSF1	Homo sapiens	185-191
16682077-3	2006	Cumulative evidence indicates that the Bcr-Abl tyrosine kinase inhibitor imatinib mesylate (Gleevec) is active for the treatment of patients with HES, particularly those expressing the FIP1L1-PDGFR-alpha oncoprotein.	imatinib	73-90	platelet derived growth factor receptor alpha	Homo sapiens	192-203
16682077-3	2006	Cumulative evidence indicates that the Bcr-Abl tyrosine kinase inhibitor imatinib mesylate (Gleevec) is active for the treatment of patients with HES, particularly those expressing the FIP1L1-PDGFR-alpha oncoprotein.	imatinib	92-99	factor interacting with PAPOLA and CPSF1	Homo sapiens	185-191
16682077-3	2006	Cumulative evidence indicates that the Bcr-Abl tyrosine kinase inhibitor imatinib mesylate (Gleevec) is active for the treatment of patients with HES, particularly those expressing the FIP1L1-PDGFR-alpha oncoprotein.	imatinib	92-99	platelet derived growth factor receptor alpha	Homo sapiens	192-203
16682077-8	2006	We conclude that AMN107 and imatinib are active and equipotent against cells expressing the FIP1L1-PDGFR-alpha fusion gene.	imatinib	28-36	platelet derived growth factor receptor alpha	Homo sapiens	99-110
17178293-3	2006	The dysregulated KIT protein is oncogenic and is an ideal target for imatinib, a KIT-selective inhibitor.	imatinib	69-77	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	81-84
16849647-5	2006	Moreover, the BCR/ABL tyrosine kinase inhibitors imatinib (STI571) and nilotinib (AMN107) decreased histamine levels and HDC mRNA expression in BCR/ABL-transformed Ba/F3 cells, in the CML-derived basophil cell line KU812, and in primary CML cells.	imatinib	49-57	BCR activator of RhoGEF and GTPase	Mus musculus	14-17
17533744-10	2006	CONCLUSION: In vitro, STI571 promotes the activation/maturation of DCs derived from BMMNCs of patients with CMI, and decreases VEGF production by the leukemic cells.	imatinib	22-28	vascular endothelial growth factor A	Homo sapiens	127-131
16840725-0	2006	Newly identified c-KIT receptor tyrosine kinase ITD in childhood AML induces ligand-independent growth and is responsive to a synergistic effect of imatinib and rapamycin.	imatinib	148-156	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	17-22
17146202-0	2006	Dose modification of imatinib by monitoring the level of BCR-ABL transcript in chronic myelogenous leukemia.	imatinib	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
17146202-3	2006	Recently, Imatinib mesylate targeting to a BCR-ABL chimeric protein has been developed, and shown to achieve complete remission at a high rate.	imatinib	10-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
16741250-6	2006	However, inhibition of c-Abl with imatinib suppressed CD154-induced expression of p73, p73-induced expression of Bid and CD95, and blocked the sensitization of p53-deficient CLL cells to CD95-mediated or F-ara-A-induced apoptosis.	imatinib	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-28
16741250-6	2006	However, inhibition of c-Abl with imatinib suppressed CD154-induced expression of p73, p73-induced expression of Bid and CD95, and blocked the sensitization of p53-deficient CLL cells to CD95-mediated or F-ara-A-induced apoptosis.	imatinib	34-42	CD40 ligand	Homo sapiens	54-59
16849647-5	2006	Moreover, the BCR/ABL tyrosine kinase inhibitors imatinib (STI571) and nilotinib (AMN107) decreased histamine levels and HDC mRNA expression in BCR/ABL-transformed Ba/F3 cells, in the CML-derived basophil cell line KU812, and in primary CML cells.	imatinib	49-57	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	18-21
16741250-6	2006	However, inhibition of c-Abl with imatinib suppressed CD154-induced expression of p73, p73-induced expression of Bid and CD95, and blocked the sensitization of p53-deficient CLL cells to CD95-mediated or F-ara-A-induced apoptosis.	imatinib	34-42	tumor protein p73	Homo sapiens	82-85
16741250-6	2006	However, inhibition of c-Abl with imatinib suppressed CD154-induced expression of p73, p73-induced expression of Bid and CD95, and blocked the sensitization of p53-deficient CLL cells to CD95-mediated or F-ara-A-induced apoptosis.	imatinib	34-42	tumor protein p73	Homo sapiens	87-90
16849647-5	2006	Moreover, the BCR/ABL tyrosine kinase inhibitors imatinib (STI571) and nilotinib (AMN107) decreased histamine levels and HDC mRNA expression in BCR/ABL-transformed Ba/F3 cells, in the CML-derived basophil cell line KU812, and in primary CML cells.	imatinib	49-57	histidine decarboxylase	Mus musculus	121-124
16741250-6	2006	However, inhibition of c-Abl with imatinib suppressed CD154-induced expression of p73, p73-induced expression of Bid and CD95, and blocked the sensitization of p53-deficient CLL cells to CD95-mediated or F-ara-A-induced apoptosis.	imatinib	34-42	tumor protein p53	Homo sapiens	160-163
16849647-5	2006	Moreover, the BCR/ABL tyrosine kinase inhibitors imatinib (STI571) and nilotinib (AMN107) decreased histamine levels and HDC mRNA expression in BCR/ABL-transformed Ba/F3 cells, in the CML-derived basophil cell line KU812, and in primary CML cells.	imatinib	49-57	BCR activator of RhoGEF and GTPase	Mus musculus	14-21
16741250-6	2006	However, inhibition of c-Abl with imatinib suppressed CD154-induced expression of p73, p73-induced expression of Bid and CD95, and blocked the sensitization of p53-deficient CLL cells to CD95-mediated or F-ara-A-induced apoptosis.	imatinib	34-42	Fas cell surface death receptor	Homo sapiens	187-191
16741250-7	2006	Conversely, CLL cells transduced with an imatinib-resistant c-Abl mutant could be induced by CD154 to express p73 and Bid even when treated with imatinib.	imatinib	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-65
16741250-7	2006	Conversely, CLL cells transduced with an imatinib-resistant c-Abl mutant could be induced by CD154 to express p73 and Bid even when treated with imatinib.	imatinib	41-49	CD40 ligand	Homo sapiens	93-98
16741250-7	2006	Conversely, CLL cells transduced with an imatinib-resistant c-Abl mutant could be induced by CD154 to express p73 and Bid even when treated with imatinib.	imatinib	41-49	tumor protein p73	Homo sapiens	110-113
16873673-1	2006	The NUP214-ABL1 fusion gene in T-cell acute lymphoblastic leukemia (T-ALL) has recently been identified as a possible target for imatinib and related tyrosine kinase inhibitors, but exact data regarding the prognostic impact and frequency of the several putative NUP214-ABL1 mRNA transcripts are still missing.	imatinib	129-137	nucleoporin 214	Homo sapiens	4-10
16873673-1	2006	The NUP214-ABL1 fusion gene in T-cell acute lymphoblastic leukemia (T-ALL) has recently been identified as a possible target for imatinib and related tyrosine kinase inhibitors, but exact data regarding the prognostic impact and frequency of the several putative NUP214-ABL1 mRNA transcripts are still missing.	imatinib	129-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-15
16873673-1	2006	The NUP214-ABL1 fusion gene in T-cell acute lymphoblastic leukemia (T-ALL) has recently been identified as a possible target for imatinib and related tyrosine kinase inhibitors, but exact data regarding the prognostic impact and frequency of the several putative NUP214-ABL1 mRNA transcripts are still missing.	imatinib	129-137	nucleoporin 214	Homo sapiens	263-269
16873673-1	2006	The NUP214-ABL1 fusion gene in T-cell acute lymphoblastic leukemia (T-ALL) has recently been identified as a possible target for imatinib and related tyrosine kinase inhibitors, but exact data regarding the prognostic impact and frequency of the several putative NUP214-ABL1 mRNA transcripts are still missing.	imatinib	129-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	270-274
16849647-5	2006	Moreover, the BCR/ABL tyrosine kinase inhibitors imatinib (STI571) and nilotinib (AMN107) decreased histamine levels and HDC mRNA expression in BCR/ABL-transformed Ba/F3 cells, in the CML-derived basophil cell line KU812, and in primary CML cells.	imatinib	59-65	BCR activator of RhoGEF and GTPase	Mus musculus	14-17
16849647-5	2006	Moreover, the BCR/ABL tyrosine kinase inhibitors imatinib (STI571) and nilotinib (AMN107) decreased histamine levels and HDC mRNA expression in BCR/ABL-transformed Ba/F3 cells, in the CML-derived basophil cell line KU812, and in primary CML cells.	imatinib	59-65	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	18-21
16849647-5	2006	Moreover, the BCR/ABL tyrosine kinase inhibitors imatinib (STI571) and nilotinib (AMN107) decreased histamine levels and HDC mRNA expression in BCR/ABL-transformed Ba/F3 cells, in the CML-derived basophil cell line KU812, and in primary CML cells.	imatinib	59-65	histidine decarboxylase	Mus musculus	121-124
16741250-7	2006	Conversely, CLL cells transduced with an imatinib-resistant c-Abl mutant could be induced by CD154 to express p73 and Bid even when treated with imatinib.	imatinib	41-49	BH3 interacting domain death agonist	Homo sapiens	118-121
16849647-5	2006	Moreover, the BCR/ABL tyrosine kinase inhibitors imatinib (STI571) and nilotinib (AMN107) decreased histamine levels and HDC mRNA expression in BCR/ABL-transformed Ba/F3 cells, in the CML-derived basophil cell line KU812, and in primary CML cells.	imatinib	59-65	BCR activator of RhoGEF and GTPase	Mus musculus	14-21
16741250-7	2006	Conversely, CLL cells transduced with an imatinib-resistant c-Abl mutant could be induced by CD154 to express p73 and Bid even when treated with imatinib.	imatinib	145-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-65
16741250-7	2006	Conversely, CLL cells transduced with an imatinib-resistant c-Abl mutant could be induced by CD154 to express p73 and Bid even when treated with imatinib.	imatinib	145-153	CD40 ligand	Homo sapiens	93-98
16917119-3	2006	METHODS: In fully mismatched rat tracheal allografts, we used imatinib and PTK/ZK, either alone or in combination, to block PDGF and VEGF receptor protein tyrosine kinase (RTK) action, respectively.	imatinib	62-70	vascular endothelial growth factor A	Rattus norvegicus	133-137
16973134-2	2006	Imatinib mesylate, known as Gleevec or STI-571, is a molecule that inhibits the function of various receptors with tyrosine kinase activity, such as Abl, the bcr-abl chimeric product, KIT, and platelet-derived growth factor (PDGF) receptors.	imatinib	0-17	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	149-152
16741250-7	2006	Conversely, CLL cells transduced with an imatinib-resistant c-Abl mutant could be induced by CD154 to express p73 and Bid even when treated with imatinib.	imatinib	145-153	tumor protein p73	Homo sapiens	110-113
16741250-7	2006	Conversely, CLL cells transduced with an imatinib-resistant c-Abl mutant could be induced by CD154 to express p73 and Bid even when treated with imatinib.	imatinib	145-153	BH3 interacting domain death agonist	Homo sapiens	118-121
16973134-2	2006	Imatinib mesylate, known as Gleevec or STI-571, is a molecule that inhibits the function of various receptors with tyrosine kinase activity, such as Abl, the bcr-abl chimeric product, KIT, and platelet-derived growth factor (PDGF) receptors.	imatinib	0-17	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	162-165
16973134-2	2006	Imatinib mesylate, known as Gleevec or STI-571, is a molecule that inhibits the function of various receptors with tyrosine kinase activity, such as Abl, the bcr-abl chimeric product, KIT, and platelet-derived growth factor (PDGF) receptors.	imatinib	0-17	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	184-187
16388897-0	2006	BNP as a marker of the heart failure in the treatment of imatinib mesylate.	imatinib	57-74	natriuretic peptide B	Homo sapiens	0-3
16908071-0	2006	Identification of a c-kit exon 8 internal tandem duplication in a feline mast cell tumor case and its favorable response to the tyrosine kinase inhibitor imatinib mesylate.	imatinib	154-171	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	20-25
17108134-4	2006	We hypothesized a sequential blockade strategy that is designed to decrease the expression of the Bcr-Abl protein, with the goal of complementing the action of imatinib on kinase activity.	imatinib	160-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
17108134-8	2006	Imatinib directly inhibited the kinase activity of Bcr-Abl.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
17108134-11	2006	Imatinib-resistant Ba/F3 cells that were transfected to express the E255K and T315I mutations of Bcr-Abl were not cross-resistant to flavopiridol and HHT.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
17008009-9	2006	The binding affinity of imatinib to human serum albumin (nKa approximately 3 x 10(4)M(-1)) is low.	imatinib	24-32	albumin	Homo sapiens	42-55
17077147-3	2006	We find that SRC kinases activated by BCR-ABL remain fully active in imatinib-treated mouse leukemic cells, suggesting that imatinib does not inactivate all BCR-ABL-activated signaling pathways.	imatinib	69-77	Rous sarcoma oncogene	Mus musculus	13-16
17077147-3	2006	We find that SRC kinases activated by BCR-ABL remain fully active in imatinib-treated mouse leukemic cells, suggesting that imatinib does not inactivate all BCR-ABL-activated signaling pathways.	imatinib	124-132	Rous sarcoma oncogene	Mus musculus	13-16
17077147-4	2006	This SRC pathway is essential for leukemic cells to survive imatinib treatment and for CML transition to lymphoid blast crisis.	imatinib	60-68	Rous sarcoma oncogene	Mus musculus	5-8
17008009-9	2006	The binding affinity of imatinib to human serum albumin (nKa approximately 3 x 10(4)M(-1)) is low.	imatinib	24-32	tachykinin precursor 1	Homo sapiens	57-60
17085664-9	2006	The limited spectrum of TKI-resistant mutations in EGFR, which binds to erlotinib in the active conformation, contrasts with a wider range of second-site mutations seen with acquired resistance to imatinib, which binds to ABL and KIT, respectively, in closed conformations.	imatinib	197-205	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	222-225
17085669-0	2006	Antileukemic activity of lysophosphatidic acid acyltransferase-beta inhibitor CT32228 in chronic myelogenous leukemia sensitive and resistant to imatinib.	imatinib	145-153	1-acylglycerol-3-phosphate O-acyltransferase 2	Homo sapiens	25-67
17085664-9	2006	The limited spectrum of TKI-resistant mutations in EGFR, which binds to erlotinib in the active conformation, contrasts with a wider range of second-site mutations seen with acquired resistance to imatinib, which binds to ABL and KIT, respectively, in closed conformations.	imatinib	197-205	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	230-233
17101065-2	2006	Imatinib, a specific inhibitor of the aberrant KIT protein, is an approved, well-tolerated oral drug for the management of metastatic or inoperable GIST.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	47-50
17419150-0	2006	Beyond imatinib: second generation c-KIT inhibitors for the management of gastrointestinal stromal tumors.	imatinib	7-15	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	35-40
17419150-3	2006	Therapeutically, metastatic GISTs are effectively treated by imatinib, a tyrosine kinase inhibitor (TKI) with activity against KIT and platelet-derived growth factor receptor.	imatinib	61-69	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	127-130
17032555-7	2006	Imatinib, a potent inhibitor of KIT activity, is now standard front-line therapy for advanced GIST.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	32-35
16988578-4	2006	This is attributed, in 40-50% of cases, to the development of BCR-ABL (breakpoint cluster region/Abelson oncogene) tyrosine kinase domain mutations that impair imatinib binding.	imatinib	160-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
17064224-2	2006	Targeting BCR-ABL by imatinib has revolutionised the clinical course of CML.	imatinib	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
16942767-9	2006	In contrast, under defined conditions in organ cultures of metanephric kidneys, c-kit-positive cells, including the Flk-1-positive subset, undergo apoptosis after treatment with STI-571, an inhibitor of c-kit tyrosine phosphorylation.	imatinib	178-185	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	80-85
16942767-9	2006	In contrast, under defined conditions in organ cultures of metanephric kidneys, c-kit-positive cells, including the Flk-1-positive subset, undergo apoptosis after treatment with STI-571, an inhibitor of c-kit tyrosine phosphorylation.	imatinib	178-185	kinase insert domain receptor	Homo sapiens	116-121
16942767-9	2006	In contrast, under defined conditions in organ cultures of metanephric kidneys, c-kit-positive cells, including the Flk-1-positive subset, undergo apoptosis after treatment with STI-571, an inhibitor of c-kit tyrosine phosphorylation.	imatinib	178-185	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	203-208
17065430-0	2006	Allele-specific polymerase chain reaction for the imatinib-resistant KIT D816V and D816F mutations in mastocytosis and acute myelogenous leukemia.	imatinib	50-58	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	69-72
17118762-2	2006	To investigate this issue, we administered imatinib (30 mg/kg per day) orally to P230 BCR/ABL-expressing Tg mice for 30 days.	imatinib	43-51	golgin A4	Homo sapiens	81-85
17118762-10	2006	Thus, imatinib administration had the intriguing effect of replacing clones with high expression of p230 BCR/ABL complementary DNA with clones with very low expression.	imatinib	6-14	golgin A4	Homo sapiens	100-104
17118762-10	2006	Thus, imatinib administration had the intriguing effect of replacing clones with high expression of p230 BCR/ABL complementary DNA with clones with very low expression.	imatinib	6-14	BCR activator of RhoGEF and GTPase	Mus musculus	105-108
17118762-10	2006	Thus, imatinib administration had the intriguing effect of replacing clones with high expression of p230 BCR/ABL complementary DNA with clones with very low expression.	imatinib	6-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-112
17118762-11	2006	These data show that imatinib may still be capable of eliminating and eradicating clones with high p230 BCR/ABL expression and healing the disease phenotype in Tg mice.	imatinib	21-29	golgin A4	Homo sapiens	99-103
17118762-11	2006	These data show that imatinib may still be capable of eliminating and eradicating clones with high p230 BCR/ABL expression and healing the disease phenotype in Tg mice.	imatinib	21-29	BCR activator of RhoGEF and GTPase	Mus musculus	104-111
17118762-0	2006	Oral administration of imatinib to P230 BCR/ABL-expressing transgenic mice changes clones with high BCR/ABL complementary DNA expression into those with low expression.	imatinib	23-31	golgin A4	Homo sapiens	35-39
17118762-0	2006	Oral administration of imatinib to P230 BCR/ABL-expressing transgenic mice changes clones with high BCR/ABL complementary DNA expression into those with low expression.	imatinib	23-31	BCR activator of RhoGEF and GTPase	Mus musculus	40-47
17118762-0	2006	Oral administration of imatinib to P230 BCR/ABL-expressing transgenic mice changes clones with high BCR/ABL complementary DNA expression into those with low expression.	imatinib	23-31	BCR activator of RhoGEF and GTPase	Mus musculus	100-107
17065430-2	2006	The D816V substitution in the activation loop of KIT results in relative resistance to the kinase inhibitor imatinib (Gleevec).	imatinib	108-116	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	49-52
17065430-2	2006	The D816V substitution in the activation loop of KIT results in relative resistance to the kinase inhibitor imatinib (Gleevec).	imatinib	118-125	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	49-52
16797704-5	2006	AMN107 was also as effective as imatinib in inhibiting phosphorylation of c-kit in HMC-1(560) cells.	imatinib	32-40	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	74-79
17077361-0	2006	Re: Response of a KIT-positive extra-abdominal fibromatosis to imatinib mesylate and KIT genetic analysis.	imatinib	63-71	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	18-21
16546254-1	2006	Advanced-phase chronic myeloid leukemia patients treated with imatinib often relapse due to point mutations in the Abl kinase domain.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-118
16797704-7	2006	Based upon our results, AMN107 and imatinib are equipotent against mast cells with wild-type c-kit and those harboring the juxtamembrane D560G c-kit mutant but have no significant activity over the dose range tested against cells expressing the c-kit D816V mutant tyrosine kinase.	imatinib	35-43	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	93-98
17003111-0	2006	Imatinib spells BAD news for Bcr/abl-positive leukemias.	imatinib	0-8	BCR activator of RhoGEF and GTPase	Homo sapiens	29-32
17008892-0	2006	A novel Bcr-Abl splice isoform is associated with the L248V mutation in CML patients with acquired resistance to imatinib.	imatinib	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-15
17003785-0	2006	Treatment with Imatinib in NSCLC is associated with decrease of phosphorylated PDGFR-beta and VEGF expression, decrease in interstitial fluid pressure and improvement of oxygenation.	imatinib	15-23	platelet derived growth factor receptor beta	Homo sapiens	79-89
17003785-0	2006	Treatment with Imatinib in NSCLC is associated with decrease of phosphorylated PDGFR-beta and VEGF expression, decrease in interstitial fluid pressure and improvement of oxygenation.	imatinib	15-23	vascular endothelial growth factor A	Homo sapiens	94-98
17003785-5	2006	We hypothesised that Imatinib, a specific PDGFR-beta inhibitor will, in addition to p-PDGFR-beta inhibition, downregulate VEGF, decrease IFP and improve tumour oxygenation.	imatinib	21-29	platelet derived growth factor receptor beta	Homo sapiens	42-52
17003785-5	2006	We hypothesised that Imatinib, a specific PDGFR-beta inhibitor will, in addition to p-PDGFR-beta inhibition, downregulate VEGF, decrease IFP and improve tumour oxygenation.	imatinib	21-29	platelet derived growth factor receptor beta	Homo sapiens	86-96
17003785-5	2006	We hypothesised that Imatinib, a specific PDGFR-beta inhibitor will, in addition to p-PDGFR-beta inhibition, downregulate VEGF, decrease IFP and improve tumour oxygenation.	imatinib	21-29	vascular endothelial growth factor A	Homo sapiens	122-126
17003785-12	2006	Imatinib treatment resulted in significant reduction of p-PDGFR-beta, VEGF and IFP.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	58-68
17003785-12	2006	Imatinib treatment resulted in significant reduction of p-PDGFR-beta, VEGF and IFP.	imatinib	0-8	vascular endothelial growth factor A	Homo sapiens	70-74
17003785-14	2006	This study shows that p-PDGFR-beta-overexpressing tumours can be effectively treated with Imatinib to decrease tumour IFP.	imatinib	90-98	platelet derived growth factor receptor beta	Homo sapiens	24-34
17003785-15	2006	Importantly, this is the first study demonstrating that Imatinib treatment improves tumour oxygenation and downregulates tumour VEGF expression.	imatinib	56-64	vascular endothelial growth factor A	Homo sapiens	128-132
16751810-0	2006	Functional analyses and molecular modeling of two c-Kit mutations responsible for imatinib secondary resistance in GIST patients.	imatinib	82-90	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	50-55
17014709-7	2006	CONCLUSION: The PDGFR system may have a role in the pathogenesis of cervical cancer as their members are frequently expressed in this tumor and cervical cancer lines are growth inhibited by the PDGFR antagonist imatinib.	imatinib	211-219	platelet derived growth factor receptor beta	Homo sapiens	16-21
17014709-7	2006	CONCLUSION: The PDGFR system may have a role in the pathogenesis of cervical cancer as their members are frequently expressed in this tumor and cervical cancer lines are growth inhibited by the PDGFR antagonist imatinib.	imatinib	211-219	platelet derived growth factor receptor beta	Homo sapiens	194-199
17068083-4	2006	Imatinib therapy was interrupted in 14 of the 58 patients (interruption group, INT), after a median time of 11.9 months.	imatinib	0-8	inturned planar cell polarity protein	Homo sapiens	79-82
17068083-7	2006	Median PFS dated from the time of imatinib initiation in the INT group was 21.8 months (95% CI, 17.3-26.3 months), but was not reached in the CONT group (P=0.029).	imatinib	34-42	inturned planar cell polarity protein	Homo sapiens	61-64
17068083-8	2006	Following imatinib reintroduction in the INT group, 88% of patients achieved disease control.	imatinib	10-18	inturned planar cell polarity protein	Homo sapiens	41-44
18221045-1	2006	The first line therapy for chronic myeloid leukemia (CML) was dramatically altered within a few years of the introduction of Abl specific tyrosine kinase inhibitor, imatinib mesylate to the clinic.	imatinib	165-173	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-128
18221045-3	2006	Point mutations within the Abl kinase domain that interfere with imatinib mesylate binding are most critical cause of imatinib resistance.	imatinib	65-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-30
18221045-3	2006	Point mutations within the Abl kinase domain that interfere with imatinib mesylate binding are most critical cause of imatinib resistance.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-30
17294703-2	2006	Imatinib (STI571) is a highly selective inhibitor of BCR/ABL oncogenic tyrosine kinase used in leukemia treatment.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
17294703-2	2006	Imatinib (STI571) is a highly selective inhibitor of BCR/ABL oncogenic tyrosine kinase used in leukemia treatment.	imatinib	10-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
17044945-5	2006	In addition, the inhibitory effect of imatinib mesylate on stem cell factor (SCF)-induced proliferation and invasion was evaluated.	imatinib	38-55	KIT ligand	Homo sapiens	59-75
17044945-5	2006	In addition, the inhibitory effect of imatinib mesylate on stem cell factor (SCF)-induced proliferation and invasion was evaluated.	imatinib	38-55	KIT ligand	Homo sapiens	77-80
17044945-11	2006	5 muM imatinib mesylate significantly inhibited SCF-enhanced proliferation to the same extent compared with the control.	imatinib	6-23	KIT ligand	Homo sapiens	48-51
17044945-12	2006	Similarly, SCF-enhanced invasive ability was significantly inhibited by 5 muM imatinib mesylate.	imatinib	78-95	KIT ligand	Homo sapiens	11-14
17044945-15	2006	CONCLUSION: Our results demonstrated that the SCF-KIT pathway enhanced the proliferation and invasiveness in KIT-positive pancreatic cancer cell lines and that the enhanced proliferation and invasion were inhibited by imatinib mesylate.	imatinib	218-235	KIT ligand	Homo sapiens	46-49
17044945-15	2006	CONCLUSION: Our results demonstrated that the SCF-KIT pathway enhanced the proliferation and invasiveness in KIT-positive pancreatic cancer cell lines and that the enhanced proliferation and invasion were inhibited by imatinib mesylate.	imatinib	218-235	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	50-53
17044945-15	2006	CONCLUSION: Our results demonstrated that the SCF-KIT pathway enhanced the proliferation and invasiveness in KIT-positive pancreatic cancer cell lines and that the enhanced proliferation and invasion were inhibited by imatinib mesylate.	imatinib	218-235	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	109-112
16986125-0	2006	Early effects of imatinib mesylate on the expression of insulin-like growth factor binding protein-3 and positron emission tomography in patients with gastrointestinal stromal tumor.	imatinib	17-34	insulin like growth factor binding protein 3	Homo sapiens	56-100
16986125-8	2006	Western blot analysis confirmed the increase of IGFBP-3 only in imatinib-sensitive GIST882 cells.	imatinib	64-72	insulin like growth factor binding protein 3	Homo sapiens	48-55
16986125-9	2006	Up to a 7-fold induction (49% mean increase; P = .08) of IGFBP-3 mRNA was found in tumor samples from patients with low residual FDG uptake, whereas there was an up to 12-fold reduction (-102% mean decrease; P = .03) in IGFBP-3 in those patients with high residual FDG uptake after imatinib therapy.	imatinib	282-290	insulin like growth factor binding protein 3	Homo sapiens	57-64
16986125-10	2006	CONCLUSIONS: In the current study, imatinib appears to regulate numerous genes and specifically induces IGFBP-3 in GIST cells and tumor samples.	imatinib	35-43	insulin like growth factor binding protein 3	Homo sapiens	104-111
16986125-11	2006	IGFBP-3 levels also were found to be inversely correlated with residual FDG uptake in GIST patients early in imatinib therapy.	imatinib	109-117	insulin like growth factor binding protein 3	Homo sapiens	0-7
16986125-12	2006	These initial observations suggest that IGFBP-3 is an important early marker of antitumor activity of imatinib in GIST.	imatinib	102-110	insulin like growth factor binding protein 3	Homo sapiens	40-47
16953242-2	2006	Imatinib mesylate, a BCR/ABL kinase inhibitor, is effective in most of chronic phase CML patients.	imatinib	0-17	BCR activator of RhoGEF and GTPase	Homo sapiens	21-24
16953242-6	2006	We recently reported that the activity of the tumour suppressor protein phosphatase 2A (PP2A) is markedly inhibited in blast crisis CML patient cells and that molecular or pharmacologic re-activation of PP2A phosphatase led to growth suppression, enhanced apoptosis, impaired clonogenic potential and decreased in vivo leukaemogenesis of imatinib-sensitive and -resistant (T315I included) CML-BC patient cells and/or BCR/ABL+ myeloid progenitor cell lines.	imatinib	338-346	protein phosphatase 2 phosphatase activator	Homo sapiens	72-86
16953242-6	2006	We recently reported that the activity of the tumour suppressor protein phosphatase 2A (PP2A) is markedly inhibited in blast crisis CML patient cells and that molecular or pharmacologic re-activation of PP2A phosphatase led to growth suppression, enhanced apoptosis, impaired clonogenic potential and decreased in vivo leukaemogenesis of imatinib-sensitive and -resistant (T315I included) CML-BC patient cells and/or BCR/ABL+ myeloid progenitor cell lines.	imatinib	338-346	protein phosphatase 2 phosphatase activator	Homo sapiens	88-92
16953242-6	2006	We recently reported that the activity of the tumour suppressor protein phosphatase 2A (PP2A) is markedly inhibited in blast crisis CML patient cells and that molecular or pharmacologic re-activation of PP2A phosphatase led to growth suppression, enhanced apoptosis, impaired clonogenic potential and decreased in vivo leukaemogenesis of imatinib-sensitive and -resistant (T315I included) CML-BC patient cells and/or BCR/ABL+ myeloid progenitor cell lines.	imatinib	338-346	protein phosphatase 2 phosphatase activator	Homo sapiens	203-207
16954519-1	2006	PURPOSE: Gastrointestinal stromal tumors (GISTs) commonly harbor oncogenic mutations of the KIT or platelet-derived growth factor alpha (PDGFRA) kinases, which are targets for imatinib.	imatinib	176-184	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	92-95
16954519-1	2006	PURPOSE: Gastrointestinal stromal tumors (GISTs) commonly harbor oncogenic mutations of the KIT or platelet-derived growth factor alpha (PDGFRA) kinases, which are targets for imatinib.	imatinib	176-184	platelet derived growth factor receptor alpha	Homo sapiens	137-143
16954519-6	2006	Secondary kinase mutations of KIT or PDGFRA that were identified in imatinib-resistant GISTs were biochemically profiled for imatinib sensitivity.	imatinib	68-76	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	30-33
16954519-6	2006	Secondary kinase mutations of KIT or PDGFRA that were identified in imatinib-resistant GISTs were biochemically profiled for imatinib sensitivity.	imatinib	68-76	platelet derived growth factor receptor alpha	Homo sapiens	37-43
16954519-8	2006	Imatinib-resistant tumors had levels of activated KIT that were similar to or greater than those typically found in untreated GISTs.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	50-53
16954519-12	2006	Using RNAi technology, we demonstrated that imatinib-resistant GIST cells remain dependent on KIT kinase activity for activation of critical downstream signaling pathways.	imatinib	44-52	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	94-97
16997913-0	2006	Bim and Bad mediate imatinib-induced killing of Bcr/Abl+ leukemic cells, and resistance due to their loss is overcome by a BH3 mimetic.	imatinib	20-28	BCL2-like 11 (apoptosis facilitator)	Mus musculus	0-3
16997913-0	2006	Bim and Bad mediate imatinib-induced killing of Bcr/Abl+ leukemic cells, and resistance due to their loss is overcome by a BH3 mimetic.	imatinib	20-28	BCR activator of RhoGEF and GTPase	Mus musculus	48-51
16997913-1	2006	Cell killing is a critical pharmacological activity of imatinib to eradicate Bcr/Abl+ leukemias.	imatinib	55-63	BCR activator of RhoGEF and GTPase	Mus musculus	77-80
16997913-2	2006	We found that imatinib kills Bcr/Abl+ leukemic cells by triggering the Bcl-2-regulated apoptotic pathway.	imatinib	14-22	BCR activator of RhoGEF and GTPase	Mus musculus	29-32
16997913-2	2006	We found that imatinib kills Bcr/Abl+ leukemic cells by triggering the Bcl-2-regulated apoptotic pathway.	imatinib	14-22	B cell leukemia/lymphoma 2	Mus musculus	71-76
16997913-3	2006	Imatinib activated several proapoptotic BH3-only proteins: bim and bmf transcription was increased, and both Bim and Bad were activated posttranslationally.	imatinib	0-8	BCL2-like 11 (apoptosis facilitator)	Mus musculus	59-62
16997913-3	2006	Imatinib activated several proapoptotic BH3-only proteins: bim and bmf transcription was increased, and both Bim and Bad were activated posttranslationally.	imatinib	0-8	BCL2 modifying factor	Mus musculus	67-70
16997913-3	2006	Imatinib activated several proapoptotic BH3-only proteins: bim and bmf transcription was increased, and both Bim and Bad were activated posttranslationally.	imatinib	0-8	BCL2-like 11 (apoptosis facilitator)	Mus musculus	109-112
16997913-4	2006	Studies using RNAi and cells from gene-targeted mice revealed that Bim plays a major role in imatinib-induced apoptosis of Bcr/Abl+ leukemic cells and that the combined loss of Bim and Bad abrogates this killing.	imatinib	93-101	BCL2-like 11 (apoptosis facilitator)	Mus musculus	67-70
16997913-4	2006	Studies using RNAi and cells from gene-targeted mice revealed that Bim plays a major role in imatinib-induced apoptosis of Bcr/Abl+ leukemic cells and that the combined loss of Bim and Bad abrogates this killing.	imatinib	93-101	BCR activator of RhoGEF and GTPase	Mus musculus	123-126
16997913-4	2006	Studies using RNAi and cells from gene-targeted mice revealed that Bim plays a major role in imatinib-induced apoptosis of Bcr/Abl+ leukemic cells and that the combined loss of Bim and Bad abrogates this killing.	imatinib	93-101	BCL2-like 11 (apoptosis facilitator)	Mus musculus	177-180
16997913-6	2006	Resistance to imatinib caused by Bcl-2 overexpression or loss of Bim (plus Bad) could be overcome by cotreatment with the BH3 mimetic ABT-737.	imatinib	14-22	B cell leukemia/lymphoma 2	Mus musculus	33-38
16997913-6	2006	Resistance to imatinib caused by Bcl-2 overexpression or loss of Bim (plus Bad) could be overcome by cotreatment with the BH3 mimetic ABT-737.	imatinib	14-22	BCL2-like 11 (apoptosis facilitator)	Mus musculus	65-68
16997913-7	2006	These results demonstrate that Bim and Bad account for most, perhaps all, imatinib-induced killing of Bcr/Abl+ leukemic cells and suggest previously undescribed drug combination strategies for cancer therapy.	imatinib	74-82	BCL2-like 11 (apoptosis facilitator)	Mus musculus	31-34
16997913-7	2006	These results demonstrate that Bim and Bad account for most, perhaps all, imatinib-induced killing of Bcr/Abl+ leukemic cells and suggest previously undescribed drug combination strategies for cancer therapy.	imatinib	74-82	BCR activator of RhoGEF and GTPase	Mus musculus	102-105
16965435-1	2006	Fip1-like 1/platelet-derived growth factor receptor-alpha (FIP1L1/PDGFRA)-positive hypereosinophilic syndrome is a rare disorder with a poor prognosis if untreated and for which treatment with imatinib mesilate is highly effective.	imatinib	193-210	platelet derived growth factor receptor alpha	Homo sapiens	12-57
17090188-15	2006	Kit/PDGFRA tyrosine kinase inhibitor imatinib has been successfully used in the treatment of metastatic GISTs for more than 5 years.	imatinib	37-45	platelet derived growth factor receptor alpha	Homo sapiens	4-10
16796694-1	2006	OBJECTIVE: To determine the biological effects of imatinib mesylate (STI-571, Gleevec; Novartis Pharmaceuticals, Inc., East Hanover, NJ, USA), as measured by prostate-specific antigen (PSA) kinetics in men with biochemical relapse of prostate cancer after definitive local therapy.	imatinib	50-67	kallikrein related peptidase 3	Homo sapiens	158-189
16965435-1	2006	Fip1-like 1/platelet-derived growth factor receptor-alpha (FIP1L1/PDGFRA)-positive hypereosinophilic syndrome is a rare disorder with a poor prognosis if untreated and for which treatment with imatinib mesilate is highly effective.	imatinib	193-210	factor interacting with PAPOLA and CPSF1	Homo sapiens	59-65
16965435-1	2006	Fip1-like 1/platelet-derived growth factor receptor-alpha (FIP1L1/PDGFRA)-positive hypereosinophilic syndrome is a rare disorder with a poor prognosis if untreated and for which treatment with imatinib mesilate is highly effective.	imatinib	193-210	platelet derived growth factor receptor alpha	Homo sapiens	66-72
16965955-0	2006	Imatinib resistant chronic myelogenous leukemia, BCR-ABL positive by chromosome and FISH analyses but negative by PCR, in a child progressing to acute basophilic leukemia: cytogenetic follow-up.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
16964380-11	2006	Therefore, in the subset of CRC patients with concomitant KIT/SCF expression, the activity of Imatinib mesylate, a selective inhibitor of specific tyrosine kinases including KIT, may be exploited in combination with standard therapy.	imatinib	94-111	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	58-61
16969080-0	2006	Regulation and targeting of Eg5, a mitotic motor protein in blast crisis CML: overcoming imatinib resistance.	imatinib	89-97	kinesin family member 11	Homo sapiens	28-31
16969080-1	2006	Patients with blast crisis (BC) CML frequently become resistant to Imatinib, a Bcr-Abl tyrosine kinase-targeting agent.	imatinib	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
16969080-5	2006	Inhibition of Bcr-Abl by Imatinib downregulated Eg5 expression in Imatinib-sensitive KBM5 and HL-60p185 cells, but not in Imatinib-resistant KBM5-STI571, harboring a T315I mutation, and Bcr-Abl-negative HL-60 cells.	imatinib	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
16969080-5	2006	Inhibition of Bcr-Abl by Imatinib downregulated Eg5 expression in Imatinib-sensitive KBM5 and HL-60p185 cells, but not in Imatinib-resistant KBM5-STI571, harboring a T315I mutation, and Bcr-Abl-negative HL-60 cells.	imatinib	25-33	kinesin family member 11	Homo sapiens	48-51
16969080-5	2006	Inhibition of Bcr-Abl by Imatinib downregulated Eg5 expression in Imatinib-sensitive KBM5 and HL-60p185 cells, but not in Imatinib-resistant KBM5-STI571, harboring a T315I mutation, and Bcr-Abl-negative HL-60 cells.	imatinib	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-193
16969080-5	2006	Inhibition of Bcr-Abl by Imatinib downregulated Eg5 expression in Imatinib-sensitive KBM5 and HL-60p185 cells, but not in Imatinib-resistant KBM5-STI571, harboring a T315I mutation, and Bcr-Abl-negative HL-60 cells.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
16969080-5	2006	Inhibition of Bcr-Abl by Imatinib downregulated Eg5 expression in Imatinib-sensitive KBM5 and HL-60p185 cells, but not in Imatinib-resistant KBM5-STI571, harboring a T315I mutation, and Bcr-Abl-negative HL-60 cells.	imatinib	66-74	kinesin family member 11	Homo sapiens	48-51
16969080-5	2006	Inhibition of Bcr-Abl by Imatinib downregulated Eg5 expression in Imatinib-sensitive KBM5 and HL-60p185 cells, but not in Imatinib-resistant KBM5-STI571, harboring a T315I mutation, and Bcr-Abl-negative HL-60 cells.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
16969080-5	2006	Inhibition of Bcr-Abl by Imatinib downregulated Eg5 expression in Imatinib-sensitive KBM5 and HL-60p185 cells, but not in Imatinib-resistant KBM5-STI571, harboring a T315I mutation, and Bcr-Abl-negative HL-60 cells.	imatinib	66-74	kinesin family member 11	Homo sapiens	48-51
16969080-6	2006	Blocking Eg5 expression with antisense oligonucleotide (Eg5-ASO) or inhibiting its activity with the small-molecule Eg5 inhibitor, S-trityl-L-cysteine induced G(2)/M cell cycle block and subsequent cell death in both Imatinib-sensitive and -resistant cells.	imatinib	217-225	kinesin family member 11	Homo sapiens	9-12
16961463-3	2006	An understanding of the mechanisms by which BCR-ABL contributes to the pathogenesis of chronic myeloid leukaemia led to the development of imatinib, the first of several tyrosine kinase inhibitors to enter clinical trials.	imatinib	139-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
17076652-1	2006	Imatinib mesylate, Abl tyrosine kinase inhibitor, has improved the treatment of Bcr-Abl-positive leukemia such as chronic myeloid leukemia (CML) and Philadelphia chromosome positive acute lymphoblastic leukemia (Ph(+)ALL).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-22
17076652-1	2006	Imatinib mesylate, Abl tyrosine kinase inhibitor, has improved the treatment of Bcr-Abl-positive leukemia such as chronic myeloid leukemia (CML) and Philadelphia chromosome positive acute lymphoblastic leukemia (Ph(+)ALL).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
17076652-3	2006	Several novel tyrosine kinase inhibitors, which have been developed to override imatinib resistance mechanisms such as overexpression of Bcr-Abl and point mutations within the Abl kinase domain, are currently competing.	imatinib	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-144
17076652-3	2006	Several novel tyrosine kinase inhibitors, which have been developed to override imatinib resistance mechanisms such as overexpression of Bcr-Abl and point mutations within the Abl kinase domain, are currently competing.	imatinib	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-144
16969080-9	2006	Inhibition of Eg5 expression or its activity blocks cell cycle progression and induces cell death independent of the cellular response to Imatinib.	imatinib	138-146	kinesin family member 11	Homo sapiens	14-17
16969080-10	2006	Therefore, Eg5 could be a potential therapeutic target for the treatment of BC CML, in particular Imatinib-resistant BC CML.	imatinib	98-106	kinesin family member 11	Homo sapiens	11-14
16845659-0	2006	Transient response to imatinib in a chronic eosinophilic leukemia associated with ins(9;4)(q33;q12q25) and a CDK5RAP2-PDGFRA fusion gene.	imatinib	22-30	CDK5 regulatory subunit associated protein 2	Homo sapiens	109-117
16845659-0	2006	Transient response to imatinib in a chronic eosinophilic leukemia associated with ins(9;4)(q33;q12q25) and a CDK5RAP2-PDGFRA fusion gene.	imatinib	22-30	platelet derived growth factor receptor alpha	Homo sapiens	118-124
16845659-1	2006	Chronic myeloproliferative disorders with rearrangements of the platelet-derived growth factor receptor A (PDGFRA) gene at chromosome band 4q12 have shown excellent responses to targeted therapy with imatinib.	imatinib	200-208	platelet derived growth factor receptor alpha	Homo sapiens	64-105
16845659-1	2006	Chronic myeloproliferative disorders with rearrangements of the platelet-derived growth factor receptor A (PDGFRA) gene at chromosome band 4q12 have shown excellent responses to targeted therapy with imatinib.	imatinib	200-208	platelet derived growth factor receptor alpha	Homo sapiens	107-113
16845659-8	2006	Despite achieving complete cytogenetic and molecular remission on imatinib, the patient relapsed with imatinib-resistant acute myeloid leukemia that was characterized by a normal karyotype, absence of detectable CDK5RAP2-PDGFRA mRNA, and a newly acquired G12D NRAS mutation.	imatinib	102-110	platelet derived growth factor receptor alpha	Homo sapiens	221-227
16845659-8	2006	Despite achieving complete cytogenetic and molecular remission on imatinib, the patient relapsed with imatinib-resistant acute myeloid leukemia that was characterized by a normal karyotype, absence of detectable CDK5RAP2-PDGFRA mRNA, and a newly acquired G12D NRAS mutation.	imatinib	102-110	NRAS proto-oncogene, GTPase	Homo sapiens	260-264
16964380-11	2006	Therefore, in the subset of CRC patients with concomitant KIT/SCF expression, the activity of Imatinib mesylate, a selective inhibitor of specific tyrosine kinases including KIT, may be exploited in combination with standard therapy.	imatinib	94-111	KIT ligand	Homo sapiens	62-65
16964380-11	2006	Therefore, in the subset of CRC patients with concomitant KIT/SCF expression, the activity of Imatinib mesylate, a selective inhibitor of specific tyrosine kinases including KIT, may be exploited in combination with standard therapy.	imatinib	94-111	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	174-177
16460801-1	2006	Imatinib mesylate has recently been reported to have clinical activity in the treatment of polycythemia vera (PV), suggesting the involvement of one of the kinases targeted by this inhibitor, including c-Kit and PDGFR.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	202-207
16981009-2	2006	Imatinib mesylate (imatinib) is a tyrosine kinase inhibitor developed to treat Bcr/Abl-expressing leukemias and subsequently found to treat c-Kit-expressing gastrointestinal stromal tumors.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	140-145
16981009-2	2006	Imatinib mesylate (imatinib) is a tyrosine kinase inhibitor developed to treat Bcr/Abl-expressing leukemias and subsequently found to treat c-Kit-expressing gastrointestinal stromal tumors.	imatinib	19-27	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	140-145
16981009-4	2006	We further show that micromolar concentrations of imatinib abrogate multiple signal transduction pathways implicated in RA pathogenesis, including mast cell c-Kit signaling and TNF-alpha release, macrophage c-Fms activation and cytokine production, and fibroblast PDGFR signaling and proliferation.	imatinib	50-58	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	157-162
16981009-4	2006	We further show that micromolar concentrations of imatinib abrogate multiple signal transduction pathways implicated in RA pathogenesis, including mast cell c-Kit signaling and TNF-alpha release, macrophage c-Fms activation and cytokine production, and fibroblast PDGFR signaling and proliferation.	imatinib	50-58	tumor necrosis factor	Homo sapiens	177-186
16981009-4	2006	We further show that micromolar concentrations of imatinib abrogate multiple signal transduction pathways implicated in RA pathogenesis, including mast cell c-Kit signaling and TNF-alpha release, macrophage c-Fms activation and cytokine production, and fibroblast PDGFR signaling and proliferation.	imatinib	50-58	colony stimulating factor 1 receptor	Homo sapiens	207-212
16981009-4	2006	We further show that micromolar concentrations of imatinib abrogate multiple signal transduction pathways implicated in RA pathogenesis, including mast cell c-Kit signaling and TNF-alpha release, macrophage c-Fms activation and cytokine production, and fibroblast PDGFR signaling and proliferation.	imatinib	50-58	platelet derived growth factor receptor beta	Homo sapiens	264-269
16981009-5	2006	In our studies, imatinib attenuated PDGFR signaling in fibroblast-like synoviocytes (FLSs) and TNF-alpha production in synovial fluid mononuclear cells (SFMCs) derived from human RA patients.	imatinib	16-24	platelet derived growth factor receptor beta	Homo sapiens	36-41
16855631-0	2006	Frequency and clinical significance of BCR-ABL mutations in patients with chronic myeloid leukemia treated with imatinib mesylate.	imatinib	112-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
16855631-1	2006	Mutations of the BCR-ABL kinase domain are a common mechanism of resistance to imatinib in chronic myeloid leukemia.	imatinib	79-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
16952195-7	2006	Moreover, DM p27 strongly inhibits the growth of imatinib-resistant CML cells, compared to the T157A p27 (SM p27).	imatinib	49-57	dynactin subunit 6	Homo sapiens	13-16
16460801-1	2006	Imatinib mesylate has recently been reported to have clinical activity in the treatment of polycythemia vera (PV), suggesting the involvement of one of the kinases targeted by this inhibitor, including c-Kit and PDGFR.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	212-217
16924245-4	2006	More recently, imatinib has been used to inhibit KIT in gastrointestinal (GI) stromal tumor, a mesenchymal tumor that arises in the GI tract.	imatinib	15-23	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	49-52
16481037-0	2006	Adaphostin and bortezomib induce oxidative injury and apoptosis in imatinib mesylate-resistant hematopoietic cells expressing mutant forms of Bcr/Abl.	imatinib	67-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
16481037-5	2006	These findings indicate that adaphostin+/-bortezomib circumvent imatinib resistance due to Bcr/Abl point mutations most likely through ROS generation.	imatinib	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
16533530-3	2006	A moderate overexpression of p14(ARF) with a normal expression of p16(INK4a) was observed in imatinib-resistant patients.	imatinib	93-101	cyclin dependent kinase inhibitor 2A	Homo sapiens	29-32
16533530-3	2006	A moderate overexpression of p14(ARF) with a normal expression of p16(INK4a) was observed in imatinib-resistant patients.	imatinib	93-101	cyclin dependent kinase inhibitor 2A	Homo sapiens	70-75
16533530-4	2006	Although protein expression did not consistently match mRNA levels, a role for the two cell cycle regulators in the IFN-alpha signaling pathway is suggested as well as a relation with the resistance to IFN-alpha or imatinib therapy.	imatinib	215-223	interferon alpha 1	Homo sapiens	116-125
16919263-2	2006	We used imatinib mesylate (Glivec) to investigate whether c-kit activity of Cajal-like cells in human myometrium is involved in spontaneous rhythmic contractions of human uterine smooth muscle, taking intestinal smooth muscle as a reference tissue.	imatinib	8-25	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	58-63
17013383-5	2006	Based on a mathematical modeling approach that quantitatively explains a broad range of phenomena, we show for two independent datasets that clinically observed BCR-ABL1 transcript dynamics during imatinib treatment of CML can consistently be explained by a selective functional effect of imatinib on proliferative leukemia stem cells.	imatinib	197-205	BCR activator of RhoGEF and GTPase	Homo sapiens	161-169
17013383-5	2006	Based on a mathematical modeling approach that quantitatively explains a broad range of phenomena, we show for two independent datasets that clinically observed BCR-ABL1 transcript dynamics during imatinib treatment of CML can consistently be explained by a selective functional effect of imatinib on proliferative leukemia stem cells.	imatinib	289-297	BCR activator of RhoGEF and GTPase	Homo sapiens	161-169
17094575-2	2006	The phosphorylation of AKT and ERK was enhanced by co-culture with MSCs in both STI571-sensitive KBM-5 and STI571-resistant KBM-5/STI cells.	imatinib	80-86	AKT serine/threonine kinase 1	Homo sapiens	23-26
17094575-2	2006	The phosphorylation of AKT and ERK was enhanced by co-culture with MSCs in both STI571-sensitive KBM-5 and STI571-resistant KBM-5/STI cells.	imatinib	80-86	mitogen-activated protein kinase 1	Homo sapiens	31-34
17094575-2	2006	The phosphorylation of AKT and ERK was enhanced by co-culture with MSCs in both STI571-sensitive KBM-5 and STI571-resistant KBM-5/STI cells.	imatinib	107-113	AKT serine/threonine kinase 1	Homo sapiens	23-26
17094575-2	2006	The phosphorylation of AKT and ERK was enhanced by co-culture with MSCs in both STI571-sensitive KBM-5 and STI571-resistant KBM-5/STI cells.	imatinib	107-113	mitogen-activated protein kinase 1	Homo sapiens	31-34
16919263-4	2006	An inhibitory antibody directed against the extracellular domain of the platelet derived growth factor receptor (PDGFR), another target of imatinib that is expressed by the uterine muscle cells themselves, failed to affect myogenic contractions.	imatinib	139-147	platelet derived growth factor receptor beta	Homo sapiens	72-111
16919263-4	2006	An inhibitory antibody directed against the extracellular domain of the platelet derived growth factor receptor (PDGFR), another target of imatinib that is expressed by the uterine muscle cells themselves, failed to affect myogenic contractions.	imatinib	139-147	platelet derived growth factor receptor beta	Homo sapiens	113-118
16931795-0	2006	Stem cell factor deficiency is vasculoprotective: unraveling a new therapeutic potential of imatinib mesylate.	imatinib	92-109	kit ligand	Mus musculus	0-16
16931795-6	2006	Pharmacological antagonism of the SCF/c-Kit pathway with imatinib mesylate (Gleevec) or ACK2 (c-Kit antibody) also resulted in a marked reduction in intimal hyperplasia.	imatinib	57-74	kit ligand	Mus musculus	34-37
16982758-0	2006	Heat shock protein 90 inhibition in imatinib-resistant gastrointestinal stromal tumor.	imatinib	36-44	heat shock protein 90 alpha family class A member 1	Homo sapiens	0-21
16931795-6	2006	Pharmacological antagonism of the SCF/c-Kit pathway with imatinib mesylate (Gleevec) or ACK2 (c-Kit antibody) also resulted in a marked reduction in intimal hyperplasia.	imatinib	57-74	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	38-43
16982758-1	2006	Inhibition of KIT oncoproteins by imatinib induces clinical responses in most gastrointestinal stromal tumor (GIST) patients.	imatinib	34-42	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-17
16982758-3	2006	Heat shock protein 90 (HSP90) protects KIT oncoproteins from proteasome-mediated degradation, and we therefore did preclinical validations of the HSP90 inhibitor, 17-allylamino-18-demethoxy-geldanamycin (17-AAG), in an imatinib-sensitive GIST cell line (GIST882) and in novel imatinib-resistant GIST lines that are either dependent on (GIST430 and GIST48) or independent of (GIST62) KIT oncoproteins.	imatinib	276-284	heat shock protein 90 alpha family class A member 1	Homo sapiens	0-21
16982758-3	2006	Heat shock protein 90 (HSP90) protects KIT oncoproteins from proteasome-mediated degradation, and we therefore did preclinical validations of the HSP90 inhibitor, 17-allylamino-18-demethoxy-geldanamycin (17-AAG), in an imatinib-sensitive GIST cell line (GIST882) and in novel imatinib-resistant GIST lines that are either dependent on (GIST430 and GIST48) or independent of (GIST62) KIT oncoproteins.	imatinib	276-284	heat shock protein 90 alpha family class A member 1	Homo sapiens	23-28
16982758-2	2006	However, many patients develop imatinib resistance due to secondary KIT mutations.	imatinib	31-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	68-71
16931795-9	2006	Vascular injury also caused an increase in circulating SCF levels which promoted CD34(+) PC mobilization, a response that was blunted in mutant and imatinib mesylate-treated mice.	imatinib	148-165	kit ligand	Mus musculus	55-58
16982758-3	2006	Heat shock protein 90 (HSP90) protects KIT oncoproteins from proteasome-mediated degradation, and we therefore did preclinical validations of the HSP90 inhibitor, 17-allylamino-18-demethoxy-geldanamycin (17-AAG), in an imatinib-sensitive GIST cell line (GIST882) and in novel imatinib-resistant GIST lines that are either dependent on (GIST430 and GIST48) or independent of (GIST62) KIT oncoproteins.	imatinib	219-227	heat shock protein 90 alpha family class A member 1	Homo sapiens	0-21
16931795-9	2006	Vascular injury also caused an increase in circulating SCF levels which promoted CD34(+) PC mobilization, a response that was blunted in mutant and imatinib mesylate-treated mice.	imatinib	148-165	CD34 antigen	Mus musculus	81-85
16982758-3	2006	Heat shock protein 90 (HSP90) protects KIT oncoproteins from proteasome-mediated degradation, and we therefore did preclinical validations of the HSP90 inhibitor, 17-allylamino-18-demethoxy-geldanamycin (17-AAG), in an imatinib-sensitive GIST cell line (GIST882) and in novel imatinib-resistant GIST lines that are either dependent on (GIST430 and GIST48) or independent of (GIST62) KIT oncoproteins.	imatinib	219-227	heat shock protein 90 alpha family class A member 1	Homo sapiens	23-28
16982758-8	2006	The dramatic inactivation of imatinib-resistant KIT oncoproteins suggests that HSP90 inhibition provides a therapeutic solution to the challenge of heterogeneous imatinib resistance mutations in GIST patients.	imatinib	29-37	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	48-51
27265480-1	2006	It has been shown that imatinib mesylate, a drug used in the treatment of chronic myelogenous leukemia, inhibits the effect of stem cell factor, which has a central role in erythropoiesis.	imatinib	23-40	KIT ligand	Homo sapiens	127-143
16982758-8	2006	The dramatic inactivation of imatinib-resistant KIT oncoproteins suggests that HSP90 inhibition provides a therapeutic solution to the challenge of heterogeneous imatinib resistance mutations in GIST patients.	imatinib	29-37	heat shock protein 90 alpha family class A member 1	Homo sapiens	79-84
16982758-8	2006	The dramatic inactivation of imatinib-resistant KIT oncoproteins suggests that HSP90 inhibition provides a therapeutic solution to the challenge of heterogeneous imatinib resistance mutations in GIST patients.	imatinib	162-170	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	48-51
16982758-8	2006	The dramatic inactivation of imatinib-resistant KIT oncoproteins suggests that HSP90 inhibition provides a therapeutic solution to the challenge of heterogeneous imatinib resistance mutations in GIST patients.	imatinib	162-170	heat shock protein 90 alpha family class A member 1	Homo sapiens	79-84
16908931-9	2006	Because the majority of the KIT mutations we found in melanoma also occur in imatinib-responsive cancers of other types, imatinib may offer an immediate therapeutic benefit for a significant proportion of the global melanoma burden.	imatinib	77-85	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	28-31
16908931-9	2006	Because the majority of the KIT mutations we found in melanoma also occur in imatinib-responsive cancers of other types, imatinib may offer an immediate therapeutic benefit for a significant proportion of the global melanoma burden.	imatinib	121-129	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	28-31
27265480-8	2006	For both types, the inhibitory effect of imatinib mesylate was striking in the presence of all cytokines including IL-3, GM-CSF and Epo.	imatinib	41-58	interleukin 3	Homo sapiens	115-119
27265480-8	2006	For both types, the inhibitory effect of imatinib mesylate was striking in the presence of all cytokines including IL-3, GM-CSF and Epo.	imatinib	41-58	colony stimulating factor 2	Homo sapiens	121-127
27265480-8	2006	For both types, the inhibitory effect of imatinib mesylate was striking in the presence of all cytokines including IL-3, GM-CSF and Epo.	imatinib	41-58	erythropoietin	Homo sapiens	132-135
27265480-9	2006	There is no direct evidence yet that imatinib mesylate could inhibit the effect of IL-3, G-CSF, GM-CSF, Epo and IGF-I on erythropoiesis.	imatinib	37-54	interleukin 3	Homo sapiens	83-87
27265480-9	2006	There is no direct evidence yet that imatinib mesylate could inhibit the effect of IL-3, G-CSF, GM-CSF, Epo and IGF-I on erythropoiesis.	imatinib	37-54	colony stimulating factor 3	Homo sapiens	89-94
27265480-9	2006	There is no direct evidence yet that imatinib mesylate could inhibit the effect of IL-3, G-CSF, GM-CSF, Epo and IGF-I on erythropoiesis.	imatinib	37-54	colony stimulating factor 2	Homo sapiens	96-102
27265480-9	2006	There is no direct evidence yet that imatinib mesylate could inhibit the effect of IL-3, G-CSF, GM-CSF, Epo and IGF-I on erythropoiesis.	imatinib	37-54	erythropoietin	Homo sapiens	104-107
27265480-9	2006	There is no direct evidence yet that imatinib mesylate could inhibit the effect of IL-3, G-CSF, GM-CSF, Epo and IGF-I on erythropoiesis.	imatinib	37-54	insulin like growth factor 1	Homo sapiens	112-117
27265480-10	2006	Considering former studies together with results of this study, it can be argued that imatinib mesylate is effective in PV on the intersecting signal transduction mechanisms in which stem cell factor and its receptor may have a part.	imatinib	86-103	KIT ligand	Homo sapiens	183-199
16904383-2	2006	Imatinib mesylate (STI571) is a specific inhibitor of the BCR/ABL fusion tyrosine kinase that exhibits potent antileukemic effects in CML.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
17018739-4	2006	Most KIT mutations occur in untreated GISTs in the juxtamembrane exon 11 and only rarely in the kinase domain, whereas in imatinib-treated patients secondary mutations are frequent in exons encoding for the ATP/imatinib binding pocket or the kinase activation loop.	imatinib	122-130	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	5-8
17018739-4	2006	Most KIT mutations occur in untreated GISTs in the juxtamembrane exon 11 and only rarely in the kinase domain, whereas in imatinib-treated patients secondary mutations are frequent in exons encoding for the ATP/imatinib binding pocket or the kinase activation loop.	imatinib	211-219	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	5-8
16638934-3	2006	Coadministration of imatinib and induction cycle 2 (INDII) resulted in a complete remission (CR) rate of 95% and polymerase chain reaction (PCR) negativity for BCR-ABL in 52% of patients, compared with 19% in patients in the alternating treatment cohort (P = .01).	imatinib	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-167
16638934-8	2006	Both schedules of imatinib have acceptable toxicity and facilitate SCT in CR1 in the majority of patients, but concurrent administration of imatinib and chemotherapy has greater antileukemic efficacy.	imatinib	18-26	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	74-77
16670264-7	2006	In vitro treatment of human CML cell lines with imatinib or siRNA directed against BCR-ABL significantly reduced BCR-ABL while increasing CCN3 expression.	imatinib	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
16670264-7	2006	In vitro treatment of human CML cell lines with imatinib or siRNA directed against BCR-ABL significantly reduced BCR-ABL while increasing CCN3 expression.	imatinib	48-56	cellular communication network factor 3	Homo sapiens	138-142
16670264-8	2006	Cells from patients responding to imatinib showed a similar decrease in BCR-ABL and increase in CCN3.	imatinib	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
16670264-8	2006	Cells from patients responding to imatinib showed a similar decrease in BCR-ABL and increase in CCN3.	imatinib	34-42	cellular communication network factor 3	Homo sapiens	96-100
16670264-9	2006	CML CD34+ cells treated with imatinib in vitro demonstrated increased CCN3 protein.	imatinib	29-37	CD34 molecule	Homo sapiens	4-8
16670264-9	2006	CML CD34+ cells treated with imatinib in vitro demonstrated increased CCN3 protein.	imatinib	29-37	cellular communication network factor 3	Homo sapiens	70-74
16822295-1	2006	Adaphostin is a tyrphostin that was designed to inhibit Bcr/Abl tyrosine kinase by altering the binding site of peptide substrates rather than that of adenosine triphosphate, a known mechanism of imatinib mesylate (IM).	imatinib	196-213	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
16904383-2	2006	Imatinib mesylate (STI571) is a specific inhibitor of the BCR/ABL fusion tyrosine kinase that exhibits potent antileukemic effects in CML.	imatinib	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
16920991-5	2006	We found that imatinib-treated CML-chronic phase patients showing a complete cytogenetic response had NKT cells capable of producing IFN-gamma, whereas NKT cells from patients who were only partially responsive to imatinib treatment did not produce IFN-gamma.	imatinib	14-22	interferon gamma	Homo sapiens	133-142
20425349-4	2006	Imatinib mesylate, a recently introduced specific tyrosine kinase inhibitor of BCR-ABL, in combination with chemotherapy, resulted in more than 90% hematologic CR in adult Ph-positive ALL, including molecular CR in more than 50% of patients.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
17167971-0	2006	Monitoring molecular response by BCR-ABL, JH and WT-1 in Ph+ all treated with imatinib containing regimen: preliminary report of two cases.	imatinib	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
16920991-5	2006	We found that imatinib-treated CML-chronic phase patients showing a complete cytogenetic response had NKT cells capable of producing IFN-gamma, whereas NKT cells from patients who were only partially responsive to imatinib treatment did not produce IFN-gamma.	imatinib	14-22	interferon gamma	Homo sapiens	249-258
16855633-1	2006	Imatinib (imatinib mesylate, STI-571, Gleevec) is a selective BCR-ABL tyrosine kinase inhibitor that has been used as a highly effective chemoagent for treating chronic myelogenous leukemia.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
16855633-1	2006	Imatinib (imatinib mesylate, STI-571, Gleevec) is a selective BCR-ABL tyrosine kinase inhibitor that has been used as a highly effective chemoagent for treating chronic myelogenous leukemia.	imatinib	10-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
16855633-1	2006	Imatinib (imatinib mesylate, STI-571, Gleevec) is a selective BCR-ABL tyrosine kinase inhibitor that has been used as a highly effective chemoagent for treating chronic myelogenous leukemia.	imatinib	29-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
16855633-8	2006	Several genes identified in this study such as IGF1 and RAB11A have the potential to become surrogate markers useful in a clinical evaluation of imatinib-resistant patients without BCR-ABL mutation.	imatinib	145-153	insulin like growth factor 1	Homo sapiens	47-51
16406018-10	2006	Because of the availability of a superior targeted drug (imatinib), it is of importance to screen for FIP1L1/PDGFRalpha in suspected CEL with or without co-existing SM.	imatinib	57-65	factor interacting with PAPOLA and CPSF1	Homo sapiens	102-108
16855633-8	2006	Several genes identified in this study such as IGF1 and RAB11A have the potential to become surrogate markers useful in a clinical evaluation of imatinib-resistant patients without BCR-ABL mutation.	imatinib	145-153	RAB11A, member RAS oncogene family	Homo sapiens	56-62
16507320-4	2006	Treatment with the ABL tyrosine kinase inhibitor Imatinib mesylate increased PDCD5 expression in K562 and MEG-01 cells.	imatinib	49-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-22
16627755-0	2006	Functional ABCG2 is overexpressed on primary CML CD34+ cells and is inhibited by imatinib mesylate.	imatinib	81-98	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	11-16
16507320-4	2006	Treatment with the ABL tyrosine kinase inhibitor Imatinib mesylate increased PDCD5 expression in K562 and MEG-01 cells.	imatinib	49-66	programmed cell death 5	Homo sapiens	77-82
16778826-5	2006	Successful treatment of metastatic and unresectable gastrointestinal stromal tumors with KIT kinase inhibitor, imatinib mesylate (Gleevec), makes it intriguing to look at the status of KIT in solid-pseudopapillary neoplasms of the pancreas.	imatinib	111-128	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	89-92
16778826-13	2006	Experience in gastrointestinal stromal tumors and other tumors have shown that mutation-mediated activation of KIT or PDGFRA is a prerequisite for clinical response with imatinib mesylate.	imatinib	170-187	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	111-114
16778826-13	2006	Experience in gastrointestinal stromal tumors and other tumors have shown that mutation-mediated activation of KIT or PDGFRA is a prerequisite for clinical response with imatinib mesylate.	imatinib	170-187	platelet derived growth factor receptor alpha	Homo sapiens	118-124
16908864-4	2006	Analysis of tumor tissue from imatinib-treated mice showed diminished phosphatidylinositol 3-kinase (PI3-kinase) and mammalian target of rapamycin (mTOR) signaling suggesting that oncogenic Kit signaling critically contributes to the translational response in GIST.	imatinib	30-38	mechanistic target of rapamycin kinase	Homo sapiens	117-146
16908864-4	2006	Analysis of tumor tissue from imatinib-treated mice showed diminished phosphatidylinositol 3-kinase (PI3-kinase) and mammalian target of rapamycin (mTOR) signaling suggesting that oncogenic Kit signaling critically contributes to the translational response in GIST.	imatinib	30-38	mechanistic target of rapamycin kinase	Homo sapiens	148-152
16908864-5	2006	Treatment with RAD001 (everolimus), an mTOR inhibitor, diminished the translational response and cell proliferation in tumor lesions, pointing to mTOR inhibition as a therapeutic approach for imatinib-resistant GIST.	imatinib	192-200	mechanistic target of rapamycin kinase	Mus musculus	146-150
16601247-0	2006	Allogeneic stem cell transplantation for patients with chronic myeloid leukemia and acute lymphocytic leukemia after Bcr-Abl kinase mutation-related imatinib failure.	imatinib	149-157	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
16601247-1	2006	Resistance to imatinib mesylate is an emerging problem in the treatment of chronic myeloid leukemia (CML), often associated with point mutations in the Bcr-Abl kinase domain.	imatinib	14-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-159
16601247-3	2006	Ten imatinib-resistant patients with Bcr-Abl kinase mutations received a transplant: 9 had CML (3 in chronic phase, 4 in accelerated phase, and 2 in blast phase) and 1 had Philadelphia-positive acute lymphocytic leukemia (ALL).	imatinib	4-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
16601247-10	2006	Allo-SCT remains an important salvage option for patients who develop resistance to imatinib through Bcr-Abl mutations.	imatinib	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
16645167-0	2006	Sorafenib is a potent inhibitor of FIP1L1-PDGFRalpha and the imatinib-resistant FIP1L1-PDGFRalpha T674I mutant.	imatinib	61-69	factor interacting with PAPOLA and CPSF1	Homo sapiens	80-86
16614241-1	2006	In advanced-phase chronic myeloid leukemia (CML), resistance to imatinib mesylate is associated with point mutations in the BCR-ABL kinase domain.	imatinib	64-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
16645167-1	2006	The FIP1L1-PDGFRA oncogene is a common cause of chronic eosinophilic leukemia (CEL), and encodes an activated tyrosine kinase that is inhibited by imatinib.	imatinib	147-155	factor interacting with PAPOLA and CPSF1	Homo sapiens	4-10
16645167-1	2006	The FIP1L1-PDGFRA oncogene is a common cause of chronic eosinophilic leukemia (CEL), and encodes an activated tyrosine kinase that is inhibited by imatinib.	imatinib	147-155	platelet derived growth factor receptor alpha	Homo sapiens	11-17
16670262-2	2006	Patients with CML in blast crisis (CML-BC) became rapidly resistant to therapy with the breakpoint cluster region-Abelson murine leukemia (BCR/ABL) kinase inhibitor imatinib (STI571) because of mutations in the kinase domain that interfere with drug binding.	imatinib	165-173	BCR activator of RhoGEF and GTPase	Mus musculus	139-142
16645167-2	2006	FIP1L1-PDGFRA-positive patients with CEL respond to low-dose imatinib therapy, but resistance due to acquired T674I mutation has been observed.	imatinib	61-69	factor interacting with PAPOLA and CPSF1	Homo sapiens	0-6
16670262-2	2006	Patients with CML in blast crisis (CML-BC) became rapidly resistant to therapy with the breakpoint cluster region-Abelson murine leukemia (BCR/ABL) kinase inhibitor imatinib (STI571) because of mutations in the kinase domain that interfere with drug binding.	imatinib	165-173	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	143-146
16645167-2	2006	FIP1L1-PDGFRA-positive patients with CEL respond to low-dose imatinib therapy, but resistance due to acquired T674I mutation has been observed.	imatinib	61-69	platelet derived growth factor receptor alpha	Homo sapiens	7-13
16547494-8	2006	Supervised analyses of gene expression profiles and real-time PCR analyses identified expression of the chemokine CXCL12/SDF-1 (stromal cell-derived factor 1) as a predictor of imatinib sensitivity.	imatinib	177-185	C-X-C motif chemokine ligand 12	Homo sapiens	114-120
16914578-16	2006	CYP3A4 inducers, such as EIAEDs, substantially decreased plasma exposure of imatinib and should be avoided in patients receiving imatinib for chronic myelogenous leukemia and gastrointestinal stromal tumors.	imatinib	76-84	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
16914578-16	2006	CYP3A4 inducers, such as EIAEDs, substantially decreased plasma exposure of imatinib and should be avoided in patients receiving imatinib for chronic myelogenous leukemia and gastrointestinal stromal tumors.	imatinib	129-137	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
17064569-10	2006	CONCLUSION: STI571 could promote the activation/maturation of DC derived from BMMNCs of patients with CML in vitro, which might be partially responsible for the fact that the inhibitory effect of VEGF on DC NF-kappaB activation was relieved through STI571 inhibiting the overproduction of VEGF in CML.	imatinib	12-18	vascular endothelial growth factor A	Homo sapiens	196-200
17064569-10	2006	CONCLUSION: STI571 could promote the activation/maturation of DC derived from BMMNCs of patients with CML in vitro, which might be partially responsible for the fact that the inhibitory effect of VEGF on DC NF-kappaB activation was relieved through STI571 inhibiting the overproduction of VEGF in CML.	imatinib	12-18	vascular endothelial growth factor A	Homo sapiens	289-293
17064569-10	2006	CONCLUSION: STI571 could promote the activation/maturation of DC derived from BMMNCs of patients with CML in vitro, which might be partially responsible for the fact that the inhibitory effect of VEGF on DC NF-kappaB activation was relieved through STI571 inhibiting the overproduction of VEGF in CML.	imatinib	249-255	vascular endothelial growth factor A	Homo sapiens	196-200
16547494-8	2006	Supervised analyses of gene expression profiles and real-time PCR analyses identified expression of the chemokine CXCL12/SDF-1 (stromal cell-derived factor 1) as a predictor of imatinib sensitivity.	imatinib	177-185	C-X-C motif chemokine ligand 12	Homo sapiens	121-126
16547494-8	2006	Supervised analyses of gene expression profiles and real-time PCR analyses identified expression of the chemokine CXCL12/SDF-1 (stromal cell-derived factor 1) as a predictor of imatinib sensitivity.	imatinib	177-185	C-X-C motif chemokine ligand 12	Homo sapiens	128-157
16547494-9	2006	Exogenous addition of CXCL12 to imatinib-insensitive cultures conferred some imatinib sensitivity.	imatinib	32-40	C-X-C motif chemokine ligand 12	Homo sapiens	22-28
16547494-9	2006	Exogenous addition of CXCL12 to imatinib-insensitive cultures conferred some imatinib sensitivity.	imatinib	77-85	C-X-C motif chemokine ligand 12	Homo sapiens	22-28
16906325-1	2006	Imatinib (Gleevec/STI-571/CGP57148B, Novartis) is a small-molecule, tyrosine kinase inhibitor developed to target BCR-ABL, c-Kit, and PDGF-R.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
16906325-1	2006	Imatinib (Gleevec/STI-571/CGP57148B, Novartis) is a small-molecule, tyrosine kinase inhibitor developed to target BCR-ABL, c-Kit, and PDGF-R.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	123-128
16906325-1	2006	Imatinib (Gleevec/STI-571/CGP57148B, Novartis) is a small-molecule, tyrosine kinase inhibitor developed to target BCR-ABL, c-Kit, and PDGF-R.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	134-140
16906325-5	2006	Additional work has shown that new BCR-ABL kinase inhibitors with increased potency or alternate conformation-binding properties can target imatinib resistance.	imatinib	140-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
16885384-5	2006	We also show that STI-571, an inhibitor of c-Abl kinase activity, induces apoptosis of CLL cells with high c-Abl expression levels through a mechanism involving inhibition of nuclear factor kappaB.	imatinib	18-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-48
16906325-2	2006	Through inhibition of these oncogenic kinases, imatinib is effective in the treatment of BCR-ABL-positive leukemia, gastrointestinal stromal tumor, and hypereosinophilic syndrome, respectively.	imatinib	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
16858179-5	2006	The discovery of the centrality of KIT proto-oncogene mutations in the pathogenesis of this tumor, and the development of imatinib mesylate, a specific inhibitor of KIT tyrosine kinase function have revolutionized the treatment of GIST.	imatinib	122-139	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	165-168
16858179-11	2006	The benefit of adjuvant treatment with the KIT tyrosine kinase inhibitor imatinib is the subject of investigation.	imatinib	73-81	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	43-46
16885384-5	2006	We also show that STI-571, an inhibitor of c-Abl kinase activity, induces apoptosis of CLL cells with high c-Abl expression levels through a mechanism involving inhibition of nuclear factor kappaB.	imatinib	18-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-112
16890580-1	2006	OBJECTIVE: Our objective was to explore the relationships between imatinib pharmacokinetics and 9 allelic variants in 7 genes coding for adenosine triphosphate-binding cassette transporters (ABCB1 and ABCG2) and enzymes (cytochrome P450 [CYP] 2C9, CYP2C19, CYP2D6, CYP3A4, and CYP3A5) of putative relevance for imatinib.	imatinib	66-74	ATP binding cassette subfamily B member 1	Homo sapiens	191-196
16890580-1	2006	OBJECTIVE: Our objective was to explore the relationships between imatinib pharmacokinetics and 9 allelic variants in 7 genes coding for adenosine triphosphate-binding cassette transporters (ABCB1 and ABCG2) and enzymes (cytochrome P450 [CYP] 2C9, CYP2C19, CYP2D6, CYP3A4, and CYP3A5) of putative relevance for imatinib.	imatinib	66-74	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	201-206
16952848-5	2006	Imatinib mesilate is a drug that inhibits c-kit activity expressed by GIST and its activity in these tumours has been demonstrated.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	42-47
16890580-1	2006	OBJECTIVE: Our objective was to explore the relationships between imatinib pharmacokinetics and 9 allelic variants in 7 genes coding for adenosine triphosphate-binding cassette transporters (ABCB1 and ABCG2) and enzymes (cytochrome P450 [CYP] 2C9, CYP2C19, CYP2D6, CYP3A4, and CYP3A5) of putative relevance for imatinib.	imatinib	66-74	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	221-246
16890580-1	2006	OBJECTIVE: Our objective was to explore the relationships between imatinib pharmacokinetics and 9 allelic variants in 7 genes coding for adenosine triphosphate-binding cassette transporters (ABCB1 and ABCG2) and enzymes (cytochrome P450 [CYP] 2C9, CYP2C19, CYP2D6, CYP3A4, and CYP3A5) of putative relevance for imatinib.	imatinib	66-74	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	248-255
16890580-1	2006	OBJECTIVE: Our objective was to explore the relationships between imatinib pharmacokinetics and 9 allelic variants in 7 genes coding for adenosine triphosphate-binding cassette transporters (ABCB1 and ABCG2) and enzymes (cytochrome P450 [CYP] 2C9, CYP2C19, CYP2D6, CYP3A4, and CYP3A5) of putative relevance for imatinib.	imatinib	66-74	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	257-263
16890580-1	2006	OBJECTIVE: Our objective was to explore the relationships between imatinib pharmacokinetics and 9 allelic variants in 7 genes coding for adenosine triphosphate-binding cassette transporters (ABCB1 and ABCG2) and enzymes (cytochrome P450 [CYP] 2C9, CYP2C19, CYP2D6, CYP3A4, and CYP3A5) of putative relevance for imatinib.	imatinib	66-74	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	265-271
16890580-1	2006	OBJECTIVE: Our objective was to explore the relationships between imatinib pharmacokinetics and 9 allelic variants in 7 genes coding for adenosine triphosphate-binding cassette transporters (ABCB1 and ABCG2) and enzymes (cytochrome P450 [CYP] 2C9, CYP2C19, CYP2D6, CYP3A4, and CYP3A5) of putative relevance for imatinib.	imatinib	66-74	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	277-283
16890580-1	2006	OBJECTIVE: Our objective was to explore the relationships between imatinib pharmacokinetics and 9 allelic variants in 7 genes coding for adenosine triphosphate-binding cassette transporters (ABCB1 and ABCG2) and enzymes (cytochrome P450 [CYP] 2C9, CYP2C19, CYP2D6, CYP3A4, and CYP3A5) of putative relevance for imatinib.	imatinib	311-319	ATP binding cassette subfamily B member 1	Homo sapiens	191-196
16890580-2	2006	METHODS: Imatinib transport in vitro was studied by use of human embryonic kidney 293 cells transfected with wild-type ABCG2 and an ABCG2 Q141K clone.	imatinib	9-17	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	119-124
16890580-2	2006	METHODS: Imatinib transport in vitro was studied by use of human embryonic kidney 293 cells transfected with wild-type ABCG2 and an ABCG2 Q141K clone.	imatinib	9-17	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	132-137
16890580-7	2006	The apparent oral clearance of imatinib was potentially reduced in individuals with at least 1 CYP2D6*4 allele (median, 7.78 versus 10.6 L/h; P = .0695).	imatinib	31-39	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	95-101
16890580-10	2006	Further investigation is required to quantitatively assess the clinical significance of homozygous variant ABCG2 and CYP2D6 genotypes in patients treated with imatinib.	imatinib	159-167	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	107-112
16890580-10	2006	Further investigation is required to quantitatively assess the clinical significance of homozygous variant ABCG2 and CYP2D6 genotypes in patients treated with imatinib.	imatinib	159-167	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	117-123
16820883-0	2006	Enhancement of radiation sensitivity, delay of proliferative recovery after radiation and abrogation of MAPK (p44/42) signaling by imatinib in glioblastoma cells.	imatinib	131-139	interferon induced protein 44	Homo sapiens	110-113
16926141-2	2006	Upon detection of BCR-ABL transcripts after PBSCT, the patient received imatinib, leading to molecular remission.	imatinib	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
16820883-6	2006	Imatinib promoted suppression of p44/42 MAPK signaling both when added prior to and post-irradiation.	imatinib	0-8	interferon induced protein 44	Homo sapiens	33-36
16820883-7	2006	Increased sensitivity to radiation and delayed proliferative recovery in irradiated glioblastoma cells exposed to imatinib may be a consequence of the capacity of imatinib to interfere with p44/42 MAPK kinase signaling.	imatinib	114-122	interferon induced protein 44	Homo sapiens	190-193
16820883-7	2006	Increased sensitivity to radiation and delayed proliferative recovery in irradiated glioblastoma cells exposed to imatinib may be a consequence of the capacity of imatinib to interfere with p44/42 MAPK kinase signaling.	imatinib	163-171	interferon induced protein 44	Homo sapiens	190-193
18156735-12	2006	During the course of the disease of the two patients, we monitored the BCR-ABL chimeric mRNA with real-time quantitative polymerase chain reaction (RT-PCR), and it was found useful in predicting the imatinib response and progression to blast crisis of CML.	imatinib	199-207	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
16406016-0	2006	FIP1L1-PDGFRA in eosinophilic disorders: prevalence in routine clinical practice, long-term experience with imatinib therapy, and a critical review of the literature.	imatinib	108-116	factor interacting with PAPOLA and CPSF1	Homo sapiens	0-6
16406016-2	2006	In that series, all 11 FIP1L1-PDGFRA+ patients receiving imatinib achieved a complete response.	imatinib	57-65	factor interacting with PAPOLA and CPSF1	Homo sapiens	23-29
16840500-6	2006	STI571, a specific inhibitor for cytoplasmic tyrosine kinase c-Abl, can inhibit F-actin polymerization and c-Abl redistribution in the activated neutrophils.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-66
16840500-6	2006	STI571, a specific inhibitor for cytoplasmic tyrosine kinase c-Abl, can inhibit F-actin polymerization and c-Abl redistribution in the activated neutrophils.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-112
16936444-7	2006	Subsequent clinical studies now realize the hypothesis that selective inhibition of the abl tyrosine kinase activity using imatinib mesylate might be useful for the treatment of CML.	imatinib	123-140	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	88-91
16966279-1	2006	Imatinib mesylate suppresses phosphorylation of its kinase target, Bcr-Abl.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
16406016-2	2006	In that series, all 11 FIP1L1-PDGFRA+ patients receiving imatinib achieved a complete response.	imatinib	57-65	platelet derived growth factor receptor alpha	Homo sapiens	30-36
16862153-5	2006	Retroviral gene transfer of an imatinib-resistant mutant of c-Abl, alleviation of ER stress or inhibition of Jun amino-terminal kinases, which are activated as a consequence of ER stress, largely rescues cardiomyocytes from imatinib-induced death.	imatinib	31-39	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	60-65
16880519-0	2006	Kinase domain mutants of Bcr-Abl exhibit altered transformation potency, kinase activity, and substrate utilization, irrespective of sensitivity to imatinib.	imatinib	148-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
16880519-1	2006	Kinase domain (KD) mutations of Bcr-Abl interfering with imatinib binding are the major mechanism of acquired imatinib resistance in patients with Philadelphia chromosome-positive leukemia.	imatinib	57-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
16880519-1	2006	Kinase domain (KD) mutations of Bcr-Abl interfering with imatinib binding are the major mechanism of acquired imatinib resistance in patients with Philadelphia chromosome-positive leukemia.	imatinib	110-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
16862153-6	2006	Thus, cardiotoxicity is an unanticipated side effect of inhibition of c-Abl by imatinib.	imatinib	79-87	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	70-75
16862153-5	2006	Retroviral gene transfer of an imatinib-resistant mutant of c-Abl, alleviation of ER stress or inhibition of Jun amino-terminal kinases, which are activated as a consequence of ER stress, largely rescues cardiomyocytes from imatinib-induced death.	imatinib	224-232	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	60-65
16543472-0	2006	Complex interaction of BCRP/ABCG2 and imatinib in BCR-ABL-expressing cells: BCRP-mediated resistance to imatinib is attenuated by imatinib-induced reduction of BCRP expression.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
16858728-0	2006	Quantification of change in phosphorylation of BCR-ABL kinase and its substrates in response to Imatinib treatment in human chronic myelogenous leukemia cells.	imatinib	96-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
16858728-6	2006	Based on the relative intensity of isotopic peptide pairs, we demonstrate that the level of phosphorylation of BCR-ABL kinase as well as SHIP-2 and Dok-2 is reduced approximately 90% upon treatment with Imatinib, a specific inhibitor of BCR-ABL kinase.	imatinib	203-211	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
16858728-6	2006	Based on the relative intensity of isotopic peptide pairs, we demonstrate that the level of phosphorylation of BCR-ABL kinase as well as SHIP-2 and Dok-2 is reduced approximately 90% upon treatment with Imatinib, a specific inhibitor of BCR-ABL kinase.	imatinib	203-211	inositol polyphosphate phosphatase like 1	Homo sapiens	137-143
16858728-6	2006	Based on the relative intensity of isotopic peptide pairs, we demonstrate that the level of phosphorylation of BCR-ABL kinase as well as SHIP-2 and Dok-2 is reduced approximately 90% upon treatment with Imatinib, a specific inhibitor of BCR-ABL kinase.	imatinib	203-211	docking protein 2	Homo sapiens	148-153
16858728-6	2006	Based on the relative intensity of isotopic peptide pairs, we demonstrate that the level of phosphorylation of BCR-ABL kinase as well as SHIP-2 and Dok-2 is reduced approximately 90% upon treatment with Imatinib, a specific inhibitor of BCR-ABL kinase.	imatinib	203-211	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	237-244
16858728-7	2006	Furthermore, proteins, such as SHIP-1, SH2-containing protein (SHC) and Casitas B-lineage lymphoma proto-oncogene (CBL), are also regulated by Imatinib.	imatinib	143-151	inositol polyphosphate-5-phosphatase D	Homo sapiens	31-37
16858728-7	2006	Furthermore, proteins, such as SHIP-1, SH2-containing protein (SHC) and Casitas B-lineage lymphoma proto-oncogene (CBL), are also regulated by Imatinib.	imatinib	143-151	Cbl proto-oncogene	Homo sapiens	72-113
16858728-7	2006	Furthermore, proteins, such as SHIP-1, SH2-containing protein (SHC) and Casitas B-lineage lymphoma proto-oncogene (CBL), are also regulated by Imatinib.	imatinib	143-151	Cbl proto-oncogene	Homo sapiens	115-118
16537804-4	2006	AMN107 was more potent than imatinib mesylate (IM) in inhibiting Bcr-Abl tyrosine kinase (TK) activity and attenuating p-STAT5, p-AKT, Bcl-x(L), and c-Myc levels in K562 and LAMA-84 cells.	imatinib	28-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
16543472-0	2006	Complex interaction of BCRP/ABCG2 and imatinib in BCR-ABL-expressing cells: BCRP-mediated resistance to imatinib is attenuated by imatinib-induced reduction of BCRP expression.	imatinib	38-46	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	76-80
16543472-0	2006	Complex interaction of BCRP/ABCG2 and imatinib in BCR-ABL-expressing cells: BCRP-mediated resistance to imatinib is attenuated by imatinib-induced reduction of BCRP expression.	imatinib	38-46	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	76-80
16597591-0	2006	OCT-1-mediated influx is a key determinant of the intracellular uptake of imatinib but not nilotinib (AMN107): reduced OCT-1 activity is the cause of low in vitro sensitivity to imatinib.	imatinib	74-82	solute carrier family 22 member 1	Homo sapiens	0-5
16597591-0	2006	OCT-1-mediated influx is a key determinant of the intracellular uptake of imatinib but not nilotinib (AMN107): reduced OCT-1 activity is the cause of low in vitro sensitivity to imatinib.	imatinib	74-82	solute carrier family 22 member 1	Homo sapiens	119-124
16597591-0	2006	OCT-1-mediated influx is a key determinant of the intracellular uptake of imatinib but not nilotinib (AMN107): reduced OCT-1 activity is the cause of low in vitro sensitivity to imatinib.	imatinib	178-186	solute carrier family 22 member 1	Homo sapiens	0-5
16597591-0	2006	OCT-1-mediated influx is a key determinant of the intracellular uptake of imatinib but not nilotinib (AMN107): reduced OCT-1 activity is the cause of low in vitro sensitivity to imatinib.	imatinib	178-186	solute carrier family 22 member 1	Homo sapiens	119-124
16543472-0	2006	Complex interaction of BCRP/ABCG2 and imatinib in BCR-ABL-expressing cells: BCRP-mediated resistance to imatinib is attenuated by imatinib-induced reduction of BCRP expression.	imatinib	104-112	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	23-27
16543472-0	2006	Complex interaction of BCRP/ABCG2 and imatinib in BCR-ABL-expressing cells: BCRP-mediated resistance to imatinib is attenuated by imatinib-induced reduction of BCRP expression.	imatinib	104-112	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	28-33
16543472-0	2006	Complex interaction of BCRP/ABCG2 and imatinib in BCR-ABL-expressing cells: BCRP-mediated resistance to imatinib is attenuated by imatinib-induced reduction of BCRP expression.	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
16597591-2	2006	IC50(imatinib) is defined as the in vitro concentration of drug required to reduce phosphorylation of the adaptor protein Crkl by 50%.	imatinib	5-13	CRK like proto-oncogene, adaptor protein	Homo sapiens	122-126
16779792-3	2006	Imatinib mesylate is a potent inhibitor of c-kit receptor tyrosine kinase activity.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	43-48
16543472-0	2006	Complex interaction of BCRP/ABCG2 and imatinib in BCR-ABL-expressing cells: BCRP-mediated resistance to imatinib is attenuated by imatinib-induced reduction of BCRP expression.	imatinib	104-112	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	76-80
16597591-9	2006	In conclusion, whereas OCT-1-mediated influx may be a key determinant of molecular response to imatinib, it is unlikely to impact on cellular uptake and patient response to nilotinib.	imatinib	95-103	solute carrier family 22 member 1	Homo sapiens	23-28
16543472-0	2006	Complex interaction of BCRP/ABCG2 and imatinib in BCR-ABL-expressing cells: BCRP-mediated resistance to imatinib is attenuated by imatinib-induced reduction of BCRP expression.	imatinib	104-112	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	76-80
16543472-0	2006	Complex interaction of BCRP/ABCG2 and imatinib in BCR-ABL-expressing cells: BCRP-mediated resistance to imatinib is attenuated by imatinib-induced reduction of BCRP expression.	imatinib	104-112	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	23-27
16543472-0	2006	Complex interaction of BCRP/ABCG2 and imatinib in BCR-ABL-expressing cells: BCRP-mediated resistance to imatinib is attenuated by imatinib-induced reduction of BCRP expression.	imatinib	104-112	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	28-33
16543472-0	2006	Complex interaction of BCRP/ABCG2 and imatinib in BCR-ABL-expressing cells: BCRP-mediated resistance to imatinib is attenuated by imatinib-induced reduction of BCRP expression.	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
16543472-0	2006	Complex interaction of BCRP/ABCG2 and imatinib in BCR-ABL-expressing cells: BCRP-mediated resistance to imatinib is attenuated by imatinib-induced reduction of BCRP expression.	imatinib	104-112	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	76-80
16543472-0	2006	Complex interaction of BCRP/ABCG2 and imatinib in BCR-ABL-expressing cells: BCRP-mediated resistance to imatinib is attenuated by imatinib-induced reduction of BCRP expression.	imatinib	104-112	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	76-80
16543472-1	2006	Imatinib, a potent tyrosine kinase inhibitor, is effluxed from cells by the breast cancer resistance protein (BCRP/ABCG2), yet published studies to date fail to demonstrate resistance to imatinib cytotoxicity in BCRP-overexpressing cells in vitro.	imatinib	0-8	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	76-108
16543472-1	2006	Imatinib, a potent tyrosine kinase inhibitor, is effluxed from cells by the breast cancer resistance protein (BCRP/ABCG2), yet published studies to date fail to demonstrate resistance to imatinib cytotoxicity in BCRP-overexpressing cells in vitro.	imatinib	0-8	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	110-114
16543472-1	2006	Imatinib, a potent tyrosine kinase inhibitor, is effluxed from cells by the breast cancer resistance protein (BCRP/ABCG2), yet published studies to date fail to demonstrate resistance to imatinib cytotoxicity in BCRP-overexpressing cells in vitro.	imatinib	0-8	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	115-120
16543472-1	2006	Imatinib, a potent tyrosine kinase inhibitor, is effluxed from cells by the breast cancer resistance protein (BCRP/ABCG2), yet published studies to date fail to demonstrate resistance to imatinib cytotoxicity in BCRP-overexpressing cells in vitro.	imatinib	0-8	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	212-216
16543472-2	2006	We investigated cellular resistance to imatinib in BCR-ABL-expressing cells transduced and selected to overexpress BCRP (K562/BCRP-MX10).	imatinib	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
16543472-4	2006	Resistance to imatinib was completely abolished by the specific BCRP inhibitor fumitremorgin C. Studies of the mechanism of the diminished resistance to imatinib compared with mitoxantrone revealed that imatinib decreased the expression of BCRP in K562/BCRP-MX10 cells without affecting mRNA levels.	imatinib	14-22	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	64-68
16543472-4	2006	Resistance to imatinib was completely abolished by the specific BCRP inhibitor fumitremorgin C. Studies of the mechanism of the diminished resistance to imatinib compared with mitoxantrone revealed that imatinib decreased the expression of BCRP in K562/BCRP-MX10 cells without affecting mRNA levels.	imatinib	14-22	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	240-244
16543472-4	2006	Resistance to imatinib was completely abolished by the specific BCRP inhibitor fumitremorgin C. Studies of the mechanism of the diminished resistance to imatinib compared with mitoxantrone revealed that imatinib decreased the expression of BCRP in K562/BCRP-MX10 cells without affecting mRNA levels.	imatinib	14-22	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	248-262
16543472-4	2006	Resistance to imatinib was completely abolished by the specific BCRP inhibitor fumitremorgin C. Studies of the mechanism of the diminished resistance to imatinib compared with mitoxantrone revealed that imatinib decreased the expression of BCRP in K562/BCRP-MX10 cells without affecting mRNA levels.	imatinib	153-161	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	64-68
16543472-4	2006	Resistance to imatinib was completely abolished by the specific BCRP inhibitor fumitremorgin C. Studies of the mechanism of the diminished resistance to imatinib compared with mitoxantrone revealed that imatinib decreased the expression of BCRP in K562/BCRP-MX10 cells without affecting mRNA levels.	imatinib	153-161	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	240-244
16543472-4	2006	Resistance to imatinib was completely abolished by the specific BCRP inhibitor fumitremorgin C. Studies of the mechanism of the diminished resistance to imatinib compared with mitoxantrone revealed that imatinib decreased the expression of BCRP in K562/BCRP-MX10 cells without affecting mRNA levels.	imatinib	153-161	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	248-262
16543472-4	2006	Resistance to imatinib was completely abolished by the specific BCRP inhibitor fumitremorgin C. Studies of the mechanism of the diminished resistance to imatinib compared with mitoxantrone revealed that imatinib decreased the expression of BCRP in K562/BCRP-MX10 cells without affecting mRNA levels.	imatinib	153-161	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	64-68
16543472-4	2006	Resistance to imatinib was completely abolished by the specific BCRP inhibitor fumitremorgin C. Studies of the mechanism of the diminished resistance to imatinib compared with mitoxantrone revealed that imatinib decreased the expression of BCRP in K562/BCRP-MX10 cells without affecting mRNA levels.	imatinib	153-161	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	240-244
16543472-4	2006	Resistance to imatinib was completely abolished by the specific BCRP inhibitor fumitremorgin C. Studies of the mechanism of the diminished resistance to imatinib compared with mitoxantrone revealed that imatinib decreased the expression of BCRP in K562/BCRP-MX10 cells without affecting mRNA levels.	imatinib	153-161	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	248-262
16543472-6	2006	Loss of BCRP expression was accompanied by imatinib-induced reduction of phosphorylated Akt in the BCRP-expressing K562 cells.	imatinib	43-51	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	8-12
16543472-6	2006	Loss of BCRP expression was accompanied by imatinib-induced reduction of phosphorylated Akt in the BCRP-expressing K562 cells.	imatinib	43-51	AKT serine/threonine kinase 1	Homo sapiens	88-91
16543472-6	2006	Loss of BCRP expression was accompanied by imatinib-induced reduction of phosphorylated Akt in the BCRP-expressing K562 cells.	imatinib	43-51	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	99-103
16543472-8	2006	These studies show that BCRP causes measurable imatinib resistance, but this effect is attenuated by imatinib-mediated inhibition of BCR-ABL, which in turn downregulates overall BCRP levels posttranscriptionally via the PI3K-Akt pathway.	imatinib	47-55	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	24-28
16543472-8	2006	These studies show that BCRP causes measurable imatinib resistance, but this effect is attenuated by imatinib-mediated inhibition of BCR-ABL, which in turn downregulates overall BCRP levels posttranscriptionally via the PI3K-Akt pathway.	imatinib	101-109	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	24-28
16543472-8	2006	These studies show that BCRP causes measurable imatinib resistance, but this effect is attenuated by imatinib-mediated inhibition of BCR-ABL, which in turn downregulates overall BCRP levels posttranscriptionally via the PI3K-Akt pathway.	imatinib	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
16543472-8	2006	These studies show that BCRP causes measurable imatinib resistance, but this effect is attenuated by imatinib-mediated inhibition of BCR-ABL, which in turn downregulates overall BCRP levels posttranscriptionally via the PI3K-Akt pathway.	imatinib	101-109	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	178-182
16543472-8	2006	These studies show that BCRP causes measurable imatinib resistance, but this effect is attenuated by imatinib-mediated inhibition of BCR-ABL, which in turn downregulates overall BCRP levels posttranscriptionally via the PI3K-Akt pathway.	imatinib	101-109	AKT serine/threonine kinase 1	Homo sapiens	225-228
16846476-8	2006	Inhibition of BCR-ABL with imatinib mesylate led to a dose-dependent downregulation of total STAT3 protein and mRNA, suggesting that BCR-ABL is involved in the transcriptional regulation of STAT3.	imatinib	27-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
16434489-8	2006	Computer modeling suggests that the KITD816V mutation destabilizes the inactive conformation of the KIT activation loop to which imatinib binds, but it is not predicted to impair binding of KIT by dasatinib.	imatinib	129-137	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	36-39
16434489-8	2006	Computer modeling suggests that the KITD816V mutation destabilizes the inactive conformation of the KIT activation loop to which imatinib binds, but it is not predicted to impair binding of KIT by dasatinib.	imatinib	129-137	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	100-103
16917210-1	2006	Imatinib mesylate is a specific inhibitor of the Bcr-Abl protein tyrosine kinase that competes with ATP for its specific binding site in the kinase domain.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
16846476-8	2006	Inhibition of BCR-ABL with imatinib mesylate led to a dose-dependent downregulation of total STAT3 protein and mRNA, suggesting that BCR-ABL is involved in the transcriptional regulation of STAT3.	imatinib	27-44	signal transducer and activator of transcription 3	Homo sapiens	93-98
16846476-8	2006	Inhibition of BCR-ABL with imatinib mesylate led to a dose-dependent downregulation of total STAT3 protein and mRNA, suggesting that BCR-ABL is involved in the transcriptional regulation of STAT3.	imatinib	27-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
16846476-8	2006	Inhibition of BCR-ABL with imatinib mesylate led to a dose-dependent downregulation of total STAT3 protein and mRNA, suggesting that BCR-ABL is involved in the transcriptional regulation of STAT3.	imatinib	27-44	signal transducer and activator of transcription 3	Homo sapiens	190-195
16818614-5	2006	Similar to wild-type Bcr-Abl+ cells, inhibition of Jak2 by Ag490 treatment resulted in decrease of pSer Akt and c-Myc in imatinib-resistant cells.	imatinib	121-129	Janus kinase 2	Mus musculus	51-55
16803953-7	2006	A normal genetically balanced genotype was shown by comparative genomic hybridisation, which, together with the expression of c-kit, a known therapeutic target for imatinib, may have prognostic and therapeutic implications.	imatinib	164-172	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	126-131
16818614-5	2006	Similar to wild-type Bcr-Abl+ cells, inhibition of Jak2 by Ag490 treatment resulted in decrease of pSer Akt and c-Myc in imatinib-resistant cells.	imatinib	121-129	thymoma viral proto-oncogene 1	Mus musculus	104-107
16721136-4	2006	The success of the Kit tyrosine kinase inhibitor, imatinib mesylate (Gleevec, formerly STI-571), has caught the attention of the medical community.	imatinib	50-67	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	19-22
16721136-4	2006	The success of the Kit tyrosine kinase inhibitor, imatinib mesylate (Gleevec, formerly STI-571), has caught the attention of the medical community.	imatinib	69-76	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	19-22
16721136-4	2006	The success of the Kit tyrosine kinase inhibitor, imatinib mesylate (Gleevec, formerly STI-571), has caught the attention of the medical community.	imatinib	87-94	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	19-22
17022716-10	2006	CONCLUSIONS: In our experience, imatinib is an effective, well tolerated therapy for malignant [c-Kit (CD117)-positive], non-resectable and/or metastatic GIST.	imatinib	32-40	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	96-101
17022716-10	2006	CONCLUSIONS: In our experience, imatinib is an effective, well tolerated therapy for malignant [c-Kit (CD117)-positive], non-resectable and/or metastatic GIST.	imatinib	32-40	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	103-108
16575905-0	2006	Increased sensitivity to the platelet-derived growth factor (PDGF) receptor inhibitor STI571 in chemoresistant glioma cells is associated with enhanced PDGF-BB-mediated signaling and STI571-induced Akt inactivation.	imatinib	86-92	AKT serine/threonine kinase 1	Homo sapiens	198-201
16575905-0	2006	Increased sensitivity to the platelet-derived growth factor (PDGF) receptor inhibitor STI571 in chemoresistant glioma cells is associated with enhanced PDGF-BB-mediated signaling and STI571-induced Akt inactivation.	imatinib	183-189	AKT serine/threonine kinase 1	Homo sapiens	198-201
16575905-5	2006	The chemoresistant glioma U87/Pt cells were twofold more sensitive to STI571 growth-inhibitory effects than the chemosensitive U87 cells, and two- to threefold more sensitive than five unrelated glioma cell lines.	imatinib	70-76	small nucleolar RNA, C/D box 87	Homo sapiens	26-29
16575905-7	2006	Sensitization of U87/Pt cells correlated with upregulation of the PDGF-B isoform and with PDGF-BB-induced Akt overactivation, which was prevented by STI571.	imatinib	149-155	small nucleolar RNA, C/D box 87	Homo sapiens	17-20
16575905-7	2006	Sensitization of U87/Pt cells correlated with upregulation of the PDGF-B isoform and with PDGF-BB-induced Akt overactivation, which was prevented by STI571.	imatinib	149-155	platelet derived growth factor subunit B	Homo sapiens	66-72
16575905-7	2006	Sensitization of U87/Pt cells correlated with upregulation of the PDGF-B isoform and with PDGF-BB-induced Akt overactivation, which was prevented by STI571.	imatinib	149-155	AKT serine/threonine kinase 1	Homo sapiens	106-109
16575905-9	2006	In serum-containing medium, STI571 decreased phospho-Akt in U87/Pt cells, but not in U87, while activating extracellular signal-regulated kinase (Erk) in both.	imatinib	28-34	AKT serine/threonine kinase 1	Homo sapiens	53-56
16842246-0	2006	KIT immunohistochemistry and mutation status in gastrointestinal stromal tumours (GISTs) evaluated for treatment with imatinib.	imatinib	118-126	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
16842259-0	2006	Pathological response of gastrointestinal stromal tumour to imatinib treatment correlates with tumour KIT mutational status in individual tumour clones.	imatinib	60-68	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	102-105
16825513-5	2006	We also examined expression of the control genes in BCR-ABL-positive K562 cells in response to Gleevec treatment.	imatinib	95-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
16575905-9	2006	In serum-containing medium, STI571 decreased phospho-Akt in U87/Pt cells, but not in U87, while activating extracellular signal-regulated kinase (Erk) in both.	imatinib	28-34	small nucleolar RNA, C/D box 87	Homo sapiens	60-63
16575905-9	2006	In serum-containing medium, STI571 decreased phospho-Akt in U87/Pt cells, but not in U87, while activating extracellular signal-regulated kinase (Erk) in both.	imatinib	28-34	mitogen-activated protein kinase 1	Homo sapiens	107-144
16575905-9	2006	In serum-containing medium, STI571 decreased phospho-Akt in U87/Pt cells, but not in U87, while activating extracellular signal-regulated kinase (Erk) in both.	imatinib	28-34	mitogen-activated protein kinase 1	Homo sapiens	146-149
16575905-10	2006	STI571 antiproliferative effects were partially reverted by constitutively active Akt.	imatinib	0-6	AKT serine/threonine kinase 1	Homo sapiens	82-85
16786129-3	2006	Imatinib is a selective tyrosine-kinase inhibitor of ABL, KIT and PDGFR, and provides a clinical benefit in about 85% of patients with advanced GIST.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
16805961-4	2006	Because both drugs are transported via P-glycoprotein and breast cancer resistance protein and metabolized by cytochrome P450 3A2, the interaction of imatinib mesilate with these proteins may be responsible for the increased intestinal absorption of ciclosporin in rats.	imatinib	150-158	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	39-53
16805961-4	2006	Because both drugs are transported via P-glycoprotein and breast cancer resistance protein and metabolized by cytochrome P450 3A2, the interaction of imatinib mesilate with these proteins may be responsible for the increased intestinal absorption of ciclosporin in rats.	imatinib	150-158	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	110-129
16891454-10	2006	Finally, the b2a2-specific antisense gapmer used in combination with STI571 (imatinib mesylate), a tyrosine kinase inhibitor of p210(BCR/ABL), produced an enhanced antiproliferative effect in KYO-1 cells, which compared with K562 cells are refractory to STI571.	imatinib	69-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
16891454-10	2006	Finally, the b2a2-specific antisense gapmer used in combination with STI571 (imatinib mesylate), a tyrosine kinase inhibitor of p210(BCR/ABL), produced an enhanced antiproliferative effect in KYO-1 cells, which compared with K562 cells are refractory to STI571.	imatinib	77-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
16891454-10	2006	Finally, the b2a2-specific antisense gapmer used in combination with STI571 (imatinib mesylate), a tyrosine kinase inhibitor of p210(BCR/ABL), produced an enhanced antiproliferative effect in KYO-1 cells, which compared with K562 cells are refractory to STI571.	imatinib	254-260	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
16838646-2	2006	Recently, imatinib, the BCR/ABL antagonist, took over the first choice drug of the treatment CML.	imatinib	10-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
16786129-3	2006	Imatinib is a selective tyrosine-kinase inhibitor of ABL, KIT and PDGFR, and provides a clinical benefit in about 85% of patients with advanced GIST.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	58-61
16786129-3	2006	Imatinib is a selective tyrosine-kinase inhibitor of ABL, KIT and PDGFR, and provides a clinical benefit in about 85% of patients with advanced GIST.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	66-71
16754879-1	2006	Mutation in the ABL kinase domain is the principal mechanism of imatinib resistance in patients with chronic myelogenous leukemia.	imatinib	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-19
16614006-2	2006	However, because imatinib inhibits c-kit, the stem cell factor receptor, it could interfere with bone marrow engraftment.	imatinib	17-25	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	35-40
16614006-4	2006	Imatinib decreased the colony-forming capacity of mobilized peripheral blood human CD133(+) cells but not that of long-term culture-initiating cells.	imatinib	0-8	prominin 1	Homo sapiens	83-88
16614006-5	2006	Imatinib also decreased the proliferation of cytokine-stimulated CD133(+) cells but did not induce apoptosis of these cells.	imatinib	0-8	prominin 1	Homo sapiens	65-70
16614006-6	2006	Expression of very late antigen (VLA)-4, VLA-5, and CXCR4 of CD133(+) cells was not modified by imatinib, but imatinib decreased the ability of CD133(+) cells to migrate.	imatinib	110-118	prominin 1	Homo sapiens	61-66
16614006-6	2006	Expression of very late antigen (VLA)-4, VLA-5, and CXCR4 of CD133(+) cells was not modified by imatinib, but imatinib decreased the ability of CD133(+) cells to migrate.	imatinib	110-118	prominin 1	Homo sapiens	144-149
16784237-2	2006	c-kit activity is elevated in gastrointestinal stromal tumors (GISTs), and its therapeutic inhibition by small molecules such as imatinib is clinically validated.	imatinib	129-137	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-5
16721371-2	2006	Imatinib inhibits the tyrosine kinase activity of the BCR-ABL protein and is an effective, frontline therapy for chronic-phase CML.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
16721371-3	2006	However, accelerated or blast-crisis phase CML patients and Ph+ ALL patients often relapse due to drug resistance resulting from the emergence of imatinib-resistant point mutations within the BCR-ABL tyrosine kinase domain.	imatinib	146-154	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	192-199
16721371-5	2006	The novel, selective BCR-ABL inhibitor, AMN107, was designed to fit into the ATP-binding site of the BCR-ABL protein with higher affinity than imatinib.	imatinib	143-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
16721371-5	2006	The novel, selective BCR-ABL inhibitor, AMN107, was designed to fit into the ATP-binding site of the BCR-ABL protein with higher affinity than imatinib.	imatinib	143-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
16721371-7	2006	In preclinical studies, AMN107 demonstrated activity in vitro and in vivo against wild-type and imatinib-resistant BCR-ABL-expressing cells.	imatinib	96-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
16497976-3	2006	However, resistance to imatinib arises in later disease stages primarily because of a Bcr-Abl mutation.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
16497976-7	2006	Comparison of this Bcr-Abl signature with the profile of cells expressing an alternative imatinib-sensitive fusion kinase, FIP1L1-PDGFRalpha, revealed that these kinases signal through different pathways.	imatinib	89-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
16775234-1	2006	BACKGROUND: The BCR-ABL tyrosine kinase inhibitor imatinib is effective in Philadelphia chromosome-positive (Ph-positive) leukemias, but relapse occurs, mainly as a result of the outgrowth of leukemic subclones with imatinib-resistant BCR-ABL mutations.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
16775234-1	2006	BACKGROUND: The BCR-ABL tyrosine kinase inhibitor imatinib is effective in Philadelphia chromosome-positive (Ph-positive) leukemias, but relapse occurs, mainly as a result of the outgrowth of leukemic subclones with imatinib-resistant BCR-ABL mutations.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	235-242
16775234-1	2006	BACKGROUND: The BCR-ABL tyrosine kinase inhibitor imatinib is effective in Philadelphia chromosome-positive (Ph-positive) leukemias, but relapse occurs, mainly as a result of the outgrowth of leukemic subclones with imatinib-resistant BCR-ABL mutations.	imatinib	216-224	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
16680752-0	2006	Induction chemotherapy and post-remission imatinib therapy for de Novo BCR-ABL-positive AML.	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
16757703-1	2006	BACKGROUND: Inhibiting phosphorylation of platelet-derived growth factor receptor (PDGFR) by treatment with the PDGFR kinase inhibitor imatinib and the chemotherapeutic agent paclitaxel reduces the incidence and size of human prostate cancer bone lesions in nude mice.	imatinib	135-143	platelet derived growth factor receptor beta	Homo sapiens	42-81
16757703-1	2006	BACKGROUND: Inhibiting phosphorylation of platelet-derived growth factor receptor (PDGFR) by treatment with the PDGFR kinase inhibitor imatinib and the chemotherapeutic agent paclitaxel reduces the incidence and size of human prostate cancer bone lesions in nude mice.	imatinib	135-143	platelet derived growth factor receptor beta	Homo sapiens	83-88
16757703-1	2006	BACKGROUND: Inhibiting phosphorylation of platelet-derived growth factor receptor (PDGFR) by treatment with the PDGFR kinase inhibitor imatinib and the chemotherapeutic agent paclitaxel reduces the incidence and size of human prostate cancer bone lesions in nude mice.	imatinib	135-143	platelet derived growth factor receptor beta	Homo sapiens	112-117
16757703-12	2006	Treatment with imatinib alone had similar effects, and imatinib treatment also inhibited phosphorylation of PDGFR on tumor cells and tumor-associated endothelial cells and increased the level of apoptosis of endothelial cells, but not tumor cells.	imatinib	55-63	platelet derived growth factor receptor, beta polypeptide	Mus musculus	108-113
16757703-13	2006	Treatment with imatinib and more so with imatinib and paclitaxel decreased mean vessel density (three CD31/PECAM-1-positive cells, 95% confidence interval [CI] = 0 to 9; and control group = 38 CD31/PECAM-1-positive cells, 95% CI = 17 to 59) (P < .001), which was followed by apoptosis of tumor cells.	imatinib	15-23	platelet/endothelial cell adhesion molecule 1	Mus musculus	102-106
16757703-13	2006	Treatment with imatinib and more so with imatinib and paclitaxel decreased mean vessel density (three CD31/PECAM-1-positive cells, 95% confidence interval [CI] = 0 to 9; and control group = 38 CD31/PECAM-1-positive cells, 95% CI = 17 to 59) (P < .001), which was followed by apoptosis of tumor cells.	imatinib	15-23	platelet/endothelial cell adhesion molecule 1	Mus musculus	107-114
16757703-13	2006	Treatment with imatinib and more so with imatinib and paclitaxel decreased mean vessel density (three CD31/PECAM-1-positive cells, 95% confidence interval [CI] = 0 to 9; and control group = 38 CD31/PECAM-1-positive cells, 95% CI = 17 to 59) (P < .001), which was followed by apoptosis of tumor cells.	imatinib	15-23	platelet/endothelial cell adhesion molecule 1	Mus musculus	193-197
16757703-13	2006	Treatment with imatinib and more so with imatinib and paclitaxel decreased mean vessel density (three CD31/PECAM-1-positive cells, 95% confidence interval [CI] = 0 to 9; and control group = 38 CD31/PECAM-1-positive cells, 95% CI = 17 to 59) (P < .001), which was followed by apoptosis of tumor cells.	imatinib	15-23	platelet/endothelial cell adhesion molecule 1	Mus musculus	198-205
16757703-13	2006	Treatment with imatinib and more so with imatinib and paclitaxel decreased mean vessel density (three CD31/PECAM-1-positive cells, 95% confidence interval [CI] = 0 to 9; and control group = 38 CD31/PECAM-1-positive cells, 95% CI = 17 to 59) (P < .001), which was followed by apoptosis of tumor cells.	imatinib	41-49	platelet/endothelial cell adhesion molecule 1	Mus musculus	102-106
16757703-13	2006	Treatment with imatinib and more so with imatinib and paclitaxel decreased mean vessel density (three CD31/PECAM-1-positive cells, 95% confidence interval [CI] = 0 to 9; and control group = 38 CD31/PECAM-1-positive cells, 95% CI = 17 to 59) (P < .001), which was followed by apoptosis of tumor cells.	imatinib	41-49	platelet/endothelial cell adhesion molecule 1	Mus musculus	107-114
16757703-13	2006	Treatment with imatinib and more so with imatinib and paclitaxel decreased mean vessel density (three CD31/PECAM-1-positive cells, 95% confidence interval [CI] = 0 to 9; and control group = 38 CD31/PECAM-1-positive cells, 95% CI = 17 to 59) (P < .001), which was followed by apoptosis of tumor cells.	imatinib	41-49	platelet/endothelial cell adhesion molecule 1	Mus musculus	193-197
16757703-13	2006	Treatment with imatinib and more so with imatinib and paclitaxel decreased mean vessel density (three CD31/PECAM-1-positive cells, 95% confidence interval [CI] = 0 to 9; and control group = 38 CD31/PECAM-1-positive cells, 95% CI = 17 to 59) (P < .001), which was followed by apoptosis of tumor cells.	imatinib	41-49	platelet/endothelial cell adhesion molecule 1	Mus musculus	198-205
16740027-2	2006	GISTs exhibit activating mutations in the c-kit proto-oncogene, which render them amenable to treatment with imatinib mesylate.	imatinib	109-126	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	42-47
16467199-0	2006	BCR-ABL mRNA levels at and after the time of a complete cytogenetic response (CCR) predict the duration of CCR in imatinib mesylate-treated patients with CML.	imatinib	114-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
16740718-0	2006	The structure of Dasatinib (BMS-354825) bound to activated ABL kinase domain elucidates its inhibitory activity against imatinib-resistant ABL mutants.	imatinib	120-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-62
16740725-2	2006	Imatinib mesylate has been shown to effectively block constitutively active KIT and delay tumor growth.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	76-79
16449525-3	2006	Since we have previously demonstrated inhibition of c-fms by imatinib, we examined the effect of imatinib on OC formation and activity.	imatinib	61-69	colony stimulating factor 1 receptor	Mus musculus	52-57
16620963-3	2006	The effect was reverted in the presence of the specific Abl inhibitor imatinib (1microM) and the Src inhibitor PP2 (10microM).	imatinib	70-78	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	56-59
16740718-0	2006	The structure of Dasatinib (BMS-354825) bound to activated ABL kinase domain elucidates its inhibitory activity against imatinib-resistant ABL mutants.	imatinib	120-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-142
16740725-8	2006	In contrast, imatinib mesylate, which inhibits KIT kinase activity but does not suppress total KIT expression, fails to cause apoptosis.	imatinib	13-30	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	47-50
16740718-2	2006	Current frontline therapy for CML is imatinib, an inhibitor of BCR-ABL.	imatinib	37-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
16740718-3	2006	Although imatinib has a high rate of clinical success in early phase CML, treatment resistance is problematic, particularly in later stages of the disease, and is frequently mediated by mutations in BCR-ABL.	imatinib	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	199-206
16740718-4	2006	Dasatinib (BMS-354825) is a multitargeted tyrosine kinase inhibitor that targets oncogenic pathways and is a more potent inhibitor than imatinib against wild-type BCR-ABL.	imatinib	136-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
16740718-5	2006	It has also shown preclinical activity against all but one of the imatinib-resistant BCR-ABL mutants tested to date.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
16740718-6	2006	Analysis of the crystal structure of dasatinib-bound ABL kinase suggests that the increased binding affinity of dasatinib over imatinib is at least partially due to its ability to recognize multiple states of BCR-ABL.	imatinib	127-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
16740718-6	2006	Analysis of the crystal structure of dasatinib-bound ABL kinase suggests that the increased binding affinity of dasatinib over imatinib is at least partially due to its ability to recognize multiple states of BCR-ABL.	imatinib	127-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-216
16740718-7	2006	The structure also provides an explanation for the activity of dasatinib against imatinib-resistant BCR-ABL mutants.	imatinib	81-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
16789903-2	2006	The most extensively investigated example is chronic myeloid leukemia, where the pathogenic tyrosine kinase fusion protein Bcr-Abl is a successful target for disease control by the specific inhibitor imatinib mesylate.	imatinib	200-217	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-130
16740780-3	2006	We recently showed the cytostatic role of imatinib, an inhibitor of the SCF-KIT loop, on Ewing tumor cells, and in this study, we intend to analyze the inhibition of the insulin-like growth factor I receptor (IGF1R) loop.	imatinib	42-50	insulin like growth factor 1 receptor	Homo sapiens	209-214
16740780-8	2006	Addition of imatinib to ADW742 synergistically augmented these effects and was especially effective in inhibiting AKT/mTOR phosphorylation and reducing vascular endothelial growth factor expression in cell lines having high IGF1R activation levels.	imatinib	12-20	AKT serine/threonine kinase 1	Homo sapiens	114-117
16740780-8	2006	Addition of imatinib to ADW742 synergistically augmented these effects and was especially effective in inhibiting AKT/mTOR phosphorylation and reducing vascular endothelial growth factor expression in cell lines having high IGF1R activation levels.	imatinib	12-20	mechanistic target of rapamycin kinase	Homo sapiens	118-122
16740780-8	2006	Addition of imatinib to ADW742 synergistically augmented these effects and was especially effective in inhibiting AKT/mTOR phosphorylation and reducing vascular endothelial growth factor expression in cell lines having high IGF1R activation levels.	imatinib	12-20	vascular endothelial growth factor A	Homo sapiens	152-186
16740780-8	2006	Addition of imatinib to ADW742 synergistically augmented these effects and was especially effective in inhibiting AKT/mTOR phosphorylation and reducing vascular endothelial growth factor expression in cell lines having high IGF1R activation levels.	imatinib	12-20	insulin like growth factor 1 receptor	Homo sapiens	224-229
16740780-11	2006	Combination of ADW742 with imatinib, vincristine, and doxorubicin induces a significant reduction of tumor cell growth, mainly by the increase in apoptosis with a pattern depending on IGF1R activation levels.	imatinib	27-35	insulin like growth factor 1 receptor	Homo sapiens	184-189
16728580-0	2006	The role of imatinib mesylate (Glivec) for treatment of patients with malignant endocrine tumors positive for c-kit or PDGF-R.	imatinib	12-29	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	110-115
16865565-0	2006	Response to imatinib in KIT- and PDGFRA-wild type gastrointestinal stromal associated with neurofibromatosis type 1.	imatinib	12-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	24-27
16865565-0	2006	Response to imatinib in KIT- and PDGFRA-wild type gastrointestinal stromal associated with neurofibromatosis type 1.	imatinib	12-20	platelet derived growth factor receptor alpha	Homo sapiens	33-39
16728580-0	2006	The role of imatinib mesylate (Glivec) for treatment of patients with malignant endocrine tumors positive for c-kit or PDGF-R.	imatinib	12-29	platelet derived growth factor receptor beta	Homo sapiens	119-125
16728580-1	2006	Imatinib mesylate (IM), a small molecule that is a selective inhibitor of the ABL, platelet derived growth factor receptor (PDGFR-R) and stem cell ligand receptor (c-kit) tyrosine kinases (TK).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-81
16728580-1	2006	Imatinib mesylate (IM), a small molecule that is a selective inhibitor of the ABL, platelet derived growth factor receptor (PDGFR-R) and stem cell ligand receptor (c-kit) tyrosine kinases (TK).	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	164-169
16728580-1	2006	Imatinib mesylate (IM), a small molecule that is a selective inhibitor of the ABL, platelet derived growth factor receptor (PDGFR-R) and stem cell ligand receptor (c-kit) tyrosine kinases (TK).	imatinib	19-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-81
16728580-1	2006	Imatinib mesylate (IM), a small molecule that is a selective inhibitor of the ABL, platelet derived growth factor receptor (PDGFR-R) and stem cell ligand receptor (c-kit) tyrosine kinases (TK).	imatinib	19-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	164-169
16572205-1	2006	In chronic myeloid leukaemia, CD34(+) stem/progenitor cells appear resistant to imatinib mesylate (IM) in vitro and in vivo.	imatinib	80-97	CD34 molecule	Homo sapiens	30-34
16850123-4	2006	Imatinib mesylate is a selective tyrosine kinase inhibitor on ABL, c-Kit and PGDF-receptor, and functions through competitive inhibition at the ATP-binding site of the enzyme, which leads to growth arrest or apoptosis in cells that express BCR-ABL.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-65
16850123-4	2006	Imatinib mesylate is a selective tyrosine kinase inhibitor on ABL, c-Kit and PGDF-receptor, and functions through competitive inhibition at the ATP-binding site of the enzyme, which leads to growth arrest or apoptosis in cells that express BCR-ABL.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	67-72
16850123-4	2006	Imatinib mesylate is a selective tyrosine kinase inhibitor on ABL, c-Kit and PGDF-receptor, and functions through competitive inhibition at the ATP-binding site of the enzyme, which leads to growth arrest or apoptosis in cells that express BCR-ABL.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	240-247
16741576-10	2006	Thus, autocrine PDGFR signaling plays an essential role during cancer progression, suggesting a novel application of STI571 to therapeutically interfere with metastasis.	imatinib	117-123	platelet derived growth factor receptor beta	Homo sapiens	16-21
16642048-1	2006	The emergence of ABL point mutations is the most frequent cause for imatinib resistance in chronic myelogenous leukemia (CML) patients and can occur during any phase of the disease; however, their clinical impact remains controversial.	imatinib	68-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-20
16642048-2	2006	In this study, we retrospectively analyzed the predictive impact of 94 BCR-ABL kinase domain mutations (18 T315I, 26 P-loop, 50 in other sites) found in 89 imatinib-resistant CML patients.	imatinib	156-164	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-78
16487996-0	2006	A case of c-kit positive high-grade stromal endometrial sarcoma responding to Imatinib Mesylate.	imatinib	78-95	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	10-15
16487996-4	2006	CASE: A 41-year-old woman suffering HGES, with positive staining for CD117 (c-kit) and large abdominal and retroperitoneal mass progressing after chemotherapy, was treated with Imatinib Mesylate.	imatinib	177-194	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	69-74
16487996-4	2006	CASE: A 41-year-old woman suffering HGES, with positive staining for CD117 (c-kit) and large abdominal and retroperitoneal mass progressing after chemotherapy, was treated with Imatinib Mesylate.	imatinib	177-194	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	76-81
16598311-1	2006	The use of the tyrosine kinase inhibitor imatinib, which blocks the enzymatic action of the BCR-ABL fusion protein, has represented a critical advance in chronic myeloid leukemia (CML) treatment.	imatinib	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
16598311-9	2006	This study identifies a set of genes that may be involved in primary resistance to imatinib, suggesting BCR-ABL-independent mechanisms.	imatinib	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
16631280-6	2006	Moreover, JAK2 V617F mutation finding may permit promising therapeutic approaches in patients with PV, particularly tyrosine kinase inhibitors; preliminary series have, in fact, underscored the potential efficacy of imatinib mesylate in PV.	imatinib	216-233	Janus kinase 2	Homo sapiens	10-14
16607380-9	2006	Using an inhibitor, imatinib mesylate, that blocks SCF/c-kit-associated RTK, we find similar results as with anti-SCF for attenuating AHR and fibrotic changes, suggesting that a potential clinical treatment for chronic asthma already exists related to this pathway.	imatinib	20-37	kit ligand	Mus musculus	51-54
16607380-9	2006	Using an inhibitor, imatinib mesylate, that blocks SCF/c-kit-associated RTK, we find similar results as with anti-SCF for attenuating AHR and fibrotic changes, suggesting that a potential clinical treatment for chronic asthma already exists related to this pathway.	imatinib	20-37	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	55-60
16607380-9	2006	Using an inhibitor, imatinib mesylate, that blocks SCF/c-kit-associated RTK, we find similar results as with anti-SCF for attenuating AHR and fibrotic changes, suggesting that a potential clinical treatment for chronic asthma already exists related to this pathway.	imatinib	20-37	aryl-hydrocarbon receptor	Mus musculus	134-137
16818499-0	2006	Imatinib inhibits c-Kit-induced hypoxia-inducible factor-1alpha activity and vascular endothelial growth factor expression in small cell lung cancer cells.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	18-23
16818499-0	2006	Imatinib inhibits c-Kit-induced hypoxia-inducible factor-1alpha activity and vascular endothelial growth factor expression in small cell lung cancer cells.	imatinib	0-8	vascular endothelial growth factor A	Homo sapiens	77-111
16818499-4	2006	SCF treatment doubled VEGF mRNA expression and VEGF secretion in the absence of other exogenous growth factors, an effect efficiently blocked by imatinib.	imatinib	145-153	KIT ligand	Homo sapiens	0-3
16818499-4	2006	SCF treatment doubled VEGF mRNA expression and VEGF secretion in the absence of other exogenous growth factors, an effect efficiently blocked by imatinib.	imatinib	145-153	vascular endothelial growth factor A	Homo sapiens	22-26
16818499-11	2006	These data indicate that activation of c-Kit by SCF leads to a predominantly HIF-1alpha-mediated enhancement of VEGF expression and that inhibition of c-Kit signaling with imatinib could result in inhibition of tumor angiogenesis.	imatinib	172-180	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	151-156
17263225-3	2006	We present results of a multicenter phase II study on the use of imatinib in chronic phase after failure to interferon-alpha (IFN-alpha).	imatinib	65-73	interferon alpha 1	Homo sapiens	126-135
16631755-3	2006	Suppression of c-Abl or PKCdelta expression using SiRNAs impaired PARP cleavage, Gleevec and/or rottlerin inhibited the induction of the subG1 phase and the increase of reactive oxygen species level.	imatinib	81-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-20
16782438-0	2006	Cellular effects of imatinib on medullary thyroid cancer cells harboring multiple endocrine neoplasia Type 2A and 2B associated RET mutations.	imatinib	20-28	ret proto-oncogene	Homo sapiens	128-131
16782438-6	2006	RESULTS: Imatinib inhibited RET Y1062 phosphorylation in a dose-dependent manner after 1.5 hours of exposure.	imatinib	9-17	ret proto-oncogene	Homo sapiens	28-31
16782438-11	2006	CONCLUSIONS: Imatinib inhibits RET-mediated MTC cell growth affecting RET protein levels in vitro in a dose-dependent manner.	imatinib	13-21	ret proto-oncogene	Homo sapiens	31-34
16782438-11	2006	CONCLUSIONS: Imatinib inhibits RET-mediated MTC cell growth affecting RET protein levels in vitro in a dose-dependent manner.	imatinib	13-21	ret proto-oncogene	Homo sapiens	70-73
16782438-12	2006	The concentration of imatinib necessary to inhibit RET in vitro, however, makes it impossible to conclude that imatinib monotherapy will be a good option for systemic therapy of MTC.	imatinib	21-29	ret proto-oncogene	Homo sapiens	51-54
16707599-1	2006	PURPOSE: Most patients with chronic-phase chronic myeloid leukemia (CML) who receive imatinib achieve a complete cytogenetic remission (CCgR) and low levels of BCR-ABL transcripts.	imatinib	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-167
16707599-3	2006	EXPERIMENTAL DESIGN: To determine the potential of quantitative reverse transcription-PCR of BCR-ABL to predict cytogenetic relapse, we serially monitored residual disease in 97 CML patients with an imatinib-induced CCgR.	imatinib	199-207	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
16418324-3	2006	Expression of CEBPB was repressed in 32D-BCR/ABL cells and reinduced by imatinib (STI571) via a mechanism that appears to depend on expression of the CUG-repeat RNA-binding protein CUGBP1 and the integrity of the CUG-rich intercistronic region of c/ebpbeta mRNA.	imatinib	72-80	CCAAT/enhancer binding protein (C/EBP), beta	Mus musculus	14-19
16418324-3	2006	Expression of CEBPB was repressed in 32D-BCR/ABL cells and reinduced by imatinib (STI571) via a mechanism that appears to depend on expression of the CUG-repeat RNA-binding protein CUGBP1 and the integrity of the CUG-rich intercistronic region of c/ebpbeta mRNA.	imatinib	72-80	CUGBP, Elav-like family member 1	Mus musculus	181-187
16707466-0	2006	Resistance to imatinib of bcr/abl p190 lymphoblastic leukemia cells.	imatinib	14-22	BCR activator of RhoGEF and GTPase	Homo sapiens	26-29
16707466-0	2006	Resistance to imatinib of bcr/abl p190 lymphoblastic leukemia cells.	imatinib	14-22	contactin associated protein 1	Homo sapiens	34-38
16707466-2	2006	Treatment with the tyrosine kinase inhibitor Imatinib is currently standard for chronic myelogenous leukemia, which is also caused by Bcr/Abl.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
16707466-4	2006	In our study, we have investigated the effect of Imatinib therapy on murine P190 Bcr/Abl lymphoblastic leukemia cells.	imatinib	49-57	RAS protein-specific guanine nucleotide-releasing factor 1	Mus musculus	76-80
16707466-4	2006	In our study, we have investigated the effect of Imatinib therapy on murine P190 Bcr/Abl lymphoblastic leukemia cells.	imatinib	49-57	BCR activator of RhoGEF and GTPase	Mus musculus	81-84
16707466-8	2006	The Bcr/Abl tyrosine kinase present in the cells that were now able to multiply in the presence of 5 mumol/L Imatinib was still inhibited by the drug.	imatinib	109-117	BCR activator of RhoGEF and GTPase	Mus musculus	4-7
16707466-9	2006	In concordance with this, the Abl ATP-binding pocket domain of Bcr/Abl in the resistant cells did not contain point mutations which would make the protein Imatinib resistant.	imatinib	155-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
16707466-12	2006	Our results show that stroma selects Imatinib-resistant Bcr/Abl P190 lymphoblasts that are less dependent on Bcr/Abl tyrosine kinase activity.	imatinib	37-45	BCR activator of RhoGEF and GTPase	Homo sapiens	56-59
16707466-12	2006	Our results show that stroma selects Imatinib-resistant Bcr/Abl P190 lymphoblasts that are less dependent on Bcr/Abl tyrosine kinase activity.	imatinib	37-45	RAS protein-specific guanine nucleotide-releasing factor 1	Mus musculus	64-68
16707477-0	2006	Therapeutic effect of imatinib in gastrointestinal stromal tumors: AKT signaling dependent and independent mechanisms.	imatinib	22-30	AKT serine/threonine kinase 1	Homo sapiens	67-70
16707477-2	2006	Imatinib mesylate, a small-molecule inhibitor against several receptor tyrosine kinases, including KIT, platelet-derived growth factor receptor-alpha, and BCR-ABL, has therapeutic benefit for GISTs both via KIT and via unknown mechanisms.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	99-102
16707477-2	2006	Imatinib mesylate, a small-molecule inhibitor against several receptor tyrosine kinases, including KIT, platelet-derived growth factor receptor-alpha, and BCR-ABL, has therapeutic benefit for GISTs both via KIT and via unknown mechanisms.	imatinib	0-17	platelet derived growth factor receptor alpha	Homo sapiens	104-149
16707477-2	2006	Imatinib mesylate, a small-molecule inhibitor against several receptor tyrosine kinases, including KIT, platelet-derived growth factor receptor-alpha, and BCR-ABL, has therapeutic benefit for GISTs both via KIT and via unknown mechanisms.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-162
16707477-2	2006	Imatinib mesylate, a small-molecule inhibitor against several receptor tyrosine kinases, including KIT, platelet-derived growth factor receptor-alpha, and BCR-ABL, has therapeutic benefit for GISTs both via KIT and via unknown mechanisms.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	207-210
16707477-9	2006	Imatinib treatment markedly reduces glucose uptake via decreased levels of plasma membrane-bound Glut4 and induces apoptosis or growth arrest by inhibiting KIT activity.	imatinib	0-8	solute carrier family 2 member 4	Homo sapiens	97-102
16707477-9	2006	Imatinib treatment markedly reduces glucose uptake via decreased levels of plasma membrane-bound Glut4 and induces apoptosis or growth arrest by inhibiting KIT activity.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	156-159
16631755-3	2006	Suppression of c-Abl or PKCdelta expression using SiRNAs impaired PARP cleavage, Gleevec and/or rottlerin inhibited the induction of the subG1 phase and the increase of reactive oxygen species level.	imatinib	81-88	protein kinase C delta	Homo sapiens	24-32
16827161-0	2006	Combination treatment of imatinib-sensitive and -resistant BCR-ABL-positive CML cells with imatinib and farnesyltransferase inhibitors.	imatinib	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
16651519-3	2006	To gain insight into factors that influence the action of a prototypical targeted drug, we studied the action of imatinib (STI-571, Gleevec) against murine cells and leukemias expressing BCR-ABL, an imatinib target and the initiating oncogene for human chronic myelogenous leukemia (CML).	imatinib	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	187-194
16651519-4	2006	We show that the tumor suppressor p53 is selectively activated by imatinib in BCR-ABL-expressing cells as a result of BCR-ABL kinase inhibition.	imatinib	66-74	tumor protein p53	Homo sapiens	34-37
16651519-4	2006	We show that the tumor suppressor p53 is selectively activated by imatinib in BCR-ABL-expressing cells as a result of BCR-ABL kinase inhibition.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
16651519-4	2006	We show that the tumor suppressor p53 is selectively activated by imatinib in BCR-ABL-expressing cells as a result of BCR-ABL kinase inhibition.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
16651519-5	2006	Inactivation of p53, which can accompany disease progression in human CML, impedes the response to imatinib in vitro and in vivo without preventing BCR-ABL kinase inhibition.	imatinib	99-107	tumor protein p53	Homo sapiens	16-19
16651519-6	2006	Concordantly, p53 mutations are associated with progression to imatinib resistance in some human CMLs.	imatinib	63-71	tumor protein p53	Homo sapiens	14-17
16687713-1	2006	BACKGROUND: Imatinib mesylate inhibits several tyrosine kinases, including BCR-ABL, the C-KIT receptor, and the platelet-derived growth factor receptors alpha and beta, all of which are associated with disease.	imatinib	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
16827161-0	2006	Combination treatment of imatinib-sensitive and -resistant BCR-ABL-positive CML cells with imatinib and farnesyltransferase inhibitors.	imatinib	91-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
16827161-8	2006	Annexin V/propidium iodide staining showed enhancement of imatinib-induced apoptosis with either drug combination, both in imatinib-sensitive and -resistant cells.	imatinib	58-66	annexin A5	Homo sapiens	0-9
16827161-8	2006	Annexin V/propidium iodide staining showed enhancement of imatinib-induced apoptosis with either drug combination, both in imatinib-sensitive and -resistant cells.	imatinib	123-131	annexin A5	Homo sapiens	0-9
16728945-1	2006	The Bcr-Abl tyrosine kinase inhibitor imatinib mesylate launched the era of molecular targeted therapy and constitutes a milestone in oncology history.	imatinib	38-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
16565971-2	2006	Imatinib mesylate is an oral tyrosine kinase inhibitor that targets bcr-Abl, c-kit, platelet-derived growth factor receptor (PDGFR)-alpha, and PDGFR-beta, leading to remarkable clinical responses in several cancers.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
16565971-2	2006	Imatinib mesylate is an oral tyrosine kinase inhibitor that targets bcr-Abl, c-kit, platelet-derived growth factor receptor (PDGFR)-alpha, and PDGFR-beta, leading to remarkable clinical responses in several cancers.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	77-82
16565971-2	2006	Imatinib mesylate is an oral tyrosine kinase inhibitor that targets bcr-Abl, c-kit, platelet-derived growth factor receptor (PDGFR)-alpha, and PDGFR-beta, leading to remarkable clinical responses in several cancers.	imatinib	0-17	platelet derived growth factor receptor alpha	Homo sapiens	125-137
16565971-2	2006	Imatinib mesylate is an oral tyrosine kinase inhibitor that targets bcr-Abl, c-kit, platelet-derived growth factor receptor (PDGFR)-alpha, and PDGFR-beta, leading to remarkable clinical responses in several cancers.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	143-153
16728945-4	2006	Point mutations in the Bcr-Abl kinase domain that impair the ability of imatinib to inhibit the kinase activity represent the leading cause of resistance.	imatinib	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
16596277-1	2006	STI571 is a specific inhibitor of tyrosine kinases, such as BCR-ABL, platelet-derived growth factor receptor, and c-KIT, and has recently been approved for the treatment of chronic myeloid leukemia and gastrointestinal stromal tumors (GISTs).	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
16634808-8	2006	These results suggest that Gab adapter proteins are expressed and likely to be involved in the growth signalling of rheumatoid synovial cells and that imatinib mesylate, a key drug in the treatment of chronic myeloid leukaemia, may also be effective for the treatment of RA.	imatinib	151-168	alpha-1-B glycoprotein	Homo sapiens	27-30
16634810-2	2006	The purpose of this study was to examine the relationship between mesangial cell proliferation and phosphorylated signal transducer and activator of transcription (STAT) 3 and to determine whether the PDGF receptor tyrosine kinase inhibitor STI 571 inhibited mesangial cell proliferation via modulation of STAT3.	imatinib	241-248	signal transducer and activator of transcription 3	Homo sapiens	306-311
16564690-2	2006	Imatinib is an inhibitor of the tyrosine kinase activities of platelet-derived growth factor receptor (PDGF-r), which is involved in glioblastoma aggressiveness.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	62-101
16564690-2	2006	Imatinib is an inhibitor of the tyrosine kinase activities of platelet-derived growth factor receptor (PDGF-r), which is involved in glioblastoma aggressiveness.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	103-109
16564690-3	2006	In this study, we have investigated the link between 99mTc-(V)-DMSA, an imaging agent used in Single Photon Emission Computed Tomography, cellular accumulation and the biological effects of imatinib mediated by PDGF-r in a human glioblastoma cell line U87-MG.	imatinib	190-198	platelet derived growth factor receptor beta	Homo sapiens	211-217
16564690-5	2006	99mTc-(V)-DMSA cellular uptake studies showed that the specific action of imatinib on PDGF-r signal pathway, in the human glioblastoma cell line U87-MG, could be followed by radioactive tracer.	imatinib	74-82	platelet derived growth factor receptor beta	Homo sapiens	86-92
16564690-6	2006	Furthermore, strong correlations between cellular 99mTc-(V)-DMSA uptake and the effect of imatinib therapy on U87-MG proliferation (r=0.896), invasion (r=0.621) and migration (r=0.822) were obtained, likewise for 99mTc-(V)-DMSA uptake and PDGF-r expression (r=0.958).	imatinib	90-98	platelet derived growth factor receptor beta	Homo sapiens	239-245
16564690-7	2006	Our results show that the biological effects of imatinib therapy on tumour cells properties are linked to PDGF-r phosphorylation and could be traced with 99mTc-(V)-DMSA, which also seems to be a potential tracer to evaluate the response to imatinib therapy in glioblastoma.	imatinib	48-56	platelet derived growth factor receptor beta	Homo sapiens	106-112
16757427-1	2006	Imatinib was developed as the first molecularly targeted therapy to specifically inhibit the BCR-ABL kinase in Philadelphia chromosome (Ph)-positive chronic myeloid leukemia (CML).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
16757427-4	2006	Several mechanisms of imatinib resistance have been identified, including BCR-ABL gene amplification that leads to overexpression of the BCR-ABL protein, point mutations in the BCR-ABL kinase domain that interfere with imatinib binding, and point mutations outside of the kinase domain that allosterically inhibit imatinib binding to BCR-ABL.	imatinib	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
16757427-4	2006	Several mechanisms of imatinib resistance have been identified, including BCR-ABL gene amplification that leads to overexpression of the BCR-ABL protein, point mutations in the BCR-ABL kinase domain that interfere with imatinib binding, and point mutations outside of the kinase domain that allosterically inhibit imatinib binding to BCR-ABL.	imatinib	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-144
16757427-4	2006	Several mechanisms of imatinib resistance have been identified, including BCR-ABL gene amplification that leads to overexpression of the BCR-ABL protein, point mutations in the BCR-ABL kinase domain that interfere with imatinib binding, and point mutations outside of the kinase domain that allosterically inhibit imatinib binding to BCR-ABL.	imatinib	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-144
16757427-4	2006	Several mechanisms of imatinib resistance have been identified, including BCR-ABL gene amplification that leads to overexpression of the BCR-ABL protein, point mutations in the BCR-ABL kinase domain that interfere with imatinib binding, and point mutations outside of the kinase domain that allosterically inhibit imatinib binding to BCR-ABL.	imatinib	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-144
16624552-5	2006	The presence of exon 9-activating mutations in KIT was the strongest adverse prognostic factor for response to imatinib, increasing the relative risk of progression by 171% (P<0.0001) and the relative risk of death by 190% (P<0.0001) when compared with KIT exon 11 mutants.	imatinib	111-119	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	47-50
16624552-5	2006	The presence of exon 9-activating mutations in KIT was the strongest adverse prognostic factor for response to imatinib, increasing the relative risk of progression by 171% (P<0.0001) and the relative risk of death by 190% (P<0.0001) when compared with KIT exon 11 mutants.	imatinib	111-119	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	259-262
16596277-1	2006	STI571 is a specific inhibitor of tyrosine kinases, such as BCR-ABL, platelet-derived growth factor receptor, and c-KIT, and has recently been approved for the treatment of chronic myeloid leukemia and gastrointestinal stromal tumors (GISTs).	imatinib	0-6	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	114-119
16757427-5	2006	The need for alternative or additional treatment for imatinib-resistant BCR-ABL-positive leukemia has guided the way to the design of a second generation of targeted therapies, which has resulted mainly in the development of novel small-molecule inhibitors such as AMN107, dasatinib, NS-187, and ON012380.	imatinib	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
16757427-6	2006	The major goal of these efforts is to create new compounds that are more potent than imatinib and/or more effective against imatinib-resistant BCR-ABL clones.	imatinib	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-150
16757427-7	2006	In this review, we discuss the next generation of BCR-ABL kinase inhibitors for overcoming imatinib resistance.	imatinib	91-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
16596277-3	2006	In these cells, STI571 induced pro-caspase-12 or pro-caspase-7 cleavage and it affected caspase-3 activity and induced the endoplasmic reticulum (ER)-resident chaperone, glucose-regulated protein 78.	imatinib	16-22	caspase 3	Homo sapiens	88-97
16596278-2	2006	The aim of our current study was to elucidate the effects of dual inhibition of PDGF and TGF-beta by combination of the clinically used imatinib mesylate (STI-571) and perindopril (an ACE-inhibitor; ACE-I), respectively, on ongoing liver fibrosis development in rats.	imatinib	136-153	transforming growth factor, beta 1	Rattus norvegicus	89-97
16596278-2	2006	The aim of our current study was to elucidate the effects of dual inhibition of PDGF and TGF-beta by combination of the clinically used imatinib mesylate (STI-571) and perindopril (an ACE-inhibitor; ACE-I), respectively, on ongoing liver fibrosis development in rats.	imatinib	155-162	transforming growth factor, beta 1	Rattus norvegicus	89-97
16640460-2	2006	The recognition of an inactive conformation of Abl, in which a catalytically important Asp-Phe-Gly (DFG) motif is flipped by approximately 180 degrees with respect to the active conformation, underlies the specificity of the cancer drug imatinib, which is used to treat CML.	imatinib	237-245	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
16910417-2	2006	Most GISTs respond to imatinib mesylate, which selectively inhibits both KIT and PDGFRalpha, and is now considered standard systemic therapy for advanced GIST.	imatinib	22-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
16910417-2	2006	Most GISTs respond to imatinib mesylate, which selectively inhibits both KIT and PDGFRalpha, and is now considered standard systemic therapy for advanced GIST.	imatinib	22-39	platelet derived growth factor receptor alpha	Homo sapiens	81-91
16703880-13	2006	CONCLUSIONS: This represents the first report of c-KIT sequencing in desmoid-type fibromatoses and suggests a possible biological basis for continuing to explore the use of adjuvant imatinib mesylate therapy.	imatinib	182-199	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	49-54
16498388-0	2006	Identification of a novel imatinib responsive KIF5B-PDGFRA fusion gene following screening for PDGFRA overexpression in patients with hypereosinophilia.	imatinib	26-34	kinesin family member 5B	Homo sapiens	46-51
16498388-0	2006	Identification of a novel imatinib responsive KIF5B-PDGFRA fusion gene following screening for PDGFRA overexpression in patients with hypereosinophilia.	imatinib	26-34	platelet derived growth factor receptor alpha	Homo sapiens	52-58
16498388-0	2006	Identification of a novel imatinib responsive KIF5B-PDGFRA fusion gene following screening for PDGFRA overexpression in patients with hypereosinophilia.	imatinib	26-34	platelet derived growth factor receptor alpha	Homo sapiens	95-101
16498388-7	2006	Imatinib, a known inhibitor of PDGFRalpha, produced a complete cytogenetic response and disappearance of the KIF5B-PDGFRA fusion by PCR, from both genomic DNA and mRNA.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	31-41
16498388-7	2006	Imatinib, a known inhibitor of PDGFRalpha, produced a complete cytogenetic response and disappearance of the KIF5B-PDGFRA fusion by PCR, from both genomic DNA and mRNA.	imatinib	0-8	kinesin family member 5B	Homo sapiens	109-114
16498388-7	2006	Imatinib, a known inhibitor of PDGFRalpha, produced a complete cytogenetic response and disappearance of the KIF5B-PDGFRA fusion by PCR, from both genomic DNA and mRNA.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	115-121
16640460-6	2006	One class of mutations in BCR-Abl that confers resistance to imatinib appears more likely to destabilize the inactive Src-like conformation than the active or imatinib-bound conformations.	imatinib	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-33
16640460-6	2006	One class of mutations in BCR-Abl that confers resistance to imatinib appears more likely to destabilize the inactive Src-like conformation than the active or imatinib-bound conformations.	imatinib	61-69	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	118-121
16640460-6	2006	One class of mutations in BCR-Abl that confers resistance to imatinib appears more likely to destabilize the inactive Src-like conformation than the active or imatinib-bound conformations.	imatinib	159-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-33
16618932-4	2006	Although the ABL kinase inhibitor imatinib mesylate (Gleevec) provides highly effective treatment for BCR-ABL-positive chronic myelogenous leukemia, it has proven far less efficacious in the treatment of BCR-ABL-positive acute lymphoblastic leukemias (ALLs), many of which sustain deletions of the INK4A-ARF (CDKN2A) tumor suppressor locus.	imatinib	34-51	cyclin dependent kinase inhibitor 2A	Mus musculus	298-307
17193822-1	2006	Mutually exclusive KIT and PDGFRA mutations are central events in GIST pathogenesis, and their understanding is becoming increasingly important, because specific treatment targeting oncogenic KIT and PDGFRA activation (especially imatinib mesylate) has become available.	imatinib	230-238	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	19-22
17193822-1	2006	Mutually exclusive KIT and PDGFRA mutations are central events in GIST pathogenesis, and their understanding is becoming increasingly important, because specific treatment targeting oncogenic KIT and PDGFRA activation (especially imatinib mesylate) has become available.	imatinib	230-238	platelet derived growth factor receptor alpha	Homo sapiens	27-33
17193822-1	2006	Mutually exclusive KIT and PDGFRA mutations are central events in GIST pathogenesis, and their understanding is becoming increasingly important, because specific treatment targeting oncogenic KIT and PDGFRA activation (especially imatinib mesylate) has become available.	imatinib	230-238	platelet derived growth factor receptor alpha	Homo sapiens	200-206
17193822-15	2006	Secondary mutations usually occur in KIT kinase domains in patients after imatinib treatment resulting in resistance to this drug.	imatinib	74-82	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	37-40
16618932-4	2006	Although the ABL kinase inhibitor imatinib mesylate (Gleevec) provides highly effective treatment for BCR-ABL-positive chronic myelogenous leukemia, it has proven far less efficacious in the treatment of BCR-ABL-positive acute lymphoblastic leukemias (ALLs), many of which sustain deletions of the INK4A-ARF (CDKN2A) tumor suppressor locus.	imatinib	34-51	cyclin dependent kinase inhibitor 2A	Mus musculus	309-315
16618932-7	2006	Treatment of Arf-/-, p210(Bcr-Abl)-positive pre-B cells with imatinib together with an inhibitor of JAK kinases abrogates this resistance, suggesting that this combination may prove beneficial in the treatment of BCR-ABL-positive acute lymphoblastic leukemia.	imatinib	61-69	envoplakin	Mus musculus	21-25
16278304-1	2006	Although targeting the BCR-ABL tyrosine kinase activity by imatinib mesylate has rapidly become first-line therapy in chronic myeloid leukemia (CML), drug resistance suggests that combination therapy directed to a complementing target may significantly improve treatment results.	imatinib	59-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
16352805-2	2006	We found that patients undergoing imatinib (n = 14) or rIFNalpha (n = 7) therapy remained strongly positive for V617F JAK2, although there was a significant reduction in the median percentage of mutant alleles that correlated with hematologic response (P = .001).	imatinib	34-42	Janus kinase 2	Homo sapiens	118-122
16622127-0	2006	Response of a KIT-positive extra-abdominal fibromatosis to imatinib mesylate and KIT genetic analysis.	imatinib	59-67	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-17
16638875-10	2006	In agreement with these results, two of the three imatinib-resistant patients with the KIT-V654A mutation responded to SU11248 treatment.	imatinib	50-58	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	87-90
16638875-1	2006	PURPOSE: The majority of gastrointestinal stromal tumors harbor mutations in the receptor tyrosine kinases KIT or platelet-derived growth factor receptor A (PDGFRA), and respond to treatment with the tyrosine kinase inhibitor imatinib.	imatinib	226-234	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	107-110
16638875-11	2006	CONCLUSIONS: These studies suggest that SU11248 may be a useful therapeutic agent to treat gastrointestinal stromal tumors harboring the imatinib-resistant KIT-V654A or KIT-T670I mutations, but it has no effect on the activity of the PDGFRA-D842V mutant.	imatinib	137-145	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	156-159
16638875-1	2006	PURPOSE: The majority of gastrointestinal stromal tumors harbor mutations in the receptor tyrosine kinases KIT or platelet-derived growth factor receptor A (PDGFRA), and respond to treatment with the tyrosine kinase inhibitor imatinib.	imatinib	226-234	platelet derived growth factor receptor alpha	Homo sapiens	114-155
16638875-1	2006	PURPOSE: The majority of gastrointestinal stromal tumors harbor mutations in the receptor tyrosine kinases KIT or platelet-derived growth factor receptor A (PDGFRA), and respond to treatment with the tyrosine kinase inhibitor imatinib.	imatinib	226-234	platelet derived growth factor receptor alpha	Homo sapiens	157-163
16638875-11	2006	CONCLUSIONS: These studies suggest that SU11248 may be a useful therapeutic agent to treat gastrointestinal stromal tumors harboring the imatinib-resistant KIT-V654A or KIT-T670I mutations, but it has no effect on the activity of the PDGFRA-D842V mutant.	imatinib	137-145	platelet derived growth factor receptor alpha	Homo sapiens	234-240
16638875-3	2006	The most common mechanism of imatinib resistance involves specific mutations in the kinase domains of KIT or PDGFRA.	imatinib	29-37	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	102-105
16638875-3	2006	The most common mechanism of imatinib resistance involves specific mutations in the kinase domains of KIT or PDGFRA.	imatinib	29-37	platelet derived growth factor receptor alpha	Homo sapiens	109-115
16585609-4	2006	At diagnosis, chronic myeloid leukemia patients had abnormally high serum levels of sMICA and weak NKG2D expression on NK and CD8+ T cells, which were restored by imatinib mesylate (IM) therapy.	imatinib	163-180	killer cell lectin like receptor K1	Homo sapiens	99-104
16638875-4	2006	We tested the activity of SU11248, an orally active small-molecule tyrosine kinase inhibitor, to inhibit important imatinib-resistant KIT and PDGFRA mutants.	imatinib	115-123	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	134-137
16638875-5	2006	EXPERIMENTAL DESIGN: Primary imatinib-resistant tumor cells and cell lines expressing clinically identified imatinib-resistant KIT-V654A, KIT-T670I, or PDGFRA-D842V mutant isoforms were evaluated for sensitivity to SU11248 by Western immunoblotting and proliferation assays.	imatinib	108-116	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	127-130
16638875-5	2006	EXPERIMENTAL DESIGN: Primary imatinib-resistant tumor cells and cell lines expressing clinically identified imatinib-resistant KIT-V654A, KIT-T670I, or PDGFRA-D842V mutant isoforms were evaluated for sensitivity to SU11248 by Western immunoblotting and proliferation assays.	imatinib	108-116	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	138-141
16609011-9	2006	Lastly, comparison of the STI571-sensitive Ph+ acute lymphoblastic leukemia cell line SupB15 with a STI571-resistant subline revealed significantly decreased PTP1B activity and enhanced BCR-ABL phosphorylation in the STI571-resistant SupB15 cells.	imatinib	100-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-193
16518826-0	2006	Expression of Bcl-2 in gastrointestinal stromal tumors: correlation with progression-free survival in 81 patients treated with imatinib mesylate.	imatinib	127-144	BCL2 apoptosis regulator	Homo sapiens	14-19
16518826-3	2006	To the authors" knowledge, the current study is the first to evaluate Bcl-2 expression in pre-imatinib GIST tissue samples as a prognostic marker of progression-free survival (PFS) time in patients treated with imatinib.	imatinib	94-102	BCL2 apoptosis regulator	Homo sapiens	70-75
16518826-3	2006	To the authors" knowledge, the current study is the first to evaluate Bcl-2 expression in pre-imatinib GIST tissue samples as a prognostic marker of progression-free survival (PFS) time in patients treated with imatinib.	imatinib	211-219	BCL2 apoptosis regulator	Homo sapiens	70-75
16518826-11	2006	CONCLUSIONS: In contrast to studies performed in the preimatinib era, in which Bcl-2 was found to be a negative prognostic indicator, the current study suggests a trend toward better PFS with increasing Bcl-2 expression level in GISTs from patients subsequently treated with imatinib.	imatinib	56-64	BCL2 apoptosis regulator	Homo sapiens	203-208
16518826-12	2006	Larger studies may help elucidate the influence of Bcl-2 expression on PFS after therapy with imatinib.	imatinib	94-102	BCL2 apoptosis regulator	Homo sapiens	51-56
16609040-3	2006	Parallel studies were done in imatinib mesylate-resistant cells, including BaF3 cells transfected with plasmids encoding clinically relevant Bcr/abl mutations conferring imatinib mesylate resistance (e.g., E255K, M351T, and T315I) and primary CD34(+) bone marrow cells from patients refractory to imatinib mesylate.	imatinib	170-187	BCR activator of RhoGEF and GTPase	Mus musculus	141-144
16609040-3	2006	Parallel studies were done in imatinib mesylate-resistant cells, including BaF3 cells transfected with plasmids encoding clinically relevant Bcr/abl mutations conferring imatinib mesylate resistance (e.g., E255K, M351T, and T315I) and primary CD34(+) bone marrow cells from patients refractory to imatinib mesylate.	imatinib	170-187	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-148
16610057-1	2006	AIM: Most gastrointestinal stromal tumors (GISTs) express constitutively activated mutant isoforms of kit kinase or platelet-derived growth factor receptor alpha (PDGFRA), which are potential therapeutic targets for imatinib mesylate (Glivec).	imatinib	216-233	platelet derived growth factor receptor alpha	Homo sapiens	116-161
16610057-1	2006	AIM: Most gastrointestinal stromal tumors (GISTs) express constitutively activated mutant isoforms of kit kinase or platelet-derived growth factor receptor alpha (PDGFRA), which are potential therapeutic targets for imatinib mesylate (Glivec).	imatinib	216-233	platelet derived growth factor receptor alpha	Homo sapiens	163-169
16613680-2	2006	STI571 is a tyrosine kinase inhibitor of platelet-derived growth factor receptor beta (PDGFR-beta) which is overexpressed in esophageal carcinoma.	imatinib	0-6	platelet derived growth factor receptor beta	Homo sapiens	41-85
16613680-2	2006	STI571 is a tyrosine kinase inhibitor of platelet-derived growth factor receptor beta (PDGFR-beta) which is overexpressed in esophageal carcinoma.	imatinib	0-6	platelet derived growth factor receptor beta	Homo sapiens	87-97
16613680-7	2006	The expression of p-PDGFR-beta was detected by Western blot before and after treatment of STI571.	imatinib	90-96	platelet derived growth factor receptor beta	Homo sapiens	20-30
16613680-12	2006	CONCLUSIONS: STI-571 could induce the apoptosis of PDGFR-beta-positive esophageal carcinoma CE-48T cells.	imatinib	13-20	platelet derived growth factor receptor beta	Homo sapiens	51-61
16609011-0	2006	Inhibition of phosphotyrosine phosphatase 1B causes resistance in BCR-ABL-positive leukemia cells to the ABL kinase inhibitor STI571.	imatinib	126-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
16609011-2	2006	To investigate whether PTP1B modulates the biological effects of the abl kinase inhibitor STI571 in BCR-ABL-positive cells, we transfected Philadelphia chromosome-positive (Ph+) chronic myeloid leukemia cell-derived K562 cells with either wild-type PTP1B (K562/PTP1B), a substrate-trapping dominant-negative mutant PTP1B (K562/D181A), or empty vector (K562/mock).	imatinib	90-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
16609011-4	2006	In both K562/mock and K562/PTP1B cells, 0.25 to 1 mumol/L STI571 induced dose-dependent growth arrest and apoptosis, as measured by a decrease of cell proliferation and an increase of Annexin V-positive cells and/or of cells in the sub-G(1) apoptotic phase.	imatinib	58-64	protein tyrosine phosphatase non-receptor type 1	Homo sapiens	22-32
16609011-4	2006	In both K562/mock and K562/PTP1B cells, 0.25 to 1 mumol/L STI571 induced dose-dependent growth arrest and apoptosis, as measured by a decrease of cell proliferation and an increase of Annexin V-positive cells and/or of cells in the sub-G(1) apoptotic phase.	imatinib	58-64	annexin A5	Homo sapiens	184-193
16609011-8	2006	Pharmacologic inhibition of PTP1B activity in wild-type K562 cells, using bis(N,N-dimethylhydroxamido)hydroxooxovanadate, attenuated STI571-induced apoptosis.	imatinib	133-139	protein tyrosine phosphatase non-receptor type 1	Homo sapiens	28-33
16609011-9	2006	Lastly, comparison of the STI571-sensitive Ph+ acute lymphoblastic leukemia cell line SupB15 with a STI571-resistant subline revealed significantly decreased PTP1B activity and enhanced BCR-ABL phosphorylation in the STI571-resistant SupB15 cells.	imatinib	26-32	protein tyrosine phosphatase non-receptor type 1	Homo sapiens	158-163
16609011-9	2006	Lastly, comparison of the STI571-sensitive Ph+ acute lymphoblastic leukemia cell line SupB15 with a STI571-resistant subline revealed significantly decreased PTP1B activity and enhanced BCR-ABL phosphorylation in the STI571-resistant SupB15 cells.	imatinib	26-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-193
16609011-9	2006	Lastly, comparison of the STI571-sensitive Ph+ acute lymphoblastic leukemia cell line SupB15 with a STI571-resistant subline revealed significantly decreased PTP1B activity and enhanced BCR-ABL phosphorylation in the STI571-resistant SupB15 cells.	imatinib	100-106	protein tyrosine phosphatase non-receptor type 1	Homo sapiens	158-163
16609040-3	2006	Parallel studies were done in imatinib mesylate-resistant cells, including BaF3 cells transfected with plasmids encoding clinically relevant Bcr/abl mutations conferring imatinib mesylate resistance (e.g., E255K, M351T, and T315I) and primary CD34(+) bone marrow cells from patients refractory to imatinib mesylate.	imatinib	170-187	BCR activator of RhoGEF and GTPase	Mus musculus	141-144
16609040-3	2006	Parallel studies were done in imatinib mesylate-resistant cells, including BaF3 cells transfected with plasmids encoding clinically relevant Bcr/abl mutations conferring imatinib mesylate resistance (e.g., E255K, M351T, and T315I) and primary CD34(+) bone marrow cells from patients refractory to imatinib mesylate.	imatinib	170-187	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-148
16609011-9	2006	Lastly, comparison of the STI571-sensitive Ph+ acute lymphoblastic leukemia cell line SupB15 with a STI571-resistant subline revealed significantly decreased PTP1B activity and enhanced BCR-ABL phosphorylation in the STI571-resistant SupB15 cells.	imatinib	100-106	protein tyrosine phosphatase non-receptor type 1	Homo sapiens	158-163
16609011-9	2006	Lastly, comparison of the STI571-sensitive Ph+ acute lymphoblastic leukemia cell line SupB15 with a STI571-resistant subline revealed significantly decreased PTP1B activity and enhanced BCR-ABL phosphorylation in the STI571-resistant SupB15 cells.	imatinib	100-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-193
16609011-10	2006	In conclusion, functional PTP1B is involved in STI571-induced growth and cell cycle arrest, apoptosis, and differentiation, and attenuation of PTP1B function may contribute to resistance towards STI571.	imatinib	47-53	protein tyrosine phosphatase non-receptor type 1	Homo sapiens	26-31
16609040-0	2006	Synergistic interactions between DMAG and mitogen-activated protein kinase kinase 1/2 inhibitors in Bcr/abl+ leukemia cells sensitive and resistant to imatinib mesylate.	imatinib	151-168	mitogen-activated protein kinase kinase 1	Homo sapiens	42-85
16539879-8	2006	Specific therapy targeting the KIT receptor with imatinib has resulted in improved outcomes for patients with unresectable, metastatic, and recurrent disease.	imatinib	49-57	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	31-34
16597375-5	2006	Treatment with either arsenic or imatinib, or both, resulted in significant increases in serum creatine kinase isoenzyme (CK-MB), glutathione peroxidase (GPx), lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) activity levels.	imatinib	33-41	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	192-218
16461746-4	2006	During differentiation, imatinib induces a slight increase of DC apoptosis and prevents CD1a up-regulation in a dose-dependent manner in bcr-abl+ and normal monocyte-derived DC, but at most, 25% of DC fail to acquire CD1a.	imatinib	24-32	CD1a molecule	Homo sapiens	88-92
16461746-4	2006	During differentiation, imatinib induces a slight increase of DC apoptosis and prevents CD1a up-regulation in a dose-dependent manner in bcr-abl+ and normal monocyte-derived DC, but at most, 25% of DC fail to acquire CD1a.	imatinib	24-32	CD1a molecule	Homo sapiens	217-221
16461746-5	2006	When DC maturation is induced in the presence of imatinib, bcr-abl+ and normal monocyte-derived DC up-regulate major histocompatibility complex and costimulatory molecules, CC chemokine receptor 7 and CD83.	imatinib	49-57	C-C motif chemokine receptor 7	Homo sapiens	173-196
16461746-5	2006	When DC maturation is induced in the presence of imatinib, bcr-abl+ and normal monocyte-derived DC up-regulate major histocompatibility complex and costimulatory molecules, CC chemokine receptor 7 and CD83.	imatinib	49-57	CD83 molecule	Homo sapiens	201-205
16461746-8	2006	In sharp contrast, imatinib, when added to DC-T cell cultures, profoundly suppresses DC-mediated T cell proliferation, despite reciprocal DC-T cell activation attested by up-regulation of CD25 on T cells and of CD86 on DC.	imatinib	19-27	interleukin 2 receptor subunit alpha	Homo sapiens	188-192
16461746-8	2006	In sharp contrast, imatinib, when added to DC-T cell cultures, profoundly suppresses DC-mediated T cell proliferation, despite reciprocal DC-T cell activation attested by up-regulation of CD25 on T cells and of CD86 on DC.	imatinib	19-27	CD86 molecule	Homo sapiens	211-215
16597375-5	2006	Treatment with either arsenic or imatinib, or both, resulted in significant increases in serum creatine kinase isoenzyme (CK-MB), glutathione peroxidase (GPx), lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) activity levels.	imatinib	33-41	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	220-223
16467863-1	2006	The expansion of a leukemia clone bearing a Bcr-Abl kinase domain mutation is associated with acquired resistance to imatinib and may also predict disease progression in patients with Philadelphia-positive chronic myeloid leukemia (CML).	imatinib	117-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
16482207-1	2006	Mutations in the Bcr-Abl kinase domain are a frequent cause of imatinib resistance in patients with advanced CML or Ph+ ALL.	imatinib	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
16498395-9	2006	hTERT levels were increased in CP patients following successful treatment with imatinib, relative to untreated CP patients.	imatinib	79-87	telomerase reverse transcriptase	Homo sapiens	0-5
16183119-0	2006	A novel K509I mutation of KIT identified in familial mastocytosis-in vitro and in vivo responsiveness to imatinib therapy.	imatinib	105-113	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	26-29
16482207-3	2006	In this study, we analyzed the effects of the Bcr-Abl P-loop mutation Y253H and the highly imatinib resistant T315I mutation on kinase activity in vitro and transforming efficiency of Bcr-Abl in vitro and in vivo.	imatinib	91-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	184-191
16183119-2	2006	For those malignancies associated with KIT mutation or over-expression, imatinib offers a specific therapeutic option, yet it has no effect on D816V mutation commonly seen in sporadic mastocytosis.	imatinib	72-80	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	39-42
16482207-7	2006	Thus, the analysed Bcr-Abl mutants confer imatinib resistance, but do not induce a growth advantage in the absence of imatinib.	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
16567968-3	2006	STI571 is a new antineoplastic compound, which selectively inhibits the tyrosine kinase activity of ABL, c-Kit and platelet-derived growth factor receptor (PDGFR).	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-103
16638194-1	2006	To study the effects of tyrosine-kinase inhibitor STI571 on the adhesion of RPMI8226 cells to fibronectin (FN), cell adhesion mediated adriamycin-resistance and the Rac1 mRNA expression, the adhesion of RPMI8226 cells to fibronectin and drug resistance mediated by cell adhesion were determined by means of crystal violet staining and MTT assays respectively, Rac1 mRNA levels in RPMI8226 cells were examined by semi-quantitative RT-PCR.	imatinib	50-56	fibronectin 1	Homo sapiens	94-105
16567968-3	2006	STI571 is a new antineoplastic compound, which selectively inhibits the tyrosine kinase activity of ABL, c-Kit and platelet-derived growth factor receptor (PDGFR).	imatinib	0-6	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	105-110
16567968-3	2006	STI571 is a new antineoplastic compound, which selectively inhibits the tyrosine kinase activity of ABL, c-Kit and platelet-derived growth factor receptor (PDGFR).	imatinib	0-6	platelet derived growth factor receptor beta	Homo sapiens	115-154
16567968-3	2006	STI571 is a new antineoplastic compound, which selectively inhibits the tyrosine kinase activity of ABL, c-Kit and platelet-derived growth factor receptor (PDGFR).	imatinib	0-6	platelet derived growth factor receptor beta	Homo sapiens	156-161
16648572-4	2006	In contrast to a previous report, we have found that imatinib has activity against human CSF-1R in both assays at submicromolar concentrations.	imatinib	53-61	colony stimulating factor 1 receptor	Homo sapiens	89-95
16648572-5	2006	In enzyme assays, we have found that the inhibition of CSF-1R by both ABT-869 and imatinib are competitive with ATP, with Ki values of 3 and 120 nmol/L, respectively.	imatinib	82-90	colony stimulating factor 1 receptor	Homo sapiens	55-61
16612767-4	2006	Indeed, imatinib mesylate has become first-line therapy for patients in whom the FIP1L1-PDGFRalpha fusion gene is detected, whereas corticosteroids remain the mainstay for management of patients in whom hypereosinophilia is secondary to the overproduction of interleukin 5 by abnormal T-cells.	imatinib	8-25	factor interacting with PAPOLA and CPSF1	Homo sapiens	81-87
16612767-4	2006	Indeed, imatinib mesylate has become first-line therapy for patients in whom the FIP1L1-PDGFRalpha fusion gene is detected, whereas corticosteroids remain the mainstay for management of patients in whom hypereosinophilia is secondary to the overproduction of interleukin 5 by abnormal T-cells.	imatinib	8-25	platelet derived growth factor receptor alpha	Homo sapiens	88-98
16689455-7	2006	Imatinib mesylate (Glivec) is a small molecule that binds to the ATP pocket of ABL and blocks downstream signalling events.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-82
16689455-13	2006	Additional BCR-ABL independent chromosomal abnormalities are common in advanced phase CML and result in resistance to imatinib.	imatinib	118-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-18
16689455-14	2006	BCR-ABL kinase-domaine mutations are frequently found in imatinib resistant patients and confer diminished sensitivity to imatinib.	imatinib	57-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
16689455-14	2006	BCR-ABL kinase-domaine mutations are frequently found in imatinib resistant patients and confer diminished sensitivity to imatinib.	imatinib	122-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
16689459-19	2006	Importantly, the lack of an activating mutation of KIT tyrosine kinase is good evidence that imatinib will not be effective.	imatinib	93-101	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	51-54
16638194-2	2006	The results showed that STI571 could inhibit the adhesion of RPMI8226 cells to fibronectin.	imatinib	24-30	fibronectin 1	Homo sapiens	79-90
16638194-6	2006	Following treatment with 20 micromol/L STI571, the mean IC50 values for FN and BSA adhered cells were (0.81 +/- 0.05) micromol/L, (0.74 +/- 0.02) micromol/L respectively, there was no significant difference between them (P > 0.05).	imatinib	39-45	fibronectin 1	Homo sapiens	72-74
16638194-8	2006	It is concluded that STI571 can inhibit the adhesion of RPMI8226 cells to fibronectin, reverse cell adhesion mediated adriamycin-resistance, and downregulate Rac1 mRNA level.	imatinib	21-27	fibronectin 1	Homo sapiens	74-85
16638194-8	2006	It is concluded that STI571 can inhibit the adhesion of RPMI8226 cells to fibronectin, reverse cell adhesion mediated adriamycin-resistance, and downregulate Rac1 mRNA level.	imatinib	21-27	Rac family small GTPase 1	Homo sapiens	158-162
16291594-0	2006	Adaphostin-induced oxidative stress overcomes BCR/ABL mutation-dependent and -independent imatinib resistance.	imatinib	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
16556328-3	2006	For example Imatinib/Gleevec (primarily a bcr/abl kinase inhibitor) or SU11248 (mainly a VEGFR inhibitor) are also potent inhibitors of PDGFR and other kinases.	imatinib	12-20	kinase insert domain receptor	Homo sapiens	89-94
16556328-3	2006	For example Imatinib/Gleevec (primarily a bcr/abl kinase inhibitor) or SU11248 (mainly a VEGFR inhibitor) are also potent inhibitors of PDGFR and other kinases.	imatinib	12-20	platelet derived growth factor receptor beta	Homo sapiens	136-141
16291594-1	2006	The BCR/ABL kinase has been targeted for the treatment of chronic myelogenous leukemia (CML) by imatinib mesylate.	imatinib	96-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
16291594-3	2006	In particular, mutation of the T315 residue in the bcr/abl activation loop renders cells highly resistant to imatinib and to second-generation kinase inhibitors such as BMS-354825 or AMN107.	imatinib	109-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
16570351-0	2006	Expression of c-kit receptor in human cholangiocarcinoma and in vivo treatment with imatinib mesilate in chimeric mice.	imatinib	84-101	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-19
16551858-0	2006	Polyclonal evolution of multiple secondary KIT mutations in gastrointestinal stromal tumors under treatment with imatinib mesylate.	imatinib	113-130	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	43-46
16551858-3	2006	Both PDGFRalpha and KIT receptors are targets of the tyrosine kinase inhibitor imatinib (Glivec) which has improved the treatment of advanced GISTs significantly.	imatinib	79-87	platelet derived growth factor receptor alpha	Homo sapiens	5-15
16551858-3	2006	Both PDGFRalpha and KIT receptors are targets of the tyrosine kinase inhibitor imatinib (Glivec) which has improved the treatment of advanced GISTs significantly.	imatinib	79-87	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	20-23
16551858-3	2006	Both PDGFRalpha and KIT receptors are targets of the tyrosine kinase inhibitor imatinib (Glivec) which has improved the treatment of advanced GISTs significantly.	imatinib	89-95	platelet derived growth factor receptor alpha	Homo sapiens	5-15
16551858-3	2006	Both PDGFRalpha and KIT receptors are targets of the tyrosine kinase inhibitor imatinib (Glivec) which has improved the treatment of advanced GISTs significantly.	imatinib	89-95	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	20-23
16303243-9	2006	The kinase inhibitors gefitinib and imatinib mesylate also interact with BCRP.	imatinib	36-53	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	73-77
16303243-12	2006	Imatinib, an inhibitor of BCR-ABL tyrosine kinase, also inhibits BCRP-mediated drug transport.	imatinib	0-8	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	65-69
16570351-15	2006	After 14 d of in vitro treatment with imatinib mesilate, using the chimeric mouse model, c-kit positive Mz-ChA-2 tumors had a significantly reduced volume and mass as compared to NS treatment (P<0.05).	imatinib	38-55	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	89-94
16570351-18	2006	Imatinib mesilate exerts marked effects on tumor growth in vitro and in vitro dependent on the level of c-kit expression.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	104-109
16570351-1	2006	AIM: To investigate the c-kit expression in biliary tract cancer cell lines and histological sections from patients with extrahepatic cholangiocarcinoma (CC) and to evaluate the efficacy of in vitro and in vitro treatment with imatinib mesilate.	imatinib	227-244	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	24-29
16570351-11	2006	Imatinib mesilate at a low concentration of 5 micromol/L caused a significant growth inhibition in the c-kit positive cell line Mz-ChA-2 (31%), but not in the c-kit negative cell line EGI-1 (0%) (P<0.05).	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	103-108
16570351-11	2006	Imatinib mesilate at a low concentration of 5 micromol/L caused a significant growth inhibition in the c-kit positive cell line Mz-ChA-2 (31%), but not in the c-kit negative cell line EGI-1 (0%) (P<0.05).	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	159-164
16619531-1	2006	BACKGROUND: Gastrointestinal stromal tumours (GIST) predominantly express activating mutations of the KIT tyrosine kinase receptor and are successfully treated with imatinib mesylate, a KIT inhibitor.	imatinib	165-182	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	102-105
16403813-0	2006	Prediction of response to imatinib by prospective quantitation of BCR-ABL transcript in late chronic phase chronic myeloid leukemia patients.	imatinib	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
16403813-1	2006	Imatinib mesylate (STI571), a specific Bcr-Abl inhibitor, has shown a potent antileukemic activity in clinical studies of chronic myeloid leukemia (CML) patients.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
16403813-1	2006	Imatinib mesylate (STI571), a specific Bcr-Abl inhibitor, has shown a potent antileukemic activity in clinical studies of chronic myeloid leukemia (CML) patients.	imatinib	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
16403813-6	2006	We show that, following initiation of imatinib, the early BCR-ABL level trends in both bone marrow and peripheral blood samples made it possible to predict the subsequent cytogenetic outcome and response.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
16619531-1	2006	BACKGROUND: Gastrointestinal stromal tumours (GIST) predominantly express activating mutations of the KIT tyrosine kinase receptor and are successfully treated with imatinib mesylate, a KIT inhibitor.	imatinib	165-182	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	186-189
16619531-4	2006	RESULTS: Using the small animal PET, FDG up-take in xenografts was significantly decreased after 24 h of treatment with imatinib, which correlated with a response to treatment, e.g., with a decrease in tumour volume, the inhibition of KIT and downstream intermediate phosphorylation and arrest of tumour cell proliferation as evaluated after 7 days of treatment.	imatinib	120-128	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	235-238
16254134-8	2006	The KIT-D816V receptor expressed in Ba/F3 cells was resistant to growth inhibition by the selective PTK inhibitors imatinib and SU5614 but fully sensitive to PKC412.	imatinib	115-123	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	4-7
16435011-5	2006	Treatment with 1.0 microM imatinib, 60 microg/ml mafosfamide and 14 days of culture with cytokines eliminated BCR-ABL(+) cells from chronic phase CML patient aphereses, while preserving normal progenitors.	imatinib	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
16469036-1	2006	OBJECTIVE: To describe the effect of a specific c-kit receptor inhibitor (imatinib mesylate) on human detrusor strips in vitro and guinea-pig cystometry in vivo, and to show histological data suggesting differences in the distribution of interstitial cells of Cajal (ICC)-like cells in "normal" and overactive human detrusor, as these cells have been identified as possible mediators of spontaneous activity and excitability in bladder smooth muscle.	imatinib	74-91	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	48-53
16332440-1	2006	A series of 3-substituted benzamide derivatives structurally related to STI-571 (imatinib mesylate), a Bcr-Abl tyrosine kinase inhibitor used to treat chronic myeloid leukemia (CML), was prepared and evaluated for antiproliferative activity against the Bcr-Abl-positive leukemia cell line K562.	imatinib	72-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
16332440-1	2006	A series of 3-substituted benzamide derivatives structurally related to STI-571 (imatinib mesylate), a Bcr-Abl tyrosine kinase inhibitor used to treat chronic myeloid leukemia (CML), was prepared and evaluated for antiproliferative activity against the Bcr-Abl-positive leukemia cell line K562.	imatinib	72-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	253-260
16332440-3	2006	One of these, NS-187 (9b), is a promising new candidate Bcr-Abl inhibitor for the therapy of STI-571-resistant chronic myeloid leukemia.	imatinib	93-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
16444746-1	2006	BACKGROUND: The objective of this study was to evaluate the ability of the clinically available histone deacetylase (HDAC) inhibitor valproate to enhance the cytotoxicity of the Bcr-Abl inhibitor imatinib in imatinib-resistant cell lines.	imatinib	196-204	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185
16357008-0	2006	Mutation and expression of PDGFRA and KIT in malignant peripheral nerve sheath tumors, and its implications for imatinib sensitivity.	imatinib	112-120	platelet derived growth factor receptor alpha	Homo sapiens	27-33
16444746-1	2006	BACKGROUND: The objective of this study was to evaluate the ability of the clinically available histone deacetylase (HDAC) inhibitor valproate to enhance the cytotoxicity of the Bcr-Abl inhibitor imatinib in imatinib-resistant cell lines.	imatinib	208-216	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185
16357008-13	2006	Imatinib treatment of MPNST cell culture S462 exerted a growth inhibitory effect and prevented PDGF-AA induced PDGFRalpha phosphorylation.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	111-121
16444746-5	2006	Coexposure of cells to valproate and imatinib was associated with repression of several genes involved in Bcr-Abl transformation.	imatinib	37-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
16357008-14	2006	In summary, PDGFRA, PDGF and KIT dysregulation as well as growth inhibition of cell culture S462 by imatinib may suggest that MPNST patients benefit from treatment with imatinib.	imatinib	169-177	platelet derived growth factor receptor alpha	Homo sapiens	12-18
16444746-6	2006	In particular, the combination valproate-imatinib downregulated the expression of Bcr-Abl and the antiapoptotic protein Bcl-2, which is particularly overexpressed in imatinib-resistant clones.	imatinib	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
16357008-14	2006	In summary, PDGFRA, PDGF and KIT dysregulation as well as growth inhibition of cell culture S462 by imatinib may suggest that MPNST patients benefit from treatment with imatinib.	imatinib	169-177	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	29-32
16444746-6	2006	In particular, the combination valproate-imatinib downregulated the expression of Bcr-Abl and the antiapoptotic protein Bcl-2, which is particularly overexpressed in imatinib-resistant clones.	imatinib	41-49	BCL2 apoptosis regulator	Homo sapiens	120-125
16444746-6	2006	In particular, the combination valproate-imatinib downregulated the expression of Bcr-Abl and the antiapoptotic protein Bcl-2, which is particularly overexpressed in imatinib-resistant clones.	imatinib	166-174	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
16444746-6	2006	In particular, the combination valproate-imatinib downregulated the expression of Bcr-Abl and the antiapoptotic protein Bcl-2, which is particularly overexpressed in imatinib-resistant clones.	imatinib	166-174	BCL2 apoptosis regulator	Homo sapiens	120-125
16432052-3	2006	We investigated whether imatinib, by inhibiting the platelet-derived growth factor receptor-beta (PDGFRbeta), prevents cardiac and renal damage in TGR(mRen2)27 (Ren2) rats.	imatinib	24-32	platelet derived growth factor receptor beta	Rattus norvegicus	52-96
16432052-3	2006	We investigated whether imatinib, by inhibiting the platelet-derived growth factor receptor-beta (PDGFRbeta), prevents cardiac and renal damage in TGR(mRen2)27 (Ren2) rats.	imatinib	24-32	platelet derived growth factor receptor beta	Rattus norvegicus	98-107
16432052-10	2006	In vitro, imatinib blocked angiotensin II-induced activation of the PDGFRbeta and significantly decreased fibroblast proliferation and collagen production.	imatinib	10-18	angiotensinogen	Rattus norvegicus	27-41
16432052-10	2006	In vitro, imatinib blocked angiotensin II-induced activation of the PDGFRbeta and significantly decreased fibroblast proliferation and collagen production.	imatinib	10-18	platelet derived growth factor receptor beta	Rattus norvegicus	68-77
16432052-11	2006	In conclusion, imatinib did not affect LV hypertrophy but attenuated the decline in cardiac function and reduced renal microvascular damage associated with reduced activation of the PDGFRbeta.	imatinib	15-23	platelet derived growth factor receptor beta	Rattus norvegicus	182-191
16470567-5	2006	Therefore, this research paper investigates the role of the activity of CYP1A1, 1A2, 1B1, 3A4, 4F2 and 4F3A/B on the fate of imatinib.	imatinib	125-133	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	72-78
16505440-15	2006	Imatinib response in AF patients may be mediated by inhibition of PDGFRB kinase activity.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	66-72
16470567-6	2006	First, a study of imatinib fragmentation was effected using electrospray triple-quadrupole and linear ion trap tandem mass spectrometers (MSn).	imatinib	18-26	moesin	Homo sapiens	138-141
16470567-10	2006	Imatinib metabolites were produced in microsomal incubations containing CYP isozymes.	imatinib	0-8	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	72-75
16629079-4	2006	The treatment options have evolved rapidly with the discovery of imatinib (Gleevec) that selectively inhibits KIT.	imatinib	65-73	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	110-113
16572634-2	2006	The authors investigated the mutation of c-kit and the expression of its product KIT in IGCTs to identify tumors susceptible to imatinib mesylate, a synthetic agent targeting KIT.	imatinib	128-145	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	175-178
15893416-1	2006	Imatinib targets KIT and platelet-derived growth factor receptors (PDGFR) and is highly effective in the treatment of CML and GIST patients.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	17-20
15893416-1	2006	Imatinib targets KIT and platelet-derived growth factor receptors (PDGFR) and is highly effective in the treatment of CML and GIST patients.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	25-65
15893416-1	2006	Imatinib targets KIT and platelet-derived growth factor receptors (PDGFR) and is highly effective in the treatment of CML and GIST patients.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	67-72
15893416-8	2006	Survival and treatment responses were independent of KIT and PDGFRbeta expression in patients treated with imatinib.	imatinib	107-115	platelet derived growth factor receptor beta	Homo sapiens	61-70
16254145-0	2006	Regulation of survivin expression through Bcr-Abl/MAPK cascade: targeting survivin overcomes imatinib resistance and increases imatinib sensitivity in imatinib-responsive CML cells.	imatinib	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
16205638-5	2006	Comparing matched leukemia sample pairs from patients before and during therapy with the BCR-ABL1 kinase inhibitor STI571 (Imatinib), inhibition of BCR-ABL1 partially corrected aberrant expression of IK6 and lineage infidelity of the leukemia cells.	imatinib	115-121	BCR activator of RhoGEF and GTPase	Homo sapiens	89-97
16205638-5	2006	Comparing matched leukemia sample pairs from patients before and during therapy with the BCR-ABL1 kinase inhibitor STI571 (Imatinib), inhibition of BCR-ABL1 partially corrected aberrant expression of IK6 and lineage infidelity of the leukemia cells.	imatinib	115-121	BCR activator of RhoGEF and GTPase	Homo sapiens	148-156
16205638-5	2006	Comparing matched leukemia sample pairs from patients before and during therapy with the BCR-ABL1 kinase inhibitor STI571 (Imatinib), inhibition of BCR-ABL1 partially corrected aberrant expression of IK6 and lineage infidelity of the leukemia cells.	imatinib	123-131	BCR activator of RhoGEF and GTPase	Homo sapiens	89-97
16249386-0	2006	BCR-ABL nuclear entrapment kills human CML cells: ex vivo study on 35 patients with the combination of imatinib mesylate and leptomycin B.	imatinib	103-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
16249386-2	2006	We previously reported that the combination of the ABL kinase inhibitor imatinib mesylate (IM) and the nuclear export inhibitor leptomycin B (LMB) traps BCR-ABL inside the nucleus, triggering the death of the leukemic cells.	imatinib	72-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
16205638-5	2006	Comparing matched leukemia sample pairs from patients before and during therapy with the BCR-ABL1 kinase inhibitor STI571 (Imatinib), inhibition of BCR-ABL1 partially corrected aberrant expression of IK6 and lineage infidelity of the leukemia cells.	imatinib	123-131	BCR activator of RhoGEF and GTPase	Homo sapiens	148-156
16254145-0	2006	Regulation of survivin expression through Bcr-Abl/MAPK cascade: targeting survivin overcomes imatinib resistance and increases imatinib sensitivity in imatinib-responsive CML cells.	imatinib	127-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
16254145-0	2006	Regulation of survivin expression through Bcr-Abl/MAPK cascade: targeting survivin overcomes imatinib resistance and increases imatinib sensitivity in imatinib-responsive CML cells.	imatinib	127-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
16254145-2	2006	Inhibition of Bcr-Abl by imatinib significantly decreased survivin expression and cell viability in KBM5, but much less so in KBM5-STI571 cells.	imatinib	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
16462496-0	2006	Phase II study of imatinib mesylate in chemotherapy refractory germ cell tumors expressing KIT.	imatinib	18-35	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	91-94
16521182-0	2006	STI571 (Glivec) suppresses the expression of vascular endothelial growth factor in the gastrointestinal stromal tumor cell line, GIST-T1.	imatinib	0-6	vascular endothelial growth factor A	Homo sapiens	45-79
16521182-1	2006	AIM: To estimate whether STI571 inhibits the expression of vascular endothelial growth factor (VEGF) in the gastrointestinal stromal tumor (GIST) cells.	imatinib	25-31	vascular endothelial growth factor A	Homo sapiens	59-93
16521182-1	2006	AIM: To estimate whether STI571 inhibits the expression of vascular endothelial growth factor (VEGF) in the gastrointestinal stromal tumor (GIST) cells.	imatinib	25-31	vascular endothelial growth factor A	Homo sapiens	95-99
16521182-8	2006	RESULTS: Activation of c-KIT was inhibited by STI571 treatment.	imatinib	46-52	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	23-28
16521182-9	2006	VEGF was suppressed at both the transcriptional and translational levels in a temporal and dose-dependent manner by STI571.	imatinib	116-122	vascular endothelial growth factor A	Homo sapiens	0-4
16521182-10	2006	SCF upregulated the expression of VEGF and it was inhibited by STI571.	imatinib	63-69	KIT ligand	Homo sapiens	0-3
16521182-10	2006	SCF upregulated the expression of VEGF and it was inhibited by STI571.	imatinib	63-69	vascular endothelial growth factor A	Homo sapiens	34-38
16462496-1	2006	OBJECTIVE: This phase II study was conducted to determine the activity of imatinib (gleevec) in heavily pretreated patients with KIT-positive metastatic germ cell tumor.	imatinib	74-82	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	129-132
16462496-1	2006	OBJECTIVE: This phase II study was conducted to determine the activity of imatinib (gleevec) in heavily pretreated patients with KIT-positive metastatic germ cell tumor.	imatinib	84-91	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	129-132
16441423-7	2006	Furthermore, in the case of neoadjuvant imatinib therapy, LOH of the c-kit gene was shown in the high cellularity area in the primary lesion and metastatic liver GIST.	imatinib	40-48	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	69-74
16441423-8	2006	It is suggested that LOH of the c-kit gene is an important event that leads to imatinib resistance and metastatic progression of GIST.	imatinib	79-87	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	32-37
16289747-1	2006	Imatinib (Gleevec) is a novel chemotherapeutic agent against Bcr-Abl protein tyrozine kinase, playing a crucial role in the therapy of chronic myeloid leukemia (CML) and gastrointestinal stromal tumors (GIST).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
16213151-1	2006	Imatinib mesylate (Gleevec) was developed as the first molecularly targeted therapy that specifically inhibits the BCR-ABL tyrosine kinase activity in patients with Philadelphia chromosome positive (Ph+) chronic myeloid leukemia (CML).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
16213151-1	2006	Imatinib mesylate (Gleevec) was developed as the first molecularly targeted therapy that specifically inhibits the BCR-ABL tyrosine kinase activity in patients with Philadelphia chromosome positive (Ph+) chronic myeloid leukemia (CML).	imatinib	19-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
16213151-6	2006	The major goal of these efforts is to create new drugs that are more potent than imatinib and/or more effective against imatinib-resistant BCR-ABL clones.	imatinib	120-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-146
16343892-3	2006	To counteract this problem, two new BCR-ABL kinase inhibitors for imatinib-refractory disease are currently in clinical trials: the imatinib derivative AMN107 and the dual-specificity SRC/ABL inhibitor dasatinib.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
16343892-3	2006	To counteract this problem, two new BCR-ABL kinase inhibitors for imatinib-refractory disease are currently in clinical trials: the imatinib derivative AMN107 and the dual-specificity SRC/ABL inhibitor dasatinib.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-43
16343892-3	2006	To counteract this problem, two new BCR-ABL kinase inhibitors for imatinib-refractory disease are currently in clinical trials: the imatinib derivative AMN107 and the dual-specificity SRC/ABL inhibitor dasatinib.	imatinib	132-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
16343892-3	2006	To counteract this problem, two new BCR-ABL kinase inhibitors for imatinib-refractory disease are currently in clinical trials: the imatinib derivative AMN107 and the dual-specificity SRC/ABL inhibitor dasatinib.	imatinib	132-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-43
16632420-11	2006	Imatinib, and inhibitor of the tyrosine kinase activity of Bcr-Abl targets also the kinase of the PDGFr.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	98-103
16289747-1	2006	Imatinib (Gleevec) is a novel chemotherapeutic agent against Bcr-Abl protein tyrozine kinase, playing a crucial role in the therapy of chronic myeloid leukemia (CML) and gastrointestinal stromal tumors (GIST).	imatinib	10-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
16321856-1	2006	The present study evaluated the expression and mutations of c-kit in peripheral T-cell lymphomas (PTCLs), except for extra-nodal NK/T cell lymphomas, as a potential target for treatment with imatinib mesylate.	imatinib	191-208	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	60-65
16461309-0	2006	The role of serial BCR-ABL transcript monitoring in predicting the emergence of BCR-ABL kinase mutations in imatinib-treated patients with chronic myeloid leukemia.	imatinib	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
16461309-0	2006	The role of serial BCR-ABL transcript monitoring in predicting the emergence of BCR-ABL kinase mutations in imatinib-treated patients with chronic myeloid leukemia.	imatinib	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
16461309-1	2006	BCR-ABL kinase mutations may confer resistance to imatinib in patients with chronic myeloid leukemia (CML), and may predict a poor outcome.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
16572895-7	2006	Indirect immunofluorescence microscopy showed nearly complete down-regulation of VE cadherin in imatinib-treated cells.	imatinib	96-104	cadherin 5	Homo sapiens	81-92
16461299-13	2006	INTERPRETATION AND CONCLUSIONS: Molecular remission after imatinib treatment, i.e. BCR-ABL/ABL< 10-5 in peripheral blood, is not a rare event, particularly in patients achieving CCR at 6 months.	imatinib	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
16461299-13	2006	INTERPRETATION AND CONCLUSIONS: Molecular remission after imatinib treatment, i.e. BCR-ABL/ABL< 10-5 in peripheral blood, is not a rare event, particularly in patients achieving CCR at 6 months.	imatinib	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-90
16485879-3	2006	As an inhibitor of PDGFR, imatinib mesylate appears to have utility in the treatment of a variety of dermatological diseases.	imatinib	26-43	platelet derived growth factor receptor beta	Homo sapiens	19-24
16485879-4	2006	Imatinib has been reported to be an effective treatment for FIP1L1-PDGFRalpha+ mast cell disease, hypereosinophilic syndrome, and dermatofibrosarcoma protuberans.	imatinib	0-8	factor interacting with PAPOLA and CPSF1	Homo sapiens	60-66
16415863-2	2006	Encouraged by the clinical validation of Bcr-abl as the target for the treatment of CML by imatinib, we sought to identify pharmacological agents that could target this kinase by a distinct mechanism.	imatinib	91-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
16445822-4	2006	In 2004, imatinib therapy, a tyrosine kinase inhibitor known to be effective against gastrointestinal stromal tumors, was reported to be effective also in a case of KIT-positive FATWO.	imatinib	9-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	165-168
16391854-8	2006	pCrkL expression was abrogated in K562 cells with the addition of the tyrosine kinase inhibitor imatinib, which indicates that phosphorylation of CrkL is mediated through targets of therapeutic TK inhibition.	imatinib	96-104	CRK like proto-oncogene, adaptor protein	Homo sapiens	1-5
16476837-10	2006	Irinotecan and agents like gefitinib, erlotinib, and imatinib targeting the epidermal growth factor receptor and platelet-derived growth factor receptor have shown some promise in recurrent malignant glioma.	imatinib	53-61	epidermal growth factor receptor	Homo sapiens	76-108
16732964-6	2006	In 26 CML with allo-PBSCT and 4 CML patients on imatinib treatment, expressions of hMSH2, hMSH3 and hMLH1 mRNA was enhanced while expression of bcr-abl mRNA decreased.	imatinib	48-56	mutS homolog 2	Homo sapiens	83-88
16732964-6	2006	In 26 CML with allo-PBSCT and 4 CML patients on imatinib treatment, expressions of hMSH2, hMSH3 and hMLH1 mRNA was enhanced while expression of bcr-abl mRNA decreased.	imatinib	48-56	mutS homolog 3	Homo sapiens	90-95
16732964-6	2006	In 26 CML with allo-PBSCT and 4 CML patients on imatinib treatment, expressions of hMSH2, hMSH3 and hMLH1 mRNA was enhanced while expression of bcr-abl mRNA decreased.	imatinib	48-56	mutL homolog 1	Homo sapiens	100-105
16732964-6	2006	In 26 CML with allo-PBSCT and 4 CML patients on imatinib treatment, expressions of hMSH2, hMSH3 and hMLH1 mRNA was enhanced while expression of bcr-abl mRNA decreased.	imatinib	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
16732964-7	2006	In CML MNC after imatinib treatment and in K562 cells, expression of hMSH2, hMSH3 and hMLH1 mRNA was enhanced while tyrosine phosphorylation of BCR-ABL fusion protein decreased.	imatinib	17-25	mutS homolog 2	Homo sapiens	69-74
16732964-7	2006	In CML MNC after imatinib treatment and in K562 cells, expression of hMSH2, hMSH3 and hMLH1 mRNA was enhanced while tyrosine phosphorylation of BCR-ABL fusion protein decreased.	imatinib	17-25	mutS homolog 3	Homo sapiens	76-81
16732964-7	2006	In CML MNC after imatinib treatment and in K562 cells, expression of hMSH2, hMSH3 and hMLH1 mRNA was enhanced while tyrosine phosphorylation of BCR-ABL fusion protein decreased.	imatinib	17-25	mutL homolog 1	Homo sapiens	86-91
16732964-7	2006	In CML MNC after imatinib treatment and in K562 cells, expression of hMSH2, hMSH3 and hMLH1 mRNA was enhanced while tyrosine phosphorylation of BCR-ABL fusion protein decreased.	imatinib	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
16342249-2	2006	Imatinib inhibits KIT kinase activity.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	18-21
16344315-0	2006	High complete remission rate and promising outcome by combination of imatinib and chemotherapy for newly diagnosed BCR-ABL-positive acute lymphoblastic leukemia: a phase II study by the Japan Adult Leukemia Study Group.	imatinib	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
16344315-3	2006	PATIENTS AND METHODS: A phase II study of imatinib-combined chemotherapy was conducted for newly diagnosed BCR-ABL-positive ALL in adults.	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
16344315-11	2006	CONCLUSION: Our results demonstrated that imatinib-combined regimen is effective and feasible for newly diagnosed BCR-ABL-positive ALL.	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
16421422-1	2006	PURPOSE: Imatinib mesylate is a potent inhibitor of BCR-ABL, the constitutively active tyrosine kinase protein critical for the pathogenesis of chronic myeloid leukemia.	imatinib	9-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
16428509-0	2006	Intermittent exposure of primitive quiescent chronic myeloid leukemia cells to granulocyte-colony stimulating factor in vitro promotes their elimination by imatinib mesylate.	imatinib	156-173	colony stimulating factor 3	Homo sapiens	79-116
16393970-0	2006	The decreased susceptibility of Bcr/Abl targets to NK cell-mediated lysis in response to imatinib mesylate involves modulation of NKG2D ligands, GM1 expression, and synapse formation.	imatinib	89-106	BCR activator of RhoGEF and GTPase	Homo sapiens	32-35
16393970-0	2006	The decreased susceptibility of Bcr/Abl targets to NK cell-mediated lysis in response to imatinib mesylate involves modulation of NKG2D ligands, GM1 expression, and synapse formation.	imatinib	89-106	killer cell lectin like receptor K1	Homo sapiens	130-135
16393970-3	2006	In the present study, using UT-7/9 cells, a high level Bcr/Abl transfectant of UT-7 cells, we show that the treatment of Bcr/Abl target by imatinib mesylate (IM), a specific Abl tyrosine kinase inhibitor, hampers the formation of the NK/target immunological synapse.	imatinib	139-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
16393970-3	2006	In the present study, using UT-7/9 cells, a high level Bcr/Abl transfectant of UT-7 cells, we show that the treatment of Bcr/Abl target by imatinib mesylate (IM), a specific Abl tyrosine kinase inhibitor, hampers the formation of the NK/target immunological synapse.	imatinib	139-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
16393970-4	2006	The main effect of IM involves an induction of surface GM1 ganglioside on Bcr/Abl transfectants that prevents the redistribution of MHC-related Ag molecules in lipid rafts upon interaction with NK cells.	imatinib	19-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
16428509-2	2006	The present study was designed to investigate whether either continuous or intermittent exposure of these cells to granulocyte-colony stimulating factor (G-CSF) in vitro can overcome this limitation to the effectiveness of imatinib mesylate therapy.	imatinib	223-240	colony stimulating factor 3	Homo sapiens	115-152
16428509-2	2006	The present study was designed to investigate whether either continuous or intermittent exposure of these cells to granulocyte-colony stimulating factor (G-CSF) in vitro can overcome this limitation to the effectiveness of imatinib mesylate therapy.	imatinib	223-240	colony stimulating factor 3	Homo sapiens	154-159
16428509-7	2006	Cultures containing imatinib mesylate and intermittently added G-CSF also showed the greatest reduction in the total number of cells present after 12 days (5-fold more than imatinib mesylate alone).	imatinib	173-190	colony stimulating factor 3	Homo sapiens	63-68
16428509-8	2006	CONCLUSION: Intermittent exposure to G-CSF can enhance the effect of imatinib mesylate on CML cells by specifically targeting the primitive quiescent leukemic elements.	imatinib	69-86	colony stimulating factor 3	Homo sapiens	37-42
16428509-9	2006	A protocol for treating chronic-phase CML patients with imatinib mesylate that incorporates intermittent G-CSF exposure may offer a novel strategy for obtaining improved responses in vivo.	imatinib	56-73	colony stimulating factor 3	Homo sapiens	105-110
16781490-8	2006	Imatinib mesylate therapy might result in complete remission of SM cases with wild-type KIT, certain KIT mutations, such as F522C, or the FIP1L1-PDGFRA fusion gene, but not of D816V-KIT-bearing SM.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	88-91
16809884-2	2006	Therefore, we evaluated in vitro the combined effect of imatinib and granulocyte colony-stimulating factor (G-CSF) on proliferation and apoptosis of Bcr-Abl-expressing leukaemic cells to infer the safety of G-CSF administration.	imatinib	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
16170366-1	2006	The kinase inhibitor imatinib is used in the treatment of chronic myeloid leukaemia, where it targets the intracellular Bcr-Abl tyrosine kinase, and gastrointestinal stromal tumours, where it targets either the KIT or PDGF tyrosine kinase receptors.	imatinib	21-29	KIT proto-oncogene receptor tyrosine kinase S homeolog	Xenopus laevis	211-214
16170366-1	2006	The kinase inhibitor imatinib is used in the treatment of chronic myeloid leukaemia, where it targets the intracellular Bcr-Abl tyrosine kinase, and gastrointestinal stromal tumours, where it targets either the KIT or PDGF tyrosine kinase receptors.	imatinib	21-29	platelet derived growth factor subunit A L homeolog	Xenopus laevis	218-222
17016042-0	2006	Atypical chronic myeloid leukaemia with CD117-positive blast cells treated with imatinib: A report of two cases.	imatinib	80-88	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	40-45
17163160-8	2006	Activating mutations in two related receptor tyrosine kinases (RTKs), KIT, and platelet-derived growth factor receptor alpha (PDGFRA) is central to the pathogenesis of gastrointestinal stromal tumors (GISTs), and countering the mutational activation by specific tyrosine kinase inhibitors, such as Imatinib mesylate, is now standard treatment for metastatic GISTs.	imatinib	298-315	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	70-73
17163160-8	2006	Activating mutations in two related receptor tyrosine kinases (RTKs), KIT, and platelet-derived growth factor receptor alpha (PDGFRA) is central to the pathogenesis of gastrointestinal stromal tumors (GISTs), and countering the mutational activation by specific tyrosine kinase inhibitors, such as Imatinib mesylate, is now standard treatment for metastatic GISTs.	imatinib	298-315	platelet derived growth factor receptor alpha	Homo sapiens	79-124
17163160-8	2006	Activating mutations in two related receptor tyrosine kinases (RTKs), KIT, and platelet-derived growth factor receptor alpha (PDGFRA) is central to the pathogenesis of gastrointestinal stromal tumors (GISTs), and countering the mutational activation by specific tyrosine kinase inhibitors, such as Imatinib mesylate, is now standard treatment for metastatic GISTs.	imatinib	298-315	platelet derived growth factor receptor alpha	Homo sapiens	126-132
16482991-1	2006	Chronic myeloproliferative diseases (CMPDs) associated with t(5;12)(q33;p13) are reported to be responsive to imatinib mesylate.	imatinib	110-127	H3 histone pseudogene 6	Homo sapiens	72-75
16781490-8	2006	Imatinib mesylate therapy might result in complete remission of SM cases with wild-type KIT, certain KIT mutations, such as F522C, or the FIP1L1-PDGFRA fusion gene, but not of D816V-KIT-bearing SM.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	101-104
16781490-8	2006	Imatinib mesylate therapy might result in complete remission of SM cases with wild-type KIT, certain KIT mutations, such as F522C, or the FIP1L1-PDGFRA fusion gene, but not of D816V-KIT-bearing SM.	imatinib	0-17	factor interacting with PAPOLA and CPSF1	Homo sapiens	138-144
16781490-8	2006	Imatinib mesylate therapy might result in complete remission of SM cases with wild-type KIT, certain KIT mutations, such as F522C, or the FIP1L1-PDGFRA fusion gene, but not of D816V-KIT-bearing SM.	imatinib	0-17	platelet derived growth factor receptor alpha	Homo sapiens	145-151
16781490-8	2006	Imatinib mesylate therapy might result in complete remission of SM cases with wild-type KIT, certain KIT mutations, such as F522C, or the FIP1L1-PDGFRA fusion gene, but not of D816V-KIT-bearing SM.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	101-104
16426942-3	2006	Studies of imatinib-treated patients have determined that BCR-ABL levels measured early in therapy can predict subsequent response and the probability of acquired resistance.	imatinib	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
16426942-5	2006	Small increases in the BCR-ABL level can identify patients with kinase domain mutations that lead to imatinib resistance.	imatinib	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
16398645-0	2006	Rapid reversion of eosinophilic gastroenteritis associated with FIP1L1-PDGFRA fusion after targeted therapy with imatinib.	imatinib	113-121	platelet derived growth factor receptor alpha	Homo sapiens	71-77
16468238-3	2006	METHODS AND RESULTS: We measured the level of BCR-ABL transcripts in peripheral blood cells of 27 subjects before and in the course of the imatinib treatment.	imatinib	139-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
16397263-2	2006	The small-molecule tyrosine kinase inhibitor imatinib mesylate is a potent inhibitor of wild-type (WT) KIT and certain mutant KIT isoforms and has become the standard of care for treating patients with metastatic GIST.	imatinib	45-62	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	103-106
16397263-2	2006	The small-molecule tyrosine kinase inhibitor imatinib mesylate is a potent inhibitor of wild-type (WT) KIT and certain mutant KIT isoforms and has become the standard of care for treating patients with metastatic GIST.	imatinib	45-62	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	126-129
16397263-3	2006	However, KIT activation loop mutations involving codon D816 that are typically found in AML, systemic mastocytosis, and seminoma are insensitive to imatinib mesylate (IC50 > 5-10 micromol/L), and acquired KIT activation loop mutations can be associated with imatinib mesylate resistance in GIST.	imatinib	261-278	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	9-12
16397263-8	2006	Furthermore, dasatinib is a potent inhibitor of imatinib-resistant KIT activation loop mutants and induces apoptosis in mast cell and leukemic cell lines expressing these mutations (potency against KIT D816Y >> D816F > D816V).	imatinib	48-56	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	67-70
16468238-4	2006	The median of relative quantity of BCR-ABL in the blood before imatinib therapy was 2.55%.	imatinib	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
16755775-4	2006	Imatinib Mesylate (Glivec) is a specific inhibitor of Bcr-Abl kinase.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
16468238-8	2006	Three patients were primarily resistant to imatinib with the BCR-ABL range of 0.13%-11.7% during the treatment.	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
16755775-4	2006	Imatinib Mesylate (Glivec) is a specific inhibitor of Bcr-Abl kinase.	imatinib	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
16506600-3	2006	The first case was classified as a indolent systemic mastocytosis without any proven genetic alteration, the second one met the criteria of aggressive systemic mastocytosis with eosinophilia, where the point mutation asp816val in c-kit gene was confirmed and the patient responded unexpectedly well to Gleevec.	imatinib	302-309	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	230-235
16542054-2	2006	These include the treatment of chronic myeloid leukemia with the Bcr-Abl inhibitor imatinib and non-small-cell lung cancer with the epidermal growth factor inhibitors erlotinib and gefitinib.	imatinib	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
16699280-5	2006	Imatinib mesylate (Glivec) is an orally administered competitive inhibitor of tyrosine kinases associated with the KIT, ABL protein, licensed for the treatment of metastatic GIST since 2002 in Germany.	imatinib	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-123
18369405-6	2006	Imatinib which is known to inhibit constitutively activated BCR-ABL tyrosine kinase in chronic myelogenous leukemia also inhibits constitutive activation of mutated KIT and PDGFRA, and is now being used for metastatic or unresectable GISTs as a molecular target drug.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	165-168
18369405-6	2006	Imatinib which is known to inhibit constitutively activated BCR-ABL tyrosine kinase in chronic myelogenous leukemia also inhibits constitutive activation of mutated KIT and PDGFRA, and is now being used for metastatic or unresectable GISTs as a molecular target drug.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	173-179
18369405-7	2006	Mutational analyses of c-kit and PDGFRA genes are considered to be significant for prediction of effectiveness of imatinib and newly developed/developing other agents on GISTs.	imatinib	114-122	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	23-28
18369405-7	2006	Mutational analyses of c-kit and PDGFRA genes are considered to be significant for prediction of effectiveness of imatinib and newly developed/developing other agents on GISTs.	imatinib	114-122	platelet derived growth factor receptor alpha	Homo sapiens	33-39
16699280-5	2006	Imatinib mesylate (Glivec) is an orally administered competitive inhibitor of tyrosine kinases associated with the KIT, ABL protein, licensed for the treatment of metastatic GIST since 2002 in Germany.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	115-118
16699280-5	2006	Imatinib mesylate (Glivec) is an orally administered competitive inhibitor of tyrosine kinases associated with the KIT, ABL protein, licensed for the treatment of metastatic GIST since 2002 in Germany.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-123
16699280-5	2006	Imatinib mesylate (Glivec) is an orally administered competitive inhibitor of tyrosine kinases associated with the KIT, ABL protein, licensed for the treatment of metastatic GIST since 2002 in Germany.	imatinib	19-25	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	115-118
16542059-4	2006	One of the possible causes of imatinib-acquired resistance is associated with increased expression of the SRC-related kinase Lyn and loss of BCR-ABL dependence arising from sequence mutations.	imatinib	30-38	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	106-109
16601347-5	2006	The effect of increased concentrations of the c-kit receptor antagonist imatinib mesylate on these contractions was observed.	imatinib	72-89	mast/stem cell growth factor receptor Kit	Oryctolagus cuniculus	46-51
16542059-4	2006	One of the possible causes of imatinib-acquired resistance is associated with increased expression of the SRC-related kinase Lyn and loss of BCR-ABL dependence arising from sequence mutations.	imatinib	30-38	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	125-128
16542059-4	2006	One of the possible causes of imatinib-acquired resistance is associated with increased expression of the SRC-related kinase Lyn and loss of BCR-ABL dependence arising from sequence mutations.	imatinib	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-148
17116285-4	2006	Some protein kinase inhibitors currently undergo clinical trials or have already been successfully introduced into treatment as exemplified by Bcr-Abl, c-kit and PDGFR inhibitor imatinib mesylate (Gleevec), flavopiridol and roscovitine, inhibitors of cyclin-dependent kinases, or erlotinib and gefitinib inhibiting EGFR.	imatinib	178-195	platelet derived growth factor receptor beta	Homo sapiens	162-167
16952044-0	2006	Recurrent gastrointestinal stromal tumor (GIST) of the stomach associated with a novel c-kit mutation after imatinib treatment.	imatinib	108-116	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	87-92
16146726-3	2006	Imatinib was the first small molecule developed to inhibit BCR-ABL tyrosine kinase activity and its success introduced the current era of molecularly targeted therapies for a number of other malignancies.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
16146726-4	2006	In patients with chronic myeloid leukaemia who develop resistance to imatinib, the Bcr-Abl signaling pathway is often re-established.	imatinib	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
16601347-11	2006	CONCLUSIONS: In isolated rabbit myometrium, acute inhibition of the c-kit receptor by imatinib mesylate affects only the amplitude of spontaneous contractions at concentrations, the equivalent of x10-100 the normal therapeutic concentration.	imatinib	86-103	mast/stem cell growth factor receptor Kit	Oryctolagus cuniculus	68-73
16434384-0	2006	The role of the K247R substitution in the ABL tyrosine kinase domain in sensitivity to imatinib.	imatinib	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-45
17124063-1	2006	For chronic phase chronic myeloid leukemia (CML) patients treated with imatinib, the essential pre-therapy assessments include bone marrow morphology and cytogenetics as well as a baseline real-time quantitative PCR (RQ-PCR) for BCR-ABL.	imatinib	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	229-236
16434384-1	2006	Imatinib mesylate has become the gold standard front-line treatment of chronic myelogenous leukemia through its ability to inhibit ABL tyrosine kinase.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-134
17124065-1	2006	Although the only curative therapy for chronic myeloid leukemia remains allogeneic stem cell transplantation (allo-SCT), early to mid-term results of imatinib in newly diagnosed patients are sufficiently impressive to have displaced allo-SCT to second- or third-line treatment.	imatinib	150-158	secretin	Homo sapiens	238-241
16816921-2	2006	Imatinib mesylate inhibits the phosphorylation of c-fms, a receptor for M-CSF.	imatinib	0-17	colony stimulating factor 1 receptor	Rattus norvegicus	50-55
16306788-10	2006	Judicious decision is mandatory before applying Imatinib therapy to KIT-positive gynecologic tumors.	imatinib	48-56	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	68-71
16274936-9	2006	Histologic sections from STI571-treated mice were stained with phospho-Akt and phospho-PDGFR beta antibodies.	imatinib	25-31	thymoma viral proto-oncogene 1	Mus musculus	71-74
16274936-9	2006	Histologic sections from STI571-treated mice were stained with phospho-Akt and phospho-PDGFR beta antibodies.	imatinib	25-31	platelet derived growth factor receptor, beta polypeptide	Mus musculus	87-97
16274936-11	2006	RESULTS: STI571 penetrated the blood-brain barrier, which resulted in a reduction in phospho-PDGFR in GBM.	imatinib	9-15	platelet derived growth factor receptor, beta polypeptide	Mus musculus	93-98
16816921-2	2006	Imatinib mesylate inhibits the phosphorylation of c-fms, a receptor for M-CSF.	imatinib	0-17	colony stimulating factor 1	Rattus norvegicus	72-77
16816921-10	2006	Imatinib mesylate dose-dependently inhibited the proliferation of M-CSF-dependent osteoclast precursor cells in vitro as well as osteoclast formation induced by M-CSF and sRANKL.	imatinib	0-17	colony stimulating factor 1	Rattus norvegicus	66-71
16816921-10	2006	Imatinib mesylate dose-dependently inhibited the proliferation of M-CSF-dependent osteoclast precursor cells in vitro as well as osteoclast formation induced by M-CSF and sRANKL.	imatinib	0-17	colony stimulating factor 1	Rattus norvegicus	161-166
16321820-4	2006	Moreover, sub-clones of Philadelphia-positive cells bearing mutations that code for amino-acid substitutions in the Bcr-Abl kinase domain can be identified in patients receiving treatment with imatinib and are associated with varying degrees of resistance to this agent.	imatinib	193-201	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
16205964-2	2006	The TK inhibitor imatinib mesylate selectively targets PDGFR-alpha, -beta, c-kit, c-abl and arg and has proven successful in the treatment of chronic myeloid leukaemia.	imatinib	17-25	TXK tyrosine kinase	Homo sapiens	4-6
16205964-2	2006	The TK inhibitor imatinib mesylate selectively targets PDGFR-alpha, -beta, c-kit, c-abl and arg and has proven successful in the treatment of chronic myeloid leukaemia.	imatinib	17-25	platelet derived growth factor receptor alpha	Homo sapiens	55-73
16205964-2	2006	The TK inhibitor imatinib mesylate selectively targets PDGFR-alpha, -beta, c-kit, c-abl and arg and has proven successful in the treatment of chronic myeloid leukaemia.	imatinib	17-25	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	75-80
16205964-2	2006	The TK inhibitor imatinib mesylate selectively targets PDGFR-alpha, -beta, c-kit, c-abl and arg and has proven successful in the treatment of chronic myeloid leukaemia.	imatinib	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-87
16263821-0	2006	Wnt/beta-catenin signaling mediates antineoplastic effects of imatinib mesylate (gleevec) in anaplastic thyroid cancer.	imatinib	62-79	catenin beta 1	Homo sapiens	4-16
16263821-0	2006	Wnt/beta-catenin signaling mediates antineoplastic effects of imatinib mesylate (gleevec) in anaplastic thyroid cancer.	imatinib	81-88	catenin beta 1	Homo sapiens	4-16
16263821-2	2006	However, it is unclear whether the selective tyrosine kinase (TK) inhibitor, imatinib mesylate, is linked to the Wnt/beta-catenin cascade and is able to modulate the pathway.	imatinib	77-94	catenin beta 1	Homo sapiens	117-129
16263821-8	2006	Imatinib (10 microM for 48 h) drastically reduced beta-catenin expression and redistributed it from the nucleus to the cell membrane.	imatinib	0-8	catenin beta 1	Homo sapiens	50-62
16263821-10	2006	Furthermore, imatinib (10 microM for 48 h) attenuated T cell factor/lymphoid enhancer factor activity, reduced cyclin D1 levels and dose-dependently suppressed thyrocyte proliferation by half without affecting apoptosis.	imatinib	13-21	cyclin D1	Homo sapiens	111-120
16406868-1	2006	PURPOSE: RCCs with sarcomatoid differentiation have been reported to frequently express KIT protein, suggesting that imatinib mesylate (STI-571 or Gleevectrade mark) may be effective treatment for these aggressive tumors.	imatinib	117-125	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	88-91
16321825-1	2006	Although imatinib was designed to specifically inhibit the bcr-abl gene product, it inhibits other receptor tyrosine kinases including c-kit.	imatinib	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
16270044-1	2006	Imatinib represents at present the most attractive therapy for BCR-ABL positive leukemias, even though a percentage of CML patients develop resistance to this compound.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
16321825-1	2006	Although imatinib was designed to specifically inhibit the bcr-abl gene product, it inhibits other receptor tyrosine kinases including c-kit.	imatinib	9-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	135-140
16502579-1	2006	The major mechanism of imatinib resistance for patients with chronic myeloid leukemia (CML) is clonal expansion of leukemic cells with mutations in the Bcr-Abl fusion tyrosine kinase that reduce the capacity of imatinib to inhibit kinase activity.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-159
16502579-1	2006	The major mechanism of imatinib resistance for patients with chronic myeloid leukemia (CML) is clonal expansion of leukemic cells with mutations in the Bcr-Abl fusion tyrosine kinase that reduce the capacity of imatinib to inhibit kinase activity.	imatinib	211-219	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-159
16398673-12	2006	The effect of imatinib mesylate is different in various types of c-kit and PDGFRA gene mutations, and the secondary resistance against imatinib mesylate is often acquired by the second mutation of the identical genes.	imatinib	14-31	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	65-70
16401709-1	2006	The introduction of imatinib, an orally administered inhibitor of the KIT receptor tyrosine kinase, is prompting revision of the management algorithms that have traditionally guided the treatment of gastrointestinal stromal tumor (GIST).	imatinib	20-28	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	70-73
16401709-1	2006	The introduction of imatinib, an orally administered inhibitor of the KIT receptor tyrosine kinase, is prompting revision of the management algorithms that have traditionally guided the treatment of gastrointestinal stromal tumor (GIST).	imatinib	20-28	ret proto-oncogene	Homo sapiens	74-98
16398673-12	2006	The effect of imatinib mesylate is different in various types of c-kit and PDGFRA gene mutations, and the secondary resistance against imatinib mesylate is often acquired by the second mutation of the identical genes.	imatinib	14-31	platelet derived growth factor receptor alpha	Homo sapiens	75-81
17245319-1	2006	STI571 (imatinib; Gleevec) was developed to specifically target the tyrosine kinase activity of the Bcr-Abl protein in Philadelphia chromosome-positive chronic myeloid leukemia (CML).	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
17064855-3	2006	Elucidation of the aberrant receptor tyrosine kinase (RTK) model of GIST pathogenesis through mutations in c-kit and platelet-derived growth factor alpha PDGFRalpha proto-oncogenes has been prerequisite to the use of imatinib mesylate (STI571, Gleevec; Novartis, Switzerland), a molecular inhibitor of several tyrosine kinases, in the treatment of GISTs.	imatinib	217-234	ret proto-oncogene	Homo sapiens	28-52
17064855-3	2006	Elucidation of the aberrant receptor tyrosine kinase (RTK) model of GIST pathogenesis through mutations in c-kit and platelet-derived growth factor alpha PDGFRalpha proto-oncogenes has been prerequisite to the use of imatinib mesylate (STI571, Gleevec; Novartis, Switzerland), a molecular inhibitor of several tyrosine kinases, in the treatment of GISTs.	imatinib	217-234	ret proto-oncogene	Homo sapiens	54-57
16860492-1	2006	The use of a relatively nontoxic tyrosine kinase receptor inhibitor, imatinib mesylate (IM) (STI-571), has increasingly become a valuable therapeutic alternative in some KIT (CD117)-overexpressing neoplasms potentially because of the presence of KIT-activating mutations.	imatinib	69-86	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	170-173
16860492-1	2006	The use of a relatively nontoxic tyrosine kinase receptor inhibitor, imatinib mesylate (IM) (STI-571), has increasingly become a valuable therapeutic alternative in some KIT (CD117)-overexpressing neoplasms potentially because of the presence of KIT-activating mutations.	imatinib	69-86	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	175-180
16860492-1	2006	The use of a relatively nontoxic tyrosine kinase receptor inhibitor, imatinib mesylate (IM) (STI-571), has increasingly become a valuable therapeutic alternative in some KIT (CD117)-overexpressing neoplasms potentially because of the presence of KIT-activating mutations.	imatinib	69-86	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	246-249
16534250-1	2006	Imatinib and AMN107 are protein tyrosine kinase inhibitors which reduce KIT autophosphorylation with similar potency.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	72-75
17245319-1	2006	STI571 (imatinib; Gleevec) was developed to specifically target the tyrosine kinase activity of the Bcr-Abl protein in Philadelphia chromosome-positive chronic myeloid leukemia (CML).	imatinib	8-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
17245319-8	2006	In this review a literature overview of the alternative inhibitors which were designed to override STI571 resistance and decrease the aberrant kinase activity of Bcr-Abl protein with higher efficiency is presented.	imatinib	99-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-169
16392960-1	2006	Gleevec, a selective tyrosine kinase inhibitor, retarded the growth of anaplastic thyroid cancer cell lines in vitro and in vivo through selective inhibition of ABL tyrosine kinase activity.	imatinib	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-164
18393778-6	2006	In addition, other KIT tyrosine kinase inhibitors with anti-VEGF receptor inhibitory activity, such as SU11248, PTK787/ZK787 and AMG 706, are currently being explored as second line monotherapy for imatinib mesylate-resistant GIST.	imatinib	198-215	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	19-22
16172030-2	2005	Imatinib targets the tyrosine kinase activity of Bcr-Abl and is a first-line therapy for this malignancy.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
18393778-2	2006	STI-571 (imatinib mesylate), a selective KIT tyrosine kinase inhibitor, has changed the natural history of this disease, since it has shown high effectiveness in metastatic GIST, and it is currently under investigation also in the adjuvant and neoadjuvant setting.	imatinib	0-7	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	41-44
18393778-2	2006	STI-571 (imatinib mesylate), a selective KIT tyrosine kinase inhibitor, has changed the natural history of this disease, since it has shown high effectiveness in metastatic GIST, and it is currently under investigation also in the adjuvant and neoadjuvant setting.	imatinib	9-26	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	41-44
17072721-0	2006	Predicting the antitumor effects of STI571 by analysis of c-kit gene mutations in gastrointestinal stromal tumors of the stomach: Report of a case.	imatinib	36-42	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	58-63
17072721-5	2006	Patients with an exon 11 mutation of the c-kit gene are reported to have a high response to STI571 (imatinib mesylate, Glivec).	imatinib	92-98	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	41-46
17072721-5	2006	Patients with an exon 11 mutation of the c-kit gene are reported to have a high response to STI571 (imatinib mesylate, Glivec).	imatinib	100-117	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	41-46
17072721-7	2006	Thus, it may be important to analyze c-kit gene mutations in patients presenting with GISTs to predict the effectiveness of STI571 in suppressing GISTs, especially tumors thought to have malignant potential.	imatinib	124-130	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	37-42
17867582-10	2006	Mutational subtype in KIT or PDGF receptor alpha not only influences the biological behavior of GISTs but also their response to treatment with imatinib, a tyrosine kinase inhibitor also inhibiting ARG, PDGF receptor beta and BCR-ABL.	imatinib	144-152	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	22-25
17867582-10	2006	Mutational subtype in KIT or PDGF receptor alpha not only influences the biological behavior of GISTs but also their response to treatment with imatinib, a tyrosine kinase inhibitor also inhibiting ARG, PDGF receptor beta and BCR-ABL.	imatinib	144-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	226-233
17867582-12	2006	GISTs without detectable KIT mutation in these both exons often are resistant to imatinib.	imatinib	81-89	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	25-28
17867582-13	2006	The development of secondary resistance to imatinib in GIST patients occurs in up to 40% of cases and is partly due to secondary KIT mutations occuring additionally to the primary mutation.	imatinib	43-51	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	129-132
17013368-4	2006	Imatinib mesylate (Glivec), a specific small-molecule inhibitor of BCR-ABL, has become the standard drug therapy in all phases of the disease.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
17013368-4	2006	Imatinib mesylate (Glivec), a specific small-molecule inhibitor of BCR-ABL, has become the standard drug therapy in all phases of the disease.	imatinib	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
16172030-4	2005	This is often due to the emergence of clones expressing mutant forms of Bcr-Abl, which exhibit a decreased sensitivity towards inhibition by imatinib.	imatinib	141-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
16236241-5	2005	Similarly, inhibition of recombinant c-Abl or Bcr-Abl in cells or cell extracts by imatinib mesylate and other Bcr-Abl targeted kinase inhibitors is readily assayed.	imatinib	83-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-42
16475128-3	2005	The aim of this observational cohort study was to discriminate and quantify BCR-ABL transcripts in the peripheral blood of patients with CML who were treated with imatinib mesylate (Glivec, Novartis).	imatinib	163-180	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
16475128-7	2005	At the sixth month, there was a significant difference in the levels of the two major transcripts of BCR-ABL, B2A2 and B3A2 (P = 0.0347), indicating that B2A2 may be more sensitive to imatinib.	imatinib	184-192	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
16226710-13	2005	STI-571, a clinically effective targeted protein-tyrosine kinase inhibitor, binds to an inactive conformation of Kit.	imatinib	0-7	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	113-116
16226710-15	2005	STI-571 binds to Kit and Bcr-Abl (the oncoprotein of chronic myelogenous leukemia) at their ATP-binding sites.	imatinib	0-7	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	17-20
16226710-15	2005	STI-571 binds to Kit and Bcr-Abl (the oncoprotein of chronic myelogenous leukemia) at their ATP-binding sites.	imatinib	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
16236241-5	2005	Similarly, inhibition of recombinant c-Abl or Bcr-Abl in cells or cell extracts by imatinib mesylate and other Bcr-Abl targeted kinase inhibitors is readily assayed.	imatinib	83-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
16288076-6	2005	DISCUSSION: Imatinib mesylate is a protein tyrosine kinase inhibitor that inhibits the BCR-ABL tyrosine kinase, the receptor tyrosine kinases for platelet-derived growth factor, and stem cell factor c-kit.	imatinib	12-29	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	199-204
16105974-0	2005	NS-187, a potent and selective dual Bcr-Abl/Lyn tyrosine kinase inhibitor, is a novel agent for imatinib-resistant leukemia.	imatinib	96-104	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	44-47
16320345-0	2005	Amelioration of autoimmune nephritis by imatinib in MRL/lpr mice.	imatinib	40-48	Fas (TNF receptor superfamily member 6)	Mus musculus	56-59
16320345-10	2005	CONCLUSION: These findings indicate that imatinib has a pleiotropic therapeutic effect, namely, the inhibition of PDGF signaling and immunosuppression, on the glomerulonephritis of MRL/lpr mice, which suggests a potential application of this drug in the treatment of human lupus nephritis.	imatinib	41-49	Fas (TNF receptor superfamily member 6)	Mus musculus	185-188
16105974-1	2005	Although the Abelson (Abl) tyrosine kinase inhibitor imatinib mesylate has improved the treatment of breakpoint cluster region-Abl (Bcr-Abl)-positive leukemia, resistance is often reported in patients with advanced-stage disease.	imatinib	53-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
16105974-1	2005	Although the Abelson (Abl) tyrosine kinase inhibitor imatinib mesylate has improved the treatment of breakpoint cluster region-Abl (Bcr-Abl)-positive leukemia, resistance is often reported in patients with advanced-stage disease.	imatinib	53-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-25
16105974-1	2005	Although the Abelson (Abl) tyrosine kinase inhibitor imatinib mesylate has improved the treatment of breakpoint cluster region-Abl (Bcr-Abl)-positive leukemia, resistance is often reported in patients with advanced-stage disease.	imatinib	53-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-130
16105974-1	2005	Although the Abelson (Abl) tyrosine kinase inhibitor imatinib mesylate has improved the treatment of breakpoint cluster region-Abl (Bcr-Abl)-positive leukemia, resistance is often reported in patients with advanced-stage disease.	imatinib	53-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
16105974-2	2005	Although several Src inhibitors are more effective than imatinib and simultaneously inhibit Lyn, whose overexpression is associated with imatinib resistance, these inhibitors are less specific than imatinib.	imatinib	137-145	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	17-20
16105974-2	2005	Although several Src inhibitors are more effective than imatinib and simultaneously inhibit Lyn, whose overexpression is associated with imatinib resistance, these inhibitors are less specific than imatinib.	imatinib	137-145	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	92-95
16105974-2	2005	Although several Src inhibitors are more effective than imatinib and simultaneously inhibit Lyn, whose overexpression is associated with imatinib resistance, these inhibitors are less specific than imatinib.	imatinib	137-145	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	17-20
16105974-2	2005	Although several Src inhibitors are more effective than imatinib and simultaneously inhibit Lyn, whose overexpression is associated with imatinib resistance, these inhibitors are less specific than imatinib.	imatinib	137-145	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	92-95
16105974-3	2005	We have identified a specific dual Abl-Lyn inhibitor, NS-187 (elsewhere described as CNS-9), which is 25 to 55 times more potent than imatinib in vitro.	imatinib	134-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
16105974-3	2005	We have identified a specific dual Abl-Lyn inhibitor, NS-187 (elsewhere described as CNS-9), which is 25 to 55 times more potent than imatinib in vitro.	imatinib	134-142	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	39-42
16105974-4	2005	NS-187 is also at least 10 times as effective as imatinib in suppressing the growth of Bcr-Abl-bearing tumors and markedly extends the survival of mice bearing such tumors.	imatinib	49-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
16338660-5	2005	Using PP1, PP2, and imatinib mesylate, we show that Kit mutants are responsible for the autonomous expansion of malignant cells via Erk1/2 and PI3K/Akt activations.	imatinib	20-37	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	52-55
16319529-0	2005	BCR-ABL kinase domain mutations in chronic myeloid leukemia: not quite enough to cause resistance to imatinib therapy?	imatinib	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
16338660-5	2005	Using PP1, PP2, and imatinib mesylate, we show that Kit mutants are responsible for the autonomous expansion of malignant cells via Erk1/2 and PI3K/Akt activations.	imatinib	20-37	mitogen-activated protein kinase 3	Mus musculus	132-138
16260764-3	2005	The success of the Abl inhibitor imatinib in the treatment of chronic myelogenous leukemia has shown the potential of kinase inhibitors, but the rise of drug resistance in patients has also shown that drugs with alternative modes of binding to the kinase are needed.	imatinib	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-22
16224487-0	2005	Selecting and deselecting imatinib-resistant clones: observations made by longitudinal, quantitative monitoring of mutated BCR-ABL.	imatinib	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-130
16224487-1	2005	Resistance to imatinib during the treatment of chronic myeloid leukaemia (CML) is frequently associated with point mutations in the ABL gene encoding the ATP binding region likely to cause disease relapse.	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-135
16263579-2	2005	The aim of the present study was to evaluate plasma levels of VEGF and bFGF in a cohort of 51 chronic-phase CML patients at the time of diagnosis, as well as to investigate the effect of imatinib therapy on VEGF amounts in CML patients.	imatinib	187-195	vascular endothelial growth factor A	Homo sapiens	207-211
16263579-7	2005	The initial VEGF levels markedly decreased after 6 months of imatinib therapy in each patient (p<0.001).	imatinib	61-69	vascular endothelial growth factor A	Homo sapiens	12-16
16265655-9	2005	Use of imatinib to treat cancers without c-kit or PDGFR-alpha mutation should be approached with caution.	imatinib	7-15	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	41-46
16265655-9	2005	Use of imatinib to treat cancers without c-kit or PDGFR-alpha mutation should be approached with caution.	imatinib	7-15	platelet derived growth factor receptor alpha	Homo sapiens	50-61
16344672-1	2005	Idiopathic hypereosinophilic syndrome (HES) in children is a very rare disorder; certain clinical differences with adult HES have been described, with no pediatric case with the imatinib-responsive FIP1L1-PDGFRA fusion gene reported to date.	imatinib	178-186	factor interacting with PAPOLA and CPSF1	Homo sapiens	198-204
15927253-0	2005	Treatment of elderly patients with acute lymphoblastic leukemia--evidence for a benefit of imatinib in BCR-ABL positive patients.	imatinib	91-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
15927253-3	2005	There were 13 BCR-ABL positive patients, 9 of who received imatinib mesylate, either during induction or post-remission therapy.	imatinib	59-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
15927253-9	2005	However, there was a strong trend for BCR-ABL status to favorably predict for PFS, and for OS when only patients treated after July 2000 (when imatinib became available) were evaluated.	imatinib	143-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
15927253-11	2005	These data suggest that BCR-ABL+ ALL is becoming a relatively more favorable prognosis disease in the elderly, likely due to the influence of imatinib therapy.	imatinib	142-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
15927253-12	2005	Further regimens should explore the use of less aggressive regimens in elderly patients and should evaluate the optimal way of combining imatinib with conventional agents in BCR-ABL+ patients.	imatinib	137-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-181
16373716-0	2005	Imatinib binding and cKIT inhibition is abrogated by the cKIT kinase domain I missense mutation Val654Ala.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	57-61
16373716-4	2005	We sequenced cKIT exons from two patients with GIST after the development of imatinib resistance, revealing a point mutation in kinase domain I (exon 13), Val654Ala, which has been associated previously with relapse and resistance.	imatinib	77-85	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	13-17
16373716-5	2005	Molecular modeling of cKIT-imatinib complexes shows that this residue is located in the drug-binding site and that the Val654Ala mutation disrupts drug binding by removing hydrophobic contacts with the central diaminophenyl ring of imatinib.	imatinib	27-35	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	22-26
16373716-6	2005	Loss of these contacts results in a destabilizing effect on two key hydrogen bonds between imatinib and Asp310 and Thr670 of cKIT.	imatinib	91-99	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	125-129
16373716-8	2005	When present on the same cKIT allele as an oncogenic mutation, the Val654Ala mutation abolishes imatinib-mediated inhibition of cKIT phosphoactivation in vitro.	imatinib	96-104	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	25-29
16373716-8	2005	When present on the same cKIT allele as an oncogenic mutation, the Val654Ala mutation abolishes imatinib-mediated inhibition of cKIT phosphoactivation in vitro.	imatinib	96-104	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	128-132
16430106-11	2005	Imatinib has been successfully used also in some patients with the constitutively activated thyrosine kinase ETV6-PDGFRbeta [1] and in systemic mast cell disease associated with eosinophilia.	imatinib	0-8	ETS variant transcription factor 6	Homo sapiens	109-113
16430106-11	2005	Imatinib has been successfully used also in some patients with the constitutively activated thyrosine kinase ETV6-PDGFRbeta [1] and in systemic mast cell disease associated with eosinophilia.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	114-123
16405837-0	2005	[Analysis of ABL tyrosine kinase point mutations in imatinib treated chronic myelogenous leukemia patients].	imatinib	52-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
16405837-1	2005	OBJECTIVE: To evaluate ABL tyrosine kinase point mutations in imatinib treated chronic myelogenous leukemia (CML) patients.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-26
16405837-5	2005	RESULTS: The ABL point mutation was detected in 13 of 30 patients, 12 of them had progressed to advanced phase, The other patient who was in late chronic phase showed point mutation when she was at 45th months of imatinib treatment, but she was still in complete cytogenetic remission at 50th months and is doing well.	imatinib	213-221	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
16405837-11	2005	CONCLUSIONS: Abl kinase point mutation is one of the main mechanisms of CML secondary resistance to imatinib.	imatinib	100-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
16405837-12	2005	Long term regular monitoring of ABL kinase point mutation is necessary during imatinib treatment.	imatinib	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-35
16288027-6	2005	PDGFR phosphorylation was inhibited by STI571.	imatinib	39-45	platelet derived growth factor receptor beta	Homo sapiens	0-5
25927124-2	2005	Imatinib (Gleevec ) is an orally administered drug that competitively inhibits the BCR-ABL tyrosine kinase, a cellular enzyme that is encoded in the BCR-ABL gene.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
25927124-2	2005	Imatinib (Gleevec ) is an orally administered drug that competitively inhibits the BCR-ABL tyrosine kinase, a cellular enzyme that is encoded in the BCR-ABL gene.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
25927124-2	2005	Imatinib (Gleevec ) is an orally administered drug that competitively inhibits the BCR-ABL tyrosine kinase, a cellular enzyme that is encoded in the BCR-ABL gene.	imatinib	10-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
25927124-2	2005	Imatinib (Gleevec ) is an orally administered drug that competitively inhibits the BCR-ABL tyrosine kinase, a cellular enzyme that is encoded in the BCR-ABL gene.	imatinib	10-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
16030188-4	2005	The imatinib mesylate-resistant mutant TEL-PDGFRbeta T681I was sensitive to AMN107, whereas the analogous mutation in FIP1L1-PDGFRalpha, T674I, was resistant.	imatinib	4-12	ETS variant transcription factor 6	Homo sapiens	39-42
16087693-0	2005	A phase II trial of imatinib (ST1571) in patients with c-kit expressing relapsed small-cell lung cancer: a CALGB and NCCTG study.	imatinib	20-28	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	55-60
16087693-1	2005	BACKGROUND: The aim of the present study was to evaluate the clinical activity of imatinib mesylate in patients with recurrent and refractory c-kit-expressing small-cell lung cancer.	imatinib	82-99	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	142-147
16030188-4	2005	The imatinib mesylate-resistant mutant TEL-PDGFRbeta T681I was sensitive to AMN107, whereas the analogous mutation in FIP1L1-PDGFRalpha, T674I, was resistant.	imatinib	4-12	platelet derived growth factor receptor beta	Homo sapiens	43-52
16161057-0	2005	Imatinib mesylate lacks activity in small cell lung carcinoma expressing c-kit protein: a Phase II clinical trial.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-78
20477604-5	2005	A subgroup of patients with the myeloproliferative variant carry the new gene rearrangement FIP1L1-PDGFRA, which produces a constitutively active tyrosine kinase often responsive to antityrosine kinase therapy with imatinib mesylate.	imatinib	215-232	factor interacting with PAPOLA and CPSF1	Homo sapiens	92-98
16286244-3	2005	In imatinib-sensitive and -resistant (T315I included) BCR/ABL+ cell lines and CML-BC progenitors, molecular and/or pharmacological activation of PP2A promotes dephosphorylation of key regulators of cell proliferation and survival, suppresses BCR/ABL activity, and induces BCR/ABL degradation.	imatinib	3-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
16286244-3	2005	In imatinib-sensitive and -resistant (T315I included) BCR/ABL+ cell lines and CML-BC progenitors, molecular and/or pharmacological activation of PP2A promotes dephosphorylation of key regulators of cell proliferation and survival, suppresses BCR/ABL activity, and induces BCR/ABL degradation.	imatinib	3-11	protein phosphatase 2 phosphatase activator	Homo sapiens	145-149
16286244-4	2005	Furthermore, PP2A activation results in growth suppression, enhanced apoptosis, restored differentiation, impaired clonogenic potential, and decreased in vivo leukemogenesis of imatinib-sensitive and -resistant BCR/ABL+ cells.	imatinib	177-185	protein phosphatase 2 phosphatase activator	Homo sapiens	13-17
16286244-4	2005	Furthermore, PP2A activation results in growth suppression, enhanced apoptosis, restored differentiation, impaired clonogenic potential, and decreased in vivo leukemogenesis of imatinib-sensitive and -resistant BCR/ABL+ cells.	imatinib	177-185	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	211-218
16294026-0	2005	Activating mutations in c-KIT and PDGFRalpha are exclusively found in gastrointestinal stromal tumors and not in other tumors overexpressing these imatinib mesylate target genes.	imatinib	147-155	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	24-29
16294026-1	2005	Previous studies have shown that Imatinib mesylate (Gleevec), a selective tyrosine kinase inhibitor of c-KIT and platelet-derived growth factor receptors (PDGFR), is highly effective in c-KIT/CD117-positive gastrointestinal stromal tumors (GIST), especially in those having activating mutations in c-kit exon 11.	imatinib	33-50	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	103-108
16294026-1	2005	Previous studies have shown that Imatinib mesylate (Gleevec), a selective tyrosine kinase inhibitor of c-KIT and platelet-derived growth factor receptors (PDGFR), is highly effective in c-KIT/CD117-positive gastrointestinal stromal tumors (GIST), especially in those having activating mutations in c-kit exon 11.	imatinib	33-50	platelet derived growth factor receptor beta	Homo sapiens	113-153
16294026-1	2005	Previous studies have shown that Imatinib mesylate (Gleevec), a selective tyrosine kinase inhibitor of c-KIT and platelet-derived growth factor receptors (PDGFR), is highly effective in c-KIT/CD117-positive gastrointestinal stromal tumors (GIST), especially in those having activating mutations in c-kit exon 11.	imatinib	33-50	platelet derived growth factor receptor beta	Homo sapiens	155-160
16294026-1	2005	Previous studies have shown that Imatinib mesylate (Gleevec), a selective tyrosine kinase inhibitor of c-KIT and platelet-derived growth factor receptors (PDGFR), is highly effective in c-KIT/CD117-positive gastrointestinal stromal tumors (GIST), especially in those having activating mutations in c-kit exon 11.	imatinib	33-50	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	186-191
16294026-1	2005	Previous studies have shown that Imatinib mesylate (Gleevec), a selective tyrosine kinase inhibitor of c-KIT and platelet-derived growth factor receptors (PDGFR), is highly effective in c-KIT/CD117-positive gastrointestinal stromal tumors (GIST), especially in those having activating mutations in c-kit exon 11.	imatinib	33-50	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	298-303
16294026-3	2005	Importantly, the presence and type of these mutually exclusive c-KIT or PDGFRalpha mutations were found to be associated with the response to imatinib.	imatinib	142-150	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	63-68
16294026-3	2005	Importantly, the presence and type of these mutually exclusive c-KIT or PDGFRalpha mutations were found to be associated with the response to imatinib.	imatinib	142-150	platelet derived growth factor receptor alpha	Homo sapiens	72-82
16242052-2	2005	Imatinib was first shown to inhibit the causative molecular translocation in chronic myelogenous leukemia, BCR-ABL.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
16242052-3	2005	Because imatinib could also inhibit the activity of KIT, a 145-kD transmembrane glycoprotein, and because gastrointestinal stromal tumors (GISTs), the most common mesenchymal tumors of the digestive tract, are characterized by expression of a gain-of-function mutation in KIT, imatinib was used in therapeutic trials of GISTs beginning in 1999.	imatinib	8-16	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	52-55
16242052-3	2005	Because imatinib could also inhibit the activity of KIT, a 145-kD transmembrane glycoprotein, and because gastrointestinal stromal tumors (GISTs), the most common mesenchymal tumors of the digestive tract, are characterized by expression of a gain-of-function mutation in KIT, imatinib was used in therapeutic trials of GISTs beginning in 1999.	imatinib	8-16	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	272-275
16242052-6	2005	Clinically, GIST patients with KIT exon 11 mutations (ie, the juxtamembrane region) are the most prevalent and sensitive to imatinib.	imatinib	124-132	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	31-34
16242052-7	2005	In addition to the inhibitory effect on KIT, imatinib also inhibits the activity of mutant platelet-derived growth factor receptor-alpha (PDGFRalpha) found in a subset of GIST.	imatinib	45-53	platelet derived growth factor receptor alpha	Homo sapiens	91-136
16242052-7	2005	In addition to the inhibitory effect on KIT, imatinib also inhibits the activity of mutant platelet-derived growth factor receptor-alpha (PDGFRalpha) found in a subset of GIST.	imatinib	45-53	platelet derived growth factor receptor alpha	Homo sapiens	138-148
16242052-8	2005	What is becoming evident is that there are patients with GIST who lack mutations in KIT or PDGFRalpha, or possess "imatinib-resistant" mutations (such as exon 17 mutations in KIT and exon 18 mutations in PDGFRalpha).	imatinib	115-123	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	175-178
16242052-8	2005	What is becoming evident is that there are patients with GIST who lack mutations in KIT or PDGFRalpha, or possess "imatinib-resistant" mutations (such as exon 17 mutations in KIT and exon 18 mutations in PDGFRalpha).	imatinib	115-123	platelet derived growth factor receptor alpha	Homo sapiens	204-214
16266981-3	2005	This model comprises murine tumors of FDC-P1 cell lines expressing c-KIT mutations that render the tumors either responsive (V560G) or resistant (D816V) to the small-molecule c-KIT inhibitor, imatinib.	imatinib	192-200	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	67-72
16266981-5	2005	Using the FDC-P1 model in small animal PET, FDG uptake into tumors expressing the c-KIT V560G mutation was significantly reduced as early as 4 hours after imatinib treatment.	imatinib	155-163	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	82-87
16305488-2	2005	Imatinib mesylate binds to the inactive conformation of BCR-ABL tyrosine kinase suppressing the Philadelphia chromosome positive clone in CML.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
20477604-5	2005	A subgroup of patients with the myeloproliferative variant carry the new gene rearrangement FIP1L1-PDGFRA, which produces a constitutively active tyrosine kinase often responsive to antityrosine kinase therapy with imatinib mesylate.	imatinib	215-232	platelet derived growth factor receptor alpha	Homo sapiens	99-105
16266893-1	2005	BACKGROUND AND OBJECTIVES: Accurate quantification of BCR-ABL mRNA is of critical importance for managing patients with chronic myeloid leukemia (CML) who are receiving imatinib therapy.	imatinib	169-177	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
16291174-0	2005	Advanced-stage gastrointestinal stromal tumor treated with imatinib in a 12-year-old girl with a unique mutation of PDGFRA.	imatinib	59-67	platelet derived growth factor receptor alpha	Homo sapiens	116-122
16266912-0	2005	Reduction of glycosylated hemoglobin with stable insulin levels in a diabetic patient with chronic myeloid leukemia responsive to imatinib.	imatinib	130-138	insulin	Homo sapiens	49-56
16298826-0	2005	Use of imatinib mesylate for favorable control of hypercalcemia mediated by parathyroid hormone-related protein in a patient with chronic myelogenous leukemia at blast phase.	imatinib	7-24	parathyroid hormone like hormone	Homo sapiens	76-111
16298826-8	2005	Taken together the findings showed that production of PTHrP by blast cells was favorably controlled by imatinib therapy alone.	imatinib	103-111	parathyroid hormone like hormone	Homo sapiens	54-59
16298826-9	2005	Imatinib may prolong survival time at BP even though the patients have the complication of PTHrP-mediated hypercalcemia.	imatinib	0-8	parathyroid hormone like hormone	Homo sapiens	91-96
16357454-2	2005	Recently it has been demonstrated that a majority of GIST patients with c-kit mutations respond to therapy with imatinib, a c-kit tyrosine kinase inhibitor.	imatinib	112-120	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	72-77
16357454-2	2005	Recently it has been demonstrated that a majority of GIST patients with c-kit mutations respond to therapy with imatinib, a c-kit tyrosine kinase inhibitor.	imatinib	112-120	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	124-129
15887238-0	2005	Induction of heparin-binding EGF-like growth factor and activation of EGF receptor in imatinib mesylate-treated squamous carcinoma cells.	imatinib	86-103	heparin binding EGF like growth factor	Homo sapiens	13-51
15887238-1	2005	Imatinib mesylate is a tyrosine kinase inhibitor of the ABL, platelet-derived growth factor receptor (PDGFR), and c-kit kinases.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-59
15887238-1	2005	Imatinib mesylate is a tyrosine kinase inhibitor of the ABL, platelet-derived growth factor receptor (PDGFR), and c-kit kinases.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	61-100
15887238-1	2005	Imatinib mesylate is a tyrosine kinase inhibitor of the ABL, platelet-derived growth factor receptor (PDGFR), and c-kit kinases.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	102-107
15887238-1	2005	Imatinib mesylate is a tyrosine kinase inhibitor of the ABL, platelet-derived growth factor receptor (PDGFR), and c-kit kinases.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	114-119
15887238-4	2005	Treatment of head and neck squamous carcinoma cells with clinically relevant concentrations of imatinib-induced changes in cell morphology and growth similar to changes associated with epidermal growth factor receptor (EGFR) activation.	imatinib	95-103	epidermal growth factor receptor	Homo sapiens	185-217
15887238-4	2005	Treatment of head and neck squamous carcinoma cells with clinically relevant concentrations of imatinib-induced changes in cell morphology and growth similar to changes associated with epidermal growth factor receptor (EGFR) activation.	imatinib	95-103	epidermal growth factor receptor	Homo sapiens	219-223
15887238-5	2005	Imatinib-induced changes were blocked with the EGFR antagonist cetuximab, which suggested direct involvement of EGFR in this process.	imatinib	0-8	epidermal growth factor receptor	Homo sapiens	47-51
15887238-5	2005	Imatinib-induced changes were blocked with the EGFR antagonist cetuximab, which suggested direct involvement of EGFR in this process.	imatinib	0-8	epidermal growth factor receptor	Homo sapiens	112-116
15887238-6	2005	Western blot analysis of cells incubated with imatinib demonstrated activation of EGFR and downstream signaling that was reduced by inhibition of mitogen-activated protein/extracellular signal-regulated kinase kinase 1 (MEK1) and EGFR, but not Her2/ErbB2.	imatinib	46-54	epidermal growth factor receptor	Homo sapiens	82-86
15887238-6	2005	Western blot analysis of cells incubated with imatinib demonstrated activation of EGFR and downstream signaling that was reduced by inhibition of mitogen-activated protein/extracellular signal-regulated kinase kinase 1 (MEK1) and EGFR, but not Her2/ErbB2.	imatinib	46-54	mitogen-activated protein kinase kinase 1	Homo sapiens	146-218
15887238-6	2005	Western blot analysis of cells incubated with imatinib demonstrated activation of EGFR and downstream signaling that was reduced by inhibition of mitogen-activated protein/extracellular signal-regulated kinase kinase 1 (MEK1) and EGFR, but not Her2/ErbB2.	imatinib	46-54	mitogen-activated protein kinase kinase 1	Homo sapiens	220-224
15887238-6	2005	Western blot analysis of cells incubated with imatinib demonstrated activation of EGFR and downstream signaling that was reduced by inhibition of mitogen-activated protein/extracellular signal-regulated kinase kinase 1 (MEK1) and EGFR, but not Her2/ErbB2.	imatinib	46-54	epidermal growth factor receptor	Homo sapiens	230-234
15887238-6	2005	Western blot analysis of cells incubated with imatinib demonstrated activation of EGFR and downstream signaling that was reduced by inhibition of mitogen-activated protein/extracellular signal-regulated kinase kinase 1 (MEK1) and EGFR, but not Her2/ErbB2.	imatinib	46-54	erb-b2 receptor tyrosine kinase 2	Homo sapiens	244-248
15887238-6	2005	Western blot analysis of cells incubated with imatinib demonstrated activation of EGFR and downstream signaling that was reduced by inhibition of mitogen-activated protein/extracellular signal-regulated kinase kinase 1 (MEK1) and EGFR, but not Her2/ErbB2.	imatinib	46-54	erb-b2 receptor tyrosine kinase 2	Homo sapiens	249-254
15887238-8	2005	Inhibitors and neutralizing antibodies against heparin-binding epidermal growth factor-like growth factor (HB-EGF), and to a lesser extent transforming growth factor-alpha, reduced imatinib-mediated mitogen activated protein kinase (MAPK) activation.	imatinib	181-189	heparin binding EGF like growth factor	Homo sapiens	107-113
15887238-9	2005	Imatinib stimulated the rapid release of soluble HB-EGF and the subsequent induction of membrane-bound HB-EGF, which correlated with biphasic MAPK activation.	imatinib	0-8	heparin binding EGF like growth factor	Homo sapiens	49-55
15887238-9	2005	Imatinib stimulated the rapid release of soluble HB-EGF and the subsequent induction of membrane-bound HB-EGF, which correlated with biphasic MAPK activation.	imatinib	0-8	heparin binding EGF like growth factor	Homo sapiens	103-109
15887238-10	2005	Together, these results suggested that imatinib affects EGFR activation and signaling pathways through rapid release and increased expression of endogenous EGFR-activating ligands.	imatinib	39-47	epidermal growth factor receptor	Homo sapiens	56-60
15887238-10	2005	Together, these results suggested that imatinib affects EGFR activation and signaling pathways through rapid release and increased expression of endogenous EGFR-activating ligands.	imatinib	39-47	epidermal growth factor receptor	Homo sapiens	156-160
15887238-11	2005	Although, imatinib primarily inhibits tyrosine kinases, it also stimulates the activity of EGFR tyrosine kinase in head and neck squamous tumors.	imatinib	10-18	epidermal growth factor receptor	Homo sapiens	91-95
16334774-4	2005	He was medicated with STI571, which works by blocking proliferation of malignant cells with expression of c-kit.	imatinib	22-28	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	106-111
16151465-0	2005	A single nucleotide polymorphism in the coding region of ABL and its effects on sensitivity to imatinib.	imatinib	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-60
16151467-0	2005	Imatinib mesylate suppresses cytokine synthesis by activated CD4 T cells of patients with chronic myelogenous leukemia.	imatinib	0-17	CD4 molecule	Homo sapiens	61-64
16179913-1	2005	The Bcr-Abl inhibitor imatinib mesylate induces complete hematologic and cytogenetic remissions in most newly diagnosed chronic myeloid leukemia (CML) patients, but relatively few of them achieve molecular remission.	imatinib	22-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
16151468-0	2005	Coexistence of AML1/RUNX1 and BCR-ABL point mutations in an imatinib-resistant form of CML.	imatinib	60-68	RUNX family transcription factor 1	Homo sapiens	15-19
16151468-0	2005	Coexistence of AML1/RUNX1 and BCR-ABL point mutations in an imatinib-resistant form of CML.	imatinib	60-68	RUNX family transcription factor 1	Homo sapiens	20-25
16151468-0	2005	Coexistence of AML1/RUNX1 and BCR-ABL point mutations in an imatinib-resistant form of CML.	imatinib	60-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
15876454-0	2005	CML patient with rare b 2 a 3 (e 13 a 3) variant of BCR-ABL transcript: complete molecular response to imatinib.	imatinib	103-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
16179913-4	2005	"Dual" Src and Abl kinase inhibitors are an attractive class of compounds, since (a) these molecules are able to bind Bcr-Abl with less stringent conformational requirements with respect to imatinib, therefore allowing for efficient inhibition of several, resistance-associated mutant forms of Bcr-Abl; (b) Src kinases have been shown to be involved in Bcr-Abl-mediated leukemogenesis as well as upregulated in some patients resistant to imatinib.	imatinib	190-198	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	7-10
16179913-4	2005	"Dual" Src and Abl kinase inhibitors are an attractive class of compounds, since (a) these molecules are able to bind Bcr-Abl with less stringent conformational requirements with respect to imatinib, therefore allowing for efficient inhibition of several, resistance-associated mutant forms of Bcr-Abl; (b) Src kinases have been shown to be involved in Bcr-Abl-mediated leukemogenesis as well as upregulated in some patients resistant to imatinib.	imatinib	190-198	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
16179913-4	2005	"Dual" Src and Abl kinase inhibitors are an attractive class of compounds, since (a) these molecules are able to bind Bcr-Abl with less stringent conformational requirements with respect to imatinib, therefore allowing for efficient inhibition of several, resistance-associated mutant forms of Bcr-Abl; (b) Src kinases have been shown to be involved in Bcr-Abl-mediated leukemogenesis as well as upregulated in some patients resistant to imatinib.	imatinib	438-446	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	7-10
16179913-4	2005	"Dual" Src and Abl kinase inhibitors are an attractive class of compounds, since (a) these molecules are able to bind Bcr-Abl with less stringent conformational requirements with respect to imatinib, therefore allowing for efficient inhibition of several, resistance-associated mutant forms of Bcr-Abl; (b) Src kinases have been shown to be involved in Bcr-Abl-mediated leukemogenesis as well as upregulated in some patients resistant to imatinib.	imatinib	438-446	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
16620554-7	2005	Compared with K562/Vp16 non-SP cells, K562/Vp16 SP cells were more resistant to imatinib, which could hardly be reversed by many multidrug resistance inhibitors.	imatinib	80-88	host cell factor C1	Homo sapiens	43-47
16264277-0	2005	Detection of single nucleotide insertion of BCR/ABL region in imatinib-resistant human myelogenous leukemia SR-1 cells.	imatinib	62-70	BCR activator of RhoGEF and GTPase	Homo sapiens	44-47
16264277-0	2005	Detection of single nucleotide insertion of BCR/ABL region in imatinib-resistant human myelogenous leukemia SR-1 cells.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-51
16264277-1	2005	Imatinib mesylate is a selective Bcr/Abl kinase inhibitor and an effective anticancer agent for Bcr/Abl-positive chronic myelogenous leukemia.	imatinib	0-17	BCR activator of RhoGEF and GTPase	Homo sapiens	33-36
16264277-1	2005	Imatinib mesylate is a selective Bcr/Abl kinase inhibitor and an effective anticancer agent for Bcr/Abl-positive chronic myelogenous leukemia.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-40
16264277-1	2005	Imatinib mesylate is a selective Bcr/Abl kinase inhibitor and an effective anticancer agent for Bcr/Abl-positive chronic myelogenous leukemia.	imatinib	0-17	BCR activator of RhoGEF and GTPase	Homo sapiens	96-99
16264277-1	2005	Imatinib mesylate is a selective Bcr/Abl kinase inhibitor and an effective anticancer agent for Bcr/Abl-positive chronic myelogenous leukemia.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-103
16620554-0	2005	[Study on the mechanisms of imatinib-resistance of cancer stem-like cells in K562/Vp16 cell line].	imatinib	28-36	host cell factor C1	Homo sapiens	82-86
16620554-1	2005	OBJECTIVE: To elucidate the mechanisms of imatinib resistance involved in some chronic myeloid leukemia (CML) cells overexpressing P-glycoprotein (P-gp).	imatinib	42-50	ATP binding cassette subfamily B member 1	Homo sapiens	131-145
16264277-6	2005	We detected the new mutation of BCR/ABL, resulting in premature termination and loss of BCR/ABL fusion protein expression, which might be possible mechanism for the resistance to imatinib in SR-1 cells.	imatinib	179-187	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
16236162-3	2005	Imatinib mesylate is a FDA approved compound that inhibits tyrosine quinase receptors, as well as c-kit.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	98-103
16264277-6	2005	We detected the new mutation of BCR/ABL, resulting in premature termination and loss of BCR/ABL fusion protein expression, which might be possible mechanism for the resistance to imatinib in SR-1 cells.	imatinib	179-187	BCR activator of RhoGEF and GTPase	Homo sapiens	32-35
16264277-6	2005	We detected the new mutation of BCR/ABL, resulting in premature termination and loss of BCR/ABL fusion protein expression, which might be possible mechanism for the resistance to imatinib in SR-1 cells.	imatinib	179-187	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-39
16157305-2	2005	Imatinib mesylate inhibits Bcr-Abl tyrosine kinase, resulting in a blockage of tyrosine phosphorylation in its downstream pathways.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
16157305-5	2005	The inhibition of Bcr-Abl tyrosine kinase by 2.5 microM imatinib mesylate caused both cell cycle arrest in the G0/G1 phase and increased the portion of apoptotic cells.	imatinib	56-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
16234522-4	2005	Forty-four patients were enrolled and received the BCR-ABL tyrosine kinase inhibitor imatinib (IM) at a starting dose of 400 mg/d.	imatinib	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
16620554-1	2005	OBJECTIVE: To elucidate the mechanisms of imatinib resistance involved in some chronic myeloid leukemia (CML) cells overexpressing P-glycoprotein (P-gp).	imatinib	42-50	ATP binding cassette subfamily B member 1	Homo sapiens	147-151
16169003-4	2005	In this study, we examined the cellular signaling profiles following imatinib mesylate treatment of eight model CML and ALL cell lines that encompass three BCR-ABL junction points and multiple lineages.	imatinib	69-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
16230407-4	2005	The BCR/ABL inhibitors imatinib and AMN107 were found to promote expression of Bim in CML cells.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
15972446-1	2005	The majority of patients with systemic mast cell disease express the imatinib-resistant Asp816Val (D816V) mutation in the KIT receptor tyrosine kinase.	imatinib	69-77	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	122-125
16230407-7	2005	Interestingly, MG132 up-regulated the expression of bim mRNA and Bim protein and suppressed the growth of Ba/F3 cells containing wild-type BCR/ABL or imatinib-resistant mutants of BCR/ABL.	imatinib	150-158	BCL2-like 11 (apoptosis facilitator)	Mus musculus	52-55
16230407-7	2005	Interestingly, MG132 up-regulated the expression of bim mRNA and Bim protein and suppressed the growth of Ba/F3 cells containing wild-type BCR/ABL or imatinib-resistant mutants of BCR/ABL.	imatinib	150-158	BCR activator of RhoGEF and GTPase	Mus musculus	180-187
16230407-8	2005	To show functional significance of "Bim reexpression," a Bim-specific small interfering RNA was applied and found to rescue BCR/ABL-transformed leukemic cells from imatinib-induced cell death.	imatinib	164-172	BCL2 like 11	Homo sapiens	36-39
16230407-8	2005	To show functional significance of "Bim reexpression," a Bim-specific small interfering RNA was applied and found to rescue BCR/ABL-transformed leukemic cells from imatinib-induced cell death.	imatinib	164-172	BCL2 like 11	Homo sapiens	57-60
16230407-8	2005	To show functional significance of "Bim reexpression," a Bim-specific small interfering RNA was applied and found to rescue BCR/ABL-transformed leukemic cells from imatinib-induced cell death.	imatinib	164-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
16230407-9	2005	In summary, our data identify BCR/ABL as a Bim suppressor in CML cells and suggest that reexpression of Bim by novel tyrosine kinase inhibitors, proteasome inhibition, or by targeting signaling pathways downstream of BCR/ABL may be an attractive therapeutic approach in imatinib-resistant CML.	imatinib	270-278	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
16230407-9	2005	In summary, our data identify BCR/ABL as a Bim suppressor in CML cells and suggest that reexpression of Bim by novel tyrosine kinase inhibitors, proteasome inhibition, or by targeting signaling pathways downstream of BCR/ABL may be an attractive therapeutic approach in imatinib-resistant CML.	imatinib	270-278	BCL2 like 11	Homo sapiens	104-107
16334201-3	2005	A new targeted therapy, imatinib mesylate (Gleevec), inhibits of the dysregulated kinase activity of BCR-ABL.	imatinib	24-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
16498290-12	2005	The treatment of localized GIST is surgical resection, which must be complete; that of advanced or unresectable GIST is based on the use of a targeted therapy, imatinib, which is a pharmacological antagonist of the KIT protein.	imatinib	160-168	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	215-218
15956284-3	2005	IC50imatinib was determined in pretherapy blood samples by measuring the in vitro imatinib-induced reduction of the phosphorylated form of the adaptor protein Crkl (CT10 regulator of kinase like).	imatinib	4-12	CRK like proto-oncogene, adaptor protein	Homo sapiens	159-163
15956284-3	2005	IC50imatinib was determined in pretherapy blood samples by measuring the in vitro imatinib-induced reduction of the phosphorylated form of the adaptor protein Crkl (CT10 regulator of kinase like).	imatinib	4-12	CRK like proto-oncogene, adaptor protein	Homo sapiens	165-194
15956284-8	2005	These data provide strong evidence that intrinsic sensitivity to imatinib is variable in previously untreated patients with CML, and the actual level of BCR-ABL kinase inhibition achieved is critical to imatinib response.	imatinib	203-211	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
16230407-4	2005	The BCR/ABL inhibitors imatinib and AMN107 were found to promote expression of Bim in CML cells.	imatinib	23-31	BCL2 like 11	Homo sapiens	79-82
16157201-0	2005	Quantitative molecular monitoring of BCR-ABL and MDR1 transcripts in patients with chronic myeloid leukemia during Imatinib treatment.	imatinib	115-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
16157201-0	2005	Quantitative molecular monitoring of BCR-ABL and MDR1 transcripts in patients with chronic myeloid leukemia during Imatinib treatment.	imatinib	115-123	ATP binding cassette subfamily B member 1	Homo sapiens	49-53
16157201-1	2005	Different mechanisms could sustain Imatinib resistance, including overexpression of MDR1, a gene already known to be responsible for multidrug resistance in other hematologic malignancies.	imatinib	35-43	ATP binding cassette subfamily B member 1	Homo sapiens	84-88
16157201-6	2005	Reported data maintain that MDR1 expression would play an important role in Imatinib resistance when the disease is not fully controlled (e.g., progressive disease or during the first months of treatment).	imatinib	76-84	ATP binding cassette subfamily B member 1	Homo sapiens	28-32
16204063-0	2005	Bcr-Abl expression levels determine the rate of development of resistance to imatinib mesylate in chronic myeloid leukemia.	imatinib	77-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
16219536-1	2005	OBJECTIVE: In chronic myeloid leukemia (CML), imatinib mesylate (IM; Gleevec, Glivec) induces a G0/G1 cell-cycle block in total CD34(+) cells without causing significant apoptosis.	imatinib	46-63	CD34 molecule	Homo sapiens	128-132
16204063-4	2005	By studying cell lines that exogenously express Bcr-Abl over the range found from chronic phase to blast crisis of CML, we show that cells expressing high amounts of Bcr-Abl, as in blast crisis, are much less sensitive to imatinib and, more significantly, take a substantially shorter time for yielding a mutant subclone resistant to the inhibitor than cells with low expression levels, as in chronic phase.	imatinib	222-230	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-173
16204063-5	2005	Our data suggest that the differential levels of the Bcr-Abl oncoprotein expressed by CD34+ CML cells may reflect the extent and duration of their response to imatinib; the relatively high levels of oncoprotein in advanced-phase disease may underlie the observed rapid development of resistance.	imatinib	159-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
16204063-5	2005	Our data suggest that the differential levels of the Bcr-Abl oncoprotein expressed by CD34+ CML cells may reflect the extent and duration of their response to imatinib; the relatively high levels of oncoprotein in advanced-phase disease may underlie the observed rapid development of resistance.	imatinib	159-167	CD34 molecule	Homo sapiens	86-90
16203792-0	2005	Combined Abl inhibitor therapy for minimizing drug resistance in chronic myeloid leukemia: Src/Abl inhibitors are compatible with imatinib.	imatinib	130-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-12
16203792-0	2005	Combined Abl inhibitor therapy for minimizing drug resistance in chronic myeloid leukemia: Src/Abl inhibitors are compatible with imatinib.	imatinib	130-138	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	91-94
16203792-0	2005	Combined Abl inhibitor therapy for minimizing drug resistance in chronic myeloid leukemia: Src/Abl inhibitors are compatible with imatinib.	imatinib	130-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-98
16203792-2	2005	However, reactivation of Bcr-Abl via kinase domain mutations that reduce sensitivity to imatinib can cause relapse.	imatinib	88-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
16203792-3	2005	As combination therapy is frequently used to prevent emergence of resistance, the combination of imatinib with an inhibitor of imatinib-resistant Bcr-Abl mutants (e.g., Src/Abl inhibitors AP23848 and BMS-354825) was investigated.	imatinib	127-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	146-153
16203792-3	2005	As combination therapy is frequently used to prevent emergence of resistance, the combination of imatinib with an inhibitor of imatinib-resistant Bcr-Abl mutants (e.g., Src/Abl inhibitors AP23848 and BMS-354825) was investigated.	imatinib	127-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-153
16203792-6	2005	RESULTS: Both Src/Abl inhibitors retained full inhibitory capacity when coadministered with imatinib at concentrations above typical clinical levels.	imatinib	92-100	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	14-17
16203792-6	2005	RESULTS: Both Src/Abl inhibitors retained full inhibitory capacity when coadministered with imatinib at concentrations above typical clinical levels.	imatinib	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-21
16203792-7	2005	For cells expressing WT Bcr-Abl or the marginally imatinib-resistant mutant M351T, inclusion of imatinib at therapeutic levels enhanced the effects of the Src/Abl inhibitors.	imatinib	96-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
16203792-7	2005	For cells expressing WT Bcr-Abl or the marginally imatinib-resistant mutant M351T, inclusion of imatinib at therapeutic levels enhanced the effects of the Src/Abl inhibitors.	imatinib	96-104	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	155-158
16203792-7	2005	For cells expressing WT Bcr-Abl or the marginally imatinib-resistant mutant M351T, inclusion of imatinib at therapeutic levels enhanced the effects of the Src/Abl inhibitors.	imatinib	96-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-31
16203792-8	2005	By comparison, for the highly imatinib-resistant mutants Y253F and E255K, inclusion of imatinib at clinical levels resulted in only a slight enhancement beyond the effects of the Src/Abl inhibitors.	imatinib	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	183-186
16203792-11	2005	CONCLUSIONS: Our results indicate that Src/Abl inhibitors are compatible with imatinib and suggest that combined Abl inhibitor therapy is a feasible treatment strategy for patients with CML.	imatinib	78-86	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	39-42
16203792-11	2005	CONCLUSIONS: Our results indicate that Src/Abl inhibitors are compatible with imatinib and suggest that combined Abl inhibitor therapy is a feasible treatment strategy for patients with CML.	imatinib	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-46
16203792-11	2005	CONCLUSIONS: Our results indicate that Src/Abl inhibitors are compatible with imatinib and suggest that combined Abl inhibitor therapy is a feasible treatment strategy for patients with CML.	imatinib	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-116
16185155-9	2005	As with as other small-molecule kinase inhibitors and susceptible diseases (e.g., imatinib and chronic myeloid leukaemia), resistance to EGFR inhibitors has been reported recently, documenting the requirement for development of multi-pronged therapeutic approaches.	imatinib	82-90	epidermal growth factor receptor	Homo sapiens	137-141
15790787-6	2005	In contrast to the effects of IFNs, imatinib mesylate suppressed p70 S6 kinase activity, consistent with inhibition of BCR-ABL-mediated activation of the mTOR/p70 S6 kinase pathway.	imatinib	36-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-126
15790787-6	2005	In contrast to the effects of IFNs, imatinib mesylate suppressed p70 S6 kinase activity, consistent with inhibition of BCR-ABL-mediated activation of the mTOR/p70 S6 kinase pathway.	imatinib	36-53	mechanistic target of rapamycin kinase	Homo sapiens	154-158
15790787-7	2005	Moreover, the mTOR inhibitor rapamycin enhanced the suppressive effects of imatinib mesylate on primary leukemic granulocyte macrophage-colony-forming unit (CFU-GM) progenitors from patients with chronic myelogenous leukemia (CML).	imatinib	75-92	mechanistic target of rapamycin kinase	Homo sapiens	14-18
15790787-8	2005	Taken altogether, our data demonstrate that IFNs and imatinib mesylate differentially regulate PI 3" kinase/mTOR-dependent signaling cascades in BCR-ABL-transformed cells, consistent with distinct effects of these agents on pathways regulating mRNA translation.	imatinib	53-70	peptidase inhibitor 3	Homo sapiens	95-99
15790787-8	2005	Taken altogether, our data demonstrate that IFNs and imatinib mesylate differentially regulate PI 3" kinase/mTOR-dependent signaling cascades in BCR-ABL-transformed cells, consistent with distinct effects of these agents on pathways regulating mRNA translation.	imatinib	53-70	mechanistic target of rapamycin kinase	Homo sapiens	108-112
15790787-8	2005	Taken altogether, our data demonstrate that IFNs and imatinib mesylate differentially regulate PI 3" kinase/mTOR-dependent signaling cascades in BCR-ABL-transformed cells, consistent with distinct effects of these agents on pathways regulating mRNA translation.	imatinib	53-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-152
16203604-3	2005	Imatinib mesylate (IM) is one such therapy that also targets Abl, c-kit and PDGF-R tyrosine kinases.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-64
16203604-3	2005	Imatinib mesylate (IM) is one such therapy that also targets Abl, c-kit and PDGF-R tyrosine kinases.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	66-71
16107888-0	2005	Chronic myeloid leukemia CD34+ cells have elevated levels of phosphatidylinositol 3,4,5 trisphosphate (PtdIns(3,4,5)P3) and lack a PtdIns(3,4,5)P3 response to cytokines and chemotactic factors; effects reversed by imatinib.	imatinib	214-222	CD34 molecule	Homo sapiens	25-29
16210056-7	2005	SCF synergized with chemoattractants in causing basophil upregulation of the integrin CD11b, and this effect was inhibited by a c-kit antibody, the tyrosine kinase inhibitor imatinib mesylate (STI-571), and a phosphatidylinositol 3 kinase inhibitor but not by inhibitors of p38 mitogen-activated protein kinase or mitogen-activated protein kinase/extracellular signal-regulated kinase kinase.	imatinib	174-191	KIT ligand	Homo sapiens	0-3
16210056-7	2005	SCF synergized with chemoattractants in causing basophil upregulation of the integrin CD11b, and this effect was inhibited by a c-kit antibody, the tyrosine kinase inhibitor imatinib mesylate (STI-571), and a phosphatidylinositol 3 kinase inhibitor but not by inhibitors of p38 mitogen-activated protein kinase or mitogen-activated protein kinase/extracellular signal-regulated kinase kinase.	imatinib	174-191	integrin subunit alpha M	Homo sapiens	86-91
16210056-7	2005	SCF synergized with chemoattractants in causing basophil upregulation of the integrin CD11b, and this effect was inhibited by a c-kit antibody, the tyrosine kinase inhibitor imatinib mesylate (STI-571), and a phosphatidylinositol 3 kinase inhibitor but not by inhibitors of p38 mitogen-activated protein kinase or mitogen-activated protein kinase/extracellular signal-regulated kinase kinase.	imatinib	193-200	KIT ligand	Homo sapiens	0-3
16210056-7	2005	SCF synergized with chemoattractants in causing basophil upregulation of the integrin CD11b, and this effect was inhibited by a c-kit antibody, the tyrosine kinase inhibitor imatinib mesylate (STI-571), and a phosphatidylinositol 3 kinase inhibitor but not by inhibitors of p38 mitogen-activated protein kinase or mitogen-activated protein kinase/extracellular signal-regulated kinase kinase.	imatinib	193-200	integrin subunit alpha M	Homo sapiens	86-91
16210056-7	2005	SCF synergized with chemoattractants in causing basophil upregulation of the integrin CD11b, and this effect was inhibited by a c-kit antibody, the tyrosine kinase inhibitor imatinib mesylate (STI-571), and a phosphatidylinositol 3 kinase inhibitor but not by inhibitors of p38 mitogen-activated protein kinase or mitogen-activated protein kinase/extracellular signal-regulated kinase kinase.	imatinib	193-200	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	128-133
16136169-0	2005	Compensatory PI3-kinase/Akt/mTor activation regulates imatinib resistance development.	imatinib	54-62	AKT serine/threonine kinase 1	Homo sapiens	24-27
16136169-0	2005	Compensatory PI3-kinase/Akt/mTor activation regulates imatinib resistance development.	imatinib	54-62	mechanistic target of rapamycin kinase	Homo sapiens	28-32
16136169-1	2005	BCR/ABL-kinase mutations frequently mediate clinical resistance to the selective tyrosine kinase inhibitor Imatinib mesylate (IM, Gleevec).	imatinib	107-124	BCR activator of RhoGEF and GTPase	Homo sapiens	0-3
16136169-1	2005	BCR/ABL-kinase mutations frequently mediate clinical resistance to the selective tyrosine kinase inhibitor Imatinib mesylate (IM, Gleevec).	imatinib	107-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
16320588-5	2005	After treating with STI571 combined with neferine, the synergistic interaction on K562/A02 cells increased 4.38 folds (P < 0.05); the mdrl mRNA expression by semi-quantitative RT-PCR was significantly reduced by (45.4 +/- 2.5) % (P < 0.01); and the P-gp expression by Western blot was deregulated by 40.58% (P < 0.05).	imatinib	20-26	phosphoglycolate phosphatase	Homo sapiens	255-259
16078266-1	2005	BACKGROUND: Previous studies have shown that patients with Bcr-Abl-positive acute lymphoblastic leukemia (ALL) either have primary disease that is refractory to imatinib mesylate or develop disease recurrence after an initial response.	imatinib	161-178	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
16174751-0	2005	The kinase inhibitor imatinib mesylate inhibits TNF-{alpha} production in vitro and prevents TNF-dependent acute hepatic inflammation.	imatinib	21-38	tumor necrosis factor	Homo sapiens	48-58
16174751-0	2005	The kinase inhibitor imatinib mesylate inhibits TNF-{alpha} production in vitro and prevents TNF-dependent acute hepatic inflammation.	imatinib	21-38	tumor necrosis factor	Homo sapiens	48-51
16174751-6	2005	In line with this observation, phosphorylation of IkappaB and subsequent DNA binding of NF-kappaB, which is critically involved in TNF-alpha, but not IL-10 expression, was reduced by imatinib.	imatinib	183-191	nuclear factor kappa B subunit 1	Homo sapiens	88-97
16174751-6	2005	In line with this observation, phosphorylation of IkappaB and subsequent DNA binding of NF-kappaB, which is critically involved in TNF-alpha, but not IL-10 expression, was reduced by imatinib.	imatinib	183-191	tumor necrosis factor	Homo sapiens	131-140
16174751-7	2005	Using several murine models of acute hepatitis, we could corroborate our in vitro findings, as imatinib prevented macrophage- and TNF-alpha-dependent inflammatory damage of the liver induced by injection of either Con A or d-galactosamine/LPS by inhibition of hepatic TNF-alpha production.	imatinib	95-103	tumor necrosis factor	Mus musculus	130-139
16174751-7	2005	Using several murine models of acute hepatitis, we could corroborate our in vitro findings, as imatinib prevented macrophage- and TNF-alpha-dependent inflammatory damage of the liver induced by injection of either Con A or d-galactosamine/LPS by inhibition of hepatic TNF-alpha production.	imatinib	95-103	tumor necrosis factor	Mus musculus	268-277
16174751-9	2005	These findings suggest a potent antiinflammatory role of imatinib by modulation of TNF-alpha production in monocytes/macrophages.	imatinib	57-65	tumor necrosis factor	Homo sapiens	83-92
15914554-0	2005	High-sensitivity detection of BCR-ABL kinase domain mutations in imatinib-naive patients: correlation with clonal cytogenetic evolution but not response to therapy.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
15914554-1	2005	Mutations in the kinase domain (KD) of BCR-ABL are the leading cause of acquired imatinib resistance.	imatinib	81-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
16007188-7	2005	Treatment with the tyrosine kinase inhibitor imatinib mesylate reversed the adhesion deficient phenotype of clones expressing low levels of Bcr-Abl.	imatinib	45-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
16078266-2	2005	METHODS: The authors investigated the effects of a newly designed Bcr-Abl inhibitor, AMN107, by comparing its in vitro inhibitory potency on p190 Bcr-Abl ALL cell lines with that of imatinib.	imatinib	182-190	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
16078266-4	2005	AMN107 was also more effective than imatinib in inhibiting phosphorylation of p190 Bcr-Abl tyrosine kinase in cell lines and primary ALL cells.	imatinib	36-44	contactin associated protein 1	Homo sapiens	78-82
16078266-4	2005	AMN107 was also more effective than imatinib in inhibiting phosphorylation of p190 Bcr-Abl tyrosine kinase in cell lines and primary ALL cells.	imatinib	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
16082245-13	2005	KIT tyrosine kinase inhibitors such as imatinib mesylate are the generally accepted treatment of metastatic GISTs, and their availability has prompted an active search for other treatment targets among KIT-positive tumors such as myeloid leukemias and small cell carcinoma of the lung, with variable and often nonconvincing results.	imatinib	39-56	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
16166321-0	2005	Inhibition of the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin pathway but not the MEK/ERK pathway attenuates laminin-mediated small cell lung cancer cellular survival and resistance to imatinib mesylate or chemotherapy.	imatinib	205-222	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	18-47
16166298-0	2005	Disruption of the inhibitor of apoptosis protein survivin sensitizes Bcr-abl-positive cells to STI571-induced apoptosis.	imatinib	95-101	CD47 molecule	Homo sapiens	18-48
16166298-0	2005	Disruption of the inhibitor of apoptosis protein survivin sensitizes Bcr-abl-positive cells to STI571-induced apoptosis.	imatinib	95-101	baculoviral IAP repeat-containing 5	Mus musculus	49-57
16166298-0	2005	Disruption of the inhibitor of apoptosis protein survivin sensitizes Bcr-abl-positive cells to STI571-induced apoptosis.	imatinib	95-101	BCR activator of RhoGEF and GTPase	Homo sapiens	69-72
16166298-7	2005	Survivin disruption in Bcr-abl-transduced Mo7e cells, or in K562 cells that endogenously express Bcr-abl, by transfection with dominant-negative or antisense survivin constructs promoted apoptosis induced by the Bcr-abl tyrosine kinase inhibitor STI571, which was accompanied by caspase-dependent cleavage of Bcr-abl, mitochondrial membrane potential disruption, and enhanced mitochondrial cytochrome c release.	imatinib	246-252	baculoviral IAP repeat-containing 5	Mus musculus	0-8
16166298-8	2005	Although ectopic survivin protected K562 cells from apoptosis induced by STI571, it did not protect cells from apoptosis induced either by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) or the combination of TRAIL plus Hemin.	imatinib	73-79	baculoviral IAP repeat-containing 5	Mus musculus	17-25
16101197-3	2005	A substantial fraction of the tumors expresses c-Kit or the platelet-derived growth factor receptor beta (PDGFRbeta), both targets for imatinib mesylate.	imatinib	135-143	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	47-52
16143141-5	2005	This mutation activates KIT, and the mutant KIT is inhibited by the tyrosine kinase inhibitor imatinib mesylate.	imatinib	94-111	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	24-27
16101197-3	2005	A substantial fraction of the tumors expresses c-Kit or the platelet-derived growth factor receptor beta (PDGFRbeta), both targets for imatinib mesylate.	imatinib	135-143	platelet derived growth factor receptor beta	Homo sapiens	60-104
16101197-3	2005	A substantial fraction of the tumors expresses c-Kit or the platelet-derived growth factor receptor beta (PDGFRbeta), both targets for imatinib mesylate.	imatinib	135-143	platelet derived growth factor receptor beta	Homo sapiens	106-115
16153117-4	2005	Half-maximal inhibition (IC50) values for imatinib mesylate inhibition of GST-Crkl (SH3) phosphorylation by v-Abl in a purified system and Bcr-Abl within a K562 cell lysate were determined to be 1.5 and 20 microM, respectively.	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-113
16140951-0	2005	Effect of platelet-derived growth factor receptor-beta inhibition with STI571 on radioimmunotherapy.	imatinib	71-77	platelet derived growth factor receptor, beta polypeptide	Mus musculus	10-54
16143141-5	2005	This mutation activates KIT, and the mutant KIT is inhibited by the tyrosine kinase inhibitor imatinib mesylate.	imatinib	94-111	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	44-47
16001089-1	2005	Selective inhibition of the BCR/ABL tyrosine kinase by imatinib has become a first-line therapy for chronic myelogenous leukemia (CML).	imatinib	55-63	BCR activator of RhoGEF and GTPase	Mus musculus	28-31
16135502-0	2005	Imatinib mesylate can induce objective response in progressing, highly expressing KIT adenoid cystic carcinoma of the salivary glands.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	82-85
16001089-1	2005	Selective inhibition of the BCR/ABL tyrosine kinase by imatinib has become a first-line therapy for chronic myelogenous leukemia (CML).	imatinib	55-63	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	32-35
16038734-1	2005	Quantitative monitoring of imatinib mesylate (IM)-resistant, mutated BCR-ABL(+) cells during the follow-up of CML could be useful for optimizing therapeutic management.	imatinib	27-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
16109618-0	2005	E6a2 BCR-ABL fusion with BCR exon 5-deleted transcript in a Philadelphia positive CML responsive to Imatinib.	imatinib	100-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	5-12
16109618-0	2005	E6a2 BCR-ABL fusion with BCR exon 5-deleted transcript in a Philadelphia positive CML responsive to Imatinib.	imatinib	100-108	BCR activator of RhoGEF and GTPase	Homo sapiens	5-8
16001089-3	2005	Drug efflux by P-glycoprotein (P-gp), as well as point mutations in BCR/ABL oncoprotein, has been implicated in the mechanism of resistance to imatinib.	imatinib	143-151	phosphoglycolate phosphatase	Mus musculus	15-29
16001089-3	2005	Drug efflux by P-glycoprotein (P-gp), as well as point mutations in BCR/ABL oncoprotein, has been implicated in the mechanism of resistance to imatinib.	imatinib	143-151	phosphoglycolate phosphatase	Mus musculus	31-35
16049512-0	2005	Imatinib mesylate for refractory acute myeloblastic leukemia harboring inv(16) and a C-KIT exon 8 mutation.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	85-90
16001089-3	2005	Drug efflux by P-glycoprotein (P-gp), as well as point mutations in BCR/ABL oncoprotein, has been implicated in the mechanism of resistance to imatinib.	imatinib	143-151	BCR activator of RhoGEF and GTPase	Mus musculus	68-75
16001089-7	2005	Furthermore, K562 cells engineered to overexpress P-gp remained sensitive to imatinib-induced growth inhibition and cell death.	imatinib	77-85	phosphoglycolate phosphatase	Homo sapiens	50-54
16015387-8	2005	We demonstrate that KIT exon 8 mutations result in constitutive ligand-independent kinase activation that can be inhibited by clinically relevant concentrations of imatinib.	imatinib	164-172	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	20-23
16015388-3	2005	Similar interactions were observed in CD34+ cells from two patients with CML and in imatinib mesylate-resistant K562 cells but not in normal human CD34+ bone marrow cells.	imatinib	84-101	CD34 molecule	Homo sapiens	38-42
15996481-6	2005	We provide evidence that Abl family kinases are a major effector of ephrin-A-induced retinal ganglion cell repulsion since the Abl inhibitor, STI571, prevents both loss of growth cone lamellipodia and axon retraction.	imatinib	142-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-28
15996481-6	2005	We provide evidence that Abl family kinases are a major effector of ephrin-A-induced retinal ganglion cell repulsion since the Abl inhibitor, STI571, prevents both loss of growth cone lamellipodia and axon retraction.	imatinib	142-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-130
16142999-5	2005	The administration of new chemotherapeutic agents, such as imatinib for gastrointestinal tumors (GIST), requires the study of genetic polymorphisms possibly affecting the integrity of the target (c-KIT), which may provide valid information regarding possible developments of therapy.	imatinib	59-67	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	196-201
16077968-0	2005	Effects of imatinib vary with the types of KIT-mutation in gastrointestinal stromal tumor cell lines.	imatinib	11-19	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	43-46
16077968-2	2005	Imatinib has therapeutic potential for GISTs because of its inhibitory effect on KIT kinase activity.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	81-84
16077968-8	2005	In two types of activating mutant KIT, imatinib could inhibit the constitutive activation of both types of KIT mutant, although the antiproliferative effect on GIST882 was weaker than on GIST-T1.	imatinib	39-47	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	34-37
16077968-8	2005	In two types of activating mutant KIT, imatinib could inhibit the constitutive activation of both types of KIT mutant, although the antiproliferative effect on GIST882 was weaker than on GIST-T1.	imatinib	39-47	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	107-110
16077968-10	2005	Our results suggest that the apoptotic signal trans-duction caused by imatinib in GISTs is susceptible to various types of KIT mutation.	imatinib	70-78	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	123-126
15928335-0	2005	PDGFRA mutations in gastrointestinal stromal tumors: frequency, spectrum and in vitro sensitivity to imatinib.	imatinib	101-109	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	0-6
15927960-10	2005	In K562 cells, expression of delta(358-452), delta(389-418), and L389A/L396A c-Myb led to enhanced proliferation after STI571 treatment.	imatinib	119-125	MYB proto-oncogene, transcription factor	Homo sapiens	77-82
16061224-4	2005	DAB2 induction and megakaryocytic differentiation was abrogated when cells were co-treated with the PDGF receptor inhibitor STI571 or when the conditioned medium was derived from TPA-plus STI571-treated cells.	imatinib	124-130	DAB adaptor protein 2	Homo sapiens	0-4
16061224-4	2005	DAB2 induction and megakaryocytic differentiation was abrogated when cells were co-treated with the PDGF receptor inhibitor STI571 or when the conditioned medium was derived from TPA-plus STI571-treated cells.	imatinib	188-194	DAB adaptor protein 2	Homo sapiens	0-4
15928335-1	2005	PURPOSE: Gastrointestinal stromal tumors (GISTs) commonly harbor oncogenic mutations of the KIT tyrosine kinase, which is a target for the kinase inhibitor imatinib.	imatinib	156-164	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	92-95
15928335-2	2005	A subset of GISTs, however, contains mutations in the homologous kinase platelet derived growth factor receptor alpha (PDGFRA), and the most common of these mutations is resistant to imatinib in vitro.	imatinib	183-191	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	72-117
15928335-2	2005	A subset of GISTs, however, contains mutations in the homologous kinase platelet derived growth factor receptor alpha (PDGFRA), and the most common of these mutations is resistant to imatinib in vitro.	imatinib	183-191	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	119-125
15928335-6	2005	Transient expression of representative PDGFRA isoforms in CHO cells revealed imatinib sensitivity of exon 12 mutations (SPDHE566-571R and insertion ER561-562) and an exon 14 substitution (N659K).	imatinib	77-85	platelet-derived growth factor receptor alpha	Cricetulus griseus	39-45
15928335-10	2005	CONCLUSION: Including our cases, there are 289 reported PDGFRA-mutant GISTs, of which 181 (62.6%) had the imatinib-resistant substitution D842V.	imatinib	106-114	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	56-62
15928335-11	2005	However, our findings suggest that more than one third of GISTs with PDGFRA mutations may respond to imatinib and that mutation screening may be helpful in the management of these tumors.	imatinib	101-109	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	69-75
16046538-2	2005	Mutant forms of BCR-ABL, KIT, and the EGF receptor (EGFR) have been found that confer resistance to the drugs imatinib, gefitinib, and erlotinib.	imatinib	110-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
16046538-2	2005	Mutant forms of BCR-ABL, KIT, and the EGF receptor (EGFR) have been found that confer resistance to the drugs imatinib, gefitinib, and erlotinib.	imatinib	110-118	epidermal growth factor receptor	Homo sapiens	38-50
16046538-2	2005	Mutant forms of BCR-ABL, KIT, and the EGF receptor (EGFR) have been found that confer resistance to the drugs imatinib, gefitinib, and erlotinib.	imatinib	110-118	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	25-28
16046538-2	2005	Mutant forms of BCR-ABL, KIT, and the EGF receptor (EGFR) have been found that confer resistance to the drugs imatinib, gefitinib, and erlotinib.	imatinib	110-118	epidermal growth factor receptor	Homo sapiens	52-56
16143881-7	2005	Imatinib mesylate, a tyrosine kinase inhibitor known to inhibit the activities of BCR-ABL, KIT, and PDGFR, is currently being used for the treatment of both chronic myeloid leukemia and metastatic GIST.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
16046538-5	2005	We found that the Aurora kinase inhibitor VX-680 and the p38 inhibitor BIRB-796 inhibit the imatinib- and BMS-354825-resistant ABL(T315I) kinase.	imatinib	92-100	mitogen-activated protein kinase 14	Homo sapiens	57-60
16046538-5	2005	We found that the Aurora kinase inhibitor VX-680 and the p38 inhibitor BIRB-796 inhibit the imatinib- and BMS-354825-resistant ABL(T315I) kinase.	imatinib	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-130
16046538-6	2005	The KIT/FLT3 inhibitor SU-11248 potently inhibits the imatinib-resistant KIT(V559D/T670I) kinase, consistent with the clinical efficacy of SU-11248 against imatinib-resistant gastrointestinal tumors, and the EGFR inhibitors EKB-569 and CI-1033, but not GW-572016 and ZD-6474, potently inhibit the gefitinib- and erlotinib-resistant EGFR(L858R/T790M) kinase.	imatinib	54-62	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	4-7
16046538-6	2005	The KIT/FLT3 inhibitor SU-11248 potently inhibits the imatinib-resistant KIT(V559D/T670I) kinase, consistent with the clinical efficacy of SU-11248 against imatinib-resistant gastrointestinal tumors, and the EGFR inhibitors EKB-569 and CI-1033, but not GW-572016 and ZD-6474, potently inhibit the gefitinib- and erlotinib-resistant EGFR(L858R/T790M) kinase.	imatinib	54-62	fms related receptor tyrosine kinase 3	Homo sapiens	8-12
16046538-6	2005	The KIT/FLT3 inhibitor SU-11248 potently inhibits the imatinib-resistant KIT(V559D/T670I) kinase, consistent with the clinical efficacy of SU-11248 against imatinib-resistant gastrointestinal tumors, and the EGFR inhibitors EKB-569 and CI-1033, but not GW-572016 and ZD-6474, potently inhibit the gefitinib- and erlotinib-resistant EGFR(L858R/T790M) kinase.	imatinib	54-62	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
16046538-6	2005	The KIT/FLT3 inhibitor SU-11248 potently inhibits the imatinib-resistant KIT(V559D/T670I) kinase, consistent with the clinical efficacy of SU-11248 against imatinib-resistant gastrointestinal tumors, and the EGFR inhibitors EKB-569 and CI-1033, but not GW-572016 and ZD-6474, potently inhibit the gefitinib- and erlotinib-resistant EGFR(L858R/T790M) kinase.	imatinib	54-62	epidermal growth factor receptor	Homo sapiens	208-212
16046538-6	2005	The KIT/FLT3 inhibitor SU-11248 potently inhibits the imatinib-resistant KIT(V559D/T670I) kinase, consistent with the clinical efficacy of SU-11248 against imatinib-resistant gastrointestinal tumors, and the EGFR inhibitors EKB-569 and CI-1033, but not GW-572016 and ZD-6474, potently inhibit the gefitinib- and erlotinib-resistant EGFR(L858R/T790M) kinase.	imatinib	54-62	epidermal growth factor receptor	Homo sapiens	332-336
16046538-6	2005	The KIT/FLT3 inhibitor SU-11248 potently inhibits the imatinib-resistant KIT(V559D/T670I) kinase, consistent with the clinical efficacy of SU-11248 against imatinib-resistant gastrointestinal tumors, and the EGFR inhibitors EKB-569 and CI-1033, but not GW-572016 and ZD-6474, potently inhibit the gefitinib- and erlotinib-resistant EGFR(L858R/T790M) kinase.	imatinib	156-164	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	4-7
16046538-6	2005	The KIT/FLT3 inhibitor SU-11248 potently inhibits the imatinib-resistant KIT(V559D/T670I) kinase, consistent with the clinical efficacy of SU-11248 against imatinib-resistant gastrointestinal tumors, and the EGFR inhibitors EKB-569 and CI-1033, but not GW-572016 and ZD-6474, potently inhibit the gefitinib- and erlotinib-resistant EGFR(L858R/T790M) kinase.	imatinib	156-164	fms related receptor tyrosine kinase 3	Homo sapiens	8-12
16014680-0	2005	Inhibition of c-kit tyrosine kinase by imatinib mesylate induces apoptosis in mast cells in rheumatoid synovia: a potential approach to the treatment of arthritis.	imatinib	39-56	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-19
16014680-5	2005	Inhibition of the c-kit tyrosine kinase with imatinib mesylate (1.0-10 micromol/l) induced profound apoptosis in cultured mast cells as judged by typical apoptotic morphology, increased number of apoptotic nucleosomes, and activation of caspases 8 and 9.	imatinib	45-62	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	18-23
16014680-5	2005	Inhibition of the c-kit tyrosine kinase with imatinib mesylate (1.0-10 micromol/l) induced profound apoptosis in cultured mast cells as judged by typical apoptotic morphology, increased number of apoptotic nucleosomes, and activation of caspases 8 and 9.	imatinib	45-62	caspase 8	Homo sapiens	237-253
16167051-3	2005	The discovery that constitutive activation of the c-kit gene drives malignant behavior in GISTs exposed a weakness that was soon exploited through the application of the novel targeted therapy imatinib, a small-molecule tyrosine kinase inhibitor of Bcr-Abl, KIT, and the platelet-derived growth factor receptor-alpha and -beta.	imatinib	193-201	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	50-55
16167051-3	2005	The discovery that constitutive activation of the c-kit gene drives malignant behavior in GISTs exposed a weakness that was soon exploited through the application of the novel targeted therapy imatinib, a small-molecule tyrosine kinase inhibitor of Bcr-Abl, KIT, and the platelet-derived growth factor receptor-alpha and -beta.	imatinib	193-201	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	249-256
16167051-3	2005	The discovery that constitutive activation of the c-kit gene drives malignant behavior in GISTs exposed a weakness that was soon exploited through the application of the novel targeted therapy imatinib, a small-molecule tyrosine kinase inhibitor of Bcr-Abl, KIT, and the platelet-derived growth factor receptor-alpha and -beta.	imatinib	193-201	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	258-261
16167051-3	2005	The discovery that constitutive activation of the c-kit gene drives malignant behavior in GISTs exposed a weakness that was soon exploited through the application of the novel targeted therapy imatinib, a small-molecule tyrosine kinase inhibitor of Bcr-Abl, KIT, and the platelet-derived growth factor receptor-alpha and -beta.	imatinib	193-201	platelet derived growth factor receptor alpha	Homo sapiens	271-326
16050798-3	2005	The effectiveness of the Bcr-Abl kinase inhibitor imatinib in these conditions reduces with advancing disease and/or the development of resistance to imatinib.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
16027519-8	2005	Since gemcitabine is activated by deoxycytidine kinase (dCK), the effect of imatinib on this enzyme was investigated.	imatinib	76-84	sticky	Drosophila melanogaster	56-59
16027519-9	2005	A dose-dependent inhibition of dCK was observed, highlighting this kinase as a possible additional secondary molecular target for imatinib.	imatinib	130-138	sticky	Drosophila melanogaster	31-34
16042686-8	2005	Imatinib and IFN appear to have divergent effects on CML progenitors at different stages of maturation, with imatinib more active against differentiated CML progenitors and IFN more active against primitive CML progenitors.	imatinib	0-8	interferon alpha 1	Homo sapiens	173-176
16042686-8	2005	Imatinib and IFN appear to have divergent effects on CML progenitors at different stages of maturation, with imatinib more active against differentiated CML progenitors and IFN more active against primitive CML progenitors.	imatinib	109-117	interferon alpha 1	Homo sapiens	13-16
16050798-3	2005	The effectiveness of the Bcr-Abl kinase inhibitor imatinib in these conditions reduces with advancing disease and/or the development of resistance to imatinib.	imatinib	150-158	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
16050798-5	2005	AMN-107 was also effective against several imatinib-resistant Bcr-Abl mutants, but not T3151.	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
16050798-7	2005	In mice transduced with the E255V imatinib-resistant mutant of Bcr-Abl, AMN-107 delayed the onset of leukaemia.	imatinib	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
16143881-7	2005	Imatinib mesylate, a tyrosine kinase inhibitor known to inhibit the activities of BCR-ABL, KIT, and PDGFR, is currently being used for the treatment of both chronic myeloid leukemia and metastatic GIST.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	91-94
16143881-7	2005	Imatinib mesylate, a tyrosine kinase inhibitor known to inhibit the activities of BCR-ABL, KIT, and PDGFR, is currently being used for the treatment of both chronic myeloid leukemia and metastatic GIST.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	100-105
16143881-8	2005	The clinical response to imatinib therapy correlates with the types of mutations of KIT and PDGFRA, and the determination of KIT and PDGFRA mutations is useful for predicting the effect of imatinib.	imatinib	25-33	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	84-87
16143881-8	2005	The clinical response to imatinib therapy correlates with the types of mutations of KIT and PDGFRA, and the determination of KIT and PDGFRA mutations is useful for predicting the effect of imatinib.	imatinib	25-33	platelet derived growth factor receptor alpha	Homo sapiens	92-98
16143881-8	2005	The clinical response to imatinib therapy correlates with the types of mutations of KIT and PDGFRA, and the determination of KIT and PDGFRA mutations is useful for predicting the effect of imatinib.	imatinib	189-197	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	125-128
16143881-8	2005	The clinical response to imatinib therapy correlates with the types of mutations of KIT and PDGFRA, and the determination of KIT and PDGFRA mutations is useful for predicting the effect of imatinib.	imatinib	189-197	platelet derived growth factor receptor alpha	Homo sapiens	133-139
16143881-9	2005	Resistance to imatinib after an initial response has been reported; secondary point mutations in KIT or PDGFRA that confer imatinib resistance are the most common mechanisms responsible for acquired resistance to imatinib.	imatinib	123-131	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	97-100
16143881-9	2005	Resistance to imatinib after an initial response has been reported; secondary point mutations in KIT or PDGFRA that confer imatinib resistance are the most common mechanisms responsible for acquired resistance to imatinib.	imatinib	123-131	platelet derived growth factor receptor alpha	Homo sapiens	104-110
16143881-9	2005	Resistance to imatinib after an initial response has been reported; secondary point mutations in KIT or PDGFRA that confer imatinib resistance are the most common mechanisms responsible for acquired resistance to imatinib.	imatinib	123-131	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	97-100
16143881-9	2005	Resistance to imatinib after an initial response has been reported; secondary point mutations in KIT or PDGFRA that confer imatinib resistance are the most common mechanisms responsible for acquired resistance to imatinib.	imatinib	123-131	platelet derived growth factor receptor alpha	Homo sapiens	104-110
16093432-0	2005	T315I-mutated Bcr-Abl in chronic myeloid leukemia and imatinib: insights from a computational study.	imatinib	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
16034302-16	2005	Results of ongoing pilot phase II studies may validate the efficacy of imatinib mesylate in malignant melanoma expressing KIT.	imatinib	71-88	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	122-125
16034306-1	2005	In order to determine whether imatinib mesylate (Gleevec), a tyrosine kinase inhibitor that binds the CD-117 (c-kit) receptor, may be of value in the treatment of malignant melanoma, an immunohistochemical analysis of 40 cases of primary and metastatic melanoma was undertaken.	imatinib	30-47	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	102-108
16034306-1	2005	In order to determine whether imatinib mesylate (Gleevec), a tyrosine kinase inhibitor that binds the CD-117 (c-kit) receptor, may be of value in the treatment of malignant melanoma, an immunohistochemical analysis of 40 cases of primary and metastatic melanoma was undertaken.	imatinib	30-47	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	110-115
15704192-5	2005	She was placed on a trial of imatinib mesylate based on tumor expression of c-KIT, a tyrosine kinase targeted by this drug.	imatinib	29-37	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	76-81
16093432-2	2005	Imatinib mesylate, a selective inhibitor of Bcr-Abl, has been successful in chronic myeloid leukemia clinical trials, but short-lived remissions are usually observed in blast crisis patients.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
16093432-6	2005	Here, we present the results obtained from the application of molecular dynamics simulations to the study of the interactions between T315I Bcr-Abl and imatinib.	imatinib	152-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
16383232-1	2005	OBJECTIVE: To explore the effect of Imatinib mesylate on proliferation, differentiation and apoptosis of leukemic Kasumi-1 cells bearing c-kit mutation.	imatinib	36-53	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	137-142
16383232-6	2005	Imatinib treatment induced a decrease in the mean fluorescence value of c-kit antigen, a progressive decline in S-phase cell fraction and an increase in G0/G1 cells.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	72-77
16383232-7	2005	Treatment with 5.00 micromol/L of imatinib for 72 h induced an increase in expression of myeloid surface protein CD11, CD13 and CD15, and for 24 h induced an increase in early apoptosis cells [from 9.04% to 86.84% (P < 0.05)].	imatinib	34-42	alanyl aminopeptidase, membrane	Homo sapiens	119-123
16383232-7	2005	Treatment with 5.00 micromol/L of imatinib for 72 h induced an increase in expression of myeloid surface protein CD11, CD13 and CD15, and for 24 h induced an increase in early apoptosis cells [from 9.04% to 86.84% (P < 0.05)].	imatinib	34-42	fucosyltransferase 4	Homo sapiens	128-132
16383232-9	2005	Tyrosine phosphorylation level of c-kit protein was decreased by Imatinib treatment.	imatinib	65-73	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	34-39
16383232-10	2005	CONCLUSION: Tyrosine kinase inhibitor Imatinib mesylate treatment could inhibit proliferation of Kasumi-1 cells which bear a c-kit mutation, induce differentiation, apoptosis and G0/G1 cells accumulation.	imatinib	38-55	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	125-130
15790786-0	2005	Activation mutations of human c-KIT resistant to imatinib mesylate are sensitive to the tyrosine kinase inhibitor PKC412.	imatinib	49-66	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	30-35
15790786-2	2005	Reports of the resistance of the kinase domain mutation D816V to the adenosine triphosphate (ATP)-competitive kinase inhibitor imatinib mesylate prompted us to characterize 14 c-KIT mutations reported in association with human hematologic malignancies for transforming activity in the murine hematopoietic cell line Ba/F3 and for sensitivity to the tyrosine kinase inhibitor PKC412.	imatinib	127-144	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	176-181
15790786-4	2005	c-KIT D816Y and D816V transformed cells were sensitive to PKC412 despite resistance to imatinib mesylate.	imatinib	87-104	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-5
15790786-7	2005	These findings suggest that PKC412 may be a useful therapeutic agent for c-KIT-positive malignancies harboring the imatinib mesylate-resistant D816V or D816Y activation mutations.	imatinib	115-132	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-78
15917650-0	2005	Inhibition of c-fms by imatinib: expanding the spectrum of treatment.	imatinib	23-31	colony stimulating factor 1 receptor	Homo sapiens	14-19
16255985-10	2005	STI571, specific inhibitor of p210 bcr/abl was added into the cultured fluid of K562 cells, then Western blotting and FCM were used to detect the protein expression of Shp-2 and p210 bcr/abl, and cell apoptosis.	imatinib	0-6	protein tyrosine phosphatase non-receptor type 11	Homo sapiens	168-173
16024645-7	2005	Indeed, ABL/ABL translocation enhances the expression levels of the NKG2D ligands on dendritic cells, which is counteracted by imatinib mesylate.	imatinib	127-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-11
16024645-7	2005	Indeed, ABL/ABL translocation enhances the expression levels of the NKG2D ligands on dendritic cells, which is counteracted by imatinib mesylate.	imatinib	127-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-15
16024645-7	2005	Indeed, ABL/ABL translocation enhances the expression levels of the NKG2D ligands on dendritic cells, which is counteracted by imatinib mesylate.	imatinib	127-144	killer cell lectin like receptor K1	Homo sapiens	68-73
15922853-1	2005	Receptor tyrosine kinase (RTK) targeted agents such as trastuzumab, imatinib, bevacizumab, and gefitinib inhibitors have illustrated the utility of targeting this protein class for treatment of selected cancers.	imatinib	68-76	ret proto-oncogene	Homo sapiens	0-24
15922853-1	2005	Receptor tyrosine kinase (RTK) targeted agents such as trastuzumab, imatinib, bevacizumab, and gefitinib inhibitors have illustrated the utility of targeting this protein class for treatment of selected cancers.	imatinib	68-76	ret proto-oncogene	Homo sapiens	26-29
15970668-0	2005	Chronic imatinib mesylate exposure leads to reduced intracellular drug accumulation by induction of the ABCG2 (BCRP) and ABCB1 (MDR1) drug transport pumps.	imatinib	8-25	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	104-109
15970668-0	2005	Chronic imatinib mesylate exposure leads to reduced intracellular drug accumulation by induction of the ABCG2 (BCRP) and ABCB1 (MDR1) drug transport pumps.	imatinib	8-25	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	111-115
15970668-0	2005	Chronic imatinib mesylate exposure leads to reduced intracellular drug accumulation by induction of the ABCG2 (BCRP) and ABCB1 (MDR1) drug transport pumps.	imatinib	8-25	ATP binding cassette subfamily B member 1	Homo sapiens	121-126
15970668-0	2005	Chronic imatinib mesylate exposure leads to reduced intracellular drug accumulation by induction of the ABCG2 (BCRP) and ABCB1 (MDR1) drug transport pumps.	imatinib	8-25	ATP binding cassette subfamily B member 1	Homo sapiens	128-132
15817679-9	2005	Continued detection of bcr-abl transcripts after 2 to 3 months on imatinib identifies patients who will ultimately experience relapse and in whom additional or alternative antileukemic treatment should be initiated.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
15930891-1	2005	We evaluated the in vitro activity of imatinib on BCR-ABL-positive and -negative tumor cells from patients with adult acute lymphoblastic leukemia (ALL), and investigated in vitro interactions between imatinib and conventional agents.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
15930891-4	2005	The BCR-ABL-positive samples were significantly (p < 0.05) more sensitive to imatinib than the BCR-ABL-negative at the concentrations 0.1, 1 and 10 muM.	imatinib	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
15930891-7	2005	The study confirms that drug sensitivity to imatinib is specific for BCR-ABL-positive samples.	imatinib	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
15949566-0	2005	Coexistence of different clonal populations harboring the b3a2 (p210) and e1a2 (p190) BCR-ABL1 fusion transcripts in chronic myelogenous leukemia resistant to imatinib.	imatinib	159-167	contactin associated protein 1	Homo sapiens	80-84
15949566-0	2005	Coexistence of different clonal populations harboring the b3a2 (p210) and e1a2 (p190) BCR-ABL1 fusion transcripts in chronic myelogenous leukemia resistant to imatinib.	imatinib	159-167	BCR activator of RhoGEF and GTPase	Homo sapiens	86-94
15949566-3	2005	After treatment with imatinib, the p210 transcript could not be detected, whereas p190 was still present 6 months after initiation of imatinib therapy and progression to blast phase.	imatinib	134-142	contactin associated protein 1	Homo sapiens	82-86
15949566-6	2005	Loss of normal BCR in one cell clone may contribute to the resistance to imatinib due to the lack of BCR mediated inhibition of BCR-ABL1.	imatinib	73-81	BCR activator of RhoGEF and GTPase	Homo sapiens	15-18
15970668-2	2005	We investigated whether the intended chronic oral administration of imatinib might lead to the induction of the intestinal ABC transport proteins ABCB1, ABCC1 (MRP1), ABCC2 (MRP2) and ABCG2.	imatinib	68-76	ATP binding cassette subfamily B member 1	Homo sapiens	146-151
15970668-2	2005	We investigated whether the intended chronic oral administration of imatinib might lead to the induction of the intestinal ABC transport proteins ABCB1, ABCC1 (MRP1), ABCC2 (MRP2) and ABCG2.	imatinib	68-76	ATP binding cassette subfamily C member 1	Homo sapiens	153-158
15970668-2	2005	We investigated whether the intended chronic oral administration of imatinib might lead to the induction of the intestinal ABC transport proteins ABCB1, ABCC1 (MRP1), ABCC2 (MRP2) and ABCG2.	imatinib	68-76	ATP binding cassette subfamily C member 1	Homo sapiens	160-164
15917650-3	2005	Imatinib also inhibits the c-abl, platelet derived growth factor receptor (PDGFR), abl-related gene and stem cell factor receptor, c-kit, protein tyrosine kinases.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-32
15970668-2	2005	We investigated whether the intended chronic oral administration of imatinib might lead to the induction of the intestinal ABC transport proteins ABCB1, ABCC1 (MRP1), ABCC2 (MRP2) and ABCG2.	imatinib	68-76	ATP binding cassette subfamily C member 2	Homo sapiens	167-172
15970668-2	2005	We investigated whether the intended chronic oral administration of imatinib might lead to the induction of the intestinal ABC transport proteins ABCB1, ABCC1 (MRP1), ABCC2 (MRP2) and ABCG2.	imatinib	68-76	ATP binding cassette subfamily C member 2	Homo sapiens	174-178
15970668-2	2005	We investigated whether the intended chronic oral administration of imatinib might lead to the induction of the intestinal ABC transport proteins ABCB1, ABCC1 (MRP1), ABCC2 (MRP2) and ABCG2.	imatinib	68-76	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	184-189
15970668-3	2005	Using Caco2 cells as an in vitro model for intestinal drug transport, we found that continuous exposure (up to 100 days) with imatinib (10 microM) specifically upregulates the expression of ABCG2 (maximal approximately 17-fold) and ABCB1 (maximal approximately 5-fold).	imatinib	126-134	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	190-195
15917650-3	2005	Imatinib also inhibits the c-abl, platelet derived growth factor receptor (PDGFR), abl-related gene and stem cell factor receptor, c-kit, protein tyrosine kinases.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	34-73
15917650-3	2005	Imatinib also inhibits the c-abl, platelet derived growth factor receptor (PDGFR), abl-related gene and stem cell factor receptor, c-kit, protein tyrosine kinases.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	75-80
15917650-3	2005	Imatinib also inhibits the c-abl, platelet derived growth factor receptor (PDGFR), abl-related gene and stem cell factor receptor, c-kit, protein tyrosine kinases.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-32
15917650-3	2005	Imatinib also inhibits the c-abl, platelet derived growth factor receptor (PDGFR), abl-related gene and stem cell factor receptor, c-kit, protein tyrosine kinases.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	131-136
15917650-4	2005	It is through inhibition of c-kit that imatinib is also used clinically in the treatment of gastrointestinal stromal tumours.	imatinib	39-47	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	28-33
15970668-3	2005	Using Caco2 cells as an in vitro model for intestinal drug transport, we found that continuous exposure (up to 100 days) with imatinib (10 microM) specifically upregulates the expression of ABCG2 (maximal approximately 17-fold) and ABCB1 (maximal approximately 5-fold).	imatinib	126-134	ATP binding cassette subfamily B member 1	Homo sapiens	232-237
15970668-5	2005	Importantly, chronic imatinib exposure of Caco2 cells resulted in a approximately 50% decrease in intracellular accumulation of imatinib, probably by enhanced ABCG2- and ABCB1-mediated efflux, as a result of upregulated expression of these drug pumps.	imatinib	21-29	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	159-164
15917650-5	2005	We have recently demonstrated that imatinib also specifically targets the macrophage colony stimulating factor receptor, c-fms, at therapeutic concentrations.	imatinib	35-43	colony stimulating factor 1 receptor	Homo sapiens	121-126
15970668-5	2005	Importantly, chronic imatinib exposure of Caco2 cells resulted in a approximately 50% decrease in intracellular accumulation of imatinib, probably by enhanced ABCG2- and ABCB1-mediated efflux, as a result of upregulated expression of these drug pumps.	imatinib	21-29	ATP binding cassette subfamily B member 1	Homo sapiens	170-175
15970668-5	2005	Importantly, chronic imatinib exposure of Caco2 cells resulted in a approximately 50% decrease in intracellular accumulation of imatinib, probably by enhanced ABCG2- and ABCB1-mediated efflux, as a result of upregulated expression of these drug pumps.	imatinib	128-136	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	159-164
15970668-5	2005	Importantly, chronic imatinib exposure of Caco2 cells resulted in a approximately 50% decrease in intracellular accumulation of imatinib, probably by enhanced ABCG2- and ABCB1-mediated efflux, as a result of upregulated expression of these drug pumps.	imatinib	128-136	ATP binding cassette subfamily B member 1	Homo sapiens	170-175
15917650-6	2005	Although this finding has important implications with regard to potential side effects in patients currently receiving imatinib therapy, these results suggest that imatinib may also be useful in the treatment of diseases where c-fms is implicated.	imatinib	164-172	colony stimulating factor 1 receptor	Homo sapiens	227-232
15970668-6	2005	Both ABCG2 and ABCB1 are normally expressed in the gastrointestinal tract and it might be anticipated that drug-induced upregulation of these intestinal pumps could reduce the oral bioavailability of imatinib, representing a novel mechanism of acquired pharmacokinetic drug resistance in cancer patients that are chronically treated with imatinib.	imatinib	200-208	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	5-10
15970668-6	2005	Both ABCG2 and ABCB1 are normally expressed in the gastrointestinal tract and it might be anticipated that drug-induced upregulation of these intestinal pumps could reduce the oral bioavailability of imatinib, representing a novel mechanism of acquired pharmacokinetic drug resistance in cancer patients that are chronically treated with imatinib.	imatinib	200-208	ATP binding cassette subfamily B member 1	Homo sapiens	15-20
15970668-6	2005	Both ABCG2 and ABCB1 are normally expressed in the gastrointestinal tract and it might be anticipated that drug-induced upregulation of these intestinal pumps could reduce the oral bioavailability of imatinib, representing a novel mechanism of acquired pharmacokinetic drug resistance in cancer patients that are chronically treated with imatinib.	imatinib	338-346	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	5-10
15933471-11	2005	Finally, gastrointestinal tumors harbor specific activating mutations in KIT or PDGFRA genes, which are responsive to imatinib.	imatinib	118-126	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
15970668-6	2005	Both ABCG2 and ABCB1 are normally expressed in the gastrointestinal tract and it might be anticipated that drug-induced upregulation of these intestinal pumps could reduce the oral bioavailability of imatinib, representing a novel mechanism of acquired pharmacokinetic drug resistance in cancer patients that are chronically treated with imatinib.	imatinib	338-346	ATP binding cassette subfamily B member 1	Homo sapiens	15-20
16000593-0	2005	AMN107, a novel aminopyrimidine inhibitor of Bcr-Abl, has in vitro activity against imatinib-resistant chronic myeloid leukemia.	imatinib	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
16000593-1	2005	Resistance to or intolerance of imatinib in patients with Philadelphia chromosome-positive chronic myelogenous leukemia (CML) has encouraged the development of more potent Bcr-Abl inhibitors.	imatinib	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-179
15933471-11	2005	Finally, gastrointestinal tumors harbor specific activating mutations in KIT or PDGFRA genes, which are responsive to imatinib.	imatinib	118-126	platelet derived growth factor receptor alpha	Homo sapiens	80-86
15946589-2	2005	Imatinib (STI571, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	105-108
15946589-2	2005	Imatinib (STI571, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-113
15946589-2	2005	Imatinib (STI571, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
15933471-12	2005	Specific mutations of the KIT and PDGFRA genes have now repeatedly been found correlated to response or resistance to imatinib.	imatinib	118-126	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	26-29
15933471-12	2005	Specific mutations of the KIT and PDGFRA genes have now repeatedly been found correlated to response or resistance to imatinib.	imatinib	118-126	platelet derived growth factor receptor alpha	Homo sapiens	34-40
15902298-0	2005	Synergistic activity of imatinib and 17-AAG in imatinib-resistant CML cells overexpressing BCR-ABL--Inhibition of P-glycoprotein function by 17-AAG.	imatinib	24-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
15946589-2	2005	Imatinib (STI571, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	124-130
15946589-2	2005	Imatinib (STI571, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	136-142
15946589-4	2005	The reported mechanism of imatinib resistance in GISTs involves missense mutation in the kinase domain of KIT, including Thr670Ile, Tyr823Asp, and Val654Ala.	imatinib	26-34	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	106-109
15985189-1	2005	OBJECTIVES: To assess the clinical and cost-effectiveness of imatinib in the treatment of unresectable and/or metastatic, KIT-positive, gastrointestinal stromal tumours (GISTs), relative to current standard treatments.	imatinib	61-69	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	122-125
15985189-20	2005	CONCLUSIONS: Evidence from uncontrolled studies indicates that the treatment with imatinib brings about clinically significant shrinkage of tumour mass in about half of patients with unresectable and/or metastatic, KIT-positive GIST.	imatinib	82-90	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	215-218
15996933-3	2005	The first example of such targeted therapy is imatinib-mesylate, an inhibitor of the BCR-ABL fusion gene that is found in more than 90% of patients with Philadelphia positive (Ph+) chronic myeloid leukemia (CML) and in 20-30% of those with Ph+ acute lymphoblastic leukemia (ALL).	imatinib	46-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
15800027-9	2005	Selective inhibitor of ERK, PD098059, and c-kit inhibitors, STI571 and PP1, suppressed the combined SCF and TNF-alpha-induced ICAM-1 expression.	imatinib	60-66	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	42-47
15800027-9	2005	Selective inhibitor of ERK, PD098059, and c-kit inhibitors, STI571 and PP1, suppressed the combined SCF and TNF-alpha-induced ICAM-1 expression.	imatinib	60-66	KIT ligand	Homo sapiens	100-103
15800027-9	2005	Selective inhibitor of ERK, PD098059, and c-kit inhibitors, STI571 and PP1, suppressed the combined SCF and TNF-alpha-induced ICAM-1 expression.	imatinib	60-66	tumor necrosis factor	Homo sapiens	108-117
15800027-9	2005	Selective inhibitor of ERK, PD098059, and c-kit inhibitors, STI571 and PP1, suppressed the combined SCF and TNF-alpha-induced ICAM-1 expression.	imatinib	60-66	intercellular adhesion molecule 1	Homo sapiens	126-132
15963852-0	2005	RNAi-mediated knockdown of P-glycoprotein using a transposon-based vector system durably restores imatinib sensitivity in imatinib-resistant CML cell lines.	imatinib	98-106	ATP binding cassette subfamily B member 1	Homo sapiens	27-41
15963852-0	2005	RNAi-mediated knockdown of P-glycoprotein using a transposon-based vector system durably restores imatinib sensitivity in imatinib-resistant CML cell lines.	imatinib	122-130	ATP binding cassette subfamily B member 1	Homo sapiens	27-41
15963852-3	2005	METHODS: We constructed a nonviral, transposon-based vector system for the stable knockdown of PgP in chronic myeloid leukemia cell lines resistant to imatinib and doxorubicin.	imatinib	151-159	ATP binding cassette subfamily B member 1	Homo sapiens	95-98
15963852-7	2005	CONCLUSION: Using chronic myeloid leukemia as a model, we show that PgP-mediated resistance to imatinib and anthracyclines can be durably reversed by nonviral, transposon-based knockdown of PgP in malignant cells.	imatinib	95-103	ATP binding cassette subfamily B member 1	Homo sapiens	68-71
15963852-7	2005	CONCLUSION: Using chronic myeloid leukemia as a model, we show that PgP-mediated resistance to imatinib and anthracyclines can be durably reversed by nonviral, transposon-based knockdown of PgP in malignant cells.	imatinib	95-103	ATP binding cassette subfamily B member 1	Homo sapiens	190-193
15976348-1	2005	AIMS: Neuroblastic tumours (NTs) have been shown to respond to imatinib treatment in vivo and in vitro, possibly via inactivating the c-kit receptor.	imatinib	63-71	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	134-139
15976348-2	2005	The purpose of this study was to identify gastrointestinal stromal tumour (GIST)-type c-kit gene associated mutations in exons 9, 11, 13, and 17 in NTs to recognise a subset of tumours that would probably respond to imatinib treatment.	imatinib	216-224	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	86-91
15976348-7	2005	Oncogenic activation of c-kit in NTs presumably differs from that of GISTs, which may influence their responsiveness to imatinib treatment.	imatinib	120-128	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	24-29
15902298-0	2005	Synergistic activity of imatinib and 17-AAG in imatinib-resistant CML cells overexpressing BCR-ABL--Inhibition of P-glycoprotein function by 17-AAG.	imatinib	24-32	ATP binding cassette subfamily B member 1	Homo sapiens	114-128
15902298-0	2005	Synergistic activity of imatinib and 17-AAG in imatinib-resistant CML cells overexpressing BCR-ABL--Inhibition of P-glycoprotein function by 17-AAG.	imatinib	24-32	N-methylpurine DNA glycosylase	Homo sapiens	144-147
15902298-0	2005	Synergistic activity of imatinib and 17-AAG in imatinib-resistant CML cells overexpressing BCR-ABL--Inhibition of P-glycoprotein function by 17-AAG.	imatinib	47-55	N-methylpurine DNA glycosylase	Homo sapiens	40-43
15902298-0	2005	Synergistic activity of imatinib and 17-AAG in imatinib-resistant CML cells overexpressing BCR-ABL--Inhibition of P-glycoprotein function by 17-AAG.	imatinib	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
15902298-0	2005	Synergistic activity of imatinib and 17-AAG in imatinib-resistant CML cells overexpressing BCR-ABL--Inhibition of P-glycoprotein function by 17-AAG.	imatinib	47-55	ATP binding cassette subfamily B member 1	Homo sapiens	114-128
15902298-1	2005	Overexpression of BCR-ABL and P-glycoprotein (Pgp) are two of the known mechanisms of imatinib resistance.	imatinib	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
15902298-1	2005	Overexpression of BCR-ABL and P-glycoprotein (Pgp) are two of the known mechanisms of imatinib resistance.	imatinib	86-94	ATP binding cassette subfamily B member 1	Homo sapiens	30-44
15902298-1	2005	Overexpression of BCR-ABL and P-glycoprotein (Pgp) are two of the known mechanisms of imatinib resistance.	imatinib	86-94	ATP binding cassette subfamily B member 1	Homo sapiens	46-49
15902298-3	2005	In imatinib-sensitive cells, combination index (CI) values obtained using the method of Chou and Talalay indicated additive (CI=1) or marginally antagonistic (CI>1) effects following simultaneous treatment with imatinib and 17-AAG.	imatinib	214-222	N-methylpurine DNA glycosylase	Homo sapiens	230-233
15902298-6	2005	Annexin V/propidium iodide staining showed that the activity of imatinib plus 17-AAG is mediated by apoptosis.	imatinib	64-72	annexin A5	Homo sapiens	0-9
15902298-7	2005	Combination treatment with imatinib plus 17-AAG was more effective in reducing the BCR-ABL protein level than 17-AAG alone.	imatinib	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
15902298-7	2005	Combination treatment with imatinib plus 17-AAG was more effective in reducing the BCR-ABL protein level than 17-AAG alone.	imatinib	27-35	N-methylpurine DNA glycosylase	Homo sapiens	113-116
15902298-8	2005	Monotherapy with 17-AAG decreased P-glycoprotein activity, which may increase intracellular imatinib levels and contribute to the sensitization of CML cells to imatinib.	imatinib	92-100	N-methylpurine DNA glycosylase	Homo sapiens	20-23
15902298-8	2005	Monotherapy with 17-AAG decreased P-glycoprotein activity, which may increase intracellular imatinib levels and contribute to the sensitization of CML cells to imatinib.	imatinib	92-100	ATP binding cassette subfamily B member 1	Homo sapiens	34-48
15902298-8	2005	Monotherapy with 17-AAG decreased P-glycoprotein activity, which may increase intracellular imatinib levels and contribute to the sensitization of CML cells to imatinib.	imatinib	160-168	N-methylpurine DNA glycosylase	Homo sapiens	20-23
15902298-8	2005	Monotherapy with 17-AAG decreased P-glycoprotein activity, which may increase intracellular imatinib levels and contribute to the sensitization of CML cells to imatinib.	imatinib	160-168	ATP binding cassette subfamily B member 1	Homo sapiens	34-48
15980865-3	2005	Additionally, release of CEV from the cell requires Abl- but not Src-family tyrosine kinases, and is blocked by STI-571 (Gleevec), an Abl-family kinase inhibitor used to treat chronic myelogenous leukemia in humans.	imatinib	112-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-137
15902298-9	2005	The results suggest that combination of imatinib and 17-AAG may be useful to overcome imatinib resistance in a clinical setting.	imatinib	86-94	N-methylpurine DNA glycosylase	Homo sapiens	56-59
15867198-0	2005	ABL mutations in late chronic phase chronic myeloid leukemia patients with up-front cytogenetic resistance to imatinib are associated with a greater likelihood of progression to blast crisis and shorter survival: a study by the GIMEMA Working Party on Chronic Myeloid Leukemia.	imatinib	110-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
15822120-3	2005	Because many GISTs display a definitive response to the KIT inhibitor imatinib, accurate diagnosis of these neoplasms is of great clinical importance.	imatinib	70-78	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	56-59
16018942-5	2005	Additional therapy with imatinib (Gleevec, Novartis Pharmaceuticals Corporation, East Hanover, NJ), an inhibitor of CD117 tyrosine kinase activity, treated recurrence in one patient and effected complete remission.	imatinib	24-32	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	116-121
16052979-11	2005	The imatinib mesylate is a selective inhibitor of the KIT tyrosine kinase receptor and it also blocks the activity of the PDGFRA kinase.	imatinib	4-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	54-57
15867198-1	2005	PURPOSE: Point mutations within the ABL kinase domain of the BCR-ABL gene have been associated with clinical resistance to imatinib mesylate in chronic myeloid leukemia (CML) patients.	imatinib	123-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-39
15867198-1	2005	PURPOSE: Point mutations within the ABL kinase domain of the BCR-ABL gene have been associated with clinical resistance to imatinib mesylate in chronic myeloid leukemia (CML) patients.	imatinib	123-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
15713800-6	2005	EML1-ABL1 and breakpoint cluster region (BCR)-ABL1 were equally sensitive to the tyrosine kinase inhibitor imatinib.	imatinib	107-115	EMAP like 1	Homo sapiens	0-4
15778488-6	2005	Simultaneous VEGF gene transfer and platelet-derived growth factor receptor inhibition with imatinib preserved respiratory epithelium and totally prevented luminal occlusion.	imatinib	92-100	vascular endothelial growth factor A	Rattus norvegicus	13-17
15713800-6	2005	EML1-ABL1 and breakpoint cluster region (BCR)-ABL1 were equally sensitive to the tyrosine kinase inhibitor imatinib.	imatinib	107-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	5-9
15713800-7	2005	These data further demonstrate the involvement of ABL1 fusions in the pathogenesis of T-ALL and identify EML1-ABL1 as a novel therapeutic target of imatinib.	imatinib	148-156	EMAP like 1	Homo sapiens	105-109
15713800-7	2005	These data further demonstrate the involvement of ABL1 fusions in the pathogenesis of T-ALL and identify EML1-ABL1 as a novel therapeutic target of imatinib.	imatinib	148-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-114
15958710-5	2005	Recent studies demonstrate that in vitro exposure of mobilized human CD34(+) progenitors to imatinib inhibits their differentiation into dendritic cells.	imatinib	92-100	CD34 molecule	Homo sapiens	69-73
15933063-0	2005	Analysis of total phosphotyrosine levels in CD34+ cells from CML patients to predict the response to imatinib mesylate treatment.	imatinib	101-118	CD34 molecule	Homo sapiens	44-48
15735062-1	2005	Imatinib mesylate is a potent and specific tyrosine kinase inhibitor against c-ABL, BCR-ABL, and c-KIT, and has been demonstrated to be highly active in chronic myeloid leukemia and gastrointestinal stromal tumors.	imatinib	0-17	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	77-82
15735062-1	2005	Imatinib mesylate is a potent and specific tyrosine kinase inhibitor against c-ABL, BCR-ABL, and c-KIT, and has been demonstrated to be highly active in chronic myeloid leukemia and gastrointestinal stromal tumors.	imatinib	0-17	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	97-102
15735062-3	2005	Imatinib inhibited the growth of primary murine lung fibroblasts and the autophosphorylation of PDGFR-beta induced by PDGF.	imatinib	0-8	platelet derived growth factor receptor, beta polypeptide	Mus musculus	96-106
15899391-0	2005	BCR-ABL gene amplification and overexpression in a patient with chronic myeloid leukemia treated with imatinib.	imatinib	102-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
15896338-0	2005	Relative importance of apoptosis and cell cycle blockage in the synergistic effect of combined R115777 and imatinib treatment in BCR/ABL-positive cell lines.	imatinib	107-115	BCR activator of RhoGEF and GTPase	Homo sapiens	129-132
15896338-1	2005	The combination of imatinib and a farnesyltransferase inhibitor might be effective for reducing the number of BCR/ABL-positive leukemia cells.	imatinib	19-27	BCR activator of RhoGEF and GTPase	Homo sapiens	110-113
15818402-0	2005	Role of poly(ADP-ribose) polymerase activity in imatinib mesylate-induced cell death.	imatinib	48-65	poly(ADP-ribose) polymerase 1	Homo sapiens	8-35
15818402-1	2005	Imatinib targets Bcr-Abl, the causative event of chronic myelogenous leukemia (CML), and addresses leukemic cells to growth arrest and cell death.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
15818402-3	2005	We investigated the role of poly(ADP-ribose) polymerase (PARP) activity in imatinib-induced cell death in Bcr-Abl-positive cells.	imatinib	75-83	poly(ADP-ribose) polymerase 1	Homo sapiens	28-55
15818402-3	2005	We investigated the role of poly(ADP-ribose) polymerase (PARP) activity in imatinib-induced cell death in Bcr-Abl-positive cells.	imatinib	75-83	poly(ADP-ribose) polymerase 1	Homo sapiens	57-61
15818402-3	2005	We investigated the role of poly(ADP-ribose) polymerase (PARP) activity in imatinib-induced cell death in Bcr-Abl-positive cells.	imatinib	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
15818402-5	2005	The effect of imatinib on PAR can be mimicked by inhibition of phosphatidylinositol 3-kinase (PI3-K) implicating a central role of the PI3-K pathway in Bcr-Abl-mediated inhibition of PAR.	imatinib	14-22	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	63-92
15894928-5	2005	STI 571 (imatinib mesylate [Gleevec]) might be an effective therapy in this case, since Gleevec targets both PDGFRA and c-kit oncoproteins.	imatinib	0-7	platelet derived growth factor receptor alpha	Homo sapiens	109-115
15894928-5	2005	STI 571 (imatinib mesylate [Gleevec]) might be an effective therapy in this case, since Gleevec targets both PDGFRA and c-kit oncoproteins.	imatinib	0-7	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	120-125
15894928-5	2005	STI 571 (imatinib mesylate [Gleevec]) might be an effective therapy in this case, since Gleevec targets both PDGFRA and c-kit oncoproteins.	imatinib	9-26	platelet derived growth factor receptor alpha	Homo sapiens	109-115
15894928-5	2005	STI 571 (imatinib mesylate [Gleevec]) might be an effective therapy in this case, since Gleevec targets both PDGFRA and c-kit oncoproteins.	imatinib	9-26	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	120-125
15899391-1	2005	Imatinib mesylate was designed as an inhibitor targeting the BCR-ABL tyrosine kinase, the molecular counterpart of the Philadelphia translocation t(9;22)(q34;q11).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
15899391-7	2005	We give further evidence that the genomic BCR-ABL amplification results in an increased level of BCR-ABL transcript linking two potent mechanisms of resistance against imatinib treatment.	imatinib	168-176	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
15899391-7	2005	We give further evidence that the genomic BCR-ABL amplification results in an increased level of BCR-ABL transcript linking two potent mechanisms of resistance against imatinib treatment.	imatinib	168-176	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
15911092-6	2005	RESULTS: The use of STI 571-mediated inhibition impaired the tyrosine phosphorylation of KIT(Asn822Lys) and its association with the p85 subunit of phosphatidylinositol 3"-kinase (p85PI3K).	imatinib	20-27	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	89-92
15930265-0	2005	In vitro activity of Bcr-Abl inhibitors AMN107 and BMS-354825 against clinically relevant imatinib-resistant Abl kinase domain mutants.	imatinib	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
15930265-0	2005	In vitro activity of Bcr-Abl inhibitors AMN107 and BMS-354825 against clinically relevant imatinib-resistant Abl kinase domain mutants.	imatinib	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-28
15930265-1	2005	Imatinib, a Bcr-Abl tyrosine kinase inhibitor, is a highly effective therapy for patients with chronic myelogenous leukemia (CML).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
15930265-3	2005	The most common mechanism of acquired imatinib resistance has been traced to Bcr-Abl kinase domain mutations with decreased imatinib sensitivity.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
15930265-3	2005	The most common mechanism of acquired imatinib resistance has been traced to Bcr-Abl kinase domain mutations with decreased imatinib sensitivity.	imatinib	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
15930265-4	2005	Thus, alternate Bcr-Abl kinase inhibitors that have activity against imatinib-resistant mutants would be useful for patients who relapse on imatinib therapy.	imatinib	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
15930265-4	2005	Thus, alternate Bcr-Abl kinase inhibitors that have activity against imatinib-resistant mutants would be useful for patients who relapse on imatinib therapy.	imatinib	140-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
15869901-2	2005	The pioneering work with the ABL inhibitor imatinib (Glivec, Gleevec) was rapidly extended to other types of leukemias as well as solid tumors, which stimulated the development of a variety of new tyrosine kinase inhibitors.	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-32
15784722-5	2005	Moreover, we observed potent cytoreductive effects of rapamycin in a patient with imatinib-resistant Bcr-Abl+ leukemia.	imatinib	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
15818402-5	2005	The effect of imatinib on PAR can be mimicked by inhibition of phosphatidylinositol 3-kinase (PI3-K) implicating a central role of the PI3-K pathway in Bcr-Abl-mediated inhibition of PAR.	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-159
15818402-8	2005	In conclusion, our results suggest that in addition to the well-documented caspase-dependent pathway, imatinib also induces a PARP-mediated death process.	imatinib	102-110	poly(ADP-ribose) polymerase 1	Homo sapiens	126-130
15911092-8	2005	STI 571 inhibited the KIT-mediated proliferation of Kasumi-1 cells in a dose-dependent manner.	imatinib	0-7	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	22-25
15800674-0	2005	Can application of serine protease inhibitors TPCK and TLCK provide evidence for possible involvement of serine protease Omi/HtrA2 in imatinib mesylate-induced cell death of BCR-ABL-positive human leukemia cells?	imatinib	134-151	HtrA serine peptidase 2	Homo sapiens	125-130
15930355-10	2005	That acquired resistance to imatinib in GIST commonly occurs via secondary gene mutation in the KIT kinase domain has implications for strategies to delay or prevent imatinib resistance and to employ newer targeted therapies.	imatinib	28-36	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	96-99
15930355-10	2005	That acquired resistance to imatinib in GIST commonly occurs via secondary gene mutation in the KIT kinase domain has implications for strategies to delay or prevent imatinib resistance and to employ newer targeted therapies.	imatinib	166-174	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	96-99
15939196-2	2005	The management of GISTs has been altered significantly by the development of imatinib mesylate, a tyrosine kinase inhibitor with activity against KIT and platelet-derived growth factor receptors.	imatinib	77-94	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	146-149
15953881-9	2005	The mechanism by which imatinib induces gynecomastia and hydrocele is thought to be associated with an inhibition of c-KIT and platelet-derive growth factor.	imatinib	23-31	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	117-122
15815728-1	2005	Imatinib mesylate, a Bcr-Abl kinase inhibitor, has been very successful in the treatment of chronic myelogenous leukemia (CML).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
15815728-5	2005	Bcr-Abl kinase inhibition by imatinib did not enhance sensitivity of CML progenitors to Ara-C, VP-16, ceramide, radiation or TRAIL-induced apoptosis but did enhance arsenic and TNFalpha-induced apoptosis.	imatinib	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
15815728-6	2005	We further demonstrate that apoptosis was restricted to dividing cells, whereas nonproliferating BCR/ABL(+) CD34(+) cells were resistant to apoptosis induced by imatinib, Ara-C or arsenic, either alone or in combination.	imatinib	161-169	CD34 molecule	Homo sapiens	108-112
15895440-6	2005	Imatinib, an inhibitor of KIT kinase activity, is now the standard front-line therapy for patients with advanced GIST.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	26-29
15800674-0	2005	Can application of serine protease inhibitors TPCK and TLCK provide evidence for possible involvement of serine protease Omi/HtrA2 in imatinib mesylate-induced cell death of BCR-ABL-positive human leukemia cells?	imatinib	134-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-181
15815724-0	2005	Imatinib induces apoptosis in CLL lymphocytes with high expression of Par-4.	imatinib	0-8	Prader Willi/Angelman region RNA 4	Homo sapiens	70-75
15770664-4	2005	In JURL-MK1 cells, the apoptosis is faster in comparison with K562 cells: the caspase-3 activity reaches the peak value (20 to 30 fold of the control) after about 40 h and the apoptosis proceeds to its culmination point, the DNA fragmentation, within 48 h following 1 microM Imatinib addition.	imatinib	275-283	caspase 3	Homo sapiens	78-87
15657179-7	2005	PD166326 also prolonged the survival of mice with imatinib mesylate-resistant CML induced by the Bcr/Abl mutants P210/H396P and P210/M351T.	imatinib	50-67	BCR activator of RhoGEF and GTPase	Mus musculus	97-104
15870711-1	2005	Imatinib mesylate (IM) is a tyrosine kinase inhibitor, which inhibits phosphorylation of downstream proteins involved in BCR-ABL signal transduction.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
15870711-1	2005	Imatinib mesylate (IM) is a tyrosine kinase inhibitor, which inhibits phosphorylation of downstream proteins involved in BCR-ABL signal transduction.	imatinib	19-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
15665113-4	2005	Here, we examined the effect of OSU-03012, a celecoxib-derived phosphoinositide-dependent kinase-1 (PDK-1) inhibitor, on imatinib mesylate-induced apoptosis in 2 clinically relevant breakpoint cluster region (Bcr)-Abl mutant cell lines, Ba/F3p210(E255K) and Ba/F3p210(T315I).	imatinib	121-138	pyruvate dehydrogenase kinase 1	Homo sapiens	63-98
15665113-4	2005	Here, we examined the effect of OSU-03012, a celecoxib-derived phosphoinositide-dependent kinase-1 (PDK-1) inhibitor, on imatinib mesylate-induced apoptosis in 2 clinically relevant breakpoint cluster region (Bcr)-Abl mutant cell lines, Ba/F3p210(E255K) and Ba/F3p210(T315I).	imatinib	121-138	pyruvate dehydrogenase kinase 1	Homo sapiens	100-105
15665113-4	2005	Here, we examined the effect of OSU-03012, a celecoxib-derived phosphoinositide-dependent kinase-1 (PDK-1) inhibitor, on imatinib mesylate-induced apoptosis in 2 clinically relevant breakpoint cluster region (Bcr)-Abl mutant cell lines, Ba/F3p210(E255K) and Ba/F3p210(T315I).	imatinib	121-138	BCR activator of RhoGEF and GTPase	Homo sapiens	182-207
15665113-9	2005	Together these data provide a novel therapeutic strategy to overcome imatinib mesylate resistance, especially with the Abl mutant T315I.	imatinib	69-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-122
15665113-0	2005	Synergistic interactions between imatinib mesylate and the novel phosphoinositide-dependent kinase-1 inhibitor OSU-03012 in overcoming imatinib mesylate resistance.	imatinib	135-152	pyruvate dehydrogenase kinase 1	Homo sapiens	65-100
15812822-0	2005	Imatinib mesylate lacks activity in small cell lung carcinoma expressing c-kit protein: a phase II clinical trial.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-78
15665113-1	2005	Resistance to the Ableson protein tyrosine (Abl) kinase inhibitor imatinib mesylate has become a critical issue for patients in advanced phases of chronic myelogenous leukemia.	imatinib	66-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-21
15665113-2	2005	Imatinib-resistant tumor cells develop, in part, as a result of point mutations within the Abl kinase domain.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-94
15665113-3	2005	As protein kinase B (Akt) plays a pivotal role in Abl oncogene-mediated cell survival, we hypothesize that concurrent inhibition of Akt will sensitize resistant cells to the residual apoptotic activity of imatinib mesylate, thereby overcoming the resistance.	imatinib	205-222	AKT serine/threonine kinase 1	Homo sapiens	21-24
15665113-3	2005	As protein kinase B (Akt) plays a pivotal role in Abl oncogene-mediated cell survival, we hypothesize that concurrent inhibition of Akt will sensitize resistant cells to the residual apoptotic activity of imatinib mesylate, thereby overcoming the resistance.	imatinib	205-222	AKT serine/threonine kinase 1	Homo sapiens	132-135
15812822-1	2005	BACKGROUND: Imatinib inhibits the c-kit tyrosine kinase, which, accounts for its activity in gastrointestinal stromal tumors.	imatinib	12-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	34-39
15812822-3	2005	The authors conducted a Phase II single-institution study of imatinib in patients with recurrent SCLC whose tumor specimens expressed c-kit protein.	imatinib	61-69	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	134-139
16158966-1	2005	BACKGROUND: c-kit expression by immunohistochemistry has been utilized to identify cancer patients who can be treated with imatinib-mesylate.	imatinib	123-140	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	12-17
15618280-8	2005	STI-571 also significantly attenuated PDGF-BB-induced phosphorylation of PDGFR-beta, MEK1/2, and Akt in activated HSC.	imatinib	0-7	platelet derived growth factor receptor beta	Rattus norvegicus	73-83
15618280-8	2005	STI-571 also significantly attenuated PDGF-BB-induced phosphorylation of PDGFR-beta, MEK1/2, and Akt in activated HSC.	imatinib	0-7	mitogen activated protein kinase kinase 1	Rattus norvegicus	85-91
15618280-8	2005	STI-571 also significantly attenuated PDGF-BB-induced phosphorylation of PDGFR-beta, MEK1/2, and Akt in activated HSC.	imatinib	0-7	AKT serine/threonine kinase 1	Rattus norvegicus	97-100
15897563-2	2005	Imatinib mesylate, a tyrosine kinase inhibitor, has activity against GISTs that contain oncogenic mutations of KIT.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	111-114
15897563-3	2005	In this study, KIT and PDGFRalpha mutation status was analyzed and protein modeling approaches were used to assess the potential effect of KIT mutations in response to imatinib therapy.	imatinib	168-176	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	139-142
15637141-0	2005	Macrophage colony-stimulating factor receptor c-fms is a novel target of imatinib.	imatinib	73-81	colony stimulating factor 1	Homo sapiens	0-36
15786421-11	2005	Treatment with STI571 down-regulated the expression of PDGF-BB and PDGFR-beta in tumor cells and decreased the production of phosphorylated PDGFR-beta and phosphorylated Akt.	imatinib	15-21	platelet derived growth factor receptor beta	Homo sapiens	67-77
15786421-11	2005	Treatment with STI571 down-regulated the expression of PDGF-BB and PDGFR-beta in tumor cells and decreased the production of phosphorylated PDGFR-beta and phosphorylated Akt.	imatinib	15-21	platelet derived growth factor receptor beta	Homo sapiens	140-150
15786421-11	2005	Treatment with STI571 down-regulated the expression of PDGF-BB and PDGFR-beta in tumor cells and decreased the production of phosphorylated PDGFR-beta and phosphorylated Akt.	imatinib	15-21	AKT serine/threonine kinase 1	Homo sapiens	170-173
15786421-12	2005	Furthermore, treatment with STI571 inhibited the expression of PDGFR-beta in stromal cells.	imatinib	28-34	platelet derived growth factor receptor beta	Homo sapiens	63-73
15786421-13	2005	CONCLUSIONS: STI571 was an effective chemosensitizer of antitumor drugs, such as 5-FU and paclitaxel for gastric carcinoma, targeting the PDGF/PDGFR-signaling pathway of tumor cells and stromal cells in disease progression and angiogenesis.	imatinib	13-19	platelet derived growth factor receptor beta	Homo sapiens	143-148
15921304-6	2005	On the basis of FIP1L1-PDGFRa fusion gene hypereosinophilic syndrome would be classified as a clonal disease and in the FIP1L1-PDGFRa positive cases the tyrosine kinase inhibitor imatinib mesylate (Glivec) would be effective.	imatinib	179-196	factor interacting with PAPOLA and CPSF1	Homo sapiens	120-126
15921304-6	2005	On the basis of FIP1L1-PDGFRa fusion gene hypereosinophilic syndrome would be classified as a clonal disease and in the FIP1L1-PDGFRa positive cases the tyrosine kinase inhibitor imatinib mesylate (Glivec) would be effective.	imatinib	179-196	platelet derived growth factor receptor alpha	Homo sapiens	127-133
15921309-2	2005	Imatinib is a targeted molecule capable to inhibit tyrosine kinase active in the production of abl-bcr protein responsible for the translocation of 9 and 22 chromosome in chronic myeloid leukemia.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
15872385-2	2005	Availability of KIT- and PDGFRA-inhibitor drug imatinib mesylate has greatly raised the interest for these tumors.	imatinib	47-64	platelet derived growth factor receptor alpha	Pan troglodytes	25-31
15626746-0	2005	Identification of mcl-1 as a BCR/ABL-dependent target in chronic myeloid leukemia (CML): evidence for cooperative antileukemic effects of imatinib and mcl-1 antisense oligonucleotides.	imatinib	138-146	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	18-23
15626746-4	2005	The BCR/ABL inhibitor imatinib (=STI571) decreased the expression of MCL-1 in these cells.	imatinib	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
15626746-4	2005	The BCR/ABL inhibitor imatinib (=STI571) decreased the expression of MCL-1 in these cells.	imatinib	22-30	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	69-74
15626746-4	2005	The BCR/ABL inhibitor imatinib (=STI571) decreased the expression of MCL-1 in these cells.	imatinib	33-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
15626746-4	2005	The BCR/ABL inhibitor imatinib (=STI571) decreased the expression of MCL-1 in these cells.	imatinib	33-39	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	69-74
15626746-10	2005	Moreover, the mcl-1 ASO was found to synergize with imatinib in producing growth inhibition in these cells.	imatinib	52-60	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	14-19
15657178-4	2005	After the first imatinib cycle, the median breakpoint cluster region-Abelson oncogene locus (BCR-ABL)/ABL ratios decreased by 0.77 log in 25 (86.2%) responders, and their BCR-ABL/ABL ratios decreased further by 0.34 log after the second imatinib cycle, which included 7 molecular CR.	imatinib	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-91
15657178-4	2005	After the first imatinib cycle, the median breakpoint cluster region-Abelson oncogene locus (BCR-ABL)/ABL ratios decreased by 0.77 log in 25 (86.2%) responders, and their BCR-ABL/ABL ratios decreased further by 0.34 log after the second imatinib cycle, which included 7 molecular CR.	imatinib	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
15657178-4	2005	After the first imatinib cycle, the median breakpoint cluster region-Abelson oncogene locus (BCR-ABL)/ABL ratios decreased by 0.77 log in 25 (86.2%) responders, and their BCR-ABL/ABL ratios decreased further by 0.34 log after the second imatinib cycle, which included 7 molecular CR.	imatinib	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-100
15657178-4	2005	After the first imatinib cycle, the median breakpoint cluster region-Abelson oncogene locus (BCR-ABL)/ABL ratios decreased by 0.77 log in 25 (86.2%) responders, and their BCR-ABL/ABL ratios decreased further by 0.34 log after the second imatinib cycle, which included 7 molecular CR.	imatinib	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-178
15657178-4	2005	After the first imatinib cycle, the median breakpoint cluster region-Abelson oncogene locus (BCR-ABL)/ABL ratios decreased by 0.77 log in 25 (86.2%) responders, and their BCR-ABL/ABL ratios decreased further by 0.34 log after the second imatinib cycle, which included 7 molecular CR.	imatinib	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-105
15657178-4	2005	After the first imatinib cycle, the median breakpoint cluster region-Abelson oncogene locus (BCR-ABL)/ABL ratios decreased by 0.77 log in 25 (86.2%) responders, and their BCR-ABL/ABL ratios decreased further by 0.34 log after the second imatinib cycle, which included 7 molecular CR.	imatinib	237-245	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
15850831-4	2005	Based on recent reports demonstrating that c-ABL phosphorylates hTERT and thereby inhibits hTERT activity, a direct effect of imatinib on hTERT activity leading to telomere elongation in BCR-ABL-positive cells has been proposed by others.	imatinib	126-134	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	43-48
15850831-4	2005	Based on recent reports demonstrating that c-ABL phosphorylates hTERT and thereby inhibits hTERT activity, a direct effect of imatinib on hTERT activity leading to telomere elongation in BCR-ABL-positive cells has been proposed by others.	imatinib	126-134	telomerase reverse transcriptase	Homo sapiens	64-69
15850831-4	2005	Based on recent reports demonstrating that c-ABL phosphorylates hTERT and thereby inhibits hTERT activity, a direct effect of imatinib on hTERT activity leading to telomere elongation in BCR-ABL-positive cells has been proposed by others.	imatinib	126-134	telomerase reverse transcriptase	Homo sapiens	91-96
15850831-4	2005	Based on recent reports demonstrating that c-ABL phosphorylates hTERT and thereby inhibits hTERT activity, a direct effect of imatinib on hTERT activity leading to telomere elongation in BCR-ABL-positive cells has been proposed by others.	imatinib	126-134	telomerase reverse transcriptase	Homo sapiens	91-96
15850831-7	2005	RESULTS: When BaF3 and BaF3p185 cells were treated with imatinib (the latter being rescued with IL-3), no effect on either telomerase activity or telomere length was observed.	imatinib	56-64	interleukin 3	Mus musculus	96-100
15918555-9	2005	Interestingly, recent molecular-targeted drugs, such as imatinib and gefitinib, were very recently found to be substrates for P-glycoprotein and/or BCRP.	imatinib	56-64	ATP binding cassette subfamily B member 1	Homo sapiens	126-140
15918555-9	2005	Interestingly, recent molecular-targeted drugs, such as imatinib and gefitinib, were very recently found to be substrates for P-glycoprotein and/or BCRP.	imatinib	56-64	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	148-152
15966213-1	2005	Imatinib, an inhibitor of the tyrosine kinase activity of c-kit, was used as an adjuvant chemotherapy in two patients who underwent curative surgery for recurrent gastrointestinal stromal tumors.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	58-63
15722647-2	2005	Imatinib is a novel and potent inhibitor of c-Kit tyrosine kinase and a new therapeutic agent for gastrointestinal stromal tumors (GIST) which presumably arise from ICCs.	imatinib	0-8	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	44-49
15722647-9	2005	These results demonstrate that imatinib affects bowel contractions, and suggest that the c-Kit signaling of ICCs plays an essential role in the spontaneous movements in circular muscles of the mouse small intestine.	imatinib	31-39	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	89-94
16479834-0	2005	[Oncogene Fip1-likeL/PDGFRalpha as a target for imatinib in patients with hypereosinophilic syndrome and chronic eosinophilic leukemia.	imatinib	48-56	factor interacting with PAPOLA and CPSF1	Homo sapiens	10-14
16479834-0	2005	[Oncogene Fip1-likeL/PDGFRalpha as a target for imatinib in patients with hypereosinophilic syndrome and chronic eosinophilic leukemia.	imatinib	48-56	platelet derived growth factor receptor alpha	Homo sapiens	21-31
16042351-10	2005	For the first time the role of STI571 was investigated, a specific inhibitor of BCR/ABL oncogenic protein approved for leukemia treatment in the NHEJ pathway.	imatinib	31-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
15846297-1	2005	This two-centre phase-II trial aimed at investigating the efficacy of imatinib in metastasised melanoma patients in correlation to the tumour expression profile of the imatinib targets c-kit and platelet-derived growth factor receptor (PDGF-R).	imatinib	70-78	platelet derived growth factor receptor beta	Homo sapiens	195-234
15846297-1	2005	This two-centre phase-II trial aimed at investigating the efficacy of imatinib in metastasised melanoma patients in correlation to the tumour expression profile of the imatinib targets c-kit and platelet-derived growth factor receptor (PDGF-R).	imatinib	70-78	platelet derived growth factor receptor beta	Homo sapiens	236-242
15846297-1	2005	This two-centre phase-II trial aimed at investigating the efficacy of imatinib in metastasised melanoma patients in correlation to the tumour expression profile of the imatinib targets c-kit and platelet-derived growth factor receptor (PDGF-R).	imatinib	168-176	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	185-190
15637141-0	2005	Macrophage colony-stimulating factor receptor c-fms is a novel target of imatinib.	imatinib	73-81	colony stimulating factor 1 receptor	Homo sapiens	46-51
15637141-2	2005	Imatinib also inhibits the c-abl, platelet-derived growth factor (PDGF) receptor, abl-related gene (ARG) and stem-cell factor (SCF) receptor tyrosine kinases, and has been used clinically to inhibit the growth of malignant cells in patients with CML and gastrointestinal stromal tumors (GISTs).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-32
15637141-2	2005	Imatinib also inhibits the c-abl, platelet-derived growth factor (PDGF) receptor, abl-related gene (ARG) and stem-cell factor (SCF) receptor tyrosine kinases, and has been used clinically to inhibit the growth of malignant cells in patients with CML and gastrointestinal stromal tumors (GISTs).	imatinib	0-8	KIT ligand	Homo sapiens	109-125
15604220-0	2005	Synergy between imatinib and mycophenolic acid in inducing apoptosis in cell lines expressing Bcr-Abl.	imatinib	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
15637141-2	2005	Imatinib also inhibits the c-abl, platelet-derived growth factor (PDGF) receptor, abl-related gene (ARG) and stem-cell factor (SCF) receptor tyrosine kinases, and has been used clinically to inhibit the growth of malignant cells in patients with CML and gastrointestinal stromal tumors (GISTs).	imatinib	0-8	KIT ligand	Homo sapiens	127-130
15604220-2	2005	Imatinib mesylate, a specific Bcr-Abl tyrosine kinase inhibitor, has been highly successful in the treatment of chronic myelogenous leukemia (CML).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
15637141-5	2005	Here, we demonstrate for the first time that imatinib targets the macrophage colony-stimulating factor (M-CSF) receptor c-fms.	imatinib	45-53	colony stimulating factor 1	Homo sapiens	66-102
15604220-5	2005	Studies of signaling pathways downstream of Bcr-Abl demonstrated that the addition of MPA to imatinib reduced the phosphorylation of both Stat5 and Lyn, a Src kinase family member.	imatinib	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
15604220-5	2005	Studies of signaling pathways downstream of Bcr-Abl demonstrated that the addition of MPA to imatinib reduced the phosphorylation of both Stat5 and Lyn, a Src kinase family member.	imatinib	93-101	signal transducer and activator of transcription 5A	Homo sapiens	138-143
15637141-5	2005	Here, we demonstrate for the first time that imatinib targets the macrophage colony-stimulating factor (M-CSF) receptor c-fms.	imatinib	45-53	colony stimulating factor 1	Homo sapiens	104-109
15604220-5	2005	Studies of signaling pathways downstream of Bcr-Abl demonstrated that the addition of MPA to imatinib reduced the phosphorylation of both Stat5 and Lyn, a Src kinase family member.	imatinib	93-101	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	148-151
15637141-5	2005	Here, we demonstrate for the first time that imatinib targets the macrophage colony-stimulating factor (M-CSF) receptor c-fms.	imatinib	45-53	colony stimulating factor 1 receptor	Homo sapiens	120-125
15637141-6	2005	Phosphorylation of c-fms was inhibited by therapeutic concentrations of imatinib, and this was not due to down-regulation in c-fms expression.	imatinib	72-80	colony stimulating factor 1 receptor	Homo sapiens	19-24
15637141-7	2005	Imatinib was also found to inhibit M-CSF-induced proliferation of a cytokine-dependent cell line, further supporting the hypothesis that imatinib affects the growth and development of monocyte and/or macrophages through inhibition of c-fms signaling.	imatinib	0-8	colony stimulating factor 1	Homo sapiens	35-40
15637141-7	2005	Imatinib was also found to inhibit M-CSF-induced proliferation of a cytokine-dependent cell line, further supporting the hypothesis that imatinib affects the growth and development of monocyte and/or macrophages through inhibition of c-fms signaling.	imatinib	0-8	colony stimulating factor 1 receptor	Homo sapiens	234-239
15637141-7	2005	Imatinib was also found to inhibit M-CSF-induced proliferation of a cytokine-dependent cell line, further supporting the hypothesis that imatinib affects the growth and development of monocyte and/or macrophages through inhibition of c-fms signaling.	imatinib	137-145	colony stimulating factor 1	Homo sapiens	35-40
15747376-0	2005	Response and resistance in 300 patients with BCR-ABL-positive leukemias treated with imatinib in a single center: a 4.5-year follow-up.	imatinib	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
15637141-7	2005	Imatinib was also found to inhibit M-CSF-induced proliferation of a cytokine-dependent cell line, further supporting the hypothesis that imatinib affects the growth and development of monocyte and/or macrophages through inhibition of c-fms signaling.	imatinib	137-145	colony stimulating factor 1 receptor	Homo sapiens	234-239
15637141-9	2005	Imatinib should now be assessed for activity in diseases where c-fms activation is implicated, including breast and ovarian cancer and inflammatory conditions.	imatinib	0-8	colony stimulating factor 1 receptor	Homo sapiens	63-68
15840387-0	2005	Imatinib (STI571) induces DNA damage in BCR/ABL-expressing leukemic cells but not in normal lymphocytes.	imatinib	0-8	BCR activator of RhoGEF and GTPase	Homo sapiens	40-43
15840387-0	2005	Imatinib (STI571) induces DNA damage in BCR/ABL-expressing leukemic cells but not in normal lymphocytes.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-47
15840387-0	2005	Imatinib (STI571) induces DNA damage in BCR/ABL-expressing leukemic cells but not in normal lymphocytes.	imatinib	10-16	BCR activator of RhoGEF and GTPase	Homo sapiens	40-43
15840387-0	2005	Imatinib (STI571) induces DNA damage in BCR/ABL-expressing leukemic cells but not in normal lymphocytes.	imatinib	10-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-47
15840387-3	2005	Using the alkaline comet assay we showed that STI571 at concentrations ranging from 0.2 to 2 microM induced DNA damage in human leukemic K562 and BV173 cells expressing the BCR/ABL oncogene, whereas it had no effect in normal human lymphocytes and leukemic CCRF-CEM cells without the expression of BCR/ABL.	imatinib	46-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	173-180
15840387-3	2005	Using the alkaline comet assay we showed that STI571 at concentrations ranging from 0.2 to 2 microM induced DNA damage in human leukemic K562 and BV173 cells expressing the BCR/ABL oncogene, whereas it had no effect in normal human lymphocytes and leukemic CCRF-CEM cells without the expression of BCR/ABL.	imatinib	46-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	298-305
15815732-3	2005	Imatinib mesylate is a recently introduced KIT tyrosine kinase inhibitor with effect on metastatic GIST.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	43-46
15805252-0	2005	The effect of Bcrp1 (Abcg2) on the in vivo pharmacokinetics and brain penetration of imatinib mesylate (Gleevec): implications for the use of breast cancer resistance protein and P-glycoprotein inhibitors to enable the brain penetration of imatinib in patients.	imatinib	85-102	BCR pseudogene 1	Homo sapiens	14-19
15618470-5	2005	Mutations in the kinase domain (KD) of BCR-ABL that impair imatinib binding have been identified as the leading cause of resistance.	imatinib	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
15692843-2	2005	It was hoped that the introduction of imatinib mesylate (IM), a specific tyrosine kinase inhibitor that targets the Bcr-Abl oncogene product, would provide long-term remission or even cure for those patients without a donor, but studies have shown that IM does not eliminate leukaemic stem cells in CML patients.	imatinib	38-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
15746584-2	2005	DFSPs have specific chromosomal abnormalities involving the platelet-derived growth factor beta-chain locus (PDGFB) which may render these tumors responsive to targeted therapy with the tyrosine kinase inhibitor imatinib mesylate.	imatinib	212-220	platelet derived growth factor subunit B	Homo sapiens	109-114
15746584-9	2005	We conclude that sustained complete remission of metastatic DFSP with specific FISH abnormalities involving the PDGFB locus can be obtained with imatinib mesylate with minimal toxicity for the patient.	imatinib	145-153	platelet derived growth factor subunit B	Homo sapiens	112-117
15805252-4	2005	Previously, imatinib was shown to potently inhibit human breast cancer resistance protein (BCRP; ABCG2).	imatinib	12-20	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	97-102
15805252-5	2005	Here, we show that imatinib is efficiently transported by mouse Bcrp1 in transfected Madin-Darby canine kidney strain II (MDCKII) monolayers.	imatinib	19-27	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	64-69
15805252-7	2005	imatinib is significantly decreased 1.6-fold in Bcrp1 knockout mice compared with wild-type mice.	imatinib	0-8	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	48-53
15805252-0	2005	The effect of Bcrp1 (Abcg2) on the in vivo pharmacokinetics and brain penetration of imatinib mesylate (Gleevec): implications for the use of breast cancer resistance protein and P-glycoprotein inhibitors to enable the brain penetration of imatinib in patients.	imatinib	85-102	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	21-26
15805252-9	2005	imatinib was significantly 2.5-fold increased in Bcrp1 knockout mice compared with control mice.	imatinib	0-8	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	49-54
15805252-10	2005	We tested the hypothesis that P-gp and BCRP inhibitors, such as elacridar and pantoprazole, improve the brain penetration of imatinib.	imatinib	125-133	phosphoglycolate phosphatase	Mus musculus	30-34
15805252-0	2005	The effect of Bcrp1 (Abcg2) on the in vivo pharmacokinetics and brain penetration of imatinib mesylate (Gleevec): implications for the use of breast cancer resistance protein and P-glycoprotein inhibitors to enable the brain penetration of imatinib in patients.	imatinib	85-102	ATP binding cassette subfamily B member 1	Homo sapiens	179-193
15805252-10	2005	We tested the hypothesis that P-gp and BCRP inhibitors, such as elacridar and pantoprazole, improve the brain penetration of imatinib.	imatinib	125-133	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	39-43
15805252-11	2005	Firstly, we showed in vitro that pantoprazole and elacridar inhibit the Bcrp1-mediated transport of imatinib in MDCKII-Bcrp1 cells.	imatinib	100-108	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	72-77
15846067-0	2005	Kinase-addiction and bi-phasic sensitivity-resistance of Bcr-Abl- and Raf-1-expressing cells to imatinib and geldanamycin.	imatinib	96-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
15805252-0	2005	The effect of Bcrp1 (Abcg2) on the in vivo pharmacokinetics and brain penetration of imatinib mesylate (Gleevec): implications for the use of breast cancer resistance protein and P-glycoprotein inhibitors to enable the brain penetration of imatinib in patients.	imatinib	85-93	BCR pseudogene 1	Homo sapiens	14-19
15846067-0	2005	Kinase-addiction and bi-phasic sensitivity-resistance of Bcr-Abl- and Raf-1-expressing cells to imatinib and geldanamycin.	imatinib	96-104	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	70-75
15805252-11	2005	Firstly, we showed in vitro that pantoprazole and elacridar inhibit the Bcrp1-mediated transport of imatinib in MDCKII-Bcrp1 cells.	imatinib	100-108	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	119-124
15805252-18	2005	Our results suggest that co-administration of BCRP and P-gp inhibitors may improve delivery of imatinib to malignant gliomas.	imatinib	95-103	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	46-50
15805252-0	2005	The effect of Bcrp1 (Abcg2) on the in vivo pharmacokinetics and brain penetration of imatinib mesylate (Gleevec): implications for the use of breast cancer resistance protein and P-glycoprotein inhibitors to enable the brain penetration of imatinib in patients.	imatinib	85-93	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	21-26
15805252-18	2005	Our results suggest that co-administration of BCRP and P-gp inhibitors may improve delivery of imatinib to malignant gliomas.	imatinib	95-103	phosphoglycolate phosphatase	Mus musculus	55-59
15846067-3	2005	The Bcr-Abl inhibitor imatinib (Gleevec, STI-571) released the apoptotic stream.	imatinib	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
15805252-3	2005	Imatinib is transported in vitro and in vivo by P-glycoprotein (P-gp; ABCB1), which thereby limits its distribution into the brain in mice.	imatinib	0-8	phosphoglycolate phosphatase	Mus musculus	48-62
15846067-3	2005	The Bcr-Abl inhibitor imatinib (Gleevec, STI-571) released the apoptotic stream.	imatinib	41-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
15805252-3	2005	Imatinib is transported in vitro and in vivo by P-glycoprotein (P-gp; ABCB1), which thereby limits its distribution into the brain in mice.	imatinib	0-8	phosphoglycolate phosphatase	Mus musculus	64-68
15846067-5	2005	Raf-1 and Bcr-Abl-transfected FDC-P1 hematopoietic cells were selectively sensitive to GA and imatinib, respectively.	imatinib	94-102	v-raf-leukemia viral oncogene 1	Mus musculus	0-5
15846067-5	2005	Raf-1 and Bcr-Abl-transfected FDC-P1 hematopoietic cells were selectively sensitive to GA and imatinib, respectively.	imatinib	94-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
15846067-6	2005	Remarkably, cell clones with high levels of Bcr-Abl that could not be depleted by GA were relatively resistant to both GA and imatinib.	imatinib	126-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
15805265-4	2005	In vitro STI-571 treatment of CD34(+) cells from patients in blast crisis markedly increased the CXCR4 transcript and CXCR4 membrane expression.	imatinib	9-16	CD34 molecule	Homo sapiens	30-34
15805265-4	2005	In vitro STI-571 treatment of CD34(+) cells from patients in blast crisis markedly increased the CXCR4 transcript and CXCR4 membrane expression.	imatinib	9-16	C-X-C motif chemokine receptor 4	Homo sapiens	97-102
15805265-4	2005	In vitro STI-571 treatment of CD34(+) cells from patients in blast crisis markedly increased the CXCR4 transcript and CXCR4 membrane expression.	imatinib	9-16	C-X-C motif chemokine receptor 4	Homo sapiens	118-123
15805252-3	2005	Imatinib is transported in vitro and in vivo by P-glycoprotein (P-gp; ABCB1), which thereby limits its distribution into the brain in mice.	imatinib	0-8	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	70-75
15805252-4	2005	Previously, imatinib was shown to potently inhibit human breast cancer resistance protein (BCRP; ABCG2).	imatinib	12-20	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	57-89
15805252-4	2005	Previously, imatinib was shown to potently inhibit human breast cancer resistance protein (BCRP; ABCG2).	imatinib	12-20	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	91-95
15814334-0	2005	Fluorescence in situ hybridization monitoring of BCR-ABL-positive neutrophils in chronic-phase chronic myeloid leukemia patients during the primary stage of imatinib mesylate therapy.	imatinib	157-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
15601623-5	2005	By contrast, in erythroid cells, inhibitors of Src family and c-Abl tyrosine kinases (tyrphostin AG 82, PP2, imatinib) enhanced protein kinase C (PKC)-dependent cell growth and antagonized thrombin-promoted apoptosis by specifically stimulating PKCbeta activity.	imatinib	109-117	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	47-50
15601623-5	2005	By contrast, in erythroid cells, inhibitors of Src family and c-Abl tyrosine kinases (tyrphostin AG 82, PP2, imatinib) enhanced protein kinase C (PKC)-dependent cell growth and antagonized thrombin-promoted apoptosis by specifically stimulating PKCbeta activity.	imatinib	109-117	protein kinase C beta	Homo sapiens	146-149
15601623-5	2005	By contrast, in erythroid cells, inhibitors of Src family and c-Abl tyrosine kinases (tyrphostin AG 82, PP2, imatinib) enhanced protein kinase C (PKC)-dependent cell growth and antagonized thrombin-promoted apoptosis by specifically stimulating PKCbeta activity.	imatinib	109-117	coagulation factor II, thrombin	Homo sapiens	189-197
15601623-5	2005	By contrast, in erythroid cells, inhibitors of Src family and c-Abl tyrosine kinases (tyrphostin AG 82, PP2, imatinib) enhanced protein kinase C (PKC)-dependent cell growth and antagonized thrombin-promoted apoptosis by specifically stimulating PKCbeta activity.	imatinib	109-117	protein kinase C beta	Homo sapiens	245-252
15853160-7	2005	Imatinib mesylate is an oral drug designed to inhibit the kinase enzyme activity of KIT.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	84-87
15820950-3	2005	The first BCR-ABL inhibitor to come into use in clinical practice, imatinib mesylate, is now the first-choice treatment for all newly diagnosed CML patients, but the initial striking efficacy of this drug has been overshadowed by the development of clinical resistance.	imatinib	67-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
15820950-4	2005	The most common mechanisms of resistance include (i) BCR-ABL overexpression, and (ii) BCR-ABL kinase domain mutations disrupting critical contact points between imatinib and BCR-ABL or inducing a transition to a conformation to which imatinib is unable to bind.	imatinib	161-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
15820950-4	2005	The most common mechanisms of resistance include (i) BCR-ABL overexpression, and (ii) BCR-ABL kinase domain mutations disrupting critical contact points between imatinib and BCR-ABL or inducing a transition to a conformation to which imatinib is unable to bind.	imatinib	161-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
15820950-4	2005	The most common mechanisms of resistance include (i) BCR-ABL overexpression, and (ii) BCR-ABL kinase domain mutations disrupting critical contact points between imatinib and BCR-ABL or inducing a transition to a conformation to which imatinib is unable to bind.	imatinib	234-242	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
15820950-4	2005	The most common mechanisms of resistance include (i) BCR-ABL overexpression, and (ii) BCR-ABL kinase domain mutations disrupting critical contact points between imatinib and BCR-ABL or inducing a transition to a conformation to which imatinib is unable to bind.	imatinib	234-242	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
15814334-1	2005	We describe a method for monitoring chronic myeloid leukemia (CML) patients treated with imatinib that uses fluorescence in situ hybridization (FISH) to detect BCR-ABL in peripheral blood (PB) granulocytes.	imatinib	89-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-167
15814335-0	2005	Successful treatment with imatinib mesylate in a case of minor BCR-ABL-positive acute myelogenous leukemia.	imatinib	26-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
15814335-2	2005	We describe a case of Ph chromosome-positive AML in which imatinib mesylate was used and a favorable outcome was obtained.A 64-year-old man was found to have Ph chromosome-positive, minor BCR-ABL-positive AML.	imatinib	58-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	188-195
15814335-4	2005	Because the patient had a serious concomitant infectious disease, administration of 600 mg/day of imatinib mesylate, a specific inhibitor of BCR-ABL tyrosine kinase, was started after written informed consent was obtained.	imatinib	98-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-148
15795119-14	2005	Unlike the drug eruptions caused by antibiotics, where the expression of CD4 was dominant, CD8 was dominant in drug eruptions by STI571.	imatinib	129-135	CD8a molecule	Homo sapiens	91-94
15725473-0	2005	Imatinib mesylate in the treatment of Core Binding Factor leukemias with KIT mutations.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
15703781-1	2005	We monitored BCR-ABL transcript levels by quantitative real-time PCR in 103 patients treated with imatinib for chronic myeloid leukaemia in chronic phase for a median of 30.3 months (range 5.5-49.9) after they achieved complete cytogenetic remission (CCyR).	imatinib	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
15725473-2	2005	Aim of this study is to investigate the capability of Imatinib to induce an anti-leukemic effect in Core Binding Factor (CBF)-leukemia patients presenting either with extracellular juxtamembrane or kinase KIT mutations.	imatinib	54-62	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	205-208
15703782-0	2005	Chronic myeloid leukaemia with BCR-ABL fusion genes located to both chromosomes 9, cyclic leukocytosis and nodal T-lymphoblastic transformation--durable complete remission following imatinib therapy.	imatinib	182-190	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
15811621-0	2005	Acquired resistance to imatinib in gastrointestinal stromal tumours caused by multiple KIT mutations.	imatinib	23-31	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	87-90
15725473-7	2005	Whether Imatinib, in combination with other agents, may play a role in the treatment of AML with more sensitive extracellular juxtamembrane KIT mutation remains to be determined.	imatinib	8-16	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	140-143
15625278-0	2005	Cotreatment with suberanoylanilide hydroxamic acid and 17-allylamino 17-demethoxygeldanamycin synergistically induces apoptosis in Bcr-Abl+ Cells sensitive and resistant to STI571 (imatinib mesylate) in association with down-regulation of Bcr-Abl, abrogation of signal transducer and activator of transcription 5 activity, and Bax conformational change.	imatinib	181-198	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
15625278-1	2005	Interactions between the histone deacetylase (HDAC) inhibitors suberanoylanilide hydroxamic acid (SAHA) and sodium butyrate (SB) and the heat shock protein (Hsp) 90 antagonist 17-allylamino 17-demethoxygeldanamycin (17-AAG) have been examined in Bcr-Abl(+) human leukemia cells (K562 and LAMA84), including those sensitive and resistant to STI571 (imatinib mesylate).	imatinib	340-346	heat shock protein 90 alpha family class A member 1	Homo sapiens	137-164
15572591-0	2005	Imatinib inhibits T-cell receptor-mediated T-cell proliferation and activation in a dose-dependent manner.	imatinib	0-8	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	18-33
15625278-1	2005	Interactions between the histone deacetylase (HDAC) inhibitors suberanoylanilide hydroxamic acid (SAHA) and sodium butyrate (SB) and the heat shock protein (Hsp) 90 antagonist 17-allylamino 17-demethoxygeldanamycin (17-AAG) have been examined in Bcr-Abl(+) human leukemia cells (K562 and LAMA84), including those sensitive and resistant to STI571 (imatinib mesylate).	imatinib	348-365	heat shock protein 90 alpha family class A member 1	Homo sapiens	137-164
15756436-2	2005	Imatinib mesylate is a tyrosine kinase inhibitor initially developed against the bcr-abl fusion protein of CML, but also shows therapeutic inhibitory activity against c-Kit expressed in GISTs.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
15756436-2	2005	Imatinib mesylate is a tyrosine kinase inhibitor initially developed against the bcr-abl fusion protein of CML, but also shows therapeutic inhibitory activity against c-Kit expressed in GISTs.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	167-172
15756436-4	2005	Our aim was to test NETs for c-Kit expression and hence identify patients for the consideration of therapy with imatinib mesylate.	imatinib	112-129	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	29-34
15756436-9	2005	Studies need to be performed to determine if c-kit expression by NETs can be translated into therapeutic benefit by agents such as imatinib mesylate.	imatinib	131-148	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	45-50
15688014-0	2005	Direct transcriptional regulation of Bim by FoxO3a mediates STI571-induced apoptosis in Bcr-Abl-expressing cells.	imatinib	60-66	BCL2-like 11 (apoptosis facilitator)	Mus musculus	37-40
15688014-0	2005	Direct transcriptional regulation of Bim by FoxO3a mediates STI571-induced apoptosis in Bcr-Abl-expressing cells.	imatinib	60-66	forkhead box O3	Mus musculus	44-50
15688014-0	2005	Direct transcriptional regulation of Bim by FoxO3a mediates STI571-induced apoptosis in Bcr-Abl-expressing cells.	imatinib	60-66	BCR activator of RhoGEF and GTPase	Homo sapiens	88-91
15688014-3	2005	Inhibition of Bcr-Abl kinase by STI571 results in FoxO3a activation, induction of Bim expression and apoptosis.	imatinib	32-38	BCR activator of RhoGEF and GTPase	Homo sapiens	14-17
15688014-3	2005	Inhibition of Bcr-Abl kinase by STI571 results in FoxO3a activation, induction of Bim expression and apoptosis.	imatinib	32-38	forkhead box O3	Mus musculus	50-56
15688014-3	2005	Inhibition of Bcr-Abl kinase by STI571 results in FoxO3a activation, induction of Bim expression and apoptosis.	imatinib	32-38	BCL2-like 11 (apoptosis facilitator)	Mus musculus	82-85
15688014-7	2005	Conversely, silencing of FoxO3a in Bcr-Abl-expressing cells abolishes STI571-mediated Bim induction and apoptosis.	imatinib	70-76	forkhead box O3	Mus musculus	25-31
15688014-7	2005	Conversely, silencing of FoxO3a in Bcr-Abl-expressing cells abolishes STI571-mediated Bim induction and apoptosis.	imatinib	70-76	BCR activator of RhoGEF and GTPase	Mus musculus	35-38
15688014-7	2005	Conversely, silencing of FoxO3a in Bcr-Abl-expressing cells abolishes STI571-mediated Bim induction and apoptosis.	imatinib	70-76	BCL2-like 11 (apoptosis facilitator)	Mus musculus	86-89
15688014-8	2005	Together, the results presented clearly confirm FoxO3a as a key regulator of apoptosis induced by STI571, and show that Bim is a direct transcriptional target of FoxO3a that mediates the STI571-induced apoptosis.	imatinib	98-104	forkhead box O3	Mus musculus	48-54
15688014-8	2005	Together, the results presented clearly confirm FoxO3a as a key regulator of apoptosis induced by STI571, and show that Bim is a direct transcriptional target of FoxO3a that mediates the STI571-induced apoptosis.	imatinib	187-193	BCL2-like 11 (apoptosis facilitator)	Mus musculus	120-123
15688014-8	2005	Together, the results presented clearly confirm FoxO3a as a key regulator of apoptosis induced by STI571, and show that Bim is a direct transcriptional target of FoxO3a that mediates the STI571-induced apoptosis.	imatinib	187-193	forkhead box O3	Mus musculus	162-168
15688014-9	2005	Thus, STI571 induces an accumulation of FoxO3a activity which in turn binds directly to an FHRE in the promoter to activate Bim expression and apoptosis.	imatinib	6-12	forkhead box O3	Mus musculus	40-46
15688014-9	2005	Thus, STI571 induces an accumulation of FoxO3a activity which in turn binds directly to an FHRE in the promoter to activate Bim expression and apoptosis.	imatinib	6-12	BCL2-like 11 (apoptosis facilitator)	Mus musculus	124-127
15657060-5	2005	Moreover, inhibition of c-Abl with STI571 blocked DNA damage-induced autoprocessing of caspase-9 to the p35 subunit and activation of caspase-3.	imatinib	35-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-29
15657060-5	2005	Moreover, inhibition of c-Abl with STI571 blocked DNA damage-induced autoprocessing of caspase-9 to the p35 subunit and activation of caspase-3.	imatinib	35-41	caspase 9	Homo sapiens	87-96
15657060-5	2005	Moreover, inhibition of c-Abl with STI571 blocked DNA damage-induced autoprocessing of caspase-9 to the p35 subunit and activation of caspase-3.	imatinib	35-41	interleukin 12A	Homo sapiens	104-107
15657060-5	2005	Moreover, inhibition of c-Abl with STI571 blocked DNA damage-induced autoprocessing of caspase-9 to the p35 subunit and activation of caspase-3.	imatinib	35-41	caspase 3	Homo sapiens	134-143
15572591-3	2005	Here, we investigate the effect of imatinib on T-cell receptor (TCR)-mediated activation of human T cells.	imatinib	35-43	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	47-62
15572591-3	2005	Here, we investigate the effect of imatinib on T-cell receptor (TCR)-mediated activation of human T cells.	imatinib	35-43	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	64-67
15781610-3	2005	Imatinib mesylate (Gleevec, STI-571) is an inhibitor of ABL tyrosine kinase activity that has been remarkably effective in slowing disease progression in patients with chronic phase chronic myelogenous leukemia, but the emergence of imatinib resistance underscores the need for additional therapies.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-59
15781610-3	2005	Imatinib mesylate (Gleevec, STI-571) is an inhibitor of ABL tyrosine kinase activity that has been remarkably effective in slowing disease progression in patients with chronic phase chronic myelogenous leukemia, but the emergence of imatinib resistance underscores the need for additional therapies.	imatinib	19-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-59
15781610-3	2005	Imatinib mesylate (Gleevec, STI-571) is an inhibitor of ABL tyrosine kinase activity that has been remarkably effective in slowing disease progression in patients with chronic phase chronic myelogenous leukemia, but the emergence of imatinib resistance underscores the need for additional therapies.	imatinib	28-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-59
15781610-3	2005	Imatinib mesylate (Gleevec, STI-571) is an inhibitor of ABL tyrosine kinase activity that has been remarkably effective in slowing disease progression in patients with chronic phase chronic myelogenous leukemia, but the emergence of imatinib resistance underscores the need for additional therapies.	imatinib	233-241	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-59
15572591-6	2005	Up-regulation of the activation markers CD25 and CD69 in response to TCR cross-linking was suppressed by imatinib at a mean inhibitory concentration 50% (IC50) of 5.4 microM and 7.3 microM, respectively; interleukin 2 (IL-2) production was also impaired.	imatinib	105-113	interleukin 2 receptor subunit alpha	Homo sapiens	40-44
15572591-6	2005	Up-regulation of the activation markers CD25 and CD69 in response to TCR cross-linking was suppressed by imatinib at a mean inhibitory concentration 50% (IC50) of 5.4 microM and 7.3 microM, respectively; interleukin 2 (IL-2) production was also impaired.	imatinib	105-113	CD69 molecule	Homo sapiens	49-53
15572591-6	2005	Up-regulation of the activation markers CD25 and CD69 in response to TCR cross-linking was suppressed by imatinib at a mean inhibitory concentration 50% (IC50) of 5.4 microM and 7.3 microM, respectively; interleukin 2 (IL-2) production was also impaired.	imatinib	105-113	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	69-72
15572591-6	2005	Up-regulation of the activation markers CD25 and CD69 in response to TCR cross-linking was suppressed by imatinib at a mean inhibitory concentration 50% (IC50) of 5.4 microM and 7.3 microM, respectively; interleukin 2 (IL-2) production was also impaired.	imatinib	105-113	interleukin 2	Homo sapiens	204-217
15572591-6	2005	Up-regulation of the activation markers CD25 and CD69 in response to TCR cross-linking was suppressed by imatinib at a mean inhibitory concentration 50% (IC50) of 5.4 microM and 7.3 microM, respectively; interleukin 2 (IL-2) production was also impaired.	imatinib	105-113	interleukin 2	Homo sapiens	219-223
15572591-7	2005	Analysis of the TCR-induced signaling cascade showed that imatinib substantially reduced tyrosine phosphorylation of ZAP70 and LAT in response to activation through the TCR.	imatinib	58-66	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	16-19
15572591-7	2005	Analysis of the TCR-induced signaling cascade showed that imatinib substantially reduced tyrosine phosphorylation of ZAP70 and LAT in response to activation through the TCR.	imatinib	58-66	zeta chain of T cell receptor associated protein kinase 70	Homo sapiens	117-122
15572591-7	2005	Analysis of the TCR-induced signaling cascade showed that imatinib substantially reduced tyrosine phosphorylation of ZAP70 and LAT in response to activation through the TCR.	imatinib	58-66	linker for activation of T cells	Homo sapiens	127-130
15572591-7	2005	Analysis of the TCR-induced signaling cascade showed that imatinib substantially reduced tyrosine phosphorylation of ZAP70 and LAT in response to activation through the TCR.	imatinib	58-66	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	169-172
15572591-8	2005	Sequence comparisons of all 90 tyrosine kinase genes in the human genome for homology in the adenosine triphosphate (ATP) binding pocket identified LCK, which is required for ZAP70 activation, as a likely target for imatinib.	imatinib	216-224	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	148-151
15572591-8	2005	Sequence comparisons of all 90 tyrosine kinase genes in the human genome for homology in the adenosine triphosphate (ATP) binding pocket identified LCK, which is required for ZAP70 activation, as a likely target for imatinib.	imatinib	216-224	zeta chain of T cell receptor associated protein kinase 70	Homo sapiens	175-180
15572591-9	2005	The IC50 for LCK inhibition by imatinib was 0.6 microM to 0.8 microM in an in vitro tyrosine kinase assay.	imatinib	31-39	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	13-16
15727903-1	2005	Imatinib mesylate is a small molecule inhibitor of the c-Abl, platelet-derived growth factor (PDGF) receptor and c-Kit tyrosine kinases that is approved for the treatment of Philadelphia chromosome-positive chronic myeloid leukemia (CML) and gastrointestinal stromal tumors.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-60
15345592-0	2005	Detection of BCR-ABL kinase mutations in CD34+ cells from chronic myelogenous leukemia patients in complete cytogenetic remission on imatinib mesylate treatment.	imatinib	133-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
15345592-0	2005	Detection of BCR-ABL kinase mutations in CD34+ cells from chronic myelogenous leukemia patients in complete cytogenetic remission on imatinib mesylate treatment.	imatinib	133-150	CD34 molecule	Homo sapiens	41-45
15345592-1	2005	The BCR-ABL kinase inhibitor imatinib mesylate induces complete cytogenetic response (CCR) in a high proportion of chronic myelogenous leukemia (CML) patients.	imatinib	29-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
15345592-4	2005	BCR-ABL kinase domain mutations affecting drug binding can lead to secondary resistance to imatinib.	imatinib	91-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
15345592-5	2005	We show here that kinase mutations could be detected in CD34+ cells isolated from CML patients in CCR on imatinib.	imatinib	105-113	CD34 molecule	Homo sapiens	56-60
15727903-1	2005	Imatinib mesylate is a small molecule inhibitor of the c-Abl, platelet-derived growth factor (PDGF) receptor and c-Kit tyrosine kinases that is approved for the treatment of Philadelphia chromosome-positive chronic myeloid leukemia (CML) and gastrointestinal stromal tumors.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	113-118
15727903-4	2005	Here, we demonstrate that pretreatment of a human glioblastoma cell line, RuSi RS1, with imatinib significantly enhanced the cytotoxic effect of ionizing radiation.	imatinib	89-97	retinoschisin 1	Homo sapiens	79-82
15345592-8	2005	These BCR-ABL mutations were associated with varying levels of imatinib resistance.	imatinib	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-13
15345592-11	2005	We conclude that BCR-ABL kinase mutations can be detected in CD34+ cells from CML patients in CCR on imatinib, may contribute to persistence of small populations of malignant progenitors, and could be a potential source of relapse.	imatinib	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
15727903-7	2005	Imatinib treatment of RuSi RS1 cells decreased overall levels of cellular tyrosine phosphorylation and specifically inhibited phosphorylation of PDGFR-beta, while c-Abl was not prominently activated in these cells.	imatinib	0-8	retinoschisin 1	Homo sapiens	27-30
15345592-11	2005	We conclude that BCR-ABL kinase mutations can be detected in CD34+ cells from CML patients in CCR on imatinib, may contribute to persistence of small populations of malignant progenitors, and could be a potential source of relapse.	imatinib	101-109	CD34 molecule	Homo sapiens	61-65
15727903-7	2005	Imatinib treatment of RuSi RS1 cells decreased overall levels of cellular tyrosine phosphorylation and specifically inhibited phosphorylation of PDGFR-beta, while c-Abl was not prominently activated in these cells.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	145-155
15727903-8	2005	These results suggest that imatinib may have clinical utility as a radiosensitizer in the treatment of human glioblastoma, possibly through disruption of an autocrine PDGF/PDGFR loop.	imatinib	27-35	platelet derived growth factor receptor beta	Homo sapiens	172-177
15803362-1	2005	BACKGROUND: Imatinib mesylate is a potent inhibitor of Abl, KIT, and PDGFR tyrosine kinases.	imatinib	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-58
15803362-1	2005	BACKGROUND: Imatinib mesylate is a potent inhibitor of Abl, KIT, and PDGFR tyrosine kinases.	imatinib	12-29	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	60-63
15721630-0	2005	Clonal evolution with inv(11)(p15q22) and NUP98/DDX10 fusion gene in imatinib-resistant chronic myelogenous leukemia.	imatinib	69-77	nucleoporin 98 and 96 precursor	Homo sapiens	42-47
15803362-1	2005	BACKGROUND: Imatinib mesylate is a potent inhibitor of Abl, KIT, and PDGFR tyrosine kinases.	imatinib	12-29	platelet derived growth factor receptor beta	Homo sapiens	69-74
15756019-0	2005	Effects of imatinib on monocyte-derived dendritic cells are mediated by inhibition of nuclear factor-kappaB and Akt signaling pathways.	imatinib	11-19	AKT serine/threonine kinase 1	Homo sapiens	112-115
15721630-0	2005	Clonal evolution with inv(11)(p15q22) and NUP98/DDX10 fusion gene in imatinib-resistant chronic myelogenous leukemia.	imatinib	69-77	DEAD-box helicase 10	Homo sapiens	48-53
15721630-1	2005	The BCR/ABL tyrosine kinase inhibitor imatinib has shown remarkable efficacy in treating patients with chronic myelogenous leukemia (CML).	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
15721630-6	2005	Furthermore, ex vivo treatment of leukemic cells with imatinib significantly reduced tyrosine phosphorylation of CrkL, a target of the BCR/ABL kinase.	imatinib	54-62	CRK like proto-oncogene, adaptor protein	Homo sapiens	113-117
15721630-6	2005	Furthermore, ex vivo treatment of leukemic cells with imatinib significantly reduced tyrosine phosphorylation of CrkL, a target of the BCR/ABL kinase.	imatinib	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
15721630-7	2005	These observations raise a possibility that the NUP98/DDX10 fusion might be involved in imatinib resistance as well as in acute transformation of CML.	imatinib	88-96	nucleoporin 98 and 96 precursor	Homo sapiens	48-53
15721630-7	2005	These observations raise a possibility that the NUP98/DDX10 fusion might be involved in imatinib resistance as well as in acute transformation of CML.	imatinib	88-96	DEAD-box helicase 10	Homo sapiens	54-59
15738656-2	2005	In chronic myeloid leukaemia (CML), the Bcr-Abl kinase inhibitor imatinib (STI571, Gleevec) induces impressive response rates.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
15738656-2	2005	In chronic myeloid leukaemia (CML), the Bcr-Abl kinase inhibitor imatinib (STI571, Gleevec) induces impressive response rates.	imatinib	75-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
15738656-2	2005	In chronic myeloid leukaemia (CML), the Bcr-Abl kinase inhibitor imatinib (STI571, Gleevec) induces impressive response rates.	imatinib	83-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
15738656-3	2005	However, resistance occurs especially in advanced phase CML and Ph+ ALL, primarily as a consequence of point mutations within the Bcr-Abl kinase domain that prevent imatinib from binding.	imatinib	165-173	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
15738656-7	2005	We recently developed a cell-based screening strategy that allows one to predict the pattern and relative abundance of Bcr-Abl resistance mutations emerging in the presence of imatinib or an alternative Abl-kinase inhibitor.	imatinib	176-184	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-126
15738656-8	2005	Using this strategy, the findings in inhibitor resistant sublines reflect observations made in CML patients with imatinib resistance, including Bcr-Abl mutations, amplification of the Bcr-Abl gene, and overexpression of the Bcr-Abl protein.	imatinib	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
15717993-5	2005	Imatinib mesylate (Gleevec; Novartis Pharmaceuticals Corp., East Hanover, NJ) is a tyrosine kinase inhibitor with activity against abl, c-kit, and platelet derived growth factor receptor (PDGFR), and is approved for the treatment of chronic myelogenous leukemia and gastrointestinal stromal tumor.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-134
15756019-3	2005	Imatinib is a novel tyrosine kinase inhibitor effective against Abl kinases, c-Kit, and platelet-derived growth factor receptor.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	77-82
15717993-5	2005	Imatinib mesylate (Gleevec; Novartis Pharmaceuticals Corp., East Hanover, NJ) is a tyrosine kinase inhibitor with activity against abl, c-kit, and platelet derived growth factor receptor (PDGFR), and is approved for the treatment of chronic myelogenous leukemia and gastrointestinal stromal tumor.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	136-141
15717993-5	2005	Imatinib mesylate (Gleevec; Novartis Pharmaceuticals Corp., East Hanover, NJ) is a tyrosine kinase inhibitor with activity against abl, c-kit, and platelet derived growth factor receptor (PDGFR), and is approved for the treatment of chronic myelogenous leukemia and gastrointestinal stromal tumor.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	147-186
15756019-4	2005	Using this compound, we show that human monocyte-derived dendritic cells generated in the presence of therapeutic concentrations of imatinib show a reduced expression of CD1a, MHC class I and II, and costimulatory molecules as well as decreased secretion of chemokines and cytokines resulting in an impaired capacity of dendritic cells to elicit primary T-cell responses.	imatinib	132-140	CD1a molecule	Homo sapiens	170-174
15717993-5	2005	Imatinib mesylate (Gleevec; Novartis Pharmaceuticals Corp., East Hanover, NJ) is a tyrosine kinase inhibitor with activity against abl, c-kit, and platelet derived growth factor receptor (PDGFR), and is approved for the treatment of chronic myelogenous leukemia and gastrointestinal stromal tumor.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	188-193
15756019-7	2005	Taken together, our study reveals that imatinib inhibits dendritic cell differentiation and function via Akt and nuclear factor-kappaB signal transduction.	imatinib	39-47	AKT serine/threonine kinase 1	Homo sapiens	105-108
15717993-5	2005	Imatinib mesylate (Gleevec; Novartis Pharmaceuticals Corp., East Hanover, NJ) is a tyrosine kinase inhibitor with activity against abl, c-kit, and platelet derived growth factor receptor (PDGFR), and is approved for the treatment of chronic myelogenous leukemia and gastrointestinal stromal tumor.	imatinib	19-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-134
15717993-5	2005	Imatinib mesylate (Gleevec; Novartis Pharmaceuticals Corp., East Hanover, NJ) is a tyrosine kinase inhibitor with activity against abl, c-kit, and platelet derived growth factor receptor (PDGFR), and is approved for the treatment of chronic myelogenous leukemia and gastrointestinal stromal tumor.	imatinib	19-26	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	136-141
15717993-5	2005	Imatinib mesylate (Gleevec; Novartis Pharmaceuticals Corp., East Hanover, NJ) is a tyrosine kinase inhibitor with activity against abl, c-kit, and platelet derived growth factor receptor (PDGFR), and is approved for the treatment of chronic myelogenous leukemia and gastrointestinal stromal tumor.	imatinib	19-26	platelet derived growth factor receptor beta	Homo sapiens	147-186
15717993-5	2005	Imatinib mesylate (Gleevec; Novartis Pharmaceuticals Corp., East Hanover, NJ) is a tyrosine kinase inhibitor with activity against abl, c-kit, and platelet derived growth factor receptor (PDGFR), and is approved for the treatment of chronic myelogenous leukemia and gastrointestinal stromal tumor.	imatinib	19-26	platelet derived growth factor receptor beta	Homo sapiens	188-193
15719031-1	2005	Imatinib, a potent inhibitor of the oncogenic tyrosine kinase BCR-ABL, has shown remarkable clinical activity in patients with chronic myelogenous leukaemia (CML).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
15791812-3	2005	Imatinib mesylate, a selective BCR-ABL tyrosine kinase inhibitor, was first given to a patient with CML in June 1998.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
15794712-4	2005	Imatinib is a small-molecule tyrosine kinase inhibitor of the ABL fusion gene, platelet derived growth factor receptors (PDGFR) and KIT.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	79-119
15794712-4	2005	Imatinib is a small-molecule tyrosine kinase inhibitor of the ABL fusion gene, platelet derived growth factor receptors (PDGFR) and KIT.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	121-126
15794712-4	2005	Imatinib is a small-molecule tyrosine kinase inhibitor of the ABL fusion gene, platelet derived growth factor receptors (PDGFR) and KIT.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	132-135
15794712-7	2005	The pivotal registration study for newly diagnosed CML was a large randomised trial comparing 400 mg/day of imatinib to a combination of IFN-alpha and cytarabine, which demonstrated a significantly higher complete haematological and cytogenetic response rate in the imatinib arm.	imatinib	266-274	interferon alpha 1	Homo sapiens	137-146
15618956-0	2005	Gene expression profiling of Philadelphia chromosome (Ph)-negative CD34+ hematopoietic stem and progenitor cells of patients with Ph-positive CML in major molecular remission during therapy with imatinib.	imatinib	195-203	CD34 molecule	Homo sapiens	67-71
15661271-1	2005	The tyrosine kinase inhibitor imatinib inhibits the activity of the bcr/abl fusion protein present in patients with chronic myeloid leukemia.	imatinib	30-38	BCR activator of RhoGEF and GTPase	Homo sapiens	68-71
15711537-5	2005	Many novel interactions were identified, including tight binding of the p38 inhibitor BIRB-796 to an imatinib-resistant variant of the ABL kinase, and binding of imatinib to the SRC-family kinase LCK.	imatinib	101-109	mitogen-activated protein kinase 14	Homo sapiens	72-75
15711537-5	2005	Many novel interactions were identified, including tight binding of the p38 inhibitor BIRB-796 to an imatinib-resistant variant of the ABL kinase, and binding of imatinib to the SRC-family kinase LCK.	imatinib	162-170	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	196-199
15499612-1	2005	STI571, or imatinib, selectively inhibits BCR/ABL, PDGFR and c-kit kinase activity.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
15854548-4	2005	One FIP1L1-PDGFRA fusion gene positive patient was administered with low-dose imatinib.	imatinib	78-86	factor interacting with PAPOLA and CPSF1	Homo sapiens	4-10
15854548-4	2005	One FIP1L1-PDGFRA fusion gene positive patient was administered with low-dose imatinib.	imatinib	78-86	platelet derived growth factor receptor alpha	Homo sapiens	11-17
15854548-7	2005	Continuous hematological remission was observed in one FIP1L1-PDGFRA fusion gene positive HES patient after low-dose imatinib treatment.	imatinib	117-125	factor interacting with PAPOLA and CPSF1	Homo sapiens	55-61
15854548-7	2005	Continuous hematological remission was observed in one FIP1L1-PDGFRA fusion gene positive HES patient after low-dose imatinib treatment.	imatinib	117-125	platelet derived growth factor receptor alpha	Homo sapiens	62-68
15705718-1	2005	Structural studies suggest that most point mutations in the BCR-ABL kinase domain cause resistance to the ABL kinase inhibitor imatinib by impairing the flexibility of the kinase domain, restricting its ability to adopt the inactive conformation required for optimal imatinib binding, rather than by directly interfering with drug contact residues.	imatinib	127-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
15705718-1	2005	Structural studies suggest that most point mutations in the BCR-ABL kinase domain cause resistance to the ABL kinase inhibitor imatinib by impairing the flexibility of the kinase domain, restricting its ability to adopt the inactive conformation required for optimal imatinib binding, rather than by directly interfering with drug contact residues.	imatinib	127-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-67
15705718-1	2005	Structural studies suggest that most point mutations in the BCR-ABL kinase domain cause resistance to the ABL kinase inhibitor imatinib by impairing the flexibility of the kinase domain, restricting its ability to adopt the inactive conformation required for optimal imatinib binding, rather than by directly interfering with drug contact residues.	imatinib	267-275	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
15705718-1	2005	Structural studies suggest that most point mutations in the BCR-ABL kinase domain cause resistance to the ABL kinase inhibitor imatinib by impairing the flexibility of the kinase domain, restricting its ability to adopt the inactive conformation required for optimal imatinib binding, rather than by directly interfering with drug contact residues.	imatinib	267-275	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-67
15705718-2	2005	BMS-354825, currently in clinical development for imatinib-resistant chronic myelogenous leukemia, is a dual SRC/ABL kinase inhibitor that binds ABL in both the active and inactive conformation.	imatinib	50-58	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	109-112
15705718-2	2005	BMS-354825, currently in clinical development for imatinib-resistant chronic myelogenous leukemia, is a dual SRC/ABL kinase inhibitor that binds ABL in both the active and inactive conformation.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-148
15854548-11	2005	Low-dose imatinib, that induces complete hematological and molecular genetic remission, exerts significant effects on FIP1L1-PDGFRA positive HES.	imatinib	9-17	factor interacting with PAPOLA and CPSF1	Homo sapiens	118-124
15854548-11	2005	Low-dose imatinib, that induces complete hematological and molecular genetic remission, exerts significant effects on FIP1L1-PDGFRA positive HES.	imatinib	9-17	platelet derived growth factor receptor alpha	Homo sapiens	125-131
15499612-1	2005	STI571, or imatinib, selectively inhibits BCR/ABL, PDGFR and c-kit kinase activity.	imatinib	0-6	platelet derived growth factor receptor beta	Homo sapiens	51-56
15499612-1	2005	STI571, or imatinib, selectively inhibits BCR/ABL, PDGFR and c-kit kinase activity.	imatinib	0-6	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	61-66
15499612-1	2005	STI571, or imatinib, selectively inhibits BCR/ABL, PDGFR and c-kit kinase activity.	imatinib	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
15499612-1	2005	STI571, or imatinib, selectively inhibits BCR/ABL, PDGFR and c-kit kinase activity.	imatinib	11-19	platelet derived growth factor receptor beta	Homo sapiens	51-56
15499612-1	2005	STI571, or imatinib, selectively inhibits BCR/ABL, PDGFR and c-kit kinase activity.	imatinib	11-19	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	61-66
15677719-0	2005	A non-ATP-competitive inhibitor of BCR-ABL overrides imatinib resistance.	imatinib	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
15459011-1	2005	In Philadelphia-positive (Ph(+)) leukemia, point mutations within the Bcr-Abl kinase domain emerged as a major mechanism of resistance to imatinib mesylate.	imatinib	138-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
15514006-7	2005	In the imatinib mesylate (IM)-refractory leukemia cells expressing Bcr-Abl with the T315I mutation, treatment with the combination attenuated the levels of the mutant Bcr-Abl and induced apoptosis.	imatinib	7-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
15514006-7	2005	In the imatinib mesylate (IM)-refractory leukemia cells expressing Bcr-Abl with the T315I mutation, treatment with the combination attenuated the levels of the mutant Bcr-Abl and induced apoptosis.	imatinib	7-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-174
15557593-4	2005	MATERIALS AND METHODS: Seeking to improve efficacy against otherwise intractable end-stage pancreatic islet tumors, two receptor tyrosine kinase inhibitors, imatinib and SU11248, were used to disrupt PDGFR-mediated pericyte support of tumor endothelial cells in concert with maximum-tolerated dose (MTD) or metronomic chemotherapy and/or VEGFR inhibition.	imatinib	157-165	platelet derived growth factor receptor, beta polypeptide	Mus musculus	200-205
15677719-1	2005	Imatinib, which is an inhibitor of the BCR-ABL tyrosine kinase, has been a remarkable success for the treatment of Philadelphia chromosome-positive (Ph+) chronic myelogenous leukemias (CMLs).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
15677719-2	2005	However, a significant proportion of patients chronically treated with imatinib develop resistance because of the acquisition of mutations in the kinase domain of BCR-ABL.	imatinib	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
15677719-6	2005	Kinetic studies demonstrate that this compound is not ATP-competitive but is substrate-competitive and works synergistically with imatinib in wild-type BCR-ABL inhibition.	imatinib	130-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-159
15677719-8	2005	injection of 32Dcl3 cells expressing the imatinib-resistant BCR-ABL isoform T315I.	imatinib	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
15618966-0	2005	Myeloid blast crisis evolving during imatinib treatment of an FIP1L1-PDGFR alpha-positive chronic myeloproliferative disease with prominent eosinophilia.	imatinib	37-45	platelet derived growth factor receptor alpha	Homo sapiens	69-80
15705916-0	2005	KIT/Val654 Ala receptor detected in one imatinib-resistant GIST patient.	imatinib	40-48	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
15710324-1	2005	The Abl inhibitor imatinib is a highly effective therapy for patients with chronic myeloid leukemia.	imatinib	18-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
15710324-5	2005	AMN107 is approximately 20-fold more potent than imatinib, and this translates into improved inhibitory activity against most of the common BCR-ABL mutations.	imatinib	49-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
15709206-4	2005	Treatment with STI571 resulted in inhibition of RET phosphorylation, cell proliferation, tumor growth and invasiveness.	imatinib	15-21	ret proto-oncogene	Homo sapiens	48-51
15685537-15	2005	Our findings show the sensitivity of the imatinib-resistant KIT -T670I and KIT -V654A and of PDGFRA -D842V mutants to PKC412.	imatinib	41-49	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	60-63
15685537-15	2005	Our findings show the sensitivity of the imatinib-resistant KIT -T670I and KIT -V654A and of PDGFRA -D842V mutants to PKC412.	imatinib	41-49	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	75-78
15661041-5	2005	A decrease in the response of CM to LPS was observed morphologically and functionally, with CM grown in the presence of imatinib showing decreased pseudopodia formation and inhibition of IL-6 and TNF-alpha production following LPS stimulation.	imatinib	120-128	interleukin 6	Homo sapiens	187-191
15661041-5	2005	A decrease in the response of CM to LPS was observed morphologically and functionally, with CM grown in the presence of imatinib showing decreased pseudopodia formation and inhibition of IL-6 and TNF-alpha production following LPS stimulation.	imatinib	120-128	tumor necrosis factor	Homo sapiens	196-205
15661041-6	2005	Imatinib also reduced the ability of M-CSF and GM-CSF stimulated CM to phagocytose zymosan particles, with uptake of non-opsonized zymosan by M-CSF stimulated CM (M-CM) being most affected.	imatinib	0-8	colony stimulating factor 1	Homo sapiens	37-42
15661041-6	2005	Imatinib also reduced the ability of M-CSF and GM-CSF stimulated CM to phagocytose zymosan particles, with uptake of non-opsonized zymosan by M-CSF stimulated CM (M-CM) being most affected.	imatinib	0-8	colony stimulating factor 2	Homo sapiens	47-53
15661041-6	2005	Imatinib also reduced the ability of M-CSF and GM-CSF stimulated CM to phagocytose zymosan particles, with uptake of non-opsonized zymosan by M-CSF stimulated CM (M-CM) being most affected.	imatinib	0-8	colony stimulating factor 1	Homo sapiens	48-53
15625075-0	2005	Imatinib attenuates diabetic nephropathy in apolipoprotein E-knockout mice.	imatinib	0-8	apolipoprotein E	Mus musculus	44-60
15526280-7	2005	STI571, a small molecule inhibitor for cytoplasmic tyrosine kinase c-Abl, also inhibited the alteration of F-actin-based cytoskeleton, and c-Abl was redistributed to where F-actin concentrated in the activated neutrophils.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-72
15526280-7	2005	STI571, a small molecule inhibitor for cytoplasmic tyrosine kinase c-Abl, also inhibited the alteration of F-actin-based cytoskeleton, and c-Abl was redistributed to where F-actin concentrated in the activated neutrophils.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-144
15618966-0	2005	Myeloid blast crisis evolving during imatinib treatment of an FIP1L1-PDGFR alpha-positive chronic myeloproliferative disease with prominent eosinophilia.	imatinib	37-45	factor interacting with PAPOLA and CPSF1	Homo sapiens	62-68
15454486-0	2005	Imatinib mesylate (STI-571) enhances antigen-presenting cell function and overcomes tumor-induced CD4+ T-cell tolerance.	imatinib	0-17	CD4 molecule	Homo sapiens	98-101
15454486-0	2005	Imatinib mesylate (STI-571) enhances antigen-presenting cell function and overcomes tumor-induced CD4+ T-cell tolerance.	imatinib	19-26	CD4 molecule	Homo sapiens	98-101
15454486-4	2005	Furthermore, in vivo treatment with STI-571 not only prevented the induction of tolerance in tumor-specific CD4(+) T cells, preserving their responsiveness to a subsequent immunization, but also resulted in enhanced vaccine efficacy.	imatinib	36-43	CD4 molecule	Homo sapiens	108-111
15723656-0	2005	STI571 (Glivec) inhibits the interaction between c-KIT and heat shock protein 90 of the gastrointestinal stromal tumor cell line, GIST-T1.	imatinib	0-6	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	49-54
15723656-0	2005	STI571 (Glivec) inhibits the interaction between c-KIT and heat shock protein 90 of the gastrointestinal stromal tumor cell line, GIST-T1.	imatinib	0-6	heat shock protein 90 alpha family class A member 1	Homo sapiens	59-80
15723656-2	2005	We report that STI571 (Glivec; Novartis, Basel, Switzerland), a specific inhibitor of c-KIT, inhibits the clustering of c-KIT at the cell membrane of the GIST-T1 cells.	imatinib	15-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	86-91
15723656-2	2005	We report that STI571 (Glivec; Novartis, Basel, Switzerland), a specific inhibitor of c-KIT, inhibits the clustering of c-KIT at the cell membrane of the GIST-T1 cells.	imatinib	15-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	120-125
15723656-3	2005	Furthermore, STI571 prevents the interaction between c-KIT and the molecular chaperone, heat shock protein 90 (Hsp90).	imatinib	13-19	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	53-58
15723656-3	2005	Furthermore, STI571 prevents the interaction between c-KIT and the molecular chaperone, heat shock protein 90 (Hsp90).	imatinib	13-19	heat shock protein 90 alpha family class A member 1	Homo sapiens	88-109
15723656-3	2005	Furthermore, STI571 prevents the interaction between c-KIT and the molecular chaperone, heat shock protein 90 (Hsp90).	imatinib	13-19	heat shock protein 90 alpha family class A member 1	Homo sapiens	111-116
15621812-1	2005	Imatinib, the ABL kinase inhibitor, is used not only for Philadelphia chromosome-positive (Ph + ) chronic myelogenous leukemia, but also for Ph + acute lymphoblastic leukemia (ALL), although resistance to the drug tends to develop in an early stage of the clinical course.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-17
15621812-2	2005	We describe a childhood refractory Ph + ALL patient in whom progressive resistance to imatinib was correlated with the appearance of a mutation in the BCR-ABL kinase domain and in vitro drug resistance to imatinib as determined by the methyl-thiazol-tetrazolium (MTT) assay.	imatinib	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-158
15389797-0	2005	A phase II trial of imatinib mesylate in patients with prostate specific antigen progression after local therapy for prostate cancer.	imatinib	20-37	kallikrein related peptidase 3	Homo sapiens	55-80
15389797-1	2005	PURPOSE: To test the hypothesis that progression of androgen sensitive prostate cancer is dependent on growth factors, such as platelet derived growth factor (PDGF), and inhibition of PDGF receptor (PDGF-R) with imatinib will induce anti-tumor activity.	imatinib	212-220	platelet derived growth factor receptor beta	Homo sapiens	184-197
15389797-1	2005	PURPOSE: To test the hypothesis that progression of androgen sensitive prostate cancer is dependent on growth factors, such as platelet derived growth factor (PDGF), and inhibition of PDGF receptor (PDGF-R) with imatinib will induce anti-tumor activity.	imatinib	212-220	platelet derived growth factor receptor beta	Homo sapiens	199-205
15389797-2	2005	PATIENTS AND METHODS: This phase II study evaluated imatinib in patients with androgen sensitive prostate cancer and prostate specific antigen (PSA) progression after local therapy.	imatinib	52-60	kallikrein related peptidase 3	Homo sapiens	144-147
15353483-6	2005	Inhibition of Bcr-Abl kinase by STI571 induced G1 arrest and caused a recovery of the p27 level with reduction of the small Jab1 complex from the cytoplasm.	imatinib	32-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
15822404-4	2005	Inhibitors of KIT tyrosine kinase activity can have a therapeutic role, particularly in seminomas with a c-kit mutation sensitive to imatinib mesylate.	imatinib	133-150	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	105-110
15748426-15	2005	Combination of Gleevec and arsenic agents in treating chronic myeloid leukemia has already make a figure both in clinical and laboratory research, aiming at counteracting the abnormal tyrosine kinase activity of ABL and the degradating BCR-ABL fusion protein.	imatinib	15-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	212-215
15748426-15	2005	Combination of Gleevec and arsenic agents in treating chronic myeloid leukemia has already make a figure both in clinical and laboratory research, aiming at counteracting the abnormal tyrosine kinase activity of ABL and the degradating BCR-ABL fusion protein.	imatinib	15-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	240-243
15596148-2	2005	Here we demonstrate that the inducible expression of BCR/ABL in a murine hematopoietic cell line, TonB210, leads to the activation of the Ras family small GTPase Rap1, which is inhibited by the ABL kinase inhibitor imatinib.	imatinib	215-223	BCR activator of RhoGEF and GTPase	Mus musculus	53-60
15596148-2	2005	Here we demonstrate that the inducible expression of BCR/ABL in a murine hematopoietic cell line, TonB210, leads to the activation of the Ras family small GTPase Rap1, which is inhibited by the ABL kinase inhibitor imatinib.	imatinib	215-223	RAS-related protein 1a	Mus musculus	162-166
15596148-2	2005	Here we demonstrate that the inducible expression of BCR/ABL in a murine hematopoietic cell line, TonB210, leads to the activation of the Ras family small GTPase Rap1, which is inhibited by the ABL kinase inhibitor imatinib.	imatinib	215-223	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	57-60
15596148-3	2005	The Rap1 activity in a CML cell line, K562, was also inhibited by imatinib.	imatinib	66-74	RAS-related protein 1a	Mus musculus	4-8
15659505-0	2005	Imatinib mesylate in patients with adenoid cystic cancers of the salivary glands expressing c-kit: a Princess Margaret Hospital phase II consortium study.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	92-97
15659505-1	2005	PURPOSE: This study aimed to assess the antitumor activity of imatinib in adenoid cystic carcinoma (ACC) of the salivary gland expressing c-kit.	imatinib	62-70	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	138-143
15659505-3	2005	Imatinib specifically inhibits autophosphorylation of the bcr-abl, platelet-derived growth factor receptor beta, and c-kit tyrosine kinases.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	117-122
15353483-6	2005	Inhibition of Bcr-Abl kinase by STI571 induced G1 arrest and caused a recovery of the p27 level with reduction of the small Jab1 complex from the cytoplasm.	imatinib	32-38	interferon alpha inducible protein 27	Homo sapiens	86-89
15353483-6	2005	Inhibition of Bcr-Abl kinase by STI571 induced G1 arrest and caused a recovery of the p27 level with reduction of the small Jab1 complex from the cytoplasm.	imatinib	32-38	COP9 signalosome subunit 5	Homo sapiens	124-128
15540243-0	2005	Granulocyte--colony-stimulating factor (Filgrastim) may overcome imatinib-induced neutropenia in patients with chronic-phase myelogenous leukemia.	imatinib	65-73	colony stimulating factor 3	Homo sapiens	0-38
15632213-0	2005	Imatinib mesylate in the treatment of c-kit-positive acute myeloid leukemia: is this the real target?	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	38-43
15995324-9	2005	A subset of MCD patients with associated eosinophilia who carry the FIP1L1-PDGFRA oncogene will achieve complete clinical, histological, and molecular remissions with imatinib mesylate therapy, in contrast to those with c-kit D816V mutations.	imatinib	167-184	factor interacting with PAPOLA and CPSF1	Homo sapiens	68-74
15995324-9	2005	A subset of MCD patients with associated eosinophilia who carry the FIP1L1-PDGFRA oncogene will achieve complete clinical, histological, and molecular remissions with imatinib mesylate therapy, in contrast to those with c-kit D816V mutations.	imatinib	167-184	platelet derived growth factor receptor alpha	Homo sapiens	75-81
15995325-6	2005	For example, the presence of either PDGFRA or PDGFRB mutations warrants the use of imatinib in clonal eosinophilia.	imatinib	83-91	platelet derived growth factor receptor alpha	Homo sapiens	36-42
15995325-6	2005	For example, the presence of either PDGFRA or PDGFRB mutations warrants the use of imatinib in clonal eosinophilia.	imatinib	83-91	platelet derived growth factor receptor beta	Homo sapiens	46-52
16196499-1	2005	Acquired resistance to imatinib mesylate is an increasing and continued challenge in the treatment of BCR-ABL tyrosine kinase positive leukemias as well as gastrointestinal stromal tumors.	imatinib	23-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
16196499-7	2005	The main clinical implications involve early detection of imatinib resistance and the identification of new metabolic enzyme targets with the potential of overcoming drug resistance downstream of the various genetic and BCR-ABL-expression derived mechanisms.	imatinib	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	220-227
16168125-3	2005	After the demonstration that gastrointestinal stromal tumours without c-Kit mutations harbour PDGFR-alpha-activating mutations and that PDGFR-alpha is also a therapeutic target for imatinib mesylate, the interest for this receptor has increased considerably.	imatinib	181-189	platelet derived growth factor receptor alpha	Homo sapiens	136-147
15634018-6	2005	The molecular hypotheses on imatinib binding to the Bcr-Abl oncogene fusion protein are interpreted at the site-specific level in view of the moiety basicities of imatinib.	imatinib	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
15634018-6	2005	The molecular hypotheses on imatinib binding to the Bcr-Abl oncogene fusion protein are interpreted at the site-specific level in view of the moiety basicities of imatinib.	imatinib	163-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
16227678-0	2005	Tyrosine kinase inhibitor STI571 (Imatinib) cooperates with wild-type p53 on K562 cell line to enhance its proapoptotic effects.	imatinib	26-32	TXK tyrosine kinase	Homo sapiens	0-15
16227678-0	2005	Tyrosine kinase inhibitor STI571 (Imatinib) cooperates with wild-type p53 on K562 cell line to enhance its proapoptotic effects.	imatinib	26-32	tumor protein p53	Homo sapiens	70-73
16227678-0	2005	Tyrosine kinase inhibitor STI571 (Imatinib) cooperates with wild-type p53 on K562 cell line to enhance its proapoptotic effects.	imatinib	34-42	TXK tyrosine kinase	Homo sapiens	0-15
16227678-0	2005	Tyrosine kinase inhibitor STI571 (Imatinib) cooperates with wild-type p53 on K562 cell line to enhance its proapoptotic effects.	imatinib	34-42	tumor protein p53	Homo sapiens	70-73
16227678-1	2005	In order to ascertain whether p53 has a role in chronic myeloid leukemia hematopoietic progenitor response to the innovative tyrosine kinase inhibitor STI571 (Imatinib), we overexpressed a wild type (wt) p53 construct in the K562 cell line, generated from a human blast crisis and lacking endogenous p53.	imatinib	159-167	tumor protein p53	Homo sapiens	30-33
15374841-4	2005	In particular, the treatment of the mice with imatinib significantly attenuated airway hyperreactivity and peribronchial eosinophil accumulation, and significantly reduced Th2 cytokines, interleukin-4 and interleukin-13.	imatinib	46-54	heart and neural crest derivatives expressed 2	Mus musculus	172-175
15374841-4	2005	In particular, the treatment of the mice with imatinib significantly attenuated airway hyperreactivity and peribronchial eosinophil accumulation, and significantly reduced Th2 cytokines, interleukin-4 and interleukin-13.	imatinib	46-54	interleukin 4	Mus musculus	187-200
15374841-4	2005	In particular, the treatment of the mice with imatinib significantly attenuated airway hyperreactivity and peribronchial eosinophil accumulation, and significantly reduced Th2 cytokines, interleukin-4 and interleukin-13.	imatinib	46-54	interleukin 13	Mus musculus	205-219
15374841-5	2005	In addition, chemokines previously associated with allergen-induced pulmonary disease, CCL2, CCL5, and CCL6, were significantly reduced in the lungs of the imatinib-treated animals.	imatinib	156-164	chemokine (C-C motif) ligand 2	Mus musculus	87-91
15374841-5	2005	In addition, chemokines previously associated with allergen-induced pulmonary disease, CCL2, CCL5, and CCL6, were significantly reduced in the lungs of the imatinib-treated animals.	imatinib	156-164	chemokine (C-C motif) ligand 5	Mus musculus	93-97
15374841-5	2005	In addition, chemokines previously associated with allergen-induced pulmonary disease, CCL2, CCL5, and CCL6, were significantly reduced in the lungs of the imatinib-treated animals.	imatinib	156-164	chemokine (C-C motif) ligand 6	Mus musculus	103-107
15558795-0	2005	Overproduction of BCR-ABL induces apoptosis in imatinib mesylate-resistant cell lines.	imatinib	47-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
15945512-3	2005	Imatinib mesylate, a molecularly targeted agent that inhibits the KIT receptor tyrosine kinase, has now been demonstrated to be highly effective at inducing objective responses in GIST patients, and it improves overall survival.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	66-69
15558795-1	2005	BACKGROUND: Imatinib mesylate, a BCR-ABL tyrosine kinase inhibitor, induces apoptosis in chronic myeloid leukemia cells.	imatinib	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
15558795-5	2005	RESULTS: Removal of imatinib from culture medium led to a decrease in Bcr-Abl protein expression by Day 5, which was sustained for > or = 3 weeks of imatinib deprivation.	imatinib	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
15558795-5	2005	RESULTS: Removal of imatinib from culture medium led to a decrease in Bcr-Abl protein expression by Day 5, which was sustained for > or = 3 weeks of imatinib deprivation.	imatinib	152-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
15558795-8	2005	CONCLUSIONS: Thus, imatinib removal led to apoptosis of BCR-ABL-overexpressing leukemic cells, a phenomenon that could be exploited to sensitize imatinib-resistant cells to the cytotoxic effect of other drugs.	imatinib	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
15558795-8	2005	CONCLUSIONS: Thus, imatinib removal led to apoptosis of BCR-ABL-overexpressing leukemic cells, a phenomenon that could be exploited to sensitize imatinib-resistant cells to the cytotoxic effect of other drugs.	imatinib	145-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
16373964-4	2005	In addition, signal transduction mediated by activating mutations of c-Kit and PDGFR can be effectively blocked by specific tyrosine kinase inhibitors, such as Imatinib mesylate.	imatinib	160-177	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	69-74
16373964-4	2005	In addition, signal transduction mediated by activating mutations of c-Kit and PDGFR can be effectively blocked by specific tyrosine kinase inhibitors, such as Imatinib mesylate.	imatinib	160-177	platelet derived growth factor receptor beta	Homo sapiens	79-84
15747786-5	2005	Molecular methods of detecting BCR-ABL transcripts are showing promise in confirming drug resistance and predicting patient outcomes in response to imatinib mesylate therapy.	imatinib	148-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
15671560-3	2005	This study examined the effects of STI571 (imatinib mesylate), which inhibits PDGFR tyrosine kinase signaling, on the growth of human breast cancer cells in the bone of nude mice with consequent osteolysis.	imatinib	35-41	platelet derived growth factor receptor, beta polypeptide	Mus musculus	78-83
15671560-3	2005	This study examined the effects of STI571 (imatinib mesylate), which inhibits PDGFR tyrosine kinase signaling, on the growth of human breast cancer cells in the bone of nude mice with consequent osteolysis.	imatinib	43-60	platelet derived growth factor receptor, beta polypeptide	Mus musculus	78-83
15671560-12	2005	STI571 treatment inhibited PDGFR phosphorylation in tumor cells and tumor-associated endothelial cells, coincident with increased apoptosis, reduced proliferation, and lower microvessel density in the tumors.	imatinib	0-6	platelet derived growth factor receptor, beta polypeptide	Mus musculus	27-32
15671523-1	2005	UNLABELLED: Imatinib mesylate (Gleevec, Novartis Pharmaceuticals East Manruer, NJ) received accelerated approval on May 10, 2001 for the treatment of patients with chronic myeloid leukemia (CML) in (a) chronic phase after failure of IFN-alpha therapy, (b) accelerated phase, and (c) blast crisis.	imatinib	12-29	interferon alpha 1	Homo sapiens	233-242
15671523-30	2005	CONCLUSIONS: The results confirm those of the interim analysis and suggest that imatinib mesylate represents an effective therapeutic agent for the treatment of patients with CML in chronic phase after failure of IFN-alpha therapy, in blast crisis, and in accelerated phase.	imatinib	80-97	interferon alpha 1	Homo sapiens	213-222
16122278-1	2005	Imatinib is a potent and selective inhibitor of the protein tyrosine kinase Bcr-Abl, platelet-derived growth factor receptors (PDGFRalpha and PDGFRbeta) and KIT.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
16122278-1	2005	Imatinib is a potent and selective inhibitor of the protein tyrosine kinase Bcr-Abl, platelet-derived growth factor receptors (PDGFRalpha and PDGFRbeta) and KIT.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	127-137
16101455-7	2005	Nevertheless, MEK blockade efficiently and selectively sensitizes leukemic cells to sub-optimal doses of other apoptotic stimuli, including classical cytotoxics (nucleoside analogs, microtubule-targeted drugs, gamma-irradiation), biologicals (retinoids, interferons, arsenic trioxide), and, most interestingly, other signal transduction/apoptosis modulators (UCN-01, STI571, Bcl-2 antagonists).	imatinib	367-373	mitogen-activated protein kinase kinase 7	Homo sapiens	14-17
16122278-1	2005	Imatinib is a potent and selective inhibitor of the protein tyrosine kinase Bcr-Abl, platelet-derived growth factor receptors (PDGFRalpha and PDGFRbeta) and KIT.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	142-151
16122278-1	2005	Imatinib is a potent and selective inhibitor of the protein tyrosine kinase Bcr-Abl, platelet-derived growth factor receptors (PDGFRalpha and PDGFRbeta) and KIT.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	157-160
16122278-10	2005	Imatinib is metabolised mainly by the cytochrome P450 (CYP) 3A4 or CYP3A5 and can competitively inhibit the metabolism of drugs that are CYP3A4 or CYP3A5 substrates.	imatinib	0-8	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	67-73
16122278-10	2005	Imatinib is metabolised mainly by the cytochrome P450 (CYP) 3A4 or CYP3A5 and can competitively inhibit the metabolism of drugs that are CYP3A4 or CYP3A5 substrates.	imatinib	0-8	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	137-143
16122278-10	2005	Imatinib is metabolised mainly by the cytochrome P450 (CYP) 3A4 or CYP3A5 and can competitively inhibit the metabolism of drugs that are CYP3A4 or CYP3A5 substrates.	imatinib	0-8	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	147-153
15604885-6	2005	Use of tyrosine kinase inhibitors for AML therapy is hindered by the acquisition of mutations in the kinase catalytic domain, and in the case of BCR-ABL, these mutations confer resistance to imatinib.	imatinib	191-199	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-152
15604889-0	2005	Monitoring minimal residual disease in BCR-ABL-positive chronic myeloid leukemia in the imatinib era.	imatinib	88-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
15604889-1	2005	PURPOSE OF REVIEW: The total number of leukemia cells in the body is reduced very substantially in patients with BCR-ABL-positive chronic myeloid leukemia (CML) responding to imatinib.	imatinib	175-183	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
15604889-3	2005	Most patients with newly diagnosed chronic-phase CML who receive imatinib achieve complete cytogenetic remission (CCYR) and low levels of BCR-ABL transcripts, a status that seems to predict for relatively long survival compared with previous treatments.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
15785039-8	2005	Imatinib at concentrations >5 microM inhibited cell proliferation and induced apoptosis in both c-Kit-positive and c-Kit-negative cell lines.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	99-104
16286749-6	2005	Imatinib is primarily metabolized by the cytochrome CYP3A4.	imatinib	0-8	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	52-58
16286749-7	2005	Voriconazole is a cytochrome CYP3A4 inhibitor and can lead to high plasma levels of imatinib.	imatinib	84-92	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	29-35
15785039-8	2005	Imatinib at concentrations >5 microM inhibited cell proliferation and induced apoptosis in both c-Kit-positive and c-Kit-negative cell lines.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	118-123
15589595-4	2005	Clinical evidences showing the effect of a tyrosine kinase inhibitor, STI571, in c-KIT-positive gastrointestinal tumors, the role of COX-inhibitors chemotherapy-associated in colorectal cancer patients and the successful therapeutic possibility of anti-HER2 therapy in metastatic breast carcinoma, have encouraged us to study the expression of c-KIT, COX-2 and HER-2/neu in uterine carcinosarcomas.	imatinib	70-76	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	81-86
15709888-1	2005	Imatinib mesylate is a selective and potent small-molecule inhibitor of tyrosine kinases, including Kit, platelet-derived growth factor receptor, and the BCR-Abl fusion protein.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-161
15709925-1	2005	The BCR-ABL tyrosine kinase inhibitor imatinib has greatly improved the outcome for patients with chronic myeloid leukaemia (CML).	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
15629889-0	2005	Imatinib mesylate blocks a non-Smad TGF-beta pathway and reduces renal fibrogenesis in vivo.	imatinib	0-17	transforming growth factor, beta 1	Rattus norvegicus	36-44
15629889-4	2005	Inhibition of the c-abl kinase with imatinib mesylate prevents increased proliferation after TGF-beta addition without affecting PAK2.	imatinib	36-53	transforming growth factor, beta 1	Rattus norvegicus	93-101
15629889-8	2005	In contrast, imatinib substantially inhibited an increase in the number of interstitial fibroblasts and myofibroblasts and reduced the expression and interstitial accumulation of collagen type III, collagen type IV and fibronectin.	imatinib	13-21	fibronectin 1	Rattus norvegicus	188-230
15586222-1	2005	Imatinib mesylate, an inhibitor of tyrosine kinases including BCR-ABL and KIT, inhibits the growth inhibition of small cell lung cancer (SCLC) cell lines in vitro.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
15586222-1	2005	Imatinib mesylate, an inhibitor of tyrosine kinases including BCR-ABL and KIT, inhibits the growth inhibition of small cell lung cancer (SCLC) cell lines in vitro.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	74-77
15545668-1	2005	PURPOSE: Mutated KIT and platelet-derived growth factor receptor alpha (PDGFRalpha) tyrosine kinases are the principal targets for imatinib mesylate in the treatment of gastrointestinal stromal tumors (GISTs).	imatinib	131-148	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	17-20
17462285-4	2005	Targeted therapy (imatinib) can inhibit C-KIT and thereby aberrant tumoural proliferation.	imatinib	18-26	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	40-45
17462285-15	2005	With the emergence of techniques enabling identification of the precise mutational status of the C-KIT oncogene, the imatinib/surgery sequence could be tailored to the type of C-KIT mutation.	imatinib	117-125	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	97-102
17462285-15	2005	With the emergence of techniques enabling identification of the precise mutational status of the C-KIT oncogene, the imatinib/surgery sequence could be tailored to the type of C-KIT mutation.	imatinib	117-125	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	176-181
15545668-1	2005	PURPOSE: Mutated KIT and platelet-derived growth factor receptor alpha (PDGFRalpha) tyrosine kinases are the principal targets for imatinib mesylate in the treatment of gastrointestinal stromal tumors (GISTs).	imatinib	131-148	platelet derived growth factor receptor alpha	Homo sapiens	25-70
15545668-1	2005	PURPOSE: Mutated KIT and platelet-derived growth factor receptor alpha (PDGFRalpha) tyrosine kinases are the principal targets for imatinib mesylate in the treatment of gastrointestinal stromal tumors (GISTs).	imatinib	131-148	platelet derived growth factor receptor alpha	Homo sapiens	72-82
15611260-2	2005	We studied whether inhibition of BCR-ABL1 kinase activity using STI571 can relieve this differentiation block.	imatinib	64-70	BCR activator of RhoGEF and GTPase	Homo sapiens	33-41
16304378-1	2005	The treatment of chronic myeloid leukemia (CML) has been revolutionized by the small molecule BCR-ABL-selective kinase inhibitor imatinib.	imatinib	129-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
16304378-4	2005	Our understanding of the major mechanisms of imatinib resistance has led to the clinical development of two novel BCR-ABL inhibitors that harbor significant therapeutic promise in early clinical trial experience.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
16304378-5	2005	These agents, dasatinib (BMS-354825) and AMN107, are more potent inhibitors of BCR-ABL than imatinib, and moreover, harbor activity against nearly all imatinib-resistant BCR-ABL kinase domain mutant forms tested in vitro.	imatinib	151-159	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-177
16304378-6	2005	Notably, neither of these compounds is effective against the imatinib-resistant BCR-ABL/T315I mutation.	imatinib	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
15611260-4	2005	However, STI571-treated pre-B ALL cells expressed lambda L, but almost no kappa L chains.	imatinib	9-15	prolactin regulatory element binding	Homo sapiens	24-29
16605139-13	2005	However, imatinib has been used with success in patients with SM-hypereosinophilic syndrome (HES) and the FIPL1/PDGFRA fusion gene and in a patient with mastocytosis with a mutation outside of codon 816.	imatinib	9-17	platelet derived growth factor receptor alpha	Homo sapiens	112-118
15667033-7	2005	Genetic mutations involving the platelet-derived growth factor receptor genes (PDGFR-alpha and PDGFR-beta) have been pathogenetically linked to clonal eosinophilia, and their presence predicts treatment response to imatinib.	imatinib	215-223	platelet derived growth factor receptor alpha	Homo sapiens	79-90
15667033-7	2005	Genetic mutations involving the platelet-derived growth factor receptor genes (PDGFR-alpha and PDGFR-beta) have been pathogenetically linked to clonal eosinophilia, and their presence predicts treatment response to imatinib.	imatinib	215-223	platelet derived growth factor receptor beta	Homo sapiens	95-105
15496975-0	2005	KIAA1509 is a novel PDGFRB fusion partner in imatinib-responsive myeloproliferative disease associated with a t(5;14)(q33;q32).	imatinib	45-53	coiled-coil domain containing 88C	Homo sapiens	0-8
15496975-0	2005	KIAA1509 is a novel PDGFRB fusion partner in imatinib-responsive myeloproliferative disease associated with a t(5;14)(q33;q32).	imatinib	45-53	platelet derived growth factor receptor beta	Homo sapiens	20-26
15496975-1	2005	We report the cloning of a novel PDGFRB fusion gene partner in a patient with a chronic myeloproliferative disorder characterized by t(5;14)(q33;q32), who responded to treatment with imatinib mesylate.	imatinib	183-200	platelet derived growth factor receptor beta	Homo sapiens	33-39
15510211-0	2005	Evidence for D276G and L364I Bcr-Abl mutations in Ph+ leukaemic cells obtained from patients resistant to Imatinib.	imatinib	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
15739029-12	2005	The results of current study indicate that imatinib has a significant therapy benefit in CML patients in whom treatment with IFN alpha had failed.	imatinib	43-51	interferon alpha 1	Homo sapiens	125-134
16381169-4	2005	STI571, a small molecule inhibitor of the BCR/ABL, c-Kit and platelet derived growth factor receptor tyrosine kinase, produced pronounced clinical responses in patients with BCR/ABL positive chronic myeloid leukemia and c-Kit positive gastrointestial stromal tumors.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
16015044-1	2005	OBJECTIVE: Overexpression of KIT (CD117), a tyrosine kinase receptor, has been reported in a variety of tumors, some of which are susceptible to therapy with imatinib mesylate.	imatinib	158-175	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	29-32
16015044-1	2005	OBJECTIVE: Overexpression of KIT (CD117), a tyrosine kinase receptor, has been reported in a variety of tumors, some of which are susceptible to therapy with imatinib mesylate.	imatinib	158-175	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	34-39
16319507-3	2005	The aim of this trial was to evaluate imatinib, a tyrosine kinase inhibitor of PDGFR and c-kit, in patients with advanced HCC and impaired liver function.	imatinib	38-46	platelet derived growth factor receptor beta	Homo sapiens	79-84
16319507-3	2005	The aim of this trial was to evaluate imatinib, a tyrosine kinase inhibitor of PDGFR and c-kit, in patients with advanced HCC and impaired liver function.	imatinib	38-46	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	89-94
16381169-4	2005	STI571, a small molecule inhibitor of the BCR/ABL, c-Kit and platelet derived growth factor receptor tyrosine kinase, produced pronounced clinical responses in patients with BCR/ABL positive chronic myeloid leukemia and c-Kit positive gastrointestial stromal tumors.	imatinib	0-6	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	51-56
16381169-4	2005	STI571, a small molecule inhibitor of the BCR/ABL, c-Kit and platelet derived growth factor receptor tyrosine kinase, produced pronounced clinical responses in patients with BCR/ABL positive chronic myeloid leukemia and c-Kit positive gastrointestial stromal tumors.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-181
16381169-4	2005	STI571, a small molecule inhibitor of the BCR/ABL, c-Kit and platelet derived growth factor receptor tyrosine kinase, produced pronounced clinical responses in patients with BCR/ABL positive chronic myeloid leukemia and c-Kit positive gastrointestial stromal tumors.	imatinib	0-6	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	220-225
15501042-0	2004	Urea derivatives of STI571 as inhibitors of Bcr-Abl and PDGFR kinases.	imatinib	20-26	platelet derived growth factor receptor beta	Homo sapiens	56-61
15850018-0	2005	Lack of response to imatinib mesylate as second-line therapy in a patient with c-kit positive metastatic soft tissue leiomyosarcoma.	imatinib	20-37	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	79-84
16089297-3	2005	FIP1L1-PDGFR alpha is a novel therapeutic target of the kinase inhibitor imatinib (Glivec, Novartis), which provides the basis for the treatment of these patients with this drug.	imatinib	73-81	factor interacting with PAPOLA and CPSF1	Homo sapiens	0-6
16089297-3	2005	FIP1L1-PDGFR alpha is a novel therapeutic target of the kinase inhibitor imatinib (Glivec, Novartis), which provides the basis for the treatment of these patients with this drug.	imatinib	73-81	platelet derived growth factor receptor alpha	Homo sapiens	7-18
16089297-4	2005	FIP1L1-PDGFRA positive CEL patients respond very well to imatinib therapy, some of which are remarkable responses with normalization of the blood counts within 2 weeks after start of the therapy.	imatinib	57-65	factor interacting with PAPOLA and CPSF1	Homo sapiens	0-6
16089297-4	2005	FIP1L1-PDGFRA positive CEL patients respond very well to imatinib therapy, some of which are remarkable responses with normalization of the blood counts within 2 weeks after start of the therapy.	imatinib	57-65	platelet derived growth factor receptor alpha	Homo sapiens	7-13
16089297-6	2005	All imatinib treated FIP1L1-PDGFRA positive CEL patients achieve hematological and cytogenetic remission, and the majority of patients also achieve a molecular remission with the fusion gene no longer detectable in blood, even by the most sensitive PCR techniques.	imatinib	4-12	factor interacting with PAPOLA and CPSF1	Homo sapiens	21-27
16089297-6	2005	All imatinib treated FIP1L1-PDGFRA positive CEL patients achieve hematological and cytogenetic remission, and the majority of patients also achieve a molecular remission with the fusion gene no longer detectable in blood, even by the most sensitive PCR techniques.	imatinib	4-12	platelet derived growth factor receptor alpha	Homo sapiens	28-34
15583695-1	2004	KIT and PDGFRA are receptor tyrosine kinases that can be specifically inactivated by small-molecule tyrosine kinase inhibitors, notably imatinib mesylate.	imatinib	136-144	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
15583695-1	2004	KIT and PDGFRA are receptor tyrosine kinases that can be specifically inactivated by small-molecule tyrosine kinase inhibitors, notably imatinib mesylate.	imatinib	136-144	platelet derived growth factor receptor alpha	Homo sapiens	8-14
15501042-0	2004	Urea derivatives of STI571 as inhibitors of Bcr-Abl and PDGFR kinases.	imatinib	20-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
16116902-6	2005	In detection of aberration of BCR-ABL gene the patients received stem hemopoietic cells, from June 2004 imatinib was added to chemotherapy in the period of induction and consolidation.	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
15507431-6	2004	We also demonstrate that Gleevec (STI-571, Imatinib) inhibits the isolated kinase domains of both unphosphorylated Syk and phosphorylated Abl with comparable potency.	imatinib	34-41	spleen associated tyrosine kinase	Homo sapiens	115-118
15507431-6	2004	We also demonstrate that Gleevec (STI-571, Imatinib) inhibits the isolated kinase domains of both unphosphorylated Syk and phosphorylated Abl with comparable potency.	imatinib	34-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-141
15507431-6	2004	We also demonstrate that Gleevec (STI-571, Imatinib) inhibits the isolated kinase domains of both unphosphorylated Syk and phosphorylated Abl with comparable potency.	imatinib	43-51	spleen associated tyrosine kinase	Homo sapiens	115-118
15507431-6	2004	We also demonstrate that Gleevec (STI-571, Imatinib) inhibits the isolated kinase domains of both unphosphorylated Syk and phosphorylated Abl with comparable potency.	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-141
15505216-2	2004	Imatinib mesylate has been useful in the treatment of Philadelphia chromosome-positive chronic myelogenous leukemia and B cell acute lymphoblastic leukemia through the inhibition of BCR-ABL tyrosine kinase activity.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-189
15505216-3	2004	Imatinib mesylate has also been shown to inhibit KIT, ARG, and platelet-derived growth factor receptors alpha and beta, and potentially other tyrosine kinases.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	49-52
15505216-5	2004	In contrast, imatinib mesylate effectively eliminated BCR-ABL(+) KIT(+)-expressing leukemic cells.	imatinib	13-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
15505216-5	2004	In contrast, imatinib mesylate effectively eliminated BCR-ABL(+) KIT(+)-expressing leukemic cells.	imatinib	13-30	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	65-68
15501042-2	2004	Urea derivatives, structurally related to the therapeutic agent STI571, have been identified, which potently inhibit the tyrosine kinase activity of recombinant Abl.	imatinib	64-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-164
15601563-0	2004	[Efficacy of imatinib mesylate, a specific inhibitor of BCR/ABL tyrosine kinase, on chronic myeloid leukemia in blast phase].	imatinib	13-30	BCR activator of RhoGEF and GTPase	Homo sapiens	56-79
15601563-2	2004	This study was to evaluate efficacy of imatinib mesylate, a specific inhibitor of BCR/ABL tyrosine kinase, on CML in blast phase.	imatinib	39-56	BCR activator of RhoGEF and GTPase	Homo sapiens	82-105
15618926-3	2004	c-kit expression has been demonstrated previously in primary MCCs thus raising the possibility of treating MCCs with imatinib mesylate, the tyrosine kinase inhibitor that has shown promise in the management of c-kit expressing tumors.	imatinib	117-134	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-5
15618926-3	2004	c-kit expression has been demonstrated previously in primary MCCs thus raising the possibility of treating MCCs with imatinib mesylate, the tyrosine kinase inhibitor that has shown promise in the management of c-kit expressing tumors.	imatinib	117-134	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	210-215
15583853-7	2004	PDGFR signalling is inhibited by imatinib mesylate, and this compound has clear clinical activity in patients with myeloid malignancies, GIST and DFSP.	imatinib	33-50	platelet derived growth factor receptor beta	Homo sapiens	0-5
15549490-2	2004	Imatinib offers the first effective treatment for patients with GISTs, but the therapeutic outcome strongly depends on the type of KIT mutation.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	131-134
15315971-7	2004	Additionally, incubations with transport inhibitors showed that verapamil, amantadine, and procainamide, inhibitors of the human organic cation transporter 1 (hOCT1), significantly decreased imatinib uptake into CEM cells, whereas the inhibition of hOCT2 or hOCT3 had no effect, indicating that influx into the cells is an active process likely to be mediated by hOCT1.	imatinib	191-199	solute carrier family 22 member 1	Homo sapiens	129-157
15315971-7	2004	Additionally, incubations with transport inhibitors showed that verapamil, amantadine, and procainamide, inhibitors of the human organic cation transporter 1 (hOCT1), significantly decreased imatinib uptake into CEM cells, whereas the inhibition of hOCT2 or hOCT3 had no effect, indicating that influx into the cells is an active process likely to be mediated by hOCT1.	imatinib	191-199	solute carrier family 22 member 1	Homo sapiens	159-164
15315971-7	2004	Additionally, incubations with transport inhibitors showed that verapamil, amantadine, and procainamide, inhibitors of the human organic cation transporter 1 (hOCT1), significantly decreased imatinib uptake into CEM cells, whereas the inhibition of hOCT2 or hOCT3 had no effect, indicating that influx into the cells is an active process likely to be mediated by hOCT1.	imatinib	191-199	POU class 2 homeobox 2	Homo sapiens	249-254
15315971-7	2004	Additionally, incubations with transport inhibitors showed that verapamil, amantadine, and procainamide, inhibitors of the human organic cation transporter 1 (hOCT1), significantly decreased imatinib uptake into CEM cells, whereas the inhibition of hOCT2 or hOCT3 had no effect, indicating that influx into the cells is an active process likely to be mediated by hOCT1.	imatinib	191-199	solute carrier family 22 member 3	Homo sapiens	258-263
15315971-7	2004	Additionally, incubations with transport inhibitors showed that verapamil, amantadine, and procainamide, inhibitors of the human organic cation transporter 1 (hOCT1), significantly decreased imatinib uptake into CEM cells, whereas the inhibition of hOCT2 or hOCT3 had no effect, indicating that influx into the cells is an active process likely to be mediated by hOCT1.	imatinib	191-199	solute carrier family 22 member 1	Homo sapiens	363-368
15315971-11	2004	Differential expression of influx (hOCT1) and efflux (MDR1) transporters may be a critical determinant of intracellular drug levels and, hence, resistance to imatinib.	imatinib	158-166	solute carrier family 22 member 1	Homo sapiens	35-40
15315971-11	2004	Differential expression of influx (hOCT1) and efflux (MDR1) transporters may be a critical determinant of intracellular drug levels and, hence, resistance to imatinib.	imatinib	158-166	ATP binding cassette subfamily B member 1	Homo sapiens	54-58
15650267-2	2004	Chronic myeloid leukemia (CML) has provided one of the best models, as the identification of a leukemia-specific hybrid tyrosine kinase (BCR-ABL, p210, p190) has led to the identification and the successful therapeutic application of a powerful tyrosine kinase inhibitor, imatinib.	imatinib	272-280	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-144
15650267-2	2004	Chronic myeloid leukemia (CML) has provided one of the best models, as the identification of a leukemia-specific hybrid tyrosine kinase (BCR-ABL, p210, p190) has led to the identification and the successful therapeutic application of a powerful tyrosine kinase inhibitor, imatinib.	imatinib	272-280	contactin associated protein 1	Homo sapiens	152-156
15611623-0	2004	Pharmacokinetic resistance to imatinib mesylate: role of the ABC drug pumps ABCG2 (BCRP) and ABCB1 (MDR1) in the oral bioavailability of imatinib.	imatinib	30-38	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	76-81
15611623-0	2004	Pharmacokinetic resistance to imatinib mesylate: role of the ABC drug pumps ABCG2 (BCRP) and ABCB1 (MDR1) in the oral bioavailability of imatinib.	imatinib	137-145	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	76-81
15583854-4	2004	The ICC tumors are called gastrointestinal stromal tumors (GISTs), and GISTs are a good target for the Kit inhibitor imatinib mesylate.	imatinib	117-134	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	103-106
15611623-0	2004	Pharmacokinetic resistance to imatinib mesylate: role of the ABC drug pumps ABCG2 (BCRP) and ABCB1 (MDR1) in the oral bioavailability of imatinib.	imatinib	137-145	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	83-87
15611623-0	2004	Pharmacokinetic resistance to imatinib mesylate: role of the ABC drug pumps ABCG2 (BCRP) and ABCB1 (MDR1) in the oral bioavailability of imatinib.	imatinib	137-145	ATP binding cassette subfamily B member 1	Homo sapiens	93-98
15583854-5	2004	The interrelationship between the type of Kit gain-of-function mutations and the therapeutic effect of imatinib mesylate has been well characterized in GISTs.	imatinib	103-120	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	42-45
15611623-0	2004	Pharmacokinetic resistance to imatinib mesylate: role of the ABC drug pumps ABCG2 (BCRP) and ABCB1 (MDR1) in the oral bioavailability of imatinib.	imatinib	137-145	ATP binding cassette subfamily B member 1	Homo sapiens	100-104
15844661-0	2004	Cyclooxygenase-2 induction and prostaglandin E2 accumulation in squamous cell carcinoma as a consequence of epidermal growth factor receptor activation by imatinib mesylate.	imatinib	155-172	prostaglandin-endoperoxide synthase 2	Homo sapiens	0-16
15638956-2	2004	In addition to paralleling what is already known about c-kit mutations that drive the proliferation of gastrointestinal stromal tumors and their response to imatinib, and providing the possibility of prospectively selecting patients with NSCLC who have a high probability of responding to EGFR TK inhibitors, these reports will likely have much broader implications with regard to the optimal and most expeditious means to develop rationally designed, target-based therapeutic agents--first establishing proof of principle in patients whose malignancies are dependent or driven by aberrations of the therapeutic"s target.	imatinib	157-165	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	55-60
22900354-3	2004	The present review focuses mainly on the development of PTK inhibitors in clinical trials, with special emphasis on imatinib mesylate, a rationally designed, potent oral anticancer agent and selective inhibitor for Abl tyrosine kinase, including Bcr-Abl, C-kit and platelet-derived growth factor-receptor tyrosine kinases, which has been implicated in several malignancies, including chronic myeloid leukemia and gastrointestinal stromal tumour.	imatinib	116-133	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	255-260
15844661-0	2004	Cyclooxygenase-2 induction and prostaglandin E2 accumulation in squamous cell carcinoma as a consequence of epidermal growth factor receptor activation by imatinib mesylate.	imatinib	155-172	epidermal growth factor receptor	Homo sapiens	108-140
15844661-5	2004	Imatinib induced expression of COX-2 in a dose-dependent manner with concomitant accumulation of prostaglandin E2.	imatinib	0-8	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	31-36
15844661-6	2004	COX-2 induction by imatinib was initiated through epidermal growth factor (EGF) receptor kinase activation and downstream signaling through mitogenic-activated protein kinase.	imatinib	19-27	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	0-5
15844661-6	2004	COX-2 induction by imatinib was initiated through epidermal growth factor (EGF) receptor kinase activation and downstream signaling through mitogenic-activated protein kinase.	imatinib	19-27	epidermal growth factor receptor	Homo sapiens	50-88
15844661-7	2004	COX-2 induction by imatinib was blocked by MEK1 or EGF receptor inhibition.	imatinib	19-27	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	0-5
15844661-7	2004	COX-2 induction by imatinib was blocked by MEK1 or EGF receptor inhibition.	imatinib	19-27	mitogen-activated protein kinase kinase 1	Homo sapiens	43-47
15844661-7	2004	COX-2 induction by imatinib was blocked by MEK1 or EGF receptor inhibition.	imatinib	19-27	epidermal growth factor receptor	Homo sapiens	51-63
15844661-9	2004	Imatinib failed to activate EGF receptor signals in other tumor types, suggesting that COX-2 induction in imatinib-treated cells is mediated through release of autocrine factors expressed or activated in squamous tumors.	imatinib	106-114	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	87-92
15844661-10	2004	COX-2 induction by imatinib in squamous tumors derived from the head and neck region is unique with respect to other target-specific agents and may represent one of the unintended toxic effects of imatinib described in some patients.	imatinib	19-27	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	0-5
15844661-10	2004	COX-2 induction by imatinib in squamous tumors derived from the head and neck region is unique with respect to other target-specific agents and may represent one of the unintended toxic effects of imatinib described in some patients.	imatinib	197-205	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	0-5
15621768-11	2004	Imatinib is an excellent candidate for first line treatment of Loeffler"s endocarditis, especially when the FIP1L1/PDGFA fusion gene is detected.	imatinib	0-8	factor interacting with PAPOLA and CPSF1	Homo sapiens	108-114
15496979-6	2004	Synergy between NVP-LAQ824 and imatinib was demonstrated against BCR/ABL-expressing K562 myeloid leukemia cell lines.	imatinib	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
15566522-10	2004	However, a significant decrease in epidermal growth factor receptor (EGFR) and focal adhesion kinase (FAK) phosphorylation was observed following treatment with STI-571.	imatinib	161-168	epidermal growth factor receptor	Homo sapiens	35-67
15566522-10	2004	However, a significant decrease in epidermal growth factor receptor (EGFR) and focal adhesion kinase (FAK) phosphorylation was observed following treatment with STI-571.	imatinib	161-168	epidermal growth factor receptor	Homo sapiens	69-73
15621768-11	2004	Imatinib is an excellent candidate for first line treatment of Loeffler"s endocarditis, especially when the FIP1L1/PDGFA fusion gene is detected.	imatinib	0-8	platelet derived growth factor subunit A	Homo sapiens	115-120
15678915-8	2004	On the other hand, 8 patients who received imatinib without SCT showed a remarkable decrease in bcr-abl/abl ratios.	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
15475568-2	2004	Derivatives from this compound class are effective against most of the imatinib mesylate-resistant BCR-ABL mutants isolated from advanced chronic myeloid leukemia patients.	imatinib	71-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
15573099-2	2004	However, as extensively documented for the BCR-ABL oncogene in imatinib-treated leukaemia patients, clinical resistance caused by mutations in the targeted oncogene has been observed.	imatinib	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
15678915-8	2004	On the other hand, 8 patients who received imatinib without SCT showed a remarkable decrease in bcr-abl/abl ratios.	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-82
15657578-8	2004	Imatinib mesylate inhibited FAK phosphorylation only at high doses.	imatinib	0-17	protein tyrosine kinase 2	Homo sapiens	28-31
15678915-11	2004	In conclusion, it is thought that measurement of RQ-PCR-based major bcr/abl mRNA in patients who were given imatinib and were treated with SCT is useful for the evaluation of MRD and in deciding additional treatment.	imatinib	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-75
15251980-0	2004	Imatinib mesylate (STI571) is a substrate for the breast cancer resistance protein (BCRP)/ABCG2 drug pump.	imatinib	0-17	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	50-82
15631651-10	2004	In conclusion, P21(WAF) inhibits the proliferation of K562 cell, meanwhile slightly inhibits its apoptosis induced by STI571and decrease its sensitivity to STI571.	imatinib	118-124	cyclin dependent kinase inhibitor 1A	Homo sapiens	15-23
15547187-0	2004	Development of c-Kit-expressing small-cell lung cancer in a chronic myeloid leukemia patient during imatinib treatment.	imatinib	100-108	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	15-20
15284118-7	2004	Treatment with low-dose imatinib (100 mg/d) produced complete and durable responses in all 8 FIP1L1-PDGFRA(+) cases treated.	imatinib	24-32	factor interacting with PAPOLA and CPSF1	Homo sapiens	93-99
15284118-7	2004	Treatment with low-dose imatinib (100 mg/d) produced complete and durable responses in all 8 FIP1L1-PDGFRA(+) cases treated.	imatinib	24-32	platelet derived growth factor receptor alpha	Homo sapiens	100-106
15542802-1	2004	PURPOSE: KIT is a target for imatinib mesylate (Gleevec; Novartis Pharma, Basel, Switzerland).	imatinib	29-46	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	9-12
15256429-0	2004	Real-time quantitative PCR analysis can be used as a primary screen to identify patients with CML treated with imatinib who have BCR-ABL kinase domain mutations.	imatinib	111-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
15256429-1	2004	Mutations within the BCR-ABL kinase domain in imatinib-treated chronic myeloid leukemia (CML) are the main mechanism of acquired resistance.	imatinib	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
15251980-0	2004	Imatinib mesylate (STI571) is a substrate for the breast cancer resistance protein (BCRP)/ABCG2 drug pump.	imatinib	0-17	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	84-88
15251980-0	2004	Imatinib mesylate (STI571) is a substrate for the breast cancer resistance protein (BCRP)/ABCG2 drug pump.	imatinib	0-17	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	90-95
15494718-0	2004	Tyrosine kinase inhibitor AG1024 exerts antileukaemic effects on STI571-resistant Bcr-Abl expressing cells and decreases AKT phosphorylation.	imatinib	65-71	TXK tyrosine kinase	Homo sapiens	0-15
15494718-0	2004	Tyrosine kinase inhibitor AG1024 exerts antileukaemic effects on STI571-resistant Bcr-Abl expressing cells and decreases AKT phosphorylation.	imatinib	65-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
15494718-3	2004	Targeting these abnormalities by blocking TK of BCR-ABL with STI571 provided a promising approach for the therapy of CML.	imatinib	61-67	TXK tyrosine kinase	Homo sapiens	42-44
15251980-0	2004	Imatinib mesylate (STI571) is a substrate for the breast cancer resistance protein (BCRP)/ABCG2 drug pump.	imatinib	19-25	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	50-82
15494718-3	2004	Targeting these abnormalities by blocking TK of BCR-ABL with STI571 provided a promising approach for the therapy of CML.	imatinib	61-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
15251980-0	2004	Imatinib mesylate (STI571) is a substrate for the breast cancer resistance protein (BCRP)/ABCG2 drug pump.	imatinib	19-25	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	84-88
15494718-4	2004	The recent development of resistance to STI571 illustrates, however, that the use of other TK inhibitors could be of major interest for therapeutic purposes.	imatinib	40-46	TXK tyrosine kinase	Homo sapiens	91-93
15251980-0	2004	Imatinib mesylate (STI571) is a substrate for the breast cancer resistance protein (BCRP)/ABCG2 drug pump.	imatinib	19-25	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	90-95
15251980-3	2004	Indeed, several molecular mechanisms leading to imatinib resistance have already been reported, including overexpression of the MDR1/ABCB1 drug pump.	imatinib	48-56	ATP binding cassette subfamily B member 1	Homo sapiens	128-132
15251980-3	2004	Indeed, several molecular mechanisms leading to imatinib resistance have already been reported, including overexpression of the MDR1/ABCB1 drug pump.	imatinib	48-56	ATP binding cassette subfamily B member 1	Homo sapiens	133-138
15372471-2	2004	Imatinib mesylate is a tyrosine kinase inhibitor targeting platelet-derived growth factor receptor-beta (PDGFRB), BCR-ABL, and KIT.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	59-103
15372471-2	2004	Imatinib mesylate is a tyrosine kinase inhibitor targeting platelet-derived growth factor receptor-beta (PDGFRB), BCR-ABL, and KIT.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	105-111
15251980-4	2004	We examined whether imatinib is a substrate for the breast cancer resistance protein (BCRP)/ABCG2 drug pump that is frequently overexpressed in human tumors.	imatinib	20-28	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	52-84
15372471-2	2004	Imatinib mesylate is a tyrosine kinase inhibitor targeting platelet-derived growth factor receptor-beta (PDGFRB), BCR-ABL, and KIT.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
15372471-2	2004	Imatinib mesylate is a tyrosine kinase inhibitor targeting platelet-derived growth factor receptor-beta (PDGFRB), BCR-ABL, and KIT.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	127-130
15251980-4	2004	We examined whether imatinib is a substrate for the breast cancer resistance protein (BCRP)/ABCG2 drug pump that is frequently overexpressed in human tumors.	imatinib	20-28	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	86-90
15251980-4	2004	We examined whether imatinib is a substrate for the breast cancer resistance protein (BCRP)/ABCG2 drug pump that is frequently overexpressed in human tumors.	imatinib	20-28	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	92-97
15251980-5	2004	Using a panel of well-defined BCRP-overexpressing cell lines, we provide the first evidence that imatinib is a substrate for BCRP, that it competes with mitoxantrone for drug export, and that BCRP-mediated efflux can be reversed by the fumitremorgin C analog Ko-143.	imatinib	97-105	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	30-34
15251980-5	2004	Using a panel of well-defined BCRP-overexpressing cell lines, we provide the first evidence that imatinib is a substrate for BCRP, that it competes with mitoxantrone for drug export, and that BCRP-mediated efflux can be reversed by the fumitremorgin C analog Ko-143.	imatinib	97-105	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	125-129
15251980-5	2004	Using a panel of well-defined BCRP-overexpressing cell lines, we provide the first evidence that imatinib is a substrate for BCRP, that it competes with mitoxantrone for drug export, and that BCRP-mediated efflux can be reversed by the fumitremorgin C analog Ko-143.	imatinib	97-105	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	125-129
15251980-6	2004	Since BCRP is highly expressed in the gastrointestinal tract, BCRP might not only play a role in cellular resistance of tumor cells but also influence the gastrointestinal absorption of imatinib.	imatinib	186-194	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	6-10
15251980-6	2004	Since BCRP is highly expressed in the gastrointestinal tract, BCRP might not only play a role in cellular resistance of tumor cells but also influence the gastrointestinal absorption of imatinib.	imatinib	186-194	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	62-66
15618851-6	2004	Because of the tumour"s intense expression of CD117 (c-kit), the patient is now treated with the tyrosine kinase inhibitor imatinib (STI571).	imatinib	123-131	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	46-51
15468123-5	2004	Tyrosine phosphorylation was inhibited by imatinib in a dose-dependent manner, but not modified by other inhibitors demonstrating that the staining detected is specific to Bcr-Abl phosphorylation.	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-179
15468123-6	2004	The staining of imatinib-resistant cell lines such as the mutated BaF/Bcr-AblT315I cell line or resistant CML patient cells, showed that hyperphosphorylation was not affected by imatinib treatment.	imatinib	16-24	BAF nuclear assembly factor 1	Homo sapiens	66-69
15618851-6	2004	Because of the tumour"s intense expression of CD117 (c-kit), the patient is now treated with the tyrosine kinase inhibitor imatinib (STI571).	imatinib	123-131	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	53-58
15520863-7	2004	Moreover, inhibition of c-Abl by imatinib prevented TGF-beta-induced ECM gene expression, morphologic transformation, and cell proliferation independently of any effect on Smad signaling.	imatinib	33-41	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	24-29
15539083-0	2004	A novel mechanism for imatinib mesylate (STI571) resistance in CML cell line KT-1: role of TC-PTP in modulating signals downstream from the BCR-ABL fusion protein.	imatinib	41-47	protein tyrosine phosphatase, non-receptor type 2	Mus musculus	91-97
15539083-8	2004	Furthermore, STAT5 phosphorylation was ablated by imatinib mesylate in KT-1 cells but remained elevated in KTR cells.	imatinib	50-67	signal transducer and activator of transcription 5A	Mus musculus	13-18
15539083-10	2004	Importantly, reconstitution of TC-PTP in KTR cells to levels found in parental KT-1 cells restored their sensitivity to imatinib mesylate as monitored by reduced proliferation and increased apoptosis.	imatinib	120-137	protein tyrosine phosphatase, non-receptor type 2	Mus musculus	31-37
15539083-11	2004	CONCLUSIONS: We have demonstrated that forced expression of TC-PTP in imatinib mesylate-resistant KTR cells can restore sensitivity to imatinib mesylate.	imatinib	70-87	protein tyrosine phosphatase, non-receptor type 2	Mus musculus	60-66
15539083-11	2004	CONCLUSIONS: We have demonstrated that forced expression of TC-PTP in imatinib mesylate-resistant KTR cells can restore sensitivity to imatinib mesylate.	imatinib	135-152	protein tyrosine phosphatase, non-receptor type 2	Mus musculus	60-66
15539083-12	2004	Our studies indicate that loss of TC-PTP may represent a novel mechanism by which CML cells can acquire imatinib mesylate-resistance.	imatinib	104-121	protein tyrosine phosphatase, non-receptor type 2	Mus musculus	34-40
15507676-2	2004	Screening GISTs for KIT gene mutations is important for translational research studies and for providing prognostic information on the likelihood of tumor response to treatment with the kinase inhibitor imatinib mesylate (Gleevec).	imatinib	203-220	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	20-23
15509806-3	2004	Inhibition of BCR-ABL by STI571 results in down-regulation of cyclin D2 expression, activation of FoxO3a activity, and up-regulation of BCL6 expression.	imatinib	25-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
15380338-4	2004	We examined SNPs in the PDGFR alpha and beta gene regions in STI571-treated patients with and without life-threatening edema or cerebral hygromas, and in healthy volunteers.	imatinib	61-67	platelet derived growth factor receptor alpha	Homo sapiens	24-35
15509806-3	2004	Inhibition of BCR-ABL by STI571 results in down-regulation of cyclin D2 expression, activation of FoxO3a activity, and up-regulation of BCL6 expression.	imatinib	25-31	cyclin D2	Homo sapiens	62-71
15509806-3	2004	Inhibition of BCR-ABL by STI571 results in down-regulation of cyclin D2 expression, activation of FoxO3a activity, and up-regulation of BCL6 expression.	imatinib	25-31	forkhead box O3	Homo sapiens	98-104
15509806-3	2004	Inhibition of BCR-ABL by STI571 results in down-regulation of cyclin D2 expression, activation of FoxO3a activity, and up-regulation of BCL6 expression.	imatinib	25-31	BCL6 transcription repressor	Homo sapiens	136-140
15509806-8	2004	Furthermore, silencing of FoxO3a and BCL6 in BCR-ABL-expressing cells abolishes STI571-mediated effects on cyclin D2.	imatinib	80-86	forkhead box O3	Homo sapiens	26-32
15509806-8	2004	Furthermore, silencing of FoxO3a and BCL6 in BCR-ABL-expressing cells abolishes STI571-mediated effects on cyclin D2.	imatinib	80-86	BCL6 transcription repressor	Homo sapiens	37-41
15509806-8	2004	Furthermore, silencing of FoxO3a and BCL6 in BCR-ABL-expressing cells abolishes STI571-mediated effects on cyclin D2.	imatinib	80-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
15509806-8	2004	Furthermore, silencing of FoxO3a and BCL6 in BCR-ABL-expressing cells abolishes STI571-mediated effects on cyclin D2.	imatinib	80-86	cyclin D2	Homo sapiens	107-116
15492236-7	2004	We conclude that TP53BP1-PDGFRB is a novel imatinib target in atypical chronic myeloid leukemia.	imatinib	43-51	platelet derived growth factor receptor beta	Homo sapiens	25-31
15777512-3	2004	Among them, CD117 was detected positive in 29 patients; 2 patients received imatinib mesylate before operation and 28 patients with unresectable and(or) metastatic GIST received oral imatinib mesylate daily at dose of 200-600 mg. Three patients were lost in follow-up and the objective effect was evaluated in 25 patients.	imatinib	183-200	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	12-17
15256422-2	2004	Imatinib mesylate (Gleevec, STI571), a Bcr-Abl kinase inhibitor, selectively inhibits proliferation and promotes apoptosis of CML cells.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
15256422-2	2004	Imatinib mesylate (Gleevec, STI571), a Bcr-Abl kinase inhibitor, selectively inhibits proliferation and promotes apoptosis of CML cells.	imatinib	19-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
15256422-2	2004	Imatinib mesylate (Gleevec, STI571), a Bcr-Abl kinase inhibitor, selectively inhibits proliferation and promotes apoptosis of CML cells.	imatinib	28-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
15256422-4	2004	The most common imatinib mesylate resistance mechanism involves Bcr-Abl kinase domain mutations that impart varying degrees of drug insensitivity.	imatinib	16-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
15179523-0	2004	[Regression of the Philadelphia chromosome (bcr/abl)-positive myelo- and megakaryopoiesis after Imatinib (STI571) therapy in chronic myelogenous leukemia (CML)].	imatinib	96-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
15179523-0	2004	[Regression of the Philadelphia chromosome (bcr/abl)-positive myelo- and megakaryopoiesis after Imatinib (STI571) therapy in chronic myelogenous leukemia (CML)].	imatinib	106-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
15256422-8	2004	Importantly, the low nanomolar cellular and biochemical inhibitory properties of AP23464 extend to frequently observed imatinib mesylate-resistant Bcr-Abl mutants, including nucleotide binding P-loop mutants Q252H, Y253F, E255K, C-terminal loop mutant M351T, and activation loop mutant H396P.	imatinib	119-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-154
15256422-10	2004	The potency of AP23464 against imatinib mesylate-refractory Bcr-Abl and its distinct binding mode relative to imatinib mesylate warrant further investigation of AP23464 for the treatment of CML.	imatinib	31-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
15492236-0	2004	p53-Binding protein 1 is fused to the platelet-derived growth factor receptor beta in a patient with a t(5;15)(q33;q22) and an imatinib-responsive eosinophilic myeloproliferative disorder.	imatinib	127-135	tumor protein p53 binding protein 1	Homo sapiens	0-21
15492236-0	2004	p53-Binding protein 1 is fused to the platelet-derived growth factor receptor beta in a patient with a t(5;15)(q33;q22) and an imatinib-responsive eosinophilic myeloproliferative disorder.	imatinib	127-135	platelet derived growth factor receptor beta	Homo sapiens	38-82
15492236-6	2004	Imatinib, a known inhibitor of PDGFRbeta, blocked the growth of patient colony-forming unit, granulocyte-macrophage in vitro and produced a clinically significant response before relapse and subsequent death with imatinib-resistant disease.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	31-40
15492236-6	2004	Imatinib, a known inhibitor of PDGFRbeta, blocked the growth of patient colony-forming unit, granulocyte-macrophage in vitro and produced a clinically significant response before relapse and subsequent death with imatinib-resistant disease.	imatinib	213-221	platelet derived growth factor receptor beta	Homo sapiens	31-40
15492236-7	2004	We conclude that TP53BP1-PDGFRB is a novel imatinib target in atypical chronic myeloid leukemia.	imatinib	43-51	tumor protein p53 binding protein 1	Homo sapiens	17-24
15389438-0	2004	Early prediction of molecular remission by monitoring BCR-ABL transcript levels in patients achieving a complete cytogenetic response after imatinib therapy for posttransplantation chronic myelogenous leukemia relapse.	imatinib	140-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
15326474-3	2004	For example, GISTs with KIT exon 11 mutations are typically gastric and have excellent imatinib response, whereas those with KIT exon 9 mutations generally arise in the small bowel and are less responsive to imatinib.	imatinib	87-95	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	24-27
15166033-1	2004	Imatinib mesylate is a small molecule drug that in vitro inhibits the Abelson (Abl), Arg (abl-related gene), stem cell factor receptor (Kit), and platelet-derived growth factor receptor A and B (PDGFRA and PDGFRB) tyrosine kinases.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
15166033-1	2004	Imatinib mesylate is a small molecule drug that in vitro inhibits the Abelson (Abl), Arg (abl-related gene), stem cell factor receptor (Kit), and platelet-derived growth factor receptor A and B (PDGFRA and PDGFRB) tyrosine kinases.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-82
15166033-1	2004	Imatinib mesylate is a small molecule drug that in vitro inhibits the Abelson (Abl), Arg (abl-related gene), stem cell factor receptor (Kit), and platelet-derived growth factor receptor A and B (PDGFRA and PDGFRB) tyrosine kinases.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-93
15166033-1	2004	Imatinib mesylate is a small molecule drug that in vitro inhibits the Abelson (Abl), Arg (abl-related gene), stem cell factor receptor (Kit), and platelet-derived growth factor receptor A and B (PDGFRA and PDGFRB) tyrosine kinases.	imatinib	0-17	platelet derived growth factor receptor alpha	Homo sapiens	195-201
15166033-1	2004	Imatinib mesylate is a small molecule drug that in vitro inhibits the Abelson (Abl), Arg (abl-related gene), stem cell factor receptor (Kit), and platelet-derived growth factor receptor A and B (PDGFRA and PDGFRB) tyrosine kinases.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	206-212
15381372-3	2004	We have established a novel STI571 (Gleevec/Glivec, imatinib mesylate)-resistant acute myelocytic leukemia cell line (SR-1) from an STI571-resistant blast crisis patient.	imatinib	28-34	spectrotype regulation	Mus musculus	118-122
15381372-3	2004	We have established a novel STI571 (Gleevec/Glivec, imatinib mesylate)-resistant acute myelocytic leukemia cell line (SR-1) from an STI571-resistant blast crisis patient.	imatinib	52-69	spectrotype regulation	Mus musculus	118-122
15381372-10	2004	We hope that our SR-1 cell line may be useful in molecular pathogenetic investigations of STI571-resistant CML.	imatinib	90-96	spectrotype regulation	Mus musculus	17-21
15475456-0	2004	Imatinib (STI571)-mediated changes in glucose metabolism in human leukemia BCR-ABL-positive cells.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
15470331-1	2004	OBJECTIVE: Imatinib is a potent inhibitor of the Bcr-Abl and c- kit tyrosine kinases and is approved for the treatment of Philadelphia chromosome-positive chronic myelogenous leukemia and gastrointestinal stromal tumors.	imatinib	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
15470331-2	2004	Because imatinib is predominantly metabolized by cytochrome P450 (CYP) 3A4, its pharmacokinetics may be altered when it is coadministered with drugs or herbs (eg, St John"s wort) that modulate CYP3A4 activity.	imatinib	8-16	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	193-199
15475456-0	2004	Imatinib (STI571)-mediated changes in glucose metabolism in human leukemia BCR-ABL-positive cells.	imatinib	10-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
15475456-1	2004	The therapeutic efficacy of imatinib mesylate (Gleevec) is based on its specific inhibition of the BCR-ABL oncogene protein, a widely expressed tyrosine kinase in chronic myelogenous leukemia (CML) cells.	imatinib	28-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
15475456-2	2004	The goal of this study was to evaluate glucose metabolism in BCR-ABL-positive cells that are sensitive to imatinib exposure.	imatinib	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
15475456-7	2004	In BCR-ABL-positive cells, the relevant therapeutic concentrations of imatinib (0.1-1.0 micromol/L) decreased glucose uptake from the media by suppressing glycolytic cell activity (C3-lactate at 0.25 mmol/L, 65% for K562 and 77% for CML-T1 versus control).	imatinib	70-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	3-10
15475456-11	2004	Unlike standard chemotherapeutics, imatinib, without cytocidal activity, reverses the Warburg effect in BCR-ABL-positive cells by switching from glycolysis to mitochondrial glucose metabolism, resulting in decreased glucose uptake and higher energy state.	imatinib	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
15477214-0	2004	Lack of response to imatinib mesylate in a patient with accelerated phase myeloproliferative disorder with rearrangement of the platelet-derived growth factor receptor beta-gene.	imatinib	20-37	platelet derived growth factor receptor beta	Homo sapiens	128-172
15385107-1	2004	PURPOSE: Imatinib mesylate is a tyrosine kinase inhibitor that specifically targets c-Kit, Abl, and platelet-derived growth factor receptor (PDGFR).	imatinib	9-26	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	84-89
15385107-1	2004	PURPOSE: Imatinib mesylate is a tyrosine kinase inhibitor that specifically targets c-Kit, Abl, and platelet-derived growth factor receptor (PDGFR).	imatinib	9-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-94
15385107-1	2004	PURPOSE: Imatinib mesylate is a tyrosine kinase inhibitor that specifically targets c-Kit, Abl, and platelet-derived growth factor receptor (PDGFR).	imatinib	9-26	platelet derived growth factor receptor beta	Homo sapiens	100-139
15455301-0	2004	[An alternative Abl-kinase inhibitor overcomes imatinib resistance mutations of Bcr-Abl oncogenes].	imatinib	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-19
15455301-0	2004	[An alternative Abl-kinase inhibitor overcomes imatinib resistance mutations of Bcr-Abl oncogenes].	imatinib	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
15455301-2	2004	Mutations within the Bcr-Abl kinase domain represent the major cause for clinical resistance toward imatinib.	imatinib	100-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
15455301-4	2004	METHODS: The proliferation of cells expressing wild-type and mutant forms of Bcr-Abl was measured in the presence of imatinib or the pyrido-pyrimidine SKI-DV 2 - 43.	imatinib	117-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
15455301-5	2004	RESULTS: The growth of a cell line expressing wild-type Bcr-Abl was suppressed with higher potency in the presence of SKI-DV 2 - 43 when compared to imatinib.	imatinib	149-157	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
15455301-6	2004	Moreover, SKI-DV 2 - 43 effectively suppressed mutant forms of Bcr-Abl that cause imatinib resistance in patients.	imatinib	82-90	SKI proto-oncogene	Homo sapiens	10-13
15455301-6	2004	Moreover, SKI-DV 2 - 43 effectively suppressed mutant forms of Bcr-Abl that cause imatinib resistance in patients.	imatinib	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
15455302-9	2004	CONCLUSION: Imatinib provides a potent therapeutic option in FIP1L1-PDGFRA negative patients suffering from HES.	imatinib	12-20	factor interacting with PAPOLA and CPSF1	Homo sapiens	61-67
15455302-9	2004	CONCLUSION: Imatinib provides a potent therapeutic option in FIP1L1-PDGFRA negative patients suffering from HES.	imatinib	12-20	platelet derived growth factor receptor alpha	Homo sapiens	68-74
15455305-3	2004	The systematic development of the selective BCR-ABL inhibitor imatinib was based on the discovery of the molecular pathogenesis of CML.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
15553717-3	2004	The development of a tyrosine kinase inhibitor, STI571 (imatinib mesylate, Glivec, Gleevec), which inhibits the BCR-ABL, PDGF-R alpha and c-kit receptors, has changed the management of unresectable malignant GIST and has improved the survival of patients with metastatic disease.	imatinib	48-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
15553717-3	2004	The development of a tyrosine kinase inhibitor, STI571 (imatinib mesylate, Glivec, Gleevec), which inhibits the BCR-ABL, PDGF-R alpha and c-kit receptors, has changed the management of unresectable malignant GIST and has improved the survival of patients with metastatic disease.	imatinib	48-54	platelet derived growth factor receptor alpha	Homo sapiens	121-133
15553717-3	2004	The development of a tyrosine kinase inhibitor, STI571 (imatinib mesylate, Glivec, Gleevec), which inhibits the BCR-ABL, PDGF-R alpha and c-kit receptors, has changed the management of unresectable malignant GIST and has improved the survival of patients with metastatic disease.	imatinib	48-54	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	138-143
15553717-3	2004	The development of a tyrosine kinase inhibitor, STI571 (imatinib mesylate, Glivec, Gleevec), which inhibits the BCR-ABL, PDGF-R alpha and c-kit receptors, has changed the management of unresectable malignant GIST and has improved the survival of patients with metastatic disease.	imatinib	56-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
15553717-3	2004	The development of a tyrosine kinase inhibitor, STI571 (imatinib mesylate, Glivec, Gleevec), which inhibits the BCR-ABL, PDGF-R alpha and c-kit receptors, has changed the management of unresectable malignant GIST and has improved the survival of patients with metastatic disease.	imatinib	56-73	platelet derived growth factor receptor alpha	Homo sapiens	121-133
15553717-3	2004	The development of a tyrosine kinase inhibitor, STI571 (imatinib mesylate, Glivec, Gleevec), which inhibits the BCR-ABL, PDGF-R alpha and c-kit receptors, has changed the management of unresectable malignant GIST and has improved the survival of patients with metastatic disease.	imatinib	56-73	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	138-143
15385107-1	2004	PURPOSE: Imatinib mesylate is a tyrosine kinase inhibitor that specifically targets c-Kit, Abl, and platelet-derived growth factor receptor (PDGFR).	imatinib	9-26	platelet derived growth factor receptor beta	Homo sapiens	141-146
15477214-1	2004	Imatinib mesylate has been reported to produce positive results in atypical chronic myeloproliferative disorders (CMD) with chromosomal translocations that disrupt the platelet-derived growth factor receptor beta gene (PDGFRB).	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	168-212
15477214-1	2004	Imatinib mesylate has been reported to produce positive results in atypical chronic myeloproliferative disorders (CMD) with chromosomal translocations that disrupt the platelet-derived growth factor receptor beta gene (PDGFRB).	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	219-225
15477214-2	2004	We used imatinib to treat a 49-year old man with atypical CMD in accelerated phase and the H4 (D10S170)-PDGFRB fusion gene.	imatinib	8-16	platelet derived growth factor receptor beta	Homo sapiens	104-110
15375771-5	2004	In patients with Imatinib as the only treatment morphometric analysis of CD61+ megakaryopoiesis was in keeping with a significant decrease in maturation defects implying a lesser amount of atypical micromegakaryocytes almost consistent with normalization.	imatinib	17-25	integrin subunit beta 3	Homo sapiens	73-77
15330987-3	2004	As it is possible to inhibit C-KIT by innovative kinase inhibitors like STI571, it may be an attractive target for new therapeutical approaches.	imatinib	72-78	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	29-34
15469479-1	2004	AIMS: Imatinib mesylate specifically inhibits KIT tyrosine kinase activity, and has been proven to be effective in the treatment of gastrointestinal stromal tumours.	imatinib	6-14	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	46-49
15469479-2	2004	Because other KIT-expressing malignancies might benefit from Imatinib therapy, we evaluated the distribution and expression of KIT in 1166 cases of malignant lymphoma.	imatinib	61-69	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-17
15540902-1	2004	Imatinib mesylate is a relatively new drug that targets the BCR-ABL chimeric protein, the molecular basis of chronic myeloid leukemia (CML).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
15343347-7	2004	Upon imatinib treatment, plasmatic VEGF rapidly decreased and a normal BDCA-4 expression was restored.	imatinib	5-13	vascular endothelial growth factor A	Homo sapiens	35-39
15343347-7	2004	Upon imatinib treatment, plasmatic VEGF rapidly decreased and a normal BDCA-4 expression was restored.	imatinib	5-13	neuropilin 1	Homo sapiens	71-77
15343347-9	2004	We conclude that VEGF may be a key player in blood DC deficiency in CML and we show that imatinib inhibits VEGF overproduction.	imatinib	89-97	vascular endothelial growth factor A	Homo sapiens	107-111
15361874-7	2004	The constitutively phosphorylated tyrosine kinase NUP214-ABL1 is sensitive to the tyrosine kinase inhibitor imatinib.	imatinib	108-116	nucleoporin 214	Homo sapiens	50-56
15361874-7	2004	The constitutively phosphorylated tyrosine kinase NUP214-ABL1 is sensitive to the tyrosine kinase inhibitor imatinib.	imatinib	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-61
15361874-9	2004	NUP214-ABL1 expression defines a new subgroup of individuals with T-ALL who could benefit from treatment with imatinib.	imatinib	110-118	nucleoporin 214	Homo sapiens	0-6
15361874-9	2004	NUP214-ABL1 expression defines a new subgroup of individuals with T-ALL who could benefit from treatment with imatinib.	imatinib	110-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	7-11
15553045-6	2004	G-CSF enables continuous treatment with high-dose imatinib.	imatinib	50-58	colony stimulating factor 3	Homo sapiens	0-5
15365079-8	2004	In particular, the responsiveness of GISTs to treatment with the kinase inhibitor imatinib varies substantially depending on the exonic location of the KIT or PDGFRA mutation.	imatinib	82-90	platelet derived growth factor receptor alpha	Homo sapiens	159-165
15500716-12	2004	The identification of FIP1L1-PDGFRA rearrangement is a useful molecular mark for HES diagnosis and works as the therapeutic target of imatinib.	imatinib	134-142	factor interacting with PAPOLA and CPSF1	Homo sapiens	22-28
15500716-12	2004	The identification of FIP1L1-PDGFRA rearrangement is a useful molecular mark for HES diagnosis and works as the therapeutic target of imatinib.	imatinib	134-142	platelet derived growth factor receptor alpha	Homo sapiens	29-35
15365079-8	2004	In particular, the responsiveness of GISTs to treatment with the kinase inhibitor imatinib varies substantially depending on the exonic location of the KIT or PDGFRA mutation.	imatinib	82-90	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	152-155
15456825-3	2004	Using a developing hippocampal culture as a model, we found that the inhibition of Abl kinases by STI571 leads to a remarkable simplification of dendritic branching similar to the phenotype caused by an increased activity of small GTPase RhoA.	imatinib	98-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-86
15456825-3	2004	Using a developing hippocampal culture as a model, we found that the inhibition of Abl kinases by STI571 leads to a remarkable simplification of dendritic branching similar to the phenotype caused by an increased activity of small GTPase RhoA.	imatinib	98-104	ras homolog family member A	Homo sapiens	238-242
15456825-8	2004	Suppression of the RhoA downstream effector Rho kinase reverses STI571-induced dendritic simplification, demonstrating that activity of the Rho pathway is responsible for the Abl-induced changes in dendrogenesis.	imatinib	64-70	ras homolog family member A	Homo sapiens	19-23
15456825-8	2004	Suppression of the RhoA downstream effector Rho kinase reverses STI571-induced dendritic simplification, demonstrating that activity of the Rho pathway is responsible for the Abl-induced changes in dendrogenesis.	imatinib	64-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-178
15517872-3	2004	STI571 also selectively inhibits platelet-derived growth factor receptors (PDGFRs) and c-kit.	imatinib	0-6	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	87-92
15510603-2	2004	With the introduction of Imatinib, an oral drug able to inhibit the KIT receptor tyrosine kinase, new questions arise regarding our ability to monitor treatment response with conventional methods and optimally manage such patients on treatment with new agents.	imatinib	25-33	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	68-71
15517875-8	2004	Enhanced apoptosis by the co-treatment was abrogated by ectopic expression of cyclin D1, c-Myc or active MEK CONCLUSION: The combination of FK228 with STI571 is a promising treatment for Bcr-Abl-positive CML, but the activation of the MEK/ERK pathway and its downstream target genes may bring resistance to the co-treatment in leukemic cells.	imatinib	151-157	cyclin D1	Homo sapiens	78-87
15309514-0	2004	Imatinib mesylate acts in metastatic or unresectable gastrointestinal stromal tumor by targeting KIT receptors--a review.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	97-100
15517875-8	2004	Enhanced apoptosis by the co-treatment was abrogated by ectopic expression of cyclin D1, c-Myc or active MEK CONCLUSION: The combination of FK228 with STI571 is a promising treatment for Bcr-Abl-positive CML, but the activation of the MEK/ERK pathway and its downstream target genes may bring resistance to the co-treatment in leukemic cells.	imatinib	151-157	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	89-94
15517875-8	2004	Enhanced apoptosis by the co-treatment was abrogated by ectopic expression of cyclin D1, c-Myc or active MEK CONCLUSION: The combination of FK228 with STI571 is a promising treatment for Bcr-Abl-positive CML, but the activation of the MEK/ERK pathway and its downstream target genes may bring resistance to the co-treatment in leukemic cells.	imatinib	151-157	mitogen-activated protein kinase kinase 7	Homo sapiens	105-108
15517875-8	2004	Enhanced apoptosis by the co-treatment was abrogated by ectopic expression of cyclin D1, c-Myc or active MEK CONCLUSION: The combination of FK228 with STI571 is a promising treatment for Bcr-Abl-positive CML, but the activation of the MEK/ERK pathway and its downstream target genes may bring resistance to the co-treatment in leukemic cells.	imatinib	151-157	mitogen-activated protein kinase kinase 7	Homo sapiens	235-238
15517875-8	2004	Enhanced apoptosis by the co-treatment was abrogated by ectopic expression of cyclin D1, c-Myc or active MEK CONCLUSION: The combination of FK228 with STI571 is a promising treatment for Bcr-Abl-positive CML, but the activation of the MEK/ERK pathway and its downstream target genes may bring resistance to the co-treatment in leukemic cells.	imatinib	151-157	mitogen-activated protein kinase 1	Homo sapiens	239-242
15155467-0	2004	CD19-targeting liposomes containing imatinib efficiently kill Philadelphia chromosome-positive acute lymphoblastic leukemia cells.	imatinib	36-44	CD19 molecule	Homo sapiens	0-4
15155467-7	2004	The cytocidal effect of imatinib-encapsulated CD19-liposomes (imatinib-CD19-liposomes) on Ph(+) ALL cell lines and primary leukemia cells from patients with Ph(+) ALL was much greater than that of imatinib with or without control liposomes.	imatinib	24-32	CD19 molecule	Homo sapiens	46-50
15155467-7	2004	The cytocidal effect of imatinib-encapsulated CD19-liposomes (imatinib-CD19-liposomes) on Ph(+) ALL cell lines and primary leukemia cells from patients with Ph(+) ALL was much greater than that of imatinib with or without control liposomes.	imatinib	24-32	CD19 molecule	Homo sapiens	71-75
15155467-7	2004	The cytocidal effect of imatinib-encapsulated CD19-liposomes (imatinib-CD19-liposomes) on Ph(+) ALL cell lines and primary leukemia cells from patients with Ph(+) ALL was much greater than that of imatinib with or without control liposomes.	imatinib	62-70	CD19 molecule	Homo sapiens	46-50
15155467-7	2004	The cytocidal effect of imatinib-encapsulated CD19-liposomes (imatinib-CD19-liposomes) on Ph(+) ALL cell lines and primary leukemia cells from patients with Ph(+) ALL was much greater than that of imatinib with or without control liposomes.	imatinib	62-70	CD19 molecule	Homo sapiens	71-75
15155467-7	2004	The cytocidal effect of imatinib-encapsulated CD19-liposomes (imatinib-CD19-liposomes) on Ph(+) ALL cell lines and primary leukemia cells from patients with Ph(+) ALL was much greater than that of imatinib with or without control liposomes.	imatinib	62-70	CD19 molecule	Homo sapiens	46-50
15155467-7	2004	The cytocidal effect of imatinib-encapsulated CD19-liposomes (imatinib-CD19-liposomes) on Ph(+) ALL cell lines and primary leukemia cells from patients with Ph(+) ALL was much greater than that of imatinib with or without control liposomes.	imatinib	62-70	CD19 molecule	Homo sapiens	71-75
15155467-8	2004	Importantly, the imatinib-CD19-liposomes did not affect the colony formation of CD34(+) hematopoietic cells, even at inhibitory concentration of free imatinib.	imatinib	17-25	CD19 molecule	Homo sapiens	26-30
15155467-9	2004	Taken together, these data clearly demonstrate that the imatinib-CD19-liposomes induced specific and efficient death of Ph(+) ALL cells.	imatinib	56-64	CD19 molecule	Homo sapiens	65-69
15342366-0	2004	A missense mutation in KIT kinase domain 1 correlates with imatinib resistance in gastrointestinal stromal tumors.	imatinib	59-67	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	23-26
15342366-2	2004	Imatinib is a selective tyrosine kinase inhibitor of ABL, platelet-derived growth factor receptor (PDGFR), and KIT and represents a new paradigm of targeted therapy against GISTs.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
15342366-2	2004	Imatinib is a selective tyrosine kinase inhibitor of ABL, platelet-derived growth factor receptor (PDGFR), and KIT and represents a new paradigm of targeted therapy against GISTs.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	58-97
15342366-2	2004	Imatinib is a selective tyrosine kinase inhibitor of ABL, platelet-derived growth factor receptor (PDGFR), and KIT and represents a new paradigm of targeted therapy against GISTs.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	99-104
15342366-2	2004	Imatinib is a selective tyrosine kinase inhibitor of ABL, platelet-derived growth factor receptor (PDGFR), and KIT and represents a new paradigm of targeted therapy against GISTs.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	111-114
15329907-1	2004	BACKGROUND: The objective of the current study was to verify the ability to predict response to imatinib therapy using in vitro assays to evaluate the inhibition of Wilms tumor gene (WT1) expression and colony growth after samples obtained from patients with chronic myelogenous leukemia (CML) before the start of treatment were subjected to short-term incubation with imatinib.	imatinib	96-104	WT1 transcription factor	Homo sapiens	183-186
15329907-2	2004	METHODS: WT1 transcript levels and colony growth in bone marrow (BM) samples from 23 patients with CML that was later identified as being responsive to imatinib and from 13 patients with CML that was later identified as not being responsive to imatinib were evaluated after incubation of these samples with imatinib at a concentration of 1 microM for 18 hours.	imatinib	244-252	WT1 transcription factor	Homo sapiens	9-12
15329907-2	2004	METHODS: WT1 transcript levels and colony growth in bone marrow (BM) samples from 23 patients with CML that was later identified as being responsive to imatinib and from 13 patients with CML that was later identified as not being responsive to imatinib were evaluated after incubation of these samples with imatinib at a concentration of 1 microM for 18 hours.	imatinib	244-252	WT1 transcription factor	Homo sapiens	9-12
15329907-5	2004	WT1 expression and colony growth were reduced significantly after an 18-hour incubation with imatinib in samples obtained from patients who were later identified as responders to treatment, but not in samples obtained from patients who did not experience responses to treatment.	imatinib	93-101	WT1 transcription factor	Homo sapiens	0-3
15329907-6	2004	Inhibition of WT1 expression in vitro was associated with inhibition of imatinib-induced BCR-ABL tyrosine kinase activity, a finding that also has been made in studies involving certain Philadelphia chromosome (Ph)-positive and Ph-negative cell lines.	imatinib	72-80	WT1 transcription factor	Homo sapiens	14-17
15329907-6	2004	Inhibition of WT1 expression in vitro was associated with inhibition of imatinib-induced BCR-ABL tyrosine kinase activity, a finding that also has been made in studies involving certain Philadelphia chromosome (Ph)-positive and Ph-negative cell lines.	imatinib	72-80	BCR activator of RhoGEF and GTPase	Homo sapiens	89-92
15329907-6	2004	Inhibition of WT1 expression in vitro was associated with inhibition of imatinib-induced BCR-ABL tyrosine kinase activity, a finding that also has been made in studies involving certain Philadelphia chromosome (Ph)-positive and Ph-negative cell lines.	imatinib	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-96
15342366-3	2004	Here we report for the first time that, after imatinib treatment, an additional specific and novel KIT mutation occurs in GISTs as they develop resistance to the drug.	imatinib	46-54	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	99-102
15309514-4	2004	Imatinib mesylate, a KIT tyrosine kinase inhibitor, is an oral agent that has been found to have a dramatic antitumor effect on metastatic GIST with either wild-type or mutant KIT.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	21-24
15342366-8	2004	All six rapidly progressive imatinib-resistant implants from five patients show an identical novel KIT missense mutation, 1982T-->C, that resulted in Val654Ala in KIT tyrosine kinase domain 1.	imatinib	28-36	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	99-102
15342366-8	2004	All six rapidly progressive imatinib-resistant implants from five patients show an identical novel KIT missense mutation, 1982T-->C, that resulted in Val654Ala in KIT tyrosine kinase domain 1.	imatinib	28-36	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	166-169
15329907-7	2004	CONCLUSIONS: Inhibition of WT1 transcript levels after a short period of in vitro exposure of pretherapy BM samples to imatinib was correlated with inhibition of colony growth and may represent the basis for an easy test that is capable of predicting the sensitivity of CML to treatment with imatinib for individual patients.	imatinib	119-127	WT1 transcription factor	Homo sapiens	27-30
15329907-7	2004	CONCLUSIONS: Inhibition of WT1 transcript levels after a short period of in vitro exposure of pretherapy BM samples to imatinib was correlated with inhibition of colony growth and may represent the basis for an easy test that is capable of predicting the sensitivity of CML to treatment with imatinib for individual patients.	imatinib	292-300	WT1 transcription factor	Homo sapiens	27-30
15309514-4	2004	Imatinib mesylate, a KIT tyrosine kinase inhibitor, is an oral agent that has been found to have a dramatic antitumor effect on metastatic GIST with either wild-type or mutant KIT.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	176-179
15467443-0	2004	Treatment of chronic myeloid leukemia cells with imatinib (STI571) impairs p53 accumulation in response to DNA damage.	imatinib	49-57	tumor protein p53	Homo sapiens	75-78
15467443-0	2004	Treatment of chronic myeloid leukemia cells with imatinib (STI571) impairs p53 accumulation in response to DNA damage.	imatinib	59-65	tumor protein p53	Homo sapiens	75-78
15467443-4	2004	Here, we investigated the effect of STI571 treatment of CML cells on p53 regulation.	imatinib	36-42	tumor protein p53	Homo sapiens	69-72
15467443-9	2004	CML cells expressing wild-type p53 are more resistant to treatment with STI571, but moderately more sensitive to DNA damage, than CML cells lacking p53.	imatinib	72-78	tumor protein p53	Homo sapiens	31-34
15471556-7	2004	Moreover, molecular targeting drugs such as imatinib mesylate (STI571), which is a selective inhibitor of KIT, might be promising agents for the treatment of intracranial germinomas with c-kit gene mutations.	imatinib	44-61	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	106-109
15355900-14	2004	One patient with gastrointestinal stromal tumor who had rapid progression during SU5416 treatment was subsequently treated with another KIT inhibitor, imatinib mesylate, and had a partial response lasting >36 months.	imatinib	151-168	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	136-139
15471556-7	2004	Moreover, molecular targeting drugs such as imatinib mesylate (STI571), which is a selective inhibitor of KIT, might be promising agents for the treatment of intracranial germinomas with c-kit gene mutations.	imatinib	44-61	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	187-192
15471556-7	2004	Moreover, molecular targeting drugs such as imatinib mesylate (STI571), which is a selective inhibitor of KIT, might be promising agents for the treatment of intracranial germinomas with c-kit gene mutations.	imatinib	63-69	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	106-109
15471556-7	2004	Moreover, molecular targeting drugs such as imatinib mesylate (STI571), which is a selective inhibitor of KIT, might be promising agents for the treatment of intracranial germinomas with c-kit gene mutations.	imatinib	63-69	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	187-192
15289888-1	2004	A therapeutic role of STI571 (imatinib mesylate) has been anticipated in patients with c-Kit positive neuroectodermal tumors.	imatinib	22-28	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	87-92
15503866-1	2004	STI-571 (Gleevec) is a highly successful cancer drug due to its activity as an inhibitor of the Abelson cytoplasmic tyrosine kinase (Abl), which is constitutively active in a majority of patients with chronic myelogenous leukemia.	imatinib	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-136
15503866-3	2004	This review focuses on recent developments in X-ray co-crystal structure analyses of STI-571 bound to Abl and the c-Kit receptor tyrosine kinase domain, and also three other relevant kinase inhibitor co-crystal structures.	imatinib	85-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-105
15689683-8	2004	Moreover, a unique therapeutic agent, imatinib, has been devised that specifically targets the aberrant KIT receptor and has demonstrated dramatic therapeutic efficacy in this otherwise resistant malignancy.	imatinib	38-46	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	104-107
15221957-0	2004	Different inhibitory effect of imatinib on phosphorylation of mitogen-activated protein kinase and Akt and on proliferation in cells expressing different types of mutant platelet-derived growth factor receptor-alpha.	imatinib	31-39	thymoma viral proto-oncogene 1	Mus musculus	99-102
15221957-0	2004	Different inhibitory effect of imatinib on phosphorylation of mitogen-activated protein kinase and Akt and on proliferation in cells expressing different types of mutant platelet-derived growth factor receptor-alpha.	imatinib	31-39	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	170-215
15221957-3	2004	Although the inhibitory effect of imatinib on various types of activating mutant KIT has been well examined, that on the activating mutant PDGFRA has not been fully investigated.	imatinib	34-42	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	81-84
15221957-4	2004	In the present study, we examined the effect of imatinib on autophosphorylation of mutant PDGFRA, phosphorylation of MAPK and of Akt and in vitro cell proliferation using murine Ba/F3 cells stably transfected with one of the 2 murine-type mutated PDGFRA cDNAs.	imatinib	48-56	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	90-96
15221957-5	2004	Imatinib almost completely inhibited autophosphorylation of mutant PDGFRA, phosphorylation of MAPK and Akt as well as in vitro cell proliferation at the concentration of 0.01 microM in cells expressing mutant PDGFRA with Val561 to Asp.	imatinib	0-8	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	67-73
15289888-1	2004	A therapeutic role of STI571 (imatinib mesylate) has been anticipated in patients with c-Kit positive neuroectodermal tumors.	imatinib	30-47	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	87-92
15221957-5	2004	Imatinib almost completely inhibited autophosphorylation of mutant PDGFRA, phosphorylation of MAPK and Akt as well as in vitro cell proliferation at the concentration of 0.01 microM in cells expressing mutant PDGFRA with Val561 to Asp.	imatinib	0-8	thymoma viral proto-oncogene 1	Mus musculus	103-106
15221957-5	2004	Imatinib almost completely inhibited autophosphorylation of mutant PDGFRA, phosphorylation of MAPK and Akt as well as in vitro cell proliferation at the concentration of 0.01 microM in cells expressing mutant PDGFRA with Val561 to Asp.	imatinib	0-8	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	209-215
15289888-2	2004	We examined the efficacy of STI571 to inhibit expansion of c-Kit positive neuroectodermal tumor cell lines in vitro and in a mouse model inoculated with ES (Ewing sarcoma) derived tumor cells, and investigated the molecular mechanism of STI571 action.	imatinib	28-34	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	59-64
15221957-6	2004	However, in cells expressing mutant PDGFRA with Asp842 to Val, imatinib almost completely inhibited autophosphorylation of mutant PDGFRA and phosphorylation of MAPK and Akt at 1.0 microM.	imatinib	63-71	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	36-42
15221957-6	2004	However, in cells expressing mutant PDGFRA with Asp842 to Val, imatinib almost completely inhibited autophosphorylation of mutant PDGFRA and phosphorylation of MAPK and Akt at 1.0 microM.	imatinib	63-71	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	130-136
15510830-0	2004	[Second hematologic response and disappearance of the ABL gene mutant clone by cessation of imatinib in a CML patient with resistance to imatinib].	imatinib	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-57
15221957-6	2004	However, in cells expressing mutant PDGFRA with Asp842 to Val, imatinib almost completely inhibited autophosphorylation of mutant PDGFRA and phosphorylation of MAPK and Akt at 1.0 microM.	imatinib	63-71	thymoma viral proto-oncogene 1	Mus musculus	169-172
15221957-8	2004	Ba/F3 cells expressing mutant PDGFRA are a good model to investigate the mechanism of cell proliferation or growth inhibition by imatinib in mutant PDGFRA-driven cells.	imatinib	129-137	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	30-36
15221957-8	2004	Ba/F3 cells expressing mutant PDGFRA are a good model to investigate the mechanism of cell proliferation or growth inhibition by imatinib in mutant PDGFRA-driven cells.	imatinib	129-137	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	148-154
15548358-1	2004	The platelet-derived growth factor receptor (PDGFR) is a receptor tyrosine kinase overexpressed in a subset of solid tumors and therefore is the target of drugs inhibiting this function such as imatinib mesylate (Gleevec).	imatinib	194-211	platelet derived growth factor receptor beta	Homo sapiens	45-50
15548358-1	2004	The platelet-derived growth factor receptor (PDGFR) is a receptor tyrosine kinase overexpressed in a subset of solid tumors and therefore is the target of drugs inhibiting this function such as imatinib mesylate (Gleevec).	imatinib	194-211	ret proto-oncogene	Homo sapiens	57-81
15548358-1	2004	The platelet-derived growth factor receptor (PDGFR) is a receptor tyrosine kinase overexpressed in a subset of solid tumors and therefore is the target of drugs inhibiting this function such as imatinib mesylate (Gleevec).	imatinib	213-220	platelet derived growth factor receptor beta	Homo sapiens	45-50
15548358-1	2004	The platelet-derived growth factor receptor (PDGFR) is a receptor tyrosine kinase overexpressed in a subset of solid tumors and therefore is the target of drugs inhibiting this function such as imatinib mesylate (Gleevec).	imatinib	213-220	ret proto-oncogene	Homo sapiens	57-81
15510830-0	2004	[Second hematologic response and disappearance of the ABL gene mutant clone by cessation of imatinib in a CML patient with resistance to imatinib].	imatinib	137-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-57
15510830-2	2004	However, resistance to imatinib appeared 9 months later due to an ABL gene point mutation, and the patient"s platelet count and BCR/ABL positive rate had remarkably increased.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-69
15510830-2	2004	However, resistance to imatinib appeared 9 months later due to an ABL gene point mutation, and the patient"s platelet count and BCR/ABL positive rate had remarkably increased.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
15510830-3	2004	We discontinued imatinib and used IFNalpha or hydroxyurea, resulting in the disappearance of the ABL gene mutation clone.	imatinib	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-100
15289338-8	2004	Furthermore, the BCR/ABL kinase inhibitor imatinib mesylate markedly inhibited proliferation of BCR/ABL-expressing progenitors but did not fully correct the adhesion and migration defects.	imatinib	42-59	BCR activator of RhoGEF and GTPase	Homo sapiens	17-20
15627886-12	2004	The results of this study support clinical trials targeting the c-kit receptor with specific c-kit inhibitors (e.g. imatinib).	imatinib	116-124	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	64-69
15627886-12	2004	The results of this study support clinical trials targeting the c-kit receptor with specific c-kit inhibitors (e.g. imatinib).	imatinib	116-124	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	93-98
15175350-0	2004	A Bcr/Abl-independent, Lyn-dependent form of imatinib mesylate (STI-571) resistance is associated with altered expression of Bcl-2.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	2-9
15175350-0	2004	A Bcr/Abl-independent, Lyn-dependent form of imatinib mesylate (STI-571) resistance is associated with altered expression of Bcl-2.	imatinib	45-53	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	23-26
15175350-0	2004	A Bcr/Abl-independent, Lyn-dependent form of imatinib mesylate (STI-571) resistance is associated with altered expression of Bcl-2.	imatinib	45-53	BCL2 apoptosis regulator	Homo sapiens	125-130
15175350-3	2004	Whereas basal expression of Bcl-2 protein was very low in parental cells, imatinib-resistant cells displayed a marked increase in Bcl-2 mRNA and/or protein levels.	imatinib	74-82	BCL2 apoptosis regulator	Homo sapiens	130-135
15175350-5	2004	Transient or stable transfection of LAMA84 or K562 cells with a constitutively active Lyn (Y508F), but not with a kinase-dead mutant (K275D), significantly increased Bcl-2 protein expression and protected cells from lethality of imatinib mesylate.	imatinib	229-246	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	86-89
15175350-6	2004	Ectopic expression of Bcl-2 protected K562 and LAMA84 cells from imatinib mesylate- and PP2-mediated lethality.	imatinib	65-82	BCL2 apoptosis regulator	Homo sapiens	22-27
15175350-7	2004	Conversely, interference with Bcl-2 function by co-administration of the small molecule Bcl-2 inhibitor HA14-1 or down-regulation of Bcl-2 expression by small interfering RNA or antisense strategies significantly increased mitochondrial dysfunction and apoptosis induced by imatinib mesylate and the topoisomerase inhibitor VP-16 in LAMA-R cells.	imatinib	274-291	BCL2 apoptosis regulator	Homo sapiens	30-35
15175350-9	2004	Together, these findings indicate that activation of Lyn in leukemia cells displaying a Bcr/Abl-independent form of imatinib mesylate resistance plays a functional role in Bcl-2 up-regulation and provide a theoretical basis for the development of therapeutic strategies targeting Bcl-2 in such a setting.	imatinib	116-133	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	53-56
15289315-1	2004	KIT expression is a key diagnostic feature of gastrointestinal stromal tumors (GISTs), and virtually all of the GISTs express oncogenic forms of the KIT or PDGFRA receptor tyrosine kinase proteins, which serve as therapeutic targets of imatinib mesylate (Gleevec; Novartis, Basel, Switzerland).	imatinib	236-253	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
15289315-1	2004	KIT expression is a key diagnostic feature of gastrointestinal stromal tumors (GISTs), and virtually all of the GISTs express oncogenic forms of the KIT or PDGFRA receptor tyrosine kinase proteins, which serve as therapeutic targets of imatinib mesylate (Gleevec; Novartis, Basel, Switzerland).	imatinib	236-253	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	149-152
15289315-1	2004	KIT expression is a key diagnostic feature of gastrointestinal stromal tumors (GISTs), and virtually all of the GISTs express oncogenic forms of the KIT or PDGFRA receptor tyrosine kinase proteins, which serve as therapeutic targets of imatinib mesylate (Gleevec; Novartis, Basel, Switzerland).	imatinib	236-253	platelet derived growth factor receptor alpha	Homo sapiens	156-162
15100154-3	2004	Interestingly, imatinib mesylate did not inhibit expression of T-cell activation markers CD25 and CD69, although it reduced the levels of activated nuclear factor-kappaB (NF-kappaB) and changed phosphorylation or protein levels of Lck, ERK1/2, retinoblastoma protein, and cyclin D3.	imatinib	15-32	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	231-234
15100154-3	2004	Interestingly, imatinib mesylate did not inhibit expression of T-cell activation markers CD25 and CD69, although it reduced the levels of activated nuclear factor-kappaB (NF-kappaB) and changed phosphorylation or protein levels of Lck, ERK1/2, retinoblastoma protein, and cyclin D3.	imatinib	15-32	mitogen-activated protein kinase 3	Homo sapiens	236-242
15100154-3	2004	Interestingly, imatinib mesylate did not inhibit expression of T-cell activation markers CD25 and CD69, although it reduced the levels of activated nuclear factor-kappaB (NF-kappaB) and changed phosphorylation or protein levels of Lck, ERK1/2, retinoblastoma protein, and cyclin D3.	imatinib	15-32	cyclin D3	Homo sapiens	272-281
15310776-0	2004	Platelet-derived growth factor receptor inhibitor imatinib mesylate and docetaxel: a modular phase I trial in androgen-independent prostate cancer.	imatinib	50-67	platelet derived growth factor receptor beta	Homo sapiens	0-39
15310776-1	2004	PURPOSE: To study the platelet-derived growth factor receptor (PDGFR) inhibitor imatinib mesylate in androgen-independent prostate cancer (AIPC), alone and in combination with docetaxel, we designed a modular phase I trial.	imatinib	80-97	platelet derived growth factor receptor beta	Homo sapiens	63-68
15310776-2	2004	Our goals were to (1) evaluate the toxicity and maximum-tolerated dose of docetaxel with imatinib, and (2) evaluate the decline of prostate-specific antigen (PSA) induced by imatinib alone, and imatinib and docetaxel.	imatinib	174-182	kallikrein related peptidase 3	Homo sapiens	131-162
15310776-2	2004	Our goals were to (1) evaluate the toxicity and maximum-tolerated dose of docetaxel with imatinib, and (2) evaluate the decline of prostate-specific antigen (PSA) induced by imatinib alone, and imatinib and docetaxel.	imatinib	174-182	kallikrein related peptidase 3	Homo sapiens	131-162
15304214-5	2004	In v-Abl transformants, SOCS-1 can inhibit cytokine signals, but it is more efficient at doing so when the cells are treated with STI571, an Abl kinase inhibitor.	imatinib	130-136	suppressor of cytokine signaling 1	Mus musculus	24-30
15306667-8	2004	RESULTS: The granulocyte-macrophage progenitor pool from patients with CML in blast crisis and imatinib-resistant CML was expanded, expressed BCR-ABL, and had elevated levels of nuclear beta-catenin as compared with the levels in progenitors from normal marrow.	imatinib	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
15306667-8	2004	RESULTS: The granulocyte-macrophage progenitor pool from patients with CML in blast crisis and imatinib-resistant CML was expanded, expressed BCR-ABL, and had elevated levels of nuclear beta-catenin as compared with the levels in progenitors from normal marrow.	imatinib	95-103	catenin beta 1	Homo sapiens	186-198
15324693-1	2004	The ABL inhibitor imatinib is a highly effective therapy for patients with chronic myeloid leukemia.	imatinib	18-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
15289338-8	2004	Furthermore, the BCR/ABL kinase inhibitor imatinib mesylate markedly inhibited proliferation of BCR/ABL-expressing progenitors but did not fully correct the adhesion and migration defects.	imatinib	42-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-24
15289338-8	2004	Furthermore, the BCR/ABL kinase inhibitor imatinib mesylate markedly inhibited proliferation of BCR/ABL-expressing progenitors but did not fully correct the adhesion and migration defects.	imatinib	42-59	BCR activator of RhoGEF and GTPase	Homo sapiens	96-99
15289338-8	2004	Furthermore, the BCR/ABL kinase inhibitor imatinib mesylate markedly inhibited proliferation of BCR/ABL-expressing progenitors but did not fully correct the adhesion and migration defects.	imatinib	42-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-103
15332547-3	2004	Imatinib mesylate (IM), an agent for chronic myeloid leukemia, was reported to inhibit tyrosine kinase activity of KIT and to be highly effective for GIST.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	115-118
15270663-3	2004	Imatinib (Gleevec, Novartis) is an orally administered competitive inhibitor of the tyrosine kinase domain of receptors such as KIT, ABL, and BCR-ABL fusion proteins, and the platelet-derived growth factor receptor.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	128-131
15270663-3	2004	Imatinib (Gleevec, Novartis) is an orally administered competitive inhibitor of the tyrosine kinase domain of receptors such as KIT, ABL, and BCR-ABL fusion proteins, and the platelet-derived growth factor receptor.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-136
15270663-3	2004	Imatinib (Gleevec, Novartis) is an orally administered competitive inhibitor of the tyrosine kinase domain of receptors such as KIT, ABL, and BCR-ABL fusion proteins, and the platelet-derived growth factor receptor.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	146-149
15332547-3	2004	Imatinib mesylate (IM), an agent for chronic myeloid leukemia, was reported to inhibit tyrosine kinase activity of KIT and to be highly effective for GIST.	imatinib	19-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	115-118
15339694-0	2004	Soft tissue and skeletal involvement in FIP1L1-PDGFR-alpha positive chronic eosinophilic leukemia: imatinib mesylate may induce complete molecular and imaging remission.	imatinib	99-116	factor interacting with PAPOLA and CPSF1	Homo sapiens	40-46
15197170-7	2004	Phosphorylation of PDGFR-beta was increased by Ang II in vascular smooth muscle cells, and this was inhibited by imatinib.	imatinib	113-121	platelet derived growth factor receptor beta	Rattus norvegicus	19-29
15197170-8	2004	The findings of attenuation of vascular hypertrophy and matrix deposition by imatinib indicate that transactivation of the PDGFR in vivo contributes to the growth factor-like effects of Ang II, independent of its hemodynamic effects or its ability to induce TGF-beta gene expression.	imatinib	77-85	angiotensinogen	Rattus norvegicus	186-192
15339694-0	2004	Soft tissue and skeletal involvement in FIP1L1-PDGFR-alpha positive chronic eosinophilic leukemia: imatinib mesylate may induce complete molecular and imaging remission.	imatinib	99-116	platelet derived growth factor receptor alpha	Homo sapiens	47-58
15286804-1	2004	Mutant isoforms of the KIT or PDGF receptors expressed by gastrointestinal stromal tumors (GISTs) are considered the therapeutic targets for STI571 (imatinib mesylate; Gleevec), a specific inhibitor of these tyrosine kinase receptors.	imatinib	141-147	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	23-26
15286804-1	2004	Mutant isoforms of the KIT or PDGF receptors expressed by gastrointestinal stromal tumors (GISTs) are considered the therapeutic targets for STI571 (imatinib mesylate; Gleevec), a specific inhibitor of these tyrosine kinase receptors.	imatinib	149-166	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	23-26
15105813-2	2004	Imatinib mesylate, a well-established inhibitor of bcr-abl tyrosine kinase, and currently used for the treatment of patients with chronic myeloid leukemia, also inhibits c-kit receptor kinase activity.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	170-175
15201856-0	2004	Efficacy of dual-specific Bcr-Abl and Src-family kinase inhibitors in cells sensitive and resistant to imatinib mesylate.	imatinib	103-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
15201856-0	2004	Efficacy of dual-specific Bcr-Abl and Src-family kinase inhibitors in cells sensitive and resistant to imatinib mesylate.	imatinib	103-120	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	38-41
15201856-2	2004	Resistance to imatinib can arise by multiple mechanisms including amplification or mutation of Bcr-Abl, and continuity of imatinib therapy is probably a poor option for either of these patient groups.	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
15201856-6	2004	We show that whereas the pyrido[2,3-d] pyrimidines are indeed highly potent in suppressing proliferation of Bcr-Abl-overexpressing imatinib-resistant cells, they are almost completely ineffective against cells expressing the T315I mutant.	imatinib	131-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
15215876-1	2004	Imatinib is a molecularly targeted therapy that inhibits the oncogenic fusion protein BCR-ABL, the tyrosine kinase involved in the pathogenesis of chronic myelogenous leukemia (CML).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
15215876-2	2004	Selective inhibition of BCR-ABL activity by imatinib has demonstrated efficacy in the treatment of CML, particularly in chronic phase.	imatinib	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
15215876-4	2004	Relapse with imatinib frequently depends not only on re-emergence of BCR-ABL kinase activity but may also indicate BCR-ABL-independent disease progression not amenable to imatinib inhibition.	imatinib	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
15215876-4	2004	Relapse with imatinib frequently depends not only on re-emergence of BCR-ABL kinase activity but may also indicate BCR-ABL-independent disease progression not amenable to imatinib inhibition.	imatinib	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
15273685-7	2004	Furthermore, worms treated with the c-Abl inhibitor STI-571 (Gleevec; used in human cancer therapy), two newly synthesized STI-571 variants or PD166326 had a phenotype similar to that generated by abl-1(ok171).	imatinib	52-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-41
15273685-7	2004	Furthermore, worms treated with the c-Abl inhibitor STI-571 (Gleevec; used in human cancer therapy), two newly synthesized STI-571 variants or PD166326 had a phenotype similar to that generated by abl-1(ok171).	imatinib	52-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	197-202
15273685-7	2004	Furthermore, worms treated with the c-Abl inhibitor STI-571 (Gleevec; used in human cancer therapy), two newly synthesized STI-571 variants or PD166326 had a phenotype similar to that generated by abl-1(ok171).	imatinib	123-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-41
15173174-4	2004	We show that cytoplasmic ERK2 activity protected against apoptosis caused by prolonged serum starvation, whereas ERK2 activation restricted to the nucleus antagonized apoptosis induced by the Bcr-Abl inhibitor STI571.	imatinib	210-216	mitogen-activated protein kinase 1	Homo sapiens	113-117
15173174-4	2004	We show that cytoplasmic ERK2 activity protected against apoptosis caused by prolonged serum starvation, whereas ERK2 activation restricted to the nucleus antagonized apoptosis induced by the Bcr-Abl inhibitor STI571.	imatinib	210-216	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	192-199
14976047-0	2004	Imatinib mesylate (STI571) decreases the vascular endothelial growth factor plasma concentration in patients with chronic myeloid leukemia.	imatinib	0-17	vascular endothelial growth factor A	Homo sapiens	41-75
14976047-0	2004	Imatinib mesylate (STI571) decreases the vascular endothelial growth factor plasma concentration in patients with chronic myeloid leukemia.	imatinib	19-25	vascular endothelial growth factor A	Homo sapiens	41-75
15190258-1	2004	The ABL tyrosine kinase inhibitor imatinib mesylate is highly effective in the treatment of CML and is increasingly used in the stem cell transplantation (SCT) setting.	imatinib	34-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
15190258-2	2004	Since ABL-dependent intracellular signaling molecules are involved in T-cell activation, imatinib may affect T-cell responses in vivo, thus affecting T-cell function in CML patients, disrupting immune reconstitution after allogeneic SCT and/or impeding the graft-versus-leukemia effect.	imatinib	89-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-9
15190258-4	2004	The effect is not dependent on antigen-presenting cells because CD3/CD28-induced T-cell stimulation was similarly inhibited by imatinib.	imatinib	127-135	CD28 molecule	Homo sapiens	68-72
15305431-2	2004	Beginning with the observation that imatinib mesylate (Gleevec) could elicit rapid and complete hematologic remissions in a proportion of patients with HES, a reverse bedside-to-bench translational research effort led to the discovery of FIP1L1-PDGFRA, a novel fusion gene on chromosome 4q12 whose product is an imatinib-sensitive protein tyrosine kinase.	imatinib	36-53	factor interacting with PAPOLA and CPSF1	Homo sapiens	238-244
15305431-2	2004	Beginning with the observation that imatinib mesylate (Gleevec) could elicit rapid and complete hematologic remissions in a proportion of patients with HES, a reverse bedside-to-bench translational research effort led to the discovery of FIP1L1-PDGFRA, a novel fusion gene on chromosome 4q12 whose product is an imatinib-sensitive protein tyrosine kinase.	imatinib	36-44	factor interacting with PAPOLA and CPSF1	Homo sapiens	238-244
15123710-5	2004	A 1.6-A crystal structure of c-Kit in complex with STI-571 (Imatinib or Gleevec) demonstrates that inhibitor binding disrupts this natural mechanism for maintaining c-Kit in an autoinhibited state.	imatinib	51-58	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	29-34
15123710-5	2004	A 1.6-A crystal structure of c-Kit in complex with STI-571 (Imatinib or Gleevec) demonstrates that inhibitor binding disrupts this natural mechanism for maintaining c-Kit in an autoinhibited state.	imatinib	51-58	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	165-170
15123710-5	2004	A 1.6-A crystal structure of c-Kit in complex with STI-571 (Imatinib or Gleevec) demonstrates that inhibitor binding disrupts this natural mechanism for maintaining c-Kit in an autoinhibited state.	imatinib	60-68	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	29-34
15123710-5	2004	A 1.6-A crystal structure of c-Kit in complex with STI-571 (Imatinib or Gleevec) demonstrates that inhibitor binding disrupts this natural mechanism for maintaining c-Kit in an autoinhibited state.	imatinib	60-68	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	165-170
14976047-2	2004	Recently, the therapeutic strategy in CML has been totally modified with the development of a new drug: imatinib mesylate (STI571), a specific inhibitor of Bcr/Abl tyrosine kinase activity.	imatinib	104-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
14976047-2	2004	Recently, the therapeutic strategy in CML has been totally modified with the development of a new drug: imatinib mesylate (STI571), a specific inhibitor of Bcr/Abl tyrosine kinase activity.	imatinib	123-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
14976047-3	2004	The aim of our study was to determine, in patients with CML, the capacity of imatinib mesylate to modulate one of the most potent regulators of angiogenesis, the vascular endothelial growth factor (VEGF).	imatinib	77-94	vascular endothelial growth factor A	Homo sapiens	162-196
14976047-3	2004	The aim of our study was to determine, in patients with CML, the capacity of imatinib mesylate to modulate one of the most potent regulators of angiogenesis, the vascular endothelial growth factor (VEGF).	imatinib	77-94	vascular endothelial growth factor A	Homo sapiens	198-202
14976047-6	2004	To understand the molecular mechanisms leading to the inhibition of VEGF production by imatinib, we focused our experiments on the human cell line K562, which is Bcr/Abl positive.	imatinib	87-95	vascular endothelial growth factor A	Homo sapiens	68-72
14976047-7	2004	We demonstrated that imatinib inhibits VEGF gene transcription by targeting the Sp1 and Sp3 transcription factors.	imatinib	21-29	vascular endothelial growth factor A	Homo sapiens	39-43
15039284-4	2004	In imatinib mesylate-resistant K562 cells displaying increased Bcr/Abl expression, bortezomib/flavopiridol treatment markedly increased apoptosis in association with down-regulation of Bcr/Abl and BclxL, and diminished phosphorylation of Lyn, Hck, CrkL, and Akt.	imatinib	3-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
15039284-4	2004	In imatinib mesylate-resistant K562 cells displaying increased Bcr/Abl expression, bortezomib/flavopiridol treatment markedly increased apoptosis in association with down-regulation of Bcr/Abl and BclxL, and diminished phosphorylation of Lyn, Hck, CrkL, and Akt.	imatinib	3-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	185-192
15039284-4	2004	In imatinib mesylate-resistant K562 cells displaying increased Bcr/Abl expression, bortezomib/flavopiridol treatment markedly increased apoptosis in association with down-regulation of Bcr/Abl and BclxL, and diminished phosphorylation of Lyn, Hck, CrkL, and Akt.	imatinib	3-20	BCL2 like 1	Homo sapiens	197-202
15039284-5	2004	Parallel studies were performed in imatinib mesylate-resistant LAMA84 cells exhibiting reduced expression of Bcr/Abl but a marked increase in expression/activation of Lyn and Hck.	imatinib	35-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
14976047-7	2004	We demonstrated that imatinib inhibits VEGF gene transcription by targeting the Sp1 and Sp3 transcription factors.	imatinib	21-29	Sp3 transcription factor	Homo sapiens	88-91
14976047-8	2004	Taken together, our results highlight the potential prognostic value of VEGF concentrations in evaluating the evolution of CML patients treated with imatinib.	imatinib	149-157	vascular endothelial growth factor A	Homo sapiens	72-76
15256671-0	2004	Overriding imatinib resistance with a novel ABL kinase inhibitor.	imatinib	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-47
15039284-5	2004	Parallel studies were performed in imatinib mesylate-resistant LAMA84 cells exhibiting reduced expression of Bcr/Abl but a marked increase in expression/activation of Lyn and Hck.	imatinib	35-52	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	167-170
15039284-5	2004	Parallel studies were performed in imatinib mesylate-resistant LAMA84 cells exhibiting reduced expression of Bcr/Abl but a marked increase in expression/activation of Lyn and Hck.	imatinib	35-52	HCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	175-178
15256671-1	2004	Resistance to the ABL kinase inhibitor imatinib (STI571 or Gleevec) in chronic myeloid leukemia (CML) occurs through selection for tumor cells harboring BCR-ABL kinase domain point mutations that interfere with drug binding.	imatinib	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-21
15256671-1	2004	Resistance to the ABL kinase inhibitor imatinib (STI571 or Gleevec) in chronic myeloid leukemia (CML) occurs through selection for tumor cells harboring BCR-ABL kinase domain point mutations that interfere with drug binding.	imatinib	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
15256671-1	2004	Resistance to the ABL kinase inhibitor imatinib (STI571 or Gleevec) in chronic myeloid leukemia (CML) occurs through selection for tumor cells harboring BCR-ABL kinase domain point mutations that interfere with drug binding.	imatinib	49-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-21
15256671-1	2004	Resistance to the ABL kinase inhibitor imatinib (STI571 or Gleevec) in chronic myeloid leukemia (CML) occurs through selection for tumor cells harboring BCR-ABL kinase domain point mutations that interfere with drug binding.	imatinib	49-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
15256671-1	2004	Resistance to the ABL kinase inhibitor imatinib (STI571 or Gleevec) in chronic myeloid leukemia (CML) occurs through selection for tumor cells harboring BCR-ABL kinase domain point mutations that interfere with drug binding.	imatinib	59-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-21
15256671-1	2004	Resistance to the ABL kinase inhibitor imatinib (STI571 or Gleevec) in chronic myeloid leukemia (CML) occurs through selection for tumor cells harboring BCR-ABL kinase domain point mutations that interfere with drug binding.	imatinib	59-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
15256671-2	2004	Crystallographic studies predict that most imatinib-resistant mutants should remain sensitive to inhibitors that bind ABL with less stringent conformational requirements.	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-121
15256671-3	2004	BMS-354825 is an orally bioavailable ABL kinase inhibitor with two-log increased potency relative to imatinib that retains activity against 14 of 15 imatinib-resistant BCR-ABL mutants.	imatinib	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-40
15256671-3	2004	BMS-354825 is an orally bioavailable ABL kinase inhibitor with two-log increased potency relative to imatinib that retains activity against 14 of 15 imatinib-resistant BCR-ABL mutants.	imatinib	149-157	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-40
15256671-3	2004	BMS-354825 is an orally bioavailable ABL kinase inhibitor with two-log increased potency relative to imatinib that retains activity against 14 of 15 imatinib-resistant BCR-ABL mutants.	imatinib	149-157	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	168-175
15223958-12	2004	Notably, some KIT-negative GISTs contain imatinib-sensitive KIT or PDGFRA mutations; therefore, patients with KIT-negative GISTs should not, a priori, be denied imatinib therapy.	imatinib	41-49	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-17
15215166-10	2004	Reactivity for DOG1 may aid in the diagnosis of GISTs, including PDGFRA mutants that fail to express KIT antigen, and lead to appropriate treatment with imatinib mesylate, an inhibitor of the KIT tyrosine kinase.	imatinib	153-170	anoctamin 1	Homo sapiens	15-19
15215166-10	2004	Reactivity for DOG1 may aid in the diagnosis of GISTs, including PDGFRA mutants that fail to express KIT antigen, and lead to appropriate treatment with imatinib mesylate, an inhibitor of the KIT tyrosine kinase.	imatinib	153-170	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	192-195
15194504-0	2004	The two major imatinib resistance mutations E255K and T315I enhance the activity of BCR/ABL fusion kinase.	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
15194504-1	2004	The resistance to the tyrosine kinase inhibitor imatinib in BCR/ABL-positive leukemias is mostly associated with mutations in the kinase domain of BCR/ABL, which include the most prevalent mutations E255K and T315I.	imatinib	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
15194504-1	2004	The resistance to the tyrosine kinase inhibitor imatinib in BCR/ABL-positive leukemias is mostly associated with mutations in the kinase domain of BCR/ABL, which include the most prevalent mutations E255K and T315I.	imatinib	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-154
15194504-4	2004	When expressed in COS7 cells, the BCR/ABL construct with either E255K or T315I exhibited not only the resistance to imatinib but also the increase in activity to induce autophosphorylation as well as tyrosine phosphorylation of various cellular proteins, which included STAT5.	imatinib	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
14975929-7	2004	However, the effects of both NPY and VEGF on the permeability of the RAEC monolayer were blocked with equal concentration dependence by STI571 (imatinib mesylate), which is an inhibitor of Abl tyrosine kinase in the nucleus and/or cytoplasm.	imatinib	136-142	neuropeptide Y	Rattus norvegicus	29-32
14975929-7	2004	However, the effects of both NPY and VEGF on the permeability of the RAEC monolayer were blocked with equal concentration dependence by STI571 (imatinib mesylate), which is an inhibitor of Abl tyrosine kinase in the nucleus and/or cytoplasm.	imatinib	136-142	vascular endothelial growth factor A	Rattus norvegicus	37-41
14975929-7	2004	However, the effects of both NPY and VEGF on the permeability of the RAEC monolayer were blocked with equal concentration dependence by STI571 (imatinib mesylate), which is an inhibitor of Abl tyrosine kinase in the nucleus and/or cytoplasm.	imatinib	144-161	neuropeptide Y	Rattus norvegicus	29-32
14975929-7	2004	However, the effects of both NPY and VEGF on the permeability of the RAEC monolayer were blocked with equal concentration dependence by STI571 (imatinib mesylate), which is an inhibitor of Abl tyrosine kinase in the nucleus and/or cytoplasm.	imatinib	144-161	vascular endothelial growth factor A	Rattus norvegicus	37-41
14975929-9	2004	These results indicate that the NPY Y(3)-receptor subtype is specifically linked to the effects of STI571 on endothelial cells, and that NPY, a sympathetic coneurotransmitter, may increase vascular permeability in association with altered intracellular or nuclear signal transduction.	imatinib	99-105	neuropeptide Y	Rattus norvegicus	32-35
14986065-3	2004	Molecular analysis demonstrated a constitutive activation of the platelet-derived growth factor receptor-alpha (PDGFR-A) as the mechanism of responsiveness to imatinib.	imatinib	159-167	platelet derived growth factor receptor alpha	Homo sapiens	65-110
14986065-3	2004	Molecular analysis demonstrated a constitutive activation of the platelet-derived growth factor receptor-alpha (PDGFR-A) as the mechanism of responsiveness to imatinib.	imatinib	159-167	platelet derived growth factor receptor alpha	Homo sapiens	112-119
15223958-12	2004	Notably, some KIT-negative GISTs contain imatinib-sensitive KIT or PDGFRA mutations; therefore, patients with KIT-negative GISTs should not, a priori, be denied imatinib therapy.	imatinib	41-49	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	60-63
15223958-12	2004	Notably, some KIT-negative GISTs contain imatinib-sensitive KIT or PDGFRA mutations; therefore, patients with KIT-negative GISTs should not, a priori, be denied imatinib therapy.	imatinib	41-49	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	60-63
15239791-3	2004	c-kit is selectively and competitively bound by STI-571, a newly developed tyrosine kinase inhibitor.	imatinib	48-55	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-5
15183120-0	2004	In bcr-abl-positive myeloid cells resistant to conventional chemotherapeutic agents, expression of Par-4 increases sensitivity to imatinib (STI571) and histone deacetylase-inhibitors.	imatinib	130-138	pro-apoptotic WT1 regulator	Homo sapiens	99-104
15183120-0	2004	In bcr-abl-positive myeloid cells resistant to conventional chemotherapeutic agents, expression of Par-4 increases sensitivity to imatinib (STI571) and histone deacetylase-inhibitors.	imatinib	140-146	pro-apoptotic WT1 regulator	Homo sapiens	99-104
15183120-5	2004	However, incubation with histone deacetylase (HDAC)-inhibitors Trichostatin A (TSA) and LAQ824 or the tyrosinkinase inhibitor Imatinib (STI571) increased the rate of apoptosis in Par-4-positive K562 cells.	imatinib	126-134	pro-apoptotic WT1 regulator	Homo sapiens	179-184
15183120-5	2004	However, incubation with histone deacetylase (HDAC)-inhibitors Trichostatin A (TSA) and LAQ824 or the tyrosinkinase inhibitor Imatinib (STI571) increased the rate of apoptosis in Par-4-positive K562 cells.	imatinib	136-142	pro-apoptotic WT1 regulator	Homo sapiens	179-184
15183120-6	2004	Assessing the underlying molecular mechanisms for the Par-4-induced response to HDAC-inhibitors and STI571 we provide evidence, that these effects are associated with a down-regulation of Daxx, enforced activation of caspases and enhanced cleavage of cellular inhibitor of apoptosis (cIAP)-1 and -2.	imatinib	100-106	pro-apoptotic WT1 regulator	Homo sapiens	54-59
15183120-6	2004	Assessing the underlying molecular mechanisms for the Par-4-induced response to HDAC-inhibitors and STI571 we provide evidence, that these effects are associated with a down-regulation of Daxx, enforced activation of caspases and enhanced cleavage of cellular inhibitor of apoptosis (cIAP)-1 and -2.	imatinib	100-106	death domain associated protein	Homo sapiens	188-192
15183120-6	2004	Assessing the underlying molecular mechanisms for the Par-4-induced response to HDAC-inhibitors and STI571 we provide evidence, that these effects are associated with a down-regulation of Daxx, enforced activation of caspases and enhanced cleavage of cellular inhibitor of apoptosis (cIAP)-1 and -2.	imatinib	100-106	baculoviral IAP repeat containing 2	Homo sapiens	251-298
15108021-4	2004	The PDGF/PDGFR signaling pathway was inhibited in the VAS cell lines and the FSA cell line using the tyrosine kinase inhibitor imatinib mesylate (formerly called STI-571).	imatinib	127-144	platelet derived growth factor receptor, beta polypeptide	Mus musculus	9-14
15108021-4	2004	The PDGF/PDGFR signaling pathway was inhibited in the VAS cell lines and the FSA cell line using the tyrosine kinase inhibitor imatinib mesylate (formerly called STI-571).	imatinib	162-169	platelet derived growth factor receptor, beta polypeptide	Mus musculus	9-14
15108021-5	2004	Imatinib inhibited PDGF-BB-induced autophosphorylation of PDGFR in VAS cells and feline FSA cells in vitro in a dose-dependent manner.	imatinib	0-8	platelet derived growth factor receptor, beta polypeptide	Mus musculus	58-63
15108021-9	2004	These observations suggest that imatinib inhibits PDGFR tyrosine kinase activity in feline soft tissue sarcomas in vitro and inhibits tumor growth in a xenograft model.	imatinib	32-40	platelet derived growth factor receptor, beta polypeptide	Mus musculus	50-55
15236194-0	2004	A new mutation in the KIT ATP pocket causes acquired resistance to imatinib in a gastrointestinal stromal tumor patient.	imatinib	67-75	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	22-25
15107311-0	2004	Denaturing-HPLC-based assay for detection of ABL mutations in chronic myeloid leukemia patients resistant to Imatinib.	imatinib	109-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-48
15107311-1	2004	BACKGROUND: Despite the efficacy of the BCR-ABL tyrosine kinase inhibitor Imatinib mesylate for the treatment of chronic myeloid leukemia (CML), resistance has been observed in a proportion of cases, especially those with advanced stages of the disease.	imatinib	74-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-47
15236194-1	2004	BACKGROUND & AIMS: Imatinib, a tyrosine kinase inhibitor of BCR-ABL, KIT, and platelet-derived growth factor receptor, is used in patients with chronic myelogenous leukemia (CML) and gastrointestinal stromal tumors (GIST).	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
15236194-1	2004	BACKGROUND & AIMS: Imatinib, a tyrosine kinase inhibitor of BCR-ABL, KIT, and platelet-derived growth factor receptor, is used in patients with chronic myelogenous leukemia (CML) and gastrointestinal stromal tumors (GIST).	imatinib	23-31	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
15236194-10	2004	CONCLUSIONS: This new mutation was confined to the progressing lesion; the resulting amino acidic substitution, T670I, affecting the ATP/imatinib pocket of KIT, makes it insensitive to the drug.	imatinib	137-145	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	156-159
15205332-6	2004	Oral administration of PKI166 inhibited the phosphorylation of EGF-R but not PDGF-R, whereas oral administration of STI571 inhibited the phosphorylation of PDGF-R but not EGF-R.	imatinib	116-122	platelet derived growth factor receptor beta	Homo sapiens	156-162
15245690-7	2004	RESULTS: Intention-to-treat analysis showed that imatinib was associated with complete CR at 12 months follow-up of 68% compared with 20% for the IFN-alpha plus Ara-C group.	imatinib	49-57	interferon alpha 1	Homo sapiens	146-155
15293570-1	2004	Imatinib mesylate and rituximab are molecularly targeted drugs against the BCR-ABL fusion protein and the CD20 antigen, respectively.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
15293570-1	2004	Imatinib mesylate and rituximab are molecularly targeted drugs against the BCR-ABL fusion protein and the CD20 antigen, respectively.	imatinib	0-17	keratin 20	Homo sapiens	106-110
15293570-3	2004	We have investigated the case of a patient with Philadelphia chromosome-positive and CD20+ acute lymphocytic leukemia who acquired resistance to imatinib and rituximab.	imatinib	145-153	keratin 20	Homo sapiens	85-89
15293571-2	2004	Complete hematologic response and the disappearance of the Bcr-Abl fusion signal on fluorescence in situ hybridization analysis were achieved after 10 weeks of imatinib therapy and were maintained for 26 months with no adverse effects, including recurrence of GVHD.	imatinib	160-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
15226421-4	2004	In contrast, those cells isolated from our previously established CML model mice resist apoptosis in cytokine-free medium without the induction of Bim expression, and these effects are reversed by the Abl-specific kinase inhibitor imatinib mesylate.	imatinib	231-248	BCL2-like 11 (apoptosis facilitator)	Mus musculus	147-150
15226421-5	2004	In addition, the expression levels of Bim are uniformly low in cell lines established from patients in the blast crisis phase of CML, and imatinib induced Bim in these cells.	imatinib	138-146	BCL2 like 11	Homo sapiens	38-41
15226421-5	2004	In addition, the expression levels of Bim are uniformly low in cell lines established from patients in the blast crisis phase of CML, and imatinib induced Bim in these cells.	imatinib	138-146	BCL2 like 11	Homo sapiens	155-158
15226421-6	2004	Moreover, small interfering RNA that reduces the expression level of Bim effectively rescues CML cells from apoptosis caused by imatinib.	imatinib	128-136	BCL2-like 11 (apoptosis facilitator)	Mus musculus	69-72
15283151-1	2004	Imatinib mesylate (imatinib), a selective inhibitor of BCR-ABL tyrosine kinase, has shown excellent efficacy in patients with chronic myelogenous leukemia (CML) in the chronic phase, however, it does not in those in the accelerated phase or blastic crisis.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
15283151-1	2004	Imatinib mesylate (imatinib), a selective inhibitor of BCR-ABL tyrosine kinase, has shown excellent efficacy in patients with chronic myelogenous leukemia (CML) in the chronic phase, however, it does not in those in the accelerated phase or blastic crisis.	imatinib	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
15283151-5	2004	The acquired resistance in patients who failed to respond to imatinib seemed to be induced by several point mutations in the BCR-ABL gene, which were likely to affect the binding of imatinib with BCR-ABL.	imatinib	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
15283151-5	2004	The acquired resistance in patients who failed to respond to imatinib seemed to be induced by several point mutations in the BCR-ABL gene, which were likely to affect the binding of imatinib with BCR-ABL.	imatinib	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	196-203
15283151-5	2004	The acquired resistance in patients who failed to respond to imatinib seemed to be induced by several point mutations in the BCR-ABL gene, which were likely to affect the binding of imatinib with BCR-ABL.	imatinib	182-190	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
15283151-5	2004	The acquired resistance in patients who failed to respond to imatinib seemed to be induced by several point mutations in the BCR-ABL gene, which were likely to affect the binding of imatinib with BCR-ABL.	imatinib	182-190	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	196-203
15283151-8	2004	New agents which inhibit the signaling pathway related to BCR-ABL, such as adaphostin (NSC680410), farnesyltransferase inhibitor SCH66336, MAP kinase inhibitor PD184352, PD98059, U0126, and antibiotic geldanamycin, have shown excellent activity combined with imatinib in vitro.	imatinib	259-267	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
15283152-2	2004	Recently treatment with imatinib mesylate, a molecular targeted agent that inhibits the KIT tyrosine kinase receptor showed 81.6% of outstanding clinical response (PR 53.7%, SD 27.9%).	imatinib	24-41	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	88-91
15197801-0	2004	Granulocyte-colony-stimulating factor (filgrastim) may overcome imatinib-induced neutropenia in patients with chronic-phase chronic myelogenous leukemia.	imatinib	64-72	colony stimulating factor 3	Homo sapiens	0-37
15197801-4	2004	The authors investigated the ability of granulocyte-colony-stimulating factor (filgrastim) to reverse imatinib-associated neutropenia, thereby allowing for more continuous imatinib administration.	imatinib	102-110	colony stimulating factor 3	Homo sapiens	40-77
15197801-4	2004	The authors investigated the ability of granulocyte-colony-stimulating factor (filgrastim) to reverse imatinib-associated neutropenia, thereby allowing for more continuous imatinib administration.	imatinib	172-180	colony stimulating factor 3	Homo sapiens	40-77
15359647-8	2004	Moreover, in response to Imatinib, BCR/ABL transcripts decreased and were no longer detectable after 6 months.	imatinib	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
15383930-3	2004	Blockade of c-kit by imatinib mesylate (Gleevec; Novartis Pharmaceuticals Corp, East Hanover, NJ) has been successfully used in the treatment of chronic myelogenous leukemia and gastrointestinal tumors.	imatinib	21-38	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	12-17
14715630-2	2004	In this study, we show that imatinib, a potent inhibitor of BCR/ABL tyrosine kinase activity, in the presence of Flt3-Ligand, could induce CD34+ progenitors from chronic myeloid leukemia (CML) to give rise in vitro to typical BDCA-2+ type I interferon-producing PDCs.	imatinib	28-36	fms related receptor tyrosine kinase 3 ligand	Homo sapiens	113-124
14715630-2	2004	In this study, we show that imatinib, a potent inhibitor of BCR/ABL tyrosine kinase activity, in the presence of Flt3-Ligand, could induce CD34+ progenitors from chronic myeloid leukemia (CML) to give rise in vitro to typical BDCA-2+ type I interferon-producing PDCs.	imatinib	28-36	CD34 molecule	Homo sapiens	139-143
14715630-2	2004	In this study, we show that imatinib, a potent inhibitor of BCR/ABL tyrosine kinase activity, in the presence of Flt3-Ligand, could induce CD34+ progenitors from chronic myeloid leukemia (CML) to give rise in vitro to typical BDCA-2+ type I interferon-producing PDCs.	imatinib	28-36	C-type lectin domain family 4 member C	Homo sapiens	226-232
14715630-3	2004	The effect of imatinib on PDC generation was related to up-regulation of Flt3 on leukemic CD34+ progenitors.	imatinib	14-22	fms related receptor tyrosine kinase 3	Homo sapiens	73-77
14715630-3	2004	The effect of imatinib on PDC generation was related to up-regulation of Flt3 on leukemic CD34+ progenitors.	imatinib	14-22	CD34 molecule	Homo sapiens	90-94
14976048-3	2004	Activation of phosphoinositide 3-kinase (PI3K) is essential for ABL-dependent proliferation and survival in some cell types, and global PI3K inhibitors can enhance the antileukemia effects of the Abl kinase inhibitor imatinib.	imatinib	217-225	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-67
15056660-0	2004	Role of the p38 mitogen-activated protein kinase pathway in the generation of the effects of imatinib mesylate (STI571) in BCR-ABL-expressing cells.	imatinib	93-110	mitogen-activated protein kinase 14	Homo sapiens	12-48
15056660-0	2004	Role of the p38 mitogen-activated protein kinase pathway in the generation of the effects of imatinib mesylate (STI571) in BCR-ABL-expressing cells.	imatinib	93-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-130
15056660-0	2004	Role of the p38 mitogen-activated protein kinase pathway in the generation of the effects of imatinib mesylate (STI571) in BCR-ABL-expressing cells.	imatinib	112-118	mitogen-activated protein kinase 14	Homo sapiens	12-48
15056660-0	2004	Role of the p38 mitogen-activated protein kinase pathway in the generation of the effects of imatinib mesylate (STI571) in BCR-ABL-expressing cells.	imatinib	112-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-130
15056660-1	2004	Imatinib mesylate (STI571), a specific inhibitor of the BCR-ABL tyrosine kinase, exhibits potent antileukemic effects in vitro and in vivo.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
15056660-1	2004	Imatinib mesylate (STI571), a specific inhibitor of the BCR-ABL tyrosine kinase, exhibits potent antileukemic effects in vitro and in vivo.	imatinib	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
15150562-0	2004	Late resistance to imatinib therapy in a metastatic gastrointestinal stromal tumour is associated with a second KIT mutation.	imatinib	19-27	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	112-115
15056660-3	2004	In the present study we provide evidence that treatment of CML-derived BCR-ABL-expressing leukemia cells with STI571 results in activation of the p38 mitogen-activated protein (MAP) kinase signaling pathway.	imatinib	110-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
15056660-3	2004	In the present study we provide evidence that treatment of CML-derived BCR-ABL-expressing leukemia cells with STI571 results in activation of the p38 mitogen-activated protein (MAP) kinase signaling pathway.	imatinib	110-116	mitogen-activated protein kinase 14	Homo sapiens	146-149
15056660-4	2004	Our data indicate that STI571 induces phosphorylation of the p38 and activation of its kinase domain, in KT-1 cells and other BCR-ABL-expressing cell lines.	imatinib	23-29	mitogen-activated protein kinase 14	Mus musculus	61-64
15056660-4	2004	Our data indicate that STI571 induces phosphorylation of the p38 and activation of its kinase domain, in KT-1 cells and other BCR-ABL-expressing cell lines.	imatinib	23-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
15056660-6	2004	Importantly, pharmacological inhibition of p38 reverses the growth inhibitory effects of STI571 on primary leukemic colony-forming unit granulocyte/macrophage progenitors from patients with CML.	imatinib	89-95	mitogen-activated protein kinase 14	Homo sapiens	43-46
15150562-3	2004	Mutation analysis showed that the imatinib-resistant liver tumour contained two c-kit mutations.	imatinib	34-42	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	80-85
14976048-3	2004	Activation of phosphoinositide 3-kinase (PI3K) is essential for ABL-dependent proliferation and survival in some cell types, and global PI3K inhibitors can enhance the antileukemia effects of the Abl kinase inhibitor imatinib.	imatinib	217-225	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	196-199
15199413-0	2004	Stable expression of small interfering RNA sensitizes TEL-PDGFbetaR to inhibition with imatinib or rapamycin.	imatinib	87-95	ets variant 6	Mus musculus	54-57
15160343-0	2004	Erythropoietin is effective in improving the anemia induced by imatinib mesylate therapy in patients with chronic myeloid leukemia in chronic phase.	imatinib	63-80	erythropoietin	Homo sapiens	0-14
15160343-9	2004	CONCLUSIONS: The authors concluded that erythropoietin is safe and effective in patients in chronic-phase CML who develop anemia with imatinib therapy.	imatinib	134-142	erythropoietin	Homo sapiens	40-54
15172974-3	2004	The addition of STI571 to cultures of bone endothelial cells blocked PDGF BB-induced phosphorylation in a dose-dependent manner and completely abrogated the activation of downstream targets Akt and ERK1/2.	imatinib	16-22	thymoma viral proto-oncogene 1	Mus musculus	190-193
15172974-3	2004	The addition of STI571 to cultures of bone endothelial cells blocked PDGF BB-induced phosphorylation in a dose-dependent manner and completely abrogated the activation of downstream targets Akt and ERK1/2.	imatinib	16-22	mitogen-activated protein kinase 3	Mus musculus	198-204
15239393-6	2004	At the center of these new developments are mutations involving the platelet-derived growth factor receptor genes (PDGFRA and PDGFRB), which have been pathogenetically linked to clonal eosinophilia, and their presence predicts complete as well as durable treatment responses to imatinib mesylate.	imatinib	278-295	platelet derived growth factor receptor alpha	Homo sapiens	115-121
15239393-6	2004	At the center of these new developments are mutations involving the platelet-derived growth factor receptor genes (PDGFRA and PDGFRB), which have been pathogenetically linked to clonal eosinophilia, and their presence predicts complete as well as durable treatment responses to imatinib mesylate.	imatinib	278-295	platelet derived growth factor receptor beta	Homo sapiens	126-132
15354415-7	2004	Comparison of cytogenetic results to FISH results at 3 and 6 months of imatinib treatment showed that some patients who had achieved major cytogenetic response (i.e.<35% of examined metaphases showing Ph), showed retention of a higher number of persisting Ph+ cells when examined by FISH, and they did not achieve major FISH response (i.e. <35% of examined interphase cells show the BCR-ABL fusion signal).	imatinib	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	389-396
15128424-3	2004	Imatinib mesylate was started in April 2002 after failure of IFN-alpha to induce a cytogenetic response.	imatinib	0-17	interferon alpha 1	Homo sapiens	61-70
15199413-1	2004	Small molecule inhibitors, such as imatinib, are effective therapies for tyrosine kinase fusions BCR-ABL-TEL-PDGFbetaR-mediated human leukemias, but resistance may develop.	imatinib	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
15199413-1	2004	Small molecule inhibitors, such as imatinib, are effective therapies for tyrosine kinase fusions BCR-ABL-TEL-PDGFbetaR-mediated human leukemias, but resistance may develop.	imatinib	35-43	ETS variant transcription factor 6	Homo sapiens	105-108
15199413-7	2004	TPsiRNA also inhibited an imatinib-resistant TEL-PDGFbetaR mutant, and the inhibition was enhanced by siRNA in combination with PKC412, another PDGFbetaR inhibitor.	imatinib	26-34	ets variant 6	Mus musculus	45-48
15126780-0	2004	C-kit expression in sarcomatoid renal cell carcinoma: potential therapy with imatinib.	imatinib	77-85	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-5
15126780-3	2004	A relatively nontoxic tyrosine kinase inhibitor, imatinib (STI-571) has been approved as a target therapy in neoplasms that express c-Kit.	imatinib	49-57	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	132-137
15126780-3	2004	A relatively nontoxic tyrosine kinase inhibitor, imatinib (STI-571) has been approved as a target therapy in neoplasms that express c-Kit.	imatinib	59-66	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	132-137
15044919-2	2004	The recent observations that c-kit proto-oncogene, a tyrosine kinase, is overexpressed in small cell lung cancers and that advanced c-kit-expressing gastrointestinal stromal tumors were successfully treated with a selective tyrosine kinase inhibitor STI-571 (Gleevec, imatinib mesylate) prompted us to investigate c-kit protein expression in cervical small cell carcinomas.	imatinib	250-257	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	29-49
15120940-0	2004	Ectopic cyclin D1 expression blocks STI571-induced erythroid differentiation of K562 cells.	imatinib	36-42	cyclin D1	Homo sapiens	8-17
15120940-7	2004	During STI571 treatment, ERK activity was downregulated in parental cells, while it was constantly activated in K562/D1 cells.	imatinib	7-13	mitogen-activated protein kinase 1	Homo sapiens	25-28
15085152-6	2004	The Abl kinase inhibitor imatinib mesylate and the Jak inhibitor AG490 suppressed TPO-induced aggregation of CML-CP platelets.	imatinib	25-42	thrombopoietin	Homo sapiens	82-85
15120938-0	2004	Interleukin 11 May improve thrombocytopenia associated with imatinib mesylate therapy in chronic Myelogenous leukemia.	imatinib	60-77	interleukin 11	Homo sapiens	0-14
15120938-4	2004	We report on the use of interleukin-11 in three CML patients with grade > or =3, imatinib-induced thrombocytopenia.	imatinib	84-92	interleukin 11	Homo sapiens	24-38
15120938-5	2004	In all three patients, interleukin-11 led to improved platelets, uninterrupted administration of imatinib and improved cytogenetic response.	imatinib	97-105	interleukin 11	Homo sapiens	23-37
15120938-6	2004	This observation suggests that interleukin-11 may be beneficial for patients with imatinib-induced thrombocytoepnia.	imatinib	82-90	interleukin 11	Homo sapiens	31-45
15044919-2	2004	The recent observations that c-kit proto-oncogene, a tyrosine kinase, is overexpressed in small cell lung cancers and that advanced c-kit-expressing gastrointestinal stromal tumors were successfully treated with a selective tyrosine kinase inhibitor STI-571 (Gleevec, imatinib mesylate) prompted us to investigate c-kit protein expression in cervical small cell carcinomas.	imatinib	250-257	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	29-34
15044919-2	2004	The recent observations that c-kit proto-oncogene, a tyrosine kinase, is overexpressed in small cell lung cancers and that advanced c-kit-expressing gastrointestinal stromal tumors were successfully treated with a selective tyrosine kinase inhibitor STI-571 (Gleevec, imatinib mesylate) prompted us to investigate c-kit protein expression in cervical small cell carcinomas.	imatinib	250-257	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	132-137
15044919-2	2004	The recent observations that c-kit proto-oncogene, a tyrosine kinase, is overexpressed in small cell lung cancers and that advanced c-kit-expressing gastrointestinal stromal tumors were successfully treated with a selective tyrosine kinase inhibitor STI-571 (Gleevec, imatinib mesylate) prompted us to investigate c-kit protein expression in cervical small cell carcinomas.	imatinib	259-266	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	29-49
15044919-2	2004	The recent observations that c-kit proto-oncogene, a tyrosine kinase, is overexpressed in small cell lung cancers and that advanced c-kit-expressing gastrointestinal stromal tumors were successfully treated with a selective tyrosine kinase inhibitor STI-571 (Gleevec, imatinib mesylate) prompted us to investigate c-kit protein expression in cervical small cell carcinomas.	imatinib	259-266	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	29-34
15044919-2	2004	The recent observations that c-kit proto-oncogene, a tyrosine kinase, is overexpressed in small cell lung cancers and that advanced c-kit-expressing gastrointestinal stromal tumors were successfully treated with a selective tyrosine kinase inhibitor STI-571 (Gleevec, imatinib mesylate) prompted us to investigate c-kit protein expression in cervical small cell carcinomas.	imatinib	259-266	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	132-137
15044919-2	2004	The recent observations that c-kit proto-oncogene, a tyrosine kinase, is overexpressed in small cell lung cancers and that advanced c-kit-expressing gastrointestinal stromal tumors were successfully treated with a selective tyrosine kinase inhibitor STI-571 (Gleevec, imatinib mesylate) prompted us to investigate c-kit protein expression in cervical small cell carcinomas.	imatinib	268-285	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	29-49
15044919-2	2004	The recent observations that c-kit proto-oncogene, a tyrosine kinase, is overexpressed in small cell lung cancers and that advanced c-kit-expressing gastrointestinal stromal tumors were successfully treated with a selective tyrosine kinase inhibitor STI-571 (Gleevec, imatinib mesylate) prompted us to investigate c-kit protein expression in cervical small cell carcinomas.	imatinib	268-285	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	29-34
15044919-2	2004	The recent observations that c-kit proto-oncogene, a tyrosine kinase, is overexpressed in small cell lung cancers and that advanced c-kit-expressing gastrointestinal stromal tumors were successfully treated with a selective tyrosine kinase inhibitor STI-571 (Gleevec, imatinib mesylate) prompted us to investigate c-kit protein expression in cervical small cell carcinomas.	imatinib	268-285	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	132-137
15308010-1	2004	OBJECTIVE: To establish a BCR/ABL+ cell line with resistance to imatinib, and investigate the possible mechanisms of the acquired resistance.	imatinib	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
15308010-10	2004	The mechanisms of resistance of K562/G01 cells to imatinib involved increased expression of BCR/ABL and mdr1/P-gp, amplification of BCR/ABL fusion gene, and increased activity of BCR/ABL.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
15308010-10	2004	The mechanisms of resistance of K562/G01 cells to imatinib involved increased expression of BCR/ABL and mdr1/P-gp, amplification of BCR/ABL fusion gene, and increased activity of BCR/ABL.	imatinib	50-58	ATP binding cassette subfamily B member 1	Homo sapiens	104-108
15308010-10	2004	The mechanisms of resistance of K562/G01 cells to imatinib involved increased expression of BCR/ABL and mdr1/P-gp, amplification of BCR/ABL fusion gene, and increased activity of BCR/ABL.	imatinib	50-58	phosphoglycolate phosphatase	Homo sapiens	109-113
15308010-10	2004	The mechanisms of resistance of K562/G01 cells to imatinib involved increased expression of BCR/ABL and mdr1/P-gp, amplification of BCR/ABL fusion gene, and increased activity of BCR/ABL.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
15308010-10	2004	The mechanisms of resistance of K562/G01 cells to imatinib involved increased expression of BCR/ABL and mdr1/P-gp, amplification of BCR/ABL fusion gene, and increased activity of BCR/ABL.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
14726395-0	2004	Efficacy and safety of imatinib in adult patients with c-kit-positive acute myeloid leukemia.	imatinib	23-31	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	55-60
14726395-1	2004	This phase 2 pilot study was conducted to determine the efficacy and safety of imatinib mesylate in patients with c-kit-positive acute myeloid leukemia (AML) refractory to or not eligible for chemotherapy.	imatinib	79-96	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	114-119
14726395-6	2004	Further, imatinib treatment of primary AML cells inhibited c-Kit tyrosine-phosphorylation.	imatinib	9-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	59-64
14726395-8	2004	Although some of the responses derived from relatively small reductions in leukemic blasts and may be attributable, in part, to prior chemotherapy, these cases suggest that imatinib has interesting clinical activity in a subset of patients with c-kit-positive AML.	imatinib	173-181	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	245-250
15094364-0	2004	Role of E2F and ERK1/2 in STI571-mediated smooth muscle cell growth arrest and cyclin A transcriptional repression.	imatinib	26-32	mitogen-activated protein kinase 3	Homo sapiens	16-22
15139047-5	2004	Imatinib is a selective inhibitor of PDGFRs, c-Kit, Abl and Arg protein-tyrosine kinases, as well as Bcr-Abl, the oncogenic tyrosine kinase that causes chronic myeloid leukemia.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	45-50
15139047-5	2004	Imatinib is a selective inhibitor of PDGFRs, c-Kit, Abl and Arg protein-tyrosine kinases, as well as Bcr-Abl, the oncogenic tyrosine kinase that causes chronic myeloid leukemia.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-55
15139047-5	2004	Imatinib is a selective inhibitor of PDGFRs, c-Kit, Abl and Arg protein-tyrosine kinases, as well as Bcr-Abl, the oncogenic tyrosine kinase that causes chronic myeloid leukemia.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
15139047-6	2004	The efficacy of imatinib in treating HES, systemic mast cell disease, chronic myelomonocytic leukemia associated with PDGFRbeta fusion genes, and (to a lesser extent) PV and idiopathic myelofibrosis was reviewed from institutional experience and a review of the literature.	imatinib	16-24	platelet derived growth factor receptor beta	Homo sapiens	118-127
15161712-3	2004	The purpose of this study was to determine whether imatinib mesylate, an inhibitor of c-Kit, could achieve therapeutic concentrations in tumors and in brain (a frequent site of SCLC metastasis) and interfere with SCLC tumor growth in vivo.	imatinib	51-68	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	86-91
15161712-8	2004	Imatinib blocked the constitutive activation of c-kit in SCLC tumor cell lines in vitro but had a negligible effect on SCLC xenograft growth in vivo.	imatinib	0-8	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	48-53
15094364-4	2004	STI571 abrogates PDGF-BB-dependent cyclin D1 and cyclin A protein expression and inhibits transcriptional activation of reporter genes driven by the human cyclin A gene promoter.	imatinib	0-6	cyclin D1	Homo sapiens	35-44
15094364-4	2004	STI571 abrogates PDGF-BB-dependent cyclin D1 and cyclin A protein expression and inhibits transcriptional activation of reporter genes driven by the human cyclin A gene promoter.	imatinib	0-6	cyclin A2	Homo sapiens	49-57
15007386-2	2004	KIT oncoproteins are detected early in GIST tumorigenesis, and most GIST patients respond well to treatment with the KIT kinase inhibitor imatinib mesylate (STI571, Gleevec).	imatinib	138-155	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
15007386-2	2004	KIT oncoproteins are detected early in GIST tumorigenesis, and most GIST patients respond well to treatment with the KIT kinase inhibitor imatinib mesylate (STI571, Gleevec).	imatinib	138-155	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	117-120
15094364-4	2004	STI571 abrogates PDGF-BB-dependent cyclin D1 and cyclin A protein expression and inhibits transcriptional activation of reporter genes driven by the human cyclin A gene promoter.	imatinib	0-6	cyclin A2	Homo sapiens	155-163
15007386-2	2004	KIT oncoproteins are detected early in GIST tumorigenesis, and most GIST patients respond well to treatment with the KIT kinase inhibitor imatinib mesylate (STI571, Gleevec).	imatinib	157-163	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
15094364-5	2004	Repression of cyclin A promoter activity by STI571 requires a functional E2F-binding site, and forced expression of E2F overrides this inhibitory effect.	imatinib	44-50	cyclin A2	Homo sapiens	14-22
15007386-2	2004	KIT oncoproteins are detected early in GIST tumorigenesis, and most GIST patients respond well to treatment with the KIT kinase inhibitor imatinib mesylate (STI571, Gleevec).	imatinib	157-163	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	117-120
15094364-7	2004	We also found that STI571 abrogates PDGF-BB-dependent activation of extracellular-regulated kinase 1 and 2 (ERK1/2), and forced activation of these factors impaired STI571-dependent inhibition of both cyclin A promoter activity and SMC proliferation.	imatinib	19-25	mitogen-activated protein kinase 3	Homo sapiens	108-114
15094364-7	2004	We also found that STI571 abrogates PDGF-BB-dependent activation of extracellular-regulated kinase 1 and 2 (ERK1/2), and forced activation of these factors impaired STI571-dependent inhibition of both cyclin A promoter activity and SMC proliferation.	imatinib	165-171	cyclin A2	Homo sapiens	201-209
15094364-8	2004	Thus, E2F and ERK1/2 play an important role in STI571-mediated SMC growth arrest and cyclin A transcriptional repression.	imatinib	47-53	mitogen-activated protein kinase 3	Homo sapiens	14-20
15142121-0	2004	Phosphatidylinositol-3 kinase inhibitors reproduce the selective antiproliferative effects of imatinib on chronic myeloid leukaemia progenitor cells.	imatinib	94-102	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	0-29
15105658-7	2004	Finally, it should be determined whether KIT plays a role in the tumorigenesis of ChRCC and oncocytoma and whether targeted therapy with STI-571, an inhibitor of KIT, could be effective in exceptional cases of ChRCC with metastatic extension or recurrence.	imatinib	137-144	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	162-165
15123459-6	2004	Imatinib is a potent, specific inhibitor of KIT that has demonstrated significant activity and tolerability in the treatment of malignant unresectable or metastatic GIST, inducing tumor shrinkage of 50% or more or stabilizing disease in most patients.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	44-47
14656881-6	2004	Moreover, ICSBP also overrode BCR/ABL-mediated morphology changes, chemotherapy, and imatinib resistance, as well as BCR/ABL-induced repression of differentiation.	imatinib	85-93	interferon regulatory factor 8	Mus musculus	10-15
15142121-1	2004	We investigated the role of the phosphatidylinositol-3 kinase (PI-3K) pathway in regulating the proliferation of primary chronic myeloid leukaemia (CML) progenitor cells by using imatinib to inhibit the activity of p210(Bcr-Abl).	imatinib	179-187	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	32-61
15142121-2	2004	The effect of imatinib on the expression of PI-3K pathway proteins was investigated by kinase assays and Western blotting; PI-3K was inhibited by wortmannin or LY294002, Jak2 by AG490 and farnesylation by FTI II; progenitor cell proliferation (self-renewal) was measured by growing myeloid colonies in vitro, then replating them to observe secondary colony formation.	imatinib	14-22	Janus kinase 2	Homo sapiens	170-174
15142121-3	2004	Suppression of p210(Bcr-Abl) with imatinib indirectly suppressed the activity of PI-3K and its downstream targets (Erk, Akt and p70S6 kinase), thereby implicating the PI-3K pathway in p210(Bcr-Abl)-mediated signalling in primary CML progenitor cells.	imatinib	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
15142121-3	2004	Suppression of p210(Bcr-Abl) with imatinib indirectly suppressed the activity of PI-3K and its downstream targets (Erk, Akt and p70S6 kinase), thereby implicating the PI-3K pathway in p210(Bcr-Abl)-mediated signalling in primary CML progenitor cells.	imatinib	34-42	mitogen-activated protein kinase 1	Homo sapiens	115-118
15142121-3	2004	Suppression of p210(Bcr-Abl) with imatinib indirectly suppressed the activity of PI-3K and its downstream targets (Erk, Akt and p70S6 kinase), thereby implicating the PI-3K pathway in p210(Bcr-Abl)-mediated signalling in primary CML progenitor cells.	imatinib	34-42	AKT serine/threonine kinase 1	Homo sapiens	120-123
15142121-3	2004	Suppression of p210(Bcr-Abl) with imatinib indirectly suppressed the activity of PI-3K and its downstream targets (Erk, Akt and p70S6 kinase), thereby implicating the PI-3K pathway in p210(Bcr-Abl)-mediated signalling in primary CML progenitor cells.	imatinib	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	189-196
15126530-3	2004	In chronic myeloid leukemia and gastrointestinal stromal tumors, imatinib inhibits the constitutive tyrosine kinase activity of BCR-ABL and c-KIT, respectively.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
15126353-5	2004	Exposure of these cells to the BCR/ABL tyrosine kinase inhibitor STI571 resulted in decreased expression of HO-1 mRNA and protein.	imatinib	65-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
15126353-5	2004	Exposure of these cells to the BCR/ABL tyrosine kinase inhibitor STI571 resulted in decreased expression of HO-1 mRNA and protein.	imatinib	65-71	heme oxygenase 1	Homo sapiens	108-112
15126353-8	2004	Hemin-induced expression of HO-1 was found to protect CML cells from STI571-induced cell death.	imatinib	69-75	heme oxygenase 1	Homo sapiens	28-32
15126353-10	2004	Furthermore, overexpression of HO-1 in the CML-derived cell line K562 was found to counteract STI571-induced apoptosis.	imatinib	94-100	heme oxygenase 1	Homo sapiens	31-35
15034867-10	2004	Here, we report the molecular and cytogenetic characterization of a patient with BCR-PDGFRA-positive MPD who had a complete hematologic response after treatment with imatinib mesylate.	imatinib	166-183	platelet derived growth factor receptor alpha	Homo sapiens	85-91
15206509-1	2004	Imatinib mesylate (Gleevec/Glivec, Novartis, Basel, Switzerland), formerly called STI571, is a specific and potent inhibitor of the BCR-ABL tyrosine kinase, the molecular hallmark of chronic myeloid leukaemia.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-139
15206509-1	2004	Imatinib mesylate (Gleevec/Glivec, Novartis, Basel, Switzerland), formerly called STI571, is a specific and potent inhibitor of the BCR-ABL tyrosine kinase, the molecular hallmark of chronic myeloid leukaemia.	imatinib	82-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-139
15206509-3	2004	On the other hand, imatinib is also active against other tyrosine kinases, such as ABL, the stem cell factor receptor (c-kit) and the platelet-derived growth factor receptor, whose inhibition might have potential implications for the treatment of several malignancies.	imatinib	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-86
15206509-3	2004	On the other hand, imatinib is also active against other tyrosine kinases, such as ABL, the stem cell factor receptor (c-kit) and the platelet-derived growth factor receptor, whose inhibition might have potential implications for the treatment of several malignancies.	imatinib	19-27	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	119-124
15126530-3	2004	In chronic myeloid leukemia and gastrointestinal stromal tumors, imatinib inhibits the constitutive tyrosine kinase activity of BCR-ABL and c-KIT, respectively.	imatinib	65-73	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	140-145
15126530-4	2004	Reports suggest that imatinib may also be effective against ABL and platelet-derived growth factor receptor kinase-dependent pathological conditions.	imatinib	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-63
15014528-4	2004	When BCR-ABL-transduced human CB cells were incubated with imatinib mesylate, an inhibitor of the p210BCR-ABL kinase, or when human CB cells were transduced with a BCR-ABL cDNA lacking the SH2 domain (p210DeltaSH2), factor independence was significantly reduced.	imatinib	59-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	5-12
15036941-2	2004	Complete remissions, in response to treatment with low-dose imatinib mesylate (100 mg/day or less) have now been documented in all cases of FIP1L1-PDGFRA(+) eosinophilic disorder as well as other eosinophilic disorders that carry activation mutations of the PDGFRB gene that is located on chromosome 5q33.	imatinib	60-77	platelet derived growth factor receptor alpha	Homo sapiens	147-153
15036941-2	2004	Complete remissions, in response to treatment with low-dose imatinib mesylate (100 mg/day or less) have now been documented in all cases of FIP1L1-PDGFRA(+) eosinophilic disorder as well as other eosinophilic disorders that carry activation mutations of the PDGFRB gene that is located on chromosome 5q33.	imatinib	60-77	platelet derived growth factor receptor beta	Homo sapiens	258-264
15014531-0	2004	Dendritic cells become BCR-ABL negative in chronic myeloid leukaemia patients successfully treated with imatinib.	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
15036944-0	2004	A 2-year-old with atypical CML with a t(5;12)(q33;p13) treated successfully with imatinib mesylate.	imatinib	81-98	H3 histone pseudogene 6	Homo sapiens	50-53
15036944-3	2004	Because the PDGFRB tyrosine kinase is one of the known targets of tyrosine kinase inhibitors, this patient achieved cytogenetic and molecular remission with treatment with imatinib mesylate (formerly STI571; now Gleevec in the United States and Glivec in Europe).	imatinib	172-189	platelet derived growth factor receptor beta	Homo sapiens	12-18
15036937-4	2004	Kit is a convenient target in Kit-induced tumors and inhibition of this receptor with the small molecule drug Gleevec (imatinib mesylate, STI571) in GIST has shown dramatic efficacy.	imatinib	119-136	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
15036937-4	2004	Kit is a convenient target in Kit-induced tumors and inhibition of this receptor with the small molecule drug Gleevec (imatinib mesylate, STI571) in GIST has shown dramatic efficacy.	imatinib	119-136	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	30-33
15036938-0	2004	Mechanisms of transformation by the BCR-ABL oncogene: new perspectives in the post-imatinib era.	imatinib	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
15036941-2	2004	Complete remissions, in response to treatment with low-dose imatinib mesylate (100 mg/day or less) have now been documented in all cases of FIP1L1-PDGFRA(+) eosinophilic disorder as well as other eosinophilic disorders that carry activation mutations of the PDGFRB gene that is located on chromosome 5q33.	imatinib	60-77	factor interacting with PAPOLA and CPSF1	Homo sapiens	140-146
15170967-2	2004	Imatinib (Glivec, formerly STI571) is a highly selective inhibitor of the bcr-abl tyrosine kinase which has shown a promising therapeutic activity in chronic myeloid leukemia as the first molecularly targeted antinoplastic treatment.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
15141010-2	2004	Previous data suggested that IGF-I protects cells from apoptosis induced by STI571, an efficient inhibitor of Kit signal transduction, by activating the critical phosphatidylinositol 3-kinase-Akt pathway.	imatinib	76-82	insulin like growth factor 1	Homo sapiens	29-34
15141010-2	2004	Previous data suggested that IGF-I protects cells from apoptosis induced by STI571, an efficient inhibitor of Kit signal transduction, by activating the critical phosphatidylinositol 3-kinase-Akt pathway.	imatinib	76-82	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	110-113
15141010-2	2004	Previous data suggested that IGF-I protects cells from apoptosis induced by STI571, an efficient inhibitor of Kit signal transduction, by activating the critical phosphatidylinositol 3-kinase-Akt pathway.	imatinib	76-82	AKT serine/threonine kinase 1	Homo sapiens	192-195
15141010-11	2004	However, for optimal growth inhibition of SCLC cells with an active SCF/Kit autocrine loop, a combination of a Kit inhibitor (STI571) and an IGF-IR inhibitor (NVP-ADW742) appears to be necessary.	imatinib	126-132	KIT ligand	Homo sapiens	68-71
15100500-1	2004	BACKGROUND: The new anti-cancer drug imatinib mesylate inhibits the tyrosine kinase growth factor receptor, c-KIT, and has shown spectacular activity in patients with gastrointestinal stromal tumours (GISTs).	imatinib	37-54	kinase insert domain receptor	Homo sapiens	68-106
15100500-1	2004	BACKGROUND: The new anti-cancer drug imatinib mesylate inhibits the tyrosine kinase growth factor receptor, c-KIT, and has shown spectacular activity in patients with gastrointestinal stromal tumours (GISTs).	imatinib	37-54	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	108-113
15170967-2	2004	Imatinib (Glivec, formerly STI571) is a highly selective inhibitor of the bcr-abl tyrosine kinase which has shown a promising therapeutic activity in chronic myeloid leukemia as the first molecularly targeted antinoplastic treatment.	imatinib	27-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
14985355-6	2004	STI-571, a c-kit inhibitor, dose-dependently attenuated these phosphorylations and inhibited stem cell factor-promoted survival and capillary tube formation over the same dose range.	imatinib	0-7	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	11-16
14985355-6	2004	STI-571, a c-kit inhibitor, dose-dependently attenuated these phosphorylations and inhibited stem cell factor-promoted survival and capillary tube formation over the same dose range.	imatinib	0-7	KIT ligand	Homo sapiens	93-109
15170967-2	2004	Imatinib (Glivec, formerly STI571) is a highly selective inhibitor of the bcr-abl tyrosine kinase which has shown a promising therapeutic activity in chronic myeloid leukemia as the first molecularly targeted antinoplastic treatment.	imatinib	10-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
15070699-0	2004	BCR/ABL kinase inhibition by imatinib mesylate enhances MAP kinase activity in chronic myelogenous leukemia CD34+ cells.	imatinib	29-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
15070666-2	2004	We monitored the serum levels of KIT, KIT ligand (stem cell factor, SCF), and the vascular endothelial growth factor (VEGF) in patients with advanced GISTs treated with imatinib in a prospective randomized trial.	imatinib	169-177	vascular endothelial growth factor A	Homo sapiens	118-122
15070658-8	2004	Compared with standard-dose imatinib, high-dose imatinib was associated with significantly better complete cytogenetic response (P =.0005), major molecular response (QPRC < 0.05%; P =.00001), and complete molecular response (undetectable BCR-ABL; P =.001).	imatinib	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	241-248
15070699-2	2004	The breakpoint cluster region/ABL (BCR/ABL) tyrosine kinase inhibitor imatinib mesylate (imatinib) is highly effective in inducing remissions in CML.	imatinib	70-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-33
15070666-0	2004	Serum KIT and KIT ligand levels in patients with gastrointestinal stromal tumors treated with imatinib.	imatinib	94-102	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	6-9
15070666-4	2004	After 1 and 6 months of imatinib treatment the average serum KIT levels decreased 31% and 52% from pretreatment levels, whereas SCF levels increased 11% and 33%, respectively.	imatinib	24-32	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	61-64
15070666-4	2004	After 1 and 6 months of imatinib treatment the average serum KIT levels decreased 31% and 52% from pretreatment levels, whereas SCF levels increased 11% and 33%, respectively.	imatinib	24-32	KIT ligand	Homo sapiens	128-131
15070666-0	2004	Serum KIT and KIT ligand levels in patients with gastrointestinal stromal tumors treated with imatinib.	imatinib	94-102	KIT ligand	Homo sapiens	14-24
15070699-2	2004	The breakpoint cluster region/ABL (BCR/ABL) tyrosine kinase inhibitor imatinib mesylate (imatinib) is highly effective in inducing remissions in CML.	imatinib	70-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
15070666-1	2004	Imatinib mesylate is a selective inhibitor of a few tyrosine kinases including KIT, and it is the first effective treatment for gastrointestinal stromal tumors (GISTs).	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	79-82
15070666-7	2004	A high serum SCF/KIT ratio may increase SCF-induced cell signaling with prolonged imatinib treatment, at the time when imatinib treatment is withdrawn, and in patients whose GIST has wild-type receptors.	imatinib	82-90	KIT ligand	Homo sapiens	13-16
15070666-7	2004	A high serum SCF/KIT ratio may increase SCF-induced cell signaling with prolonged imatinib treatment, at the time when imatinib treatment is withdrawn, and in patients whose GIST has wild-type receptors.	imatinib	82-90	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	17-20
15070699-2	2004	The breakpoint cluster region/ABL (BCR/ABL) tyrosine kinase inhibitor imatinib mesylate (imatinib) is highly effective in inducing remissions in CML.	imatinib	70-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-33
15070666-7	2004	A high serum SCF/KIT ratio may increase SCF-induced cell signaling with prolonged imatinib treatment, at the time when imatinib treatment is withdrawn, and in patients whose GIST has wild-type receptors.	imatinib	82-90	KIT ligand	Homo sapiens	40-43
15070666-7	2004	A high serum SCF/KIT ratio may increase SCF-induced cell signaling with prolonged imatinib treatment, at the time when imatinib treatment is withdrawn, and in patients whose GIST has wild-type receptors.	imatinib	119-127	KIT ligand	Homo sapiens	13-16
15070706-0	2004	A novel form of mastocytosis associated with a transmembrane c-kit mutation and response to imatinib.	imatinib	92-100	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	61-66
15070699-2	2004	The breakpoint cluster region/ABL (BCR/ABL) tyrosine kinase inhibitor imatinib mesylate (imatinib) is highly effective in inducing remissions in CML.	imatinib	70-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
15070706-2	2004	Transfection experiments revealed that the mutation caused ligand-independent autophosphorylation of Kit, which was inhibited by the tyrosine kinase inhibitor imatinib mesylate.	imatinib	159-176	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	101-104
15070706-5	2004	These results highlight the significance of the transmembrane region of Kit in activation of the molecule and its importance in mast cell development and suggest a role for screening for transmembrane c-kit mutations in patients with mastocytosis in association with the decision to use imatinib mesylate.	imatinib	287-295	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	72-75
15070666-7	2004	A high serum SCF/KIT ratio may increase SCF-induced cell signaling with prolonged imatinib treatment, at the time when imatinib treatment is withdrawn, and in patients whose GIST has wild-type receptors.	imatinib	119-127	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	17-20
15070666-7	2004	A high serum SCF/KIT ratio may increase SCF-induced cell signaling with prolonged imatinib treatment, at the time when imatinib treatment is withdrawn, and in patients whose GIST has wild-type receptors.	imatinib	119-127	KIT ligand	Homo sapiens	40-43
15070699-4	2004	We show that imatinib exposure resulted in a significant dose-responsive reduction in BCR/ABL kinase activity in CML CD34+ cells.	imatinib	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
15070699-5	2004	However, imatinib treatment resulted in an increase in activity of p42/44 mitogen-activated protein kinase (MAPK), an important downstream effector of BCR/ABL.	imatinib	9-17	cyclin dependent kinase 20	Homo sapiens	67-70
15070699-5	2004	However, imatinib treatment resulted in an increase in activity of p42/44 mitogen-activated protein kinase (MAPK), an important downstream effector of BCR/ABL.	imatinib	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-158
15070699-11	2004	We conclude that inhibition of BCR/ABL kinase activity in CML progenitors by imatinib results in a growth factor-dependent compensatory increase in MAPK activity and in only partial inhibition of PI-3 kinase activity.	imatinib	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
15087377-0	2004	NIN, a gene encoding a CEP110-like centrosomal protein, is fused to PDGFRB in a patient with a t(5;14)(q33;q24) and an imatinib-responsive myeloproliferative disorder.	imatinib	119-127	ninein	Homo sapiens	0-3
15087377-0	2004	NIN, a gene encoding a CEP110-like centrosomal protein, is fused to PDGFRB in a patient with a t(5;14)(q33;q24) and an imatinib-responsive myeloproliferative disorder.	imatinib	119-127	centriolar coiled-coil protein 110	Homo sapiens	23-29
15135086-3	2004	The latter cells express the BCR/ABL fusion protein, which can be a target of the tyrosine kinase inhibitor STI571.	imatinib	108-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
15135086-11	2004	The results obtained with the BCR/ABL inhibitor suggest that K562 cells could be more sensitive towards co-treatment of cisplatin and STI571.	imatinib	134-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
15087377-0	2004	NIN, a gene encoding a CEP110-like centrosomal protein, is fused to PDGFRB in a patient with a t(5;14)(q33;q24) and an imatinib-responsive myeloproliferative disorder.	imatinib	119-127	platelet derived growth factor receptor beta	Homo sapiens	68-74
15087377-4	2004	After treatment with imatinib, the patient achieved hematological and cytogenetical remission, but NIN-PDGFRB mRNA remained detectable by reverse transcription-PCR.	imatinib	21-29	platelet derived growth factor receptor beta	Homo sapiens	103-109
15057146-5	2004	The prognosis of these diseases improved enormously since the drug imatinib, a tyrosine kinase inhibitor of c-kit and bcr-abl, was introduced.	imatinib	67-75	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	108-113
15188667-6	2004	Most GISTs respond to imatinib mesylate, which selectively inhibits both KIT and PDGFRA, and is now considered as the standard systemic therapy for advanced GIST.	imatinib	22-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
15188667-6	2004	Most GISTs respond to imatinib mesylate, which selectively inhibits both KIT and PDGFRA, and is now considered as the standard systemic therapy for advanced GIST.	imatinib	22-39	platelet derived growth factor receptor alpha	Homo sapiens	81-87
15033665-7	2004	This study suggests the necessity for clinical trials confirming the utility of the tyrosine kinase inhibitor, STI571, in ovarian advanced cancer patients with c-KIT overexpression when these patients have shown no clinical response to conventional chemotherapy.	imatinib	111-117	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	160-165
15087667-12	2004	Furthermore, STI-571, targeting c-kit and PDGFR tyrosine kinase, seems to be a possible therapeutic strategy for EGISTs, especially advanced cases.	imatinib	13-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	32-37
15057146-5	2004	The prognosis of these diseases improved enormously since the drug imatinib, a tyrosine kinase inhibitor of c-kit and bcr-abl, was introduced.	imatinib	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
15042680-0	2004	Changes associated with the development of resistance to imatinib (STI571) in two leukemia cell lines expressing p210 Bcr/Abl protein.	imatinib	57-65	BCR activator of RhoGEF and GTPase	Homo sapiens	118-121
15042680-0	2004	Changes associated with the development of resistance to imatinib (STI571) in two leukemia cell lines expressing p210 Bcr/Abl protein.	imatinib	57-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-125
14726674-5	2004	Here we describe that blocking c-Kit with STI571 inhibits these malignant traits not only in DLD-1 cells but also in two early passage colorectal carcinoma cell strains.	imatinib	42-48	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	31-36
14726674-2	2004	The tyrosine kinase inhibitor STI571 (IMATINIB MESYLATE; GLEEVEC; GLIVEC) is a case in point as it has shown promise in the treatment of malignancies expressing the BCR/ABL fusion protein.	imatinib	30-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	165-172
15042680-0	2004	Changes associated with the development of resistance to imatinib (STI571) in two leukemia cell lines expressing p210 Bcr/Abl protein.	imatinib	67-73	BCR activator of RhoGEF and GTPase	Homo sapiens	118-121
14726674-2	2004	The tyrosine kinase inhibitor STI571 (IMATINIB MESYLATE; GLEEVEC; GLIVEC) is a case in point as it has shown promise in the treatment of malignancies expressing the BCR/ABL fusion protein.	imatinib	38-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	165-172
14726674-3	2004	In addition to BCR/ABL, STI571 inhibits the tyrosine kinase moieties of several cell surface receptors including the platelet-derived growth factor (PDGF) receptors and c-Kit.	imatinib	24-30	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	169-174
14726674-8	2004	In addition, STI571 treatment affected the balance of the Bcl-2 family of apoptosis regulators on favor of a pro-apoptotic phenotype.	imatinib	13-19	BCL2 apoptosis regulator	Homo sapiens	58-63
15042680-0	2004	Changes associated with the development of resistance to imatinib (STI571) in two leukemia cell lines expressing p210 Bcr/Abl protein.	imatinib	67-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-125
15042680-9	2004	The response of KBM5 cells to imatinib was characterized by a low level of apoptotic response, a marginal increase in BCR/ABL copy number, a modest increase in p210 expression, and a highly imatinib-resistant Bcr/Abl TK.	imatinib	30-38	BCR activator of RhoGEF and GTPase	Homo sapiens	118-121
15042680-9	2004	The response of KBM5 cells to imatinib was characterized by a low level of apoptotic response, a marginal increase in BCR/ABL copy number, a modest increase in p210 expression, and a highly imatinib-resistant Bcr/Abl TK.	imatinib	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-125
15042680-9	2004	The response of KBM5 cells to imatinib was characterized by a low level of apoptotic response, a marginal increase in BCR/ABL copy number, a modest increase in p210 expression, and a highly imatinib-resistant Bcr/Abl TK.	imatinib	30-38	BCR activator of RhoGEF and GTPase	Homo sapiens	209-212
15042680-9	2004	The response of KBM5 cells to imatinib was characterized by a low level of apoptotic response, a marginal increase in BCR/ABL copy number, a modest increase in p210 expression, and a highly imatinib-resistant Bcr/Abl TK.	imatinib	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	213-216
15042680-9	2004	The response of KBM5 cells to imatinib was characterized by a low level of apoptotic response, a marginal increase in BCR/ABL copy number, a modest increase in p210 expression, and a highly imatinib-resistant Bcr/Abl TK.	imatinib	30-38	TXK tyrosine kinase	Homo sapiens	217-219
15042680-12	2004	CONCLUSIONS: BCR/ABL amplification with subsequent overexpression of Bcr/Abl protein, loss of apoptotic response, or point mutation of the ATP-binding site of BCR/ABL was associated alternatively with the acquisition of the resistant phenotype, supporting the notion that multiple mechanisms are involved in the induction of resistance to imatinib.	imatinib	339-347	BCR activator of RhoGEF and GTPase	Homo sapiens	13-16
15042680-12	2004	CONCLUSIONS: BCR/ABL amplification with subsequent overexpression of Bcr/Abl protein, loss of apoptotic response, or point mutation of the ATP-binding site of BCR/ABL was associated alternatively with the acquisition of the resistant phenotype, supporting the notion that multiple mechanisms are involved in the induction of resistance to imatinib.	imatinib	339-347	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-20
15042680-12	2004	CONCLUSIONS: BCR/ABL amplification with subsequent overexpression of Bcr/Abl protein, loss of apoptotic response, or point mutation of the ATP-binding site of BCR/ABL was associated alternatively with the acquisition of the resistant phenotype, supporting the notion that multiple mechanisms are involved in the induction of resistance to imatinib.	imatinib	339-347	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
15042680-12	2004	CONCLUSIONS: BCR/ABL amplification with subsequent overexpression of Bcr/Abl protein, loss of apoptotic response, or point mutation of the ATP-binding site of BCR/ABL was associated alternatively with the acquisition of the resistant phenotype, supporting the notion that multiple mechanisms are involved in the induction of resistance to imatinib.	imatinib	339-347	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
15050748-0	2004	Ascorbic acid restores sensitivity to imatinib via suppression of Nrf2-dependent gene expression in the imatinib-resistant cell line.	imatinib	38-46	NFE2 like bZIP transcription factor 2	Homo sapiens	66-70
15059881-0	2004	Imatinib mesylate is a potent inhibitor of the ABCG2 (BCRP) transporter and reverses resistance to topotecan and SN-38 in vitro.	imatinib	0-17	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	47-52
15059881-0	2004	Imatinib mesylate is a potent inhibitor of the ABCG2 (BCRP) transporter and reverses resistance to topotecan and SN-38 in vitro.	imatinib	0-17	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	54-58
15059881-1	2004	Imatinib mesylate (Gleevec, STI571) is a kinase inhibitor selective for Bcr-Abl, activated c-Kit kinases, and platelet-derived growth factor receptor tyrosine kinase.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
15059881-1	2004	Imatinib mesylate (Gleevec, STI571) is a kinase inhibitor selective for Bcr-Abl, activated c-Kit kinases, and platelet-derived growth factor receptor tyrosine kinase.	imatinib	19-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
15059881-1	2004	Imatinib mesylate (Gleevec, STI571) is a kinase inhibitor selective for Bcr-Abl, activated c-Kit kinases, and platelet-derived growth factor receptor tyrosine kinase.	imatinib	28-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
15094158-6	2004	Along this line, based on rational drug design, imatinib, a 2-phenylaminopyrimidine derivative, has very recently been introduced and found to be an efficient inhibitor of the altered tyrosine kinase, which arises as a product of the BCR-ABL fusion transcript in Philadelphia chromosome positive (Ph+) cases of CML.	imatinib	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	234-241
15059881-5	2004	Here, we show that imatinib mesylate potently reverses ABCG2-mediated resistance to topotecan and SN-38 and significantly increases accumulation of topotecan only in cells expressing functional ABCG2.	imatinib	19-36	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	55-60
15059881-5	2004	Here, we show that imatinib mesylate potently reverses ABCG2-mediated resistance to topotecan and SN-38 and significantly increases accumulation of topotecan only in cells expressing functional ABCG2.	imatinib	19-36	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	194-199
15059881-8	2004	These results suggest that imatinib mesylate inhibits the function of ABCG2 but is not a substrate for this transporter.	imatinib	27-44	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	70-75
15050748-4	2004	In this study, we examined the involvement of Nrf2 in the acquisition of resistance to imatinib.	imatinib	87-95	NFE2 like bZIP transcription factor 2	Homo sapiens	46-50
15050748-6	2004	RESULTS: Binding of Nrf2 to the ARE of the gamma-GCS light subunit (gamma-GCSl) gene promoter was much stronger in the imatinib-resistant cell line KCL22/SR than in the parental imatinib-sensitive cell line KCL22.	imatinib	119-127	NFE2 like bZIP transcription factor 2	Homo sapiens	20-24
15050748-6	2004	RESULTS: Binding of Nrf2 to the ARE of the gamma-GCS light subunit (gamma-GCSl) gene promoter was much stronger in the imatinib-resistant cell line KCL22/SR than in the parental imatinib-sensitive cell line KCL22.	imatinib	119-127	glutamate-cysteine ligase catalytic subunit	Homo sapiens	43-52
15050748-0	2004	Ascorbic acid restores sensitivity to imatinib via suppression of Nrf2-dependent gene expression in the imatinib-resistant cell line.	imatinib	104-112	NFE2 like bZIP transcription factor 2	Homo sapiens	66-70
15050748-6	2004	RESULTS: Binding of Nrf2 to the ARE of the gamma-GCS light subunit (gamma-GCSl) gene promoter was much stronger in the imatinib-resistant cell line KCL22/SR than in the parental imatinib-sensitive cell line KCL22.	imatinib	178-186	NFE2 like bZIP transcription factor 2	Homo sapiens	20-24
15050748-6	2004	RESULTS: Binding of Nrf2 to the ARE of the gamma-GCS light subunit (gamma-GCSl) gene promoter was much stronger in the imatinib-resistant cell line KCL22/SR than in the parental imatinib-sensitive cell line KCL22.	imatinib	178-186	glutamate-cysteine ligase catalytic subunit	Homo sapiens	43-52
14961028-6	2004	Treatment of p210BCR/ABL-positive cells with the Abl-specific tyrosine kinase inhibitor STI571 reverted PYK2 splicing to a configuration more consistent with normal cells, and correlated with decreased expression of BCR/ABL-induced proteins involved in pre-mRNA processing.	imatinib	88-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-24
15050748-11	2004	CONCLUSION: Changes in the redox state caused by antioxidants such as ascorbic acid can overcome resistance to imatinib via inhibition of Nrf2-mediated gene expression.	imatinib	111-119	NFE2 like bZIP transcription factor 2	Homo sapiens	138-142
14718589-4	2004	Imatinib-mesylate concentrations, ranging from 30 to 300 microM, reversibly decreased Ca(V)3.3 current amplitude with an IC(50) value of 56.9 microM.	imatinib	0-17	immunoglobulin lambda variable 7-46	Homo sapiens	86-94
14718589-8	2004	In conclusion, imatinib-mesylate blocked the cloned Ca(V)3.3 channels by a PTK-independent mechanism.	imatinib	15-32	immunoglobulin lambda variable 7-46	Homo sapiens	52-60
14718589-8	2004	In conclusion, imatinib-mesylate blocked the cloned Ca(V)3.3 channels by a PTK-independent mechanism.	imatinib	15-32	fibroblast growth factor receptor 4	Homo sapiens	75-78
14973504-6	2004	Imatinib induced rapid complete hematological responses in 4/4 treated FIP1L1-PDGFRA (+) cases, including one female, and complete molecular remission in 2/3 evaluable cases.	imatinib	0-8	factor interacting with PAPOLA and CPSF1	Homo sapiens	71-77
14973504-6	2004	Imatinib induced rapid complete hematological responses in 4/4 treated FIP1L1-PDGFRA (+) cases, including one female, and complete molecular remission in 2/3 evaluable cases.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	78-84
15024716-13	2004	GISTs with very low levels of KIT expression may respond to imatinib mesylate therapy if the receptors are activated by specific mechanisms.	imatinib	60-68	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	30-33
15739279-3	2004	The introduction into clinical practice of imatinib, (Glivec, Gleevec, Novartis), a potent tyrosine kinase inhibitor of the Bcr-Abl protein as well as of a restricted number of other TKs, has not only produced a substantial improvement in the treatment of CML, but represents a major break-through in the perspective of opening a new era, that of molecularly targeted therapy, in the management of other types of leukemia, lymphoma and cancer in general.	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
14718589-0	2004	Imatinib-mesylate blocks recombinant T-type calcium channels expressed in human embryonic kidney-293 cells by a protein tyrosine kinase-independent mechanism.	imatinib	0-8	fibroblast growth factor receptor 4	Homo sapiens	112-135
14718589-1	2004	The 2-phenylaminopyrimidine derivative imatinib-mesylate, a powerful protein tyrosine kinase (PTK) inhibitor that targets abl, c-kit, and the platelet-derived growth factor receptors, is rapidly gaining a relevant role in the treatment of several types of neoplasms.	imatinib	39-56	fibroblast growth factor receptor 4	Homo sapiens	69-92
14718589-1	2004	The 2-phenylaminopyrimidine derivative imatinib-mesylate, a powerful protein tyrosine kinase (PTK) inhibitor that targets abl, c-kit, and the platelet-derived growth factor receptors, is rapidly gaining a relevant role in the treatment of several types of neoplasms.	imatinib	39-56	fibroblast growth factor receptor 4	Homo sapiens	94-97
14718589-1	2004	The 2-phenylaminopyrimidine derivative imatinib-mesylate, a powerful protein tyrosine kinase (PTK) inhibitor that targets abl, c-kit, and the platelet-derived growth factor receptors, is rapidly gaining a relevant role in the treatment of several types of neoplasms.	imatinib	39-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-125
14718589-1	2004	The 2-phenylaminopyrimidine derivative imatinib-mesylate, a powerful protein tyrosine kinase (PTK) inhibitor that targets abl, c-kit, and the platelet-derived growth factor receptors, is rapidly gaining a relevant role in the treatment of several types of neoplasms.	imatinib	39-56	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	127-132
15109541-0	2004	Imatinib mesylate (STI571) prevents the mutator phenotype of Bcr-Abl in hematopoietic cell lines.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
15109541-0	2004	Imatinib mesylate (STI571) prevents the mutator phenotype of Bcr-Abl in hematopoietic cell lines.	imatinib	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
15109541-3	2004	Imatinib treatment of cells expressing Bcr-Abl reversed the mutation frequency to a value comparable to that of Bcr-Abl negative cells.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
14973504-8	2004	Thus, correlating IHES/CEL genotype with phenotype, FIP1L1-PDGFRA (+) CEL emerges as a homogeneous clinicobiological entity, where imatinib can induce molecular remission.	imatinib	131-139	factor interacting with PAPOLA and CPSF1	Homo sapiens	52-58
14973504-8	2004	Thus, correlating IHES/CEL genotype with phenotype, FIP1L1-PDGFRA (+) CEL emerges as a homogeneous clinicobiological entity, where imatinib can induce molecular remission.	imatinib	131-139	platelet derived growth factor receptor alpha	Homo sapiens	59-65
14961028-6	2004	Treatment of p210BCR/ABL-positive cells with the Abl-specific tyrosine kinase inhibitor STI571 reverted PYK2 splicing to a configuration more consistent with normal cells, and correlated with decreased expression of BCR/ABL-induced proteins involved in pre-mRNA processing.	imatinib	88-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-52
14961028-6	2004	Treatment of p210BCR/ABL-positive cells with the Abl-specific tyrosine kinase inhibitor STI571 reverted PYK2 splicing to a configuration more consistent with normal cells, and correlated with decreased expression of BCR/ABL-induced proteins involved in pre-mRNA processing.	imatinib	88-94	protein tyrosine kinase 2 beta	Homo sapiens	104-108
14961028-6	2004	Treatment of p210BCR/ABL-positive cells with the Abl-specific tyrosine kinase inhibitor STI571 reverted PYK2 splicing to a configuration more consistent with normal cells, and correlated with decreased expression of BCR/ABL-induced proteins involved in pre-mRNA processing.	imatinib	88-94	BCR activator of RhoGEF and GTPase	Homo sapiens	17-20
15109543-0	2004	Differences and similarities in kinetics of BCR-ABL transcript levels in CML patients treated with imatinib mesylate for chronic or accelerated disease phase.	imatinib	99-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
15109543-1	2004	Kinetics of BCR-ABL transcript levels were determined in 19 patients with chronic myeloid leukemia (CML) treated with imatinib for chronic (CP) or accelerated phase (AP).	imatinib	118-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
14961028-6	2004	Treatment of p210BCR/ABL-positive cells with the Abl-specific tyrosine kinase inhibitor STI571 reverted PYK2 splicing to a configuration more consistent with normal cells, and correlated with decreased expression of BCR/ABL-induced proteins involved in pre-mRNA processing.	imatinib	88-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	220-223
15109543-4	2004	It is summarized that BCR-ABL transcript kinetics clearly characterize responses to imatinib treatment and are highly predictive for disease progression.	imatinib	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
14973502-4	2004	When D-HPLC was applied to 30 cDNAs from patients with imatinib resistance that had previously been characterized for KD mutations by direct sequencing of BCR-ABL RT-PCR products, there was concordance in 97% of samples.	imatinib	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-162
15031492-4	2004	We review progress with the receptor tyrosine kinases (growth factor receptors EGFR, VEGFR, and FGFR) and nonreceptor tyrosine kinases (Bcr-Abl), where advances have been made with cancer therapeutic agents such as Herceptin and Gleevec.	imatinib	229-236	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-143
15175998-2	2004	These receptor tyrosine kinases, as well as ABL and BCR-ABL, are inhibited by imatinib.	imatinib	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-47
15175998-2	2004	These receptor tyrosine kinases, as well as ABL and BCR-ABL, are inhibited by imatinib.	imatinib	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
15175998-3	2004	Tumors caused by chromosomal translocations that lead to overexpression of PDGFR ligand, resulting in continuous activation of wild-type PDGFRs, are likely to respond to imatinib, as are malignancies caused by gene amplification and overexpression of wild-type PDGFR or KIT receptors.	imatinib	170-178	platelet derived growth factor receptor beta	Homo sapiens	75-80
15175998-3	2004	Tumors caused by chromosomal translocations that lead to overexpression of PDGFR ligand, resulting in continuous activation of wild-type PDGFRs, are likely to respond to imatinib, as are malignancies caused by gene amplification and overexpression of wild-type PDGFR or KIT receptors.	imatinib	170-178	platelet derived growth factor receptor beta	Homo sapiens	137-142
15175998-3	2004	Tumors caused by chromosomal translocations that lead to overexpression of PDGFR ligand, resulting in continuous activation of wild-type PDGFRs, are likely to respond to imatinib, as are malignancies caused by gene amplification and overexpression of wild-type PDGFR or KIT receptors.	imatinib	170-178	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	270-273
15175998-4	2004	Malignancies linked to chromosomal translocations that express PDGFR or KIT fusion protein-tyrosine kinases are also likely to respond to imatinib.	imatinib	138-146	platelet derived growth factor receptor beta	Homo sapiens	63-68
15175998-4	2004	Malignancies linked to chromosomal translocations that express PDGFR or KIT fusion protein-tyrosine kinases are also likely to respond to imatinib.	imatinib	138-146	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	72-75
15175999-5	2004	Fusion of the Fip1-like 1 gene (FIP1L1) and the platelet-derived growth factor receptor alpha gene (PDGFRA) was discovered in the majority of patients with imatinib-sensitive HES, and all patients with the fusion responded to imatinib.	imatinib	156-164	factor interacting with PAPOLA and CPSF1	Homo sapiens	14-25
15175999-5	2004	Fusion of the Fip1-like 1 gene (FIP1L1) and the platelet-derived growth factor receptor alpha gene (PDGFRA) was discovered in the majority of patients with imatinib-sensitive HES, and all patients with the fusion responded to imatinib.	imatinib	156-164	factor interacting with PAPOLA and CPSF1	Homo sapiens	32-38
15175999-5	2004	Fusion of the Fip1-like 1 gene (FIP1L1) and the platelet-derived growth factor receptor alpha gene (PDGFRA) was discovered in the majority of patients with imatinib-sensitive HES, and all patients with the fusion responded to imatinib.	imatinib	156-164	platelet derived growth factor receptor alpha	Homo sapiens	48-93
15175999-5	2004	Fusion of the Fip1-like 1 gene (FIP1L1) and the platelet-derived growth factor receptor alpha gene (PDGFRA) was discovered in the majority of patients with imatinib-sensitive HES, and all patients with the fusion responded to imatinib.	imatinib	156-164	platelet derived growth factor receptor alpha	Homo sapiens	100-106
15175999-5	2004	Fusion of the Fip1-like 1 gene (FIP1L1) and the platelet-derived growth factor receptor alpha gene (PDGFRA) was discovered in the majority of patients with imatinib-sensitive HES, and all patients with the fusion responded to imatinib.	imatinib	226-234	factor interacting with PAPOLA and CPSF1	Homo sapiens	14-25
15175999-5	2004	Fusion of the Fip1-like 1 gene (FIP1L1) and the platelet-derived growth factor receptor alpha gene (PDGFRA) was discovered in the majority of patients with imatinib-sensitive HES, and all patients with the fusion responded to imatinib.	imatinib	226-234	factor interacting with PAPOLA and CPSF1	Homo sapiens	32-38
15175999-5	2004	Fusion of the Fip1-like 1 gene (FIP1L1) and the platelet-derived growth factor receptor alpha gene (PDGFRA) was discovered in the majority of patients with imatinib-sensitive HES, and all patients with the fusion responded to imatinib.	imatinib	226-234	platelet derived growth factor receptor alpha	Homo sapiens	48-93
15175999-5	2004	Fusion of the Fip1-like 1 gene (FIP1L1) and the platelet-derived growth factor receptor alpha gene (PDGFRA) was discovered in the majority of patients with imatinib-sensitive HES, and all patients with the fusion responded to imatinib.	imatinib	226-234	platelet derived growth factor receptor alpha	Homo sapiens	100-106
15175999-7	2004	The efficacy of relatively low imatinib concentrations in HES, mediated by inhibition of FIP1L1-PDGFRalpha kinase activity, causally implicates FIP1L1-PDGFRA in the pathogenesis in certain HES patients.	imatinib	31-39	factor interacting with PAPOLA and CPSF1	Homo sapiens	89-95
15175999-7	2004	The efficacy of relatively low imatinib concentrations in HES, mediated by inhibition of FIP1L1-PDGFRalpha kinase activity, causally implicates FIP1L1-PDGFRA in the pathogenesis in certain HES patients.	imatinib	31-39	factor interacting with PAPOLA and CPSF1	Homo sapiens	144-150
15175999-7	2004	The efficacy of relatively low imatinib concentrations in HES, mediated by inhibition of FIP1L1-PDGFRalpha kinase activity, causally implicates FIP1L1-PDGFRA in the pathogenesis in certain HES patients.	imatinib	31-39	platelet derived growth factor receptor alpha	Homo sapiens	151-157
15176001-4	2004	Preclinical data suggest that preferential expression of PDGFRs in endothelial cells of tumor vasculature in experimental prostate cancer bone metastases is an important target for combination therapy incorporating the PDGFR inhibitor imatinib mesylate.	imatinib	235-252	platelet derived growth factor receptor beta	Homo sapiens	57-62
15106018-11	2004	This new tyrosine kinase inhibitor, imatinib mesylate, which inhibits the c-kit receptor, has proved highly effective against GIST and has improved survival in metastatic GIST.	imatinib	36-53	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	76-79
15024050-6	2004	In agreement with these results, treatment of normal mice with the Kit tyrosine kinase inhibitor imatinib (Gleevec) leads to deficits in pro T and pro B cell development, similar to those seen in KitY567F/Y567F and KitW/W mice.	imatinib	97-105	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	67-70
14645009-1	2004	Imatinib is a tyrosine-kinase inhibitor that binds to ABL proteins and induces cytogenetic remissions in patients with chronic myeloid leukemia (CML).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-57
14645012-0	2004	A novel mechanism for imatinib mesylate-induced cell death of BCR-ABL-positive human leukemic cells: caspase-independent, necrosis-like programmed cell death mediated by serine protease activity.	imatinib	22-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
14645012-0	2004	A novel mechanism for imatinib mesylate-induced cell death of BCR-ABL-positive human leukemic cells: caspase-independent, necrosis-like programmed cell death mediated by serine protease activity.	imatinib	22-39	coagulation factor II, thrombin	Homo sapiens	170-185
14645012-2	2004	The ABL kinase inhibitor, imatinib mesylate, has been reported to induce apoptosis of BCR-ABL-positive cells in a caspase-dependent fashion.	imatinib	26-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
14645012-8	2004	However, we observed the mitochondrial release of the serine protease Omi/HtrA2 into the cytosol of the cells treated with imatinib mesylate or zVAD-fmk plus imatinib mesylate.	imatinib	123-140	coagulation factor II, thrombin	Homo sapiens	54-69
14645012-8	2004	However, we observed the mitochondrial release of the serine protease Omi/HtrA2 into the cytosol of the cells treated with imatinib mesylate or zVAD-fmk plus imatinib mesylate.	imatinib	123-140	HtrA serine peptidase 2	Homo sapiens	74-79
14645012-8	2004	However, we observed the mitochondrial release of the serine protease Omi/HtrA2 into the cytosol of the cells treated with imatinib mesylate or zVAD-fmk plus imatinib mesylate.	imatinib	158-175	coagulation factor II, thrombin	Homo sapiens	54-69
14645012-8	2004	However, we observed the mitochondrial release of the serine protease Omi/HtrA2 into the cytosol of the cells treated with imatinib mesylate or zVAD-fmk plus imatinib mesylate.	imatinib	158-175	HtrA serine peptidase 2	Homo sapiens	74-79
14645012-10	2004	Taken together, our results suggest that imatinib mesylate induces a caspase-independent, necrosis-like programmed cell death mediated by the serine protease activity of Omi/HtrA2.	imatinib	41-58	coagulation factor II, thrombin	Homo sapiens	142-157
14645012-10	2004	Taken together, our results suggest that imatinib mesylate induces a caspase-independent, necrosis-like programmed cell death mediated by the serine protease activity of Omi/HtrA2.	imatinib	41-58	HtrA serine peptidase 2	Homo sapiens	174-179
15010069-0	2004	Use of c-KIT/PDGFRA mutational analysis to predict the clinical response to imatinib in patients with advanced gastrointestinal stromal tumours entered on phase I and II studies of the EORTC Soft Tissue and Bone Sarcoma Group.	imatinib	76-84	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	7-12
14769706-0	2004	Oral imatinib mesylate (STI571/gleevec) improves the efficacy of local intravascular vascular endothelial growth factor-C gene transfer in reducing neointimal growth in hypercholesterolemic rabbits.	imatinib	5-22	vascular endothelial growth factor A	Oryctolagus cuniculus	85-119
15023347-9	2004	This binding mode, similar to that observed for the anti-leukemia drug, imatinib in complex with c-Abl kinase, may be responsible for the high selectivity of AAL993 and provides valuable insight for the design of further compounds.	imatinib	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-102
14976243-3	2004	The ABL inhibitor Imatinib (Gleevec, STI571) has remarkable efficacy for treating chronic phase CML, and FLT3 inhibitors (e.g., PKC412) show similar promise in preclinical studies.	imatinib	18-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
14976243-3	2004	The ABL inhibitor Imatinib (Gleevec, STI571) has remarkable efficacy for treating chronic phase CML, and FLT3 inhibitors (e.g., PKC412) show similar promise in preclinical studies.	imatinib	37-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
14976243-6	2004	Here, we report that the mTOR inhibitor rapamycin synergizes with Imatinib against BCR/ABL-transformed myeloid and lymphoid cells and increases survival in a murine CML model.	imatinib	66-74	mechanistic target of rapamycin kinase	Mus musculus	25-29
14976243-6	2004	Here, we report that the mTOR inhibitor rapamycin synergizes with Imatinib against BCR/ABL-transformed myeloid and lymphoid cells and increases survival in a murine CML model.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
14976243-7	2004	Rapamycin/Imatinib combinations also inhibit Imatinib-resistant mutants of BCR/ABL, and rapamycin plus PKC412 synergistically inhibits cells expressing PKC412-sensitive or -resistant leukemogenic FLT3 mutants.	imatinib	10-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
14976243-7	2004	Rapamycin/Imatinib combinations also inhibit Imatinib-resistant mutants of BCR/ABL, and rapamycin plus PKC412 synergistically inhibits cells expressing PKC412-sensitive or -resistant leukemogenic FLT3 mutants.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
14976062-0	2004	Imatinib mesylate impairs Flt3L-mediated dendritic cell expansion and antitumor effects in vivo.	imatinib	0-17	fms related receptor tyrosine kinase 3 ligand	Homo sapiens	26-31
14726714-6	2004	The identification of a novel tumor-specific target in c-KIT resulted in the development of a tyrosine kinase-inhibitor (imatinib mesylate) that provides an encouraging option for treating GISTs.	imatinib	121-138	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	55-60
15703627-3	2004	The clinical application of imatinib mesylate, a selective inhibitor of the KIT kinase activity, has provided a novel molecularly targeted therapy for these tumors.	imatinib	28-45	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	76-79
15010069-0	2004	Use of c-KIT/PDGFRA mutational analysis to predict the clinical response to imatinib in patients with advanced gastrointestinal stromal tumours entered on phase I and II studies of the EORTC Soft Tissue and Bone Sarcoma Group.	imatinib	76-84	platelet derived growth factor receptor alpha	Homo sapiens	13-19
15010069-1	2004	Previous studies have shown that activating mutations of c-KIT/PDGFRA, potential therapeutic targets for imatinib mesylate, are implicated in the pathophysiology of gastrointestinal stromal tumours (GISTs).	imatinib	105-113	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	57-62
15010069-1	2004	Previous studies have shown that activating mutations of c-KIT/PDGFRA, potential therapeutic targets for imatinib mesylate, are implicated in the pathophysiology of gastrointestinal stromal tumours (GISTs).	imatinib	105-113	platelet derived growth factor receptor alpha	Homo sapiens	63-69
15010069-11	2004	These findings indicate that the mutational status of the c-KIT/PDGFRA oncoproteins could be useful to predict the clinical response of patients imatinib therapy.	imatinib	145-153	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	58-63
15010069-11	2004	These findings indicate that the mutational status of the c-KIT/PDGFRA oncoproteins could be useful to predict the clinical response of patients imatinib therapy.	imatinib	145-153	platelet derived growth factor receptor alpha	Homo sapiens	64-70
14755542-0	2004	Different roles of p38 MAPK and ERK in STI571-induced multi-lineage differentiation of K562 cells.	imatinib	39-45	mitogen-activated protein kinase 14	Homo sapiens	19-22
15045935-3	2004	Although the first-line therapy of resectable GISTs is surgery, imatinib mesylate, a target-based molecule against KIT and PDGF-R alpha proteins, showed remarkable clinical effects and good tolerability for non-resectable GISTs.	imatinib	64-72	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	115-118
15045935-3	2004	Although the first-line therapy of resectable GISTs is surgery, imatinib mesylate, a target-based molecule against KIT and PDGF-R alpha proteins, showed remarkable clinical effects and good tolerability for non-resectable GISTs.	imatinib	64-72	platelet derived growth factor receptor alpha	Homo sapiens	123-135
14755542-0	2004	Different roles of p38 MAPK and ERK in STI571-induced multi-lineage differentiation of K562 cells.	imatinib	39-45	mitogen-activated protein kinase 1	Homo sapiens	32-35
14755542-4	2004	In this study, we demonstrated that STI571 induced the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and dephosphorylation of extracellular signal-regulated kinase (ERK) in K562 cells.	imatinib	36-42	mitogen-activated protein kinase 14	Homo sapiens	74-110
14755542-4	2004	In this study, we demonstrated that STI571 induced the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and dephosphorylation of extracellular signal-regulated kinase (ERK) in K562 cells.	imatinib	36-42	mitogen-activated protein kinase 1	Homo sapiens	112-116
14755542-4	2004	In this study, we demonstrated that STI571 induced the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and dephosphorylation of extracellular signal-regulated kinase (ERK) in K562 cells.	imatinib	36-42	mitogen-activated protein kinase 1	Homo sapiens	143-180
14755542-4	2004	In this study, we demonstrated that STI571 induced the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and dephosphorylation of extracellular signal-regulated kinase (ERK) in K562 cells.	imatinib	36-42	mitogen-activated protein kinase 1	Homo sapiens	182-185
14755542-6	2004	We also found that STI571 induced all the myeloid (CD11b, CD13), megakaryocytic (CD41a, CD42), and erythroid (glycophorin-A) markers on K562 cells.	imatinib	19-25	integrin subunit alpha M	Homo sapiens	51-56
14993251-6	2004	Conversely, leukemia subclones surviving inhibition of BCR-ABL1 by STI571 restore responsiveness to antigen receptor engagement and differentiate into immature B cells expressing immunoglobulin light chains.	imatinib	67-73	BCR activator of RhoGEF and GTPase	Homo sapiens	55-63
14755542-6	2004	We also found that STI571 induced all the myeloid (CD11b, CD13), megakaryocytic (CD41a, CD42), and erythroid (glycophorin-A) markers on K562 cells.	imatinib	19-25	alanyl aminopeptidase, membrane	Homo sapiens	58-62
14755542-6	2004	We also found that STI571 induced all the myeloid (CD11b, CD13), megakaryocytic (CD41a, CD42), and erythroid (glycophorin-A) markers on K562 cells.	imatinib	19-25	glycophorin A (MNS blood group)	Homo sapiens	110-123
14755542-7	2004	A p38 MAPK-specific inhibitor, SB203580, inhibited the STI571-induced multi-lineage differentiation of K562 cells, indicating that p38 MAPK is crucial for this differentiation.	imatinib	55-61	mitogen-activated protein kinase 14	Homo sapiens	2-5
14755542-7	2004	A p38 MAPK-specific inhibitor, SB203580, inhibited the STI571-induced multi-lineage differentiation of K562 cells, indicating that p38 MAPK is crucial for this differentiation.	imatinib	55-61	mitogen-activated protein kinase 1	Homo sapiens	6-10
14755542-7	2004	A p38 MAPK-specific inhibitor, SB203580, inhibited the STI571-induced multi-lineage differentiation of K562 cells, indicating that p38 MAPK is crucial for this differentiation.	imatinib	55-61	mitogen-activated protein kinase 14	Homo sapiens	131-134
14755542-8	2004	In contrast, SB203580 did not overcome the inhibitory effect for proliferation of K562 cells, indicating that p38 MAPK activation by STI571 does not affect cell numbers.	imatinib	133-139	mitogen-activated protein kinase 14	Homo sapiens	110-113
14755542-10	2004	STI571-induced downregulation of c-myb mRNA was prevented by the pretreatment of K562 cells by SB203580.	imatinib	0-6	MYB proto-oncogene, transcription factor	Homo sapiens	33-38
14755542-11	2004	Our data provides insights into how p38 MAPK and ERK pathways are involved in STI571-induced differentiation of K562 cells.	imatinib	78-84	mitogen-activated protein kinase 14	Homo sapiens	36-39
14755542-11	2004	Our data provides insights into how p38 MAPK and ERK pathways are involved in STI571-induced differentiation of K562 cells.	imatinib	78-84	mitogen-activated protein kinase 1	Homo sapiens	49-52
14712290-7	2004	The mechanism of action appears to involve imatinib inhibition of c-abl kinase activity with an associated decrease in CLB-induced Rad51 phosphorylation and CLB-induced Rad51 nuclear foci, suggesting that imatinib decreases Rad51-related DNA repair of CLB-induced DNA lesions.	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-71
15030167-4	2004	Herbimycin A and STI571 differentiated K562 cells accompanying with the transient down-regulated ERK.	imatinib	17-23	mitogen-activated protein kinase 1	Homo sapiens	97-100
14712293-7	2004	The expression of CEACAM1 was reversible upon imatinib treatment in BCR/ABL-expressing U937 cells as well as in BCR/ABL-positive K562 cells.	imatinib	46-54	CEA cell adhesion molecule 1	Homo sapiens	18-25
14712293-7	2004	The expression of CEACAM1 was reversible upon imatinib treatment in BCR/ABL-expressing U937 cells as well as in BCR/ABL-positive K562 cells.	imatinib	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
14724652-0	2004	P-glycoprotein-mediated drug efflux is a resistance mechanism of chronic myelogenous leukemia cells to treatment with imatinib mesylate.	imatinib	118-135	ATP binding cassette subfamily B member 1	Homo sapiens	0-14
14724652-1	2004	Imatinib (Glivec), STI571) is an intracellular acting drug that demonstrates high activity against BCR-ABL-positive chronic myelogenous leukemia (CML) or acute lymphoblastic leukemia (ALL).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
14724652-1	2004	Imatinib (Glivec), STI571) is an intracellular acting drug that demonstrates high activity against BCR-ABL-positive chronic myelogenous leukemia (CML) or acute lymphoblastic leukemia (ALL).	imatinib	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
14724652-3	2004	Here, we show by a novel high-performance liquid chromatography-based method that intracellular levels of imatinib decrease in P-glycoprotein (Pgp)-positive leukemic cells.	imatinib	106-114	ATP binding cassette subfamily B member 1	Homo sapiens	127-141
14724652-3	2004	Here, we show by a novel high-performance liquid chromatography-based method that intracellular levels of imatinib decrease in P-glycoprotein (Pgp)-positive leukemic cells.	imatinib	106-114	ATP binding cassette subfamily B member 1	Homo sapiens	143-146
14724652-4	2004	In a model of K562 cells with gradually increasing Pgp expression, a Pgp-dependent decline of intracellular imatinib levels was observed.	imatinib	108-116	ATP binding cassette subfamily B member 1	Homo sapiens	51-54
14724652-4	2004	In a model of K562 cells with gradually increasing Pgp expression, a Pgp-dependent decline of intracellular imatinib levels was observed.	imatinib	108-116	ATP binding cassette subfamily B member 1	Homo sapiens	69-72
14724652-5	2004	Decreased imatinib levels were associated with a retained phosphorylation pattern of the Bcr-Abl target Crkl and loss of effect of imatinib on cellular proliferation and apoptosis.	imatinib	10-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
14724652-5	2004	Decreased imatinib levels were associated with a retained phosphorylation pattern of the Bcr-Abl target Crkl and loss of effect of imatinib on cellular proliferation and apoptosis.	imatinib	10-18	CRK like proto-oncogene, adaptor protein	Homo sapiens	104-108
14724652-6	2004	The modulation of Pgp by cyclosporin A (CSA) readily restored imatinib cytotoxicity in these cells.	imatinib	62-70	ATP binding cassette subfamily B member 1	Homo sapiens	18-21
14724652-7	2004	Finally, we provide first data showing a biological effect of Pgp modulation in the imatinib treatment of a patient with BCR-ABL-positive ALL.	imatinib	84-92	ATP binding cassette subfamily B member 1	Homo sapiens	62-65
14724652-7	2004	Finally, we provide first data showing a biological effect of Pgp modulation in the imatinib treatment of a patient with BCR-ABL-positive ALL.	imatinib	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
14724652-8	2004	MDR1 overexpression must therefore be considered as an important clinical mechanism in the diversity of resistance development to imatinib treatment.	imatinib	130-138	ATP binding cassette subfamily B member 1	Homo sapiens	0-4
15030167-0	2004	Inactivation of ERK accelerates erythroid differentiation of K562 cells induced by herbimycin A and STI571 while activation of MEK1 interferes with it.	imatinib	100-106	mitogen-activated protein kinase 1	Homo sapiens	16-19
15030167-8	2004	These results demonstrate that the erythroid differentiation of K562 cells induced by herbimycin A or STI571 requires the down-regulation of MEK1/ ERK pathway.	imatinib	102-108	mitogen-activated protein kinase kinase 1	Homo sapiens	141-145
15030167-8	2004	These results demonstrate that the erythroid differentiation of K562 cells induced by herbimycin A or STI571 requires the down-regulation of MEK1/ ERK pathway.	imatinib	102-108	mitogen-activated protein kinase 1	Homo sapiens	147-150
15141598-2	2004	However, the advent of the targeted molecule imatinib mesylate (formerly STI-571) against the bcr-abl chimeric protein in the disease has brought the issue of managing newly diagnosed CML patients, especially those with available donors, to the crossroads.	imatinib	45-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
14677065-0	2004	Rare KIT (CD117) expression in multiple myeloma abrogates the usefulness of imatinib mesylate treatment.	imatinib	76-93	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	5-8
14677065-0	2004	Rare KIT (CD117) expression in multiple myeloma abrogates the usefulness of imatinib mesylate treatment.	imatinib	76-93	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	10-15
14677065-1	2004	BACKGROUND: Imatinib mesylate blocks the tyrosine kinase activity of KIT (CD117) and is an effective treatment for gastrointestinal stromal tumors.	imatinib	12-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	69-72
14677065-1	2004	BACKGROUND: Imatinib mesylate blocks the tyrosine kinase activity of KIT (CD117) and is an effective treatment for gastrointestinal stromal tumors.	imatinib	12-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	74-79
14504104-9	2004	In conclusion, a tumor-specific bcr-abl breakpoint peptide-derived vaccine can be safely administered and can reliably elicit measurable peptide-specific CD4 immune responses, including in patients after bone marrow transplantation, on interferon, or on imatinib mesylate.	imatinib	254-271	CD4 molecule	Homo sapiens	154-157
14755375-0	2004	Chronic myeloid leukemia with an e13a3 BCR-ABL fusion: benign course responsive to imatinib with an RT-PCR advisory.	imatinib	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
15022111-7	2004	The third case of a 40-year-old patient with a malignant GIST recurrence after surgery and exhibiting secondary resistance after one year of successful therapy with the receptor tyrosine kinase inhibitor imatinib (Gleevec), antagonizing pathogenetically relevant constitutive c-KIT activation, illustrates the potential and limitations of the only effective drug treatment for advanced GIST.	imatinib	204-212	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	276-281
15003901-0	2004	Imatinib mesylate can induce complete molecular remission in FIP1L1-PDGFR-a positive idiopathic hypereosinophilic syndrome.	imatinib	0-17	factor interacting with PAPOLA and CPSF1	Homo sapiens	61-67
14605865-1	2004	OBJECTIVE: This study was carried out to investigate the influence of CYP3A induction with rifampicin on imatinib (Gleevec) exposure.	imatinib	105-113	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	70-75
14605865-1	2004	OBJECTIVE: This study was carried out to investigate the influence of CYP3A induction with rifampicin on imatinib (Gleevec) exposure.	imatinib	115-122	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	70-75
14871965-1	2004	PURPOSE: We sought to determine whether blockade of platelet-derived growth factor receptor (PDGF-R) activation by oral administration of a PDGF-R tyrosine kinase inhibitor (STI571) alone or in combination with i.p.	imatinib	174-180	platelet derived growth factor receptor beta	Homo sapiens	52-91
14871965-7	2004	Immunohistochemical analyses revealed that PDGF-R activation was blocked by STI571 administered alone or in combination with paclitaxel.	imatinib	76-82	platelet derived growth factor receptor, beta polypeptide	Mus musculus	43-49
15003901-0	2004	Imatinib mesylate can induce complete molecular remission in FIP1L1-PDGFR-a positive idiopathic hypereosinophilic syndrome.	imatinib	0-17	platelet derived growth factor receptor alpha	Homo sapiens	68-75
14605878-1	2004	Imatinib (STI571), a 2-phenylaminopyrimidine, specifically inhibits the tyrosine kinase activity of Abl, Kit, and platelet-derived growth factor receptor.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-103
14605878-1	2004	Imatinib (STI571), a 2-phenylaminopyrimidine, specifically inhibits the tyrosine kinase activity of Abl, Kit, and platelet-derived growth factor receptor.	imatinib	10-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-103
14654084-4	2004	The Bcl-2 dowmodulation and inactivation induced by the binding to its antagonist: Bad, the release of caspase 12 from the ER membranes in its active form and of Ca(2+) from the ER pool addressed towards ER a sensor of STI571-induced pro-apoptotic signal.	imatinib	219-225	caspase 12	Mus musculus	103-113
15009722-3	2004	Imatinib mesylate was previously reported to have specific activity in inhibiting select tyrosine kinase receptors, including PDGF and c-Kit.	imatinib	0-17	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	135-140
15009722-12	2004	Immunohistochemical studies demonstrated inhibition of PDGFR phosphorylation on the tumors from mice treated with imatinib mesylate but not from control mice, suggesting that the receptors were functional and that the concentration of drug used was appropriate.	imatinib	114-131	platelet derived growth factor receptor, beta polypeptide	Mus musculus	55-60
15009722-13	2004	Our data demonstrated that imatinib mesylate blocked both PDGFR-alpha and PDGFR-beta in vivo.	imatinib	27-44	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	58-69
15009722-13	2004	Our data demonstrated that imatinib mesylate blocked both PDGFR-alpha and PDGFR-beta in vivo.	imatinib	27-44	platelet derived growth factor receptor, beta polypeptide	Mus musculus	74-84
14654084-0	2004	Endoplasmic reticulum stress initiates apoptotic death induced by STI571 inhibition of p210 bcr-abl tyrosine kinase.	imatinib	66-72	envoplakin	Mus musculus	87-91
14654084-3	2004	Here, we showed that the apoptotic death triggered by STI571, an inhibitor of the p210 bcr-abl tyrosine kinase, in murine myeloid progenitors transducing the p210 bcr-abl tyrosine kinase of Chronic Myeloid Leukemia (CML) proceeds from ER stress.	imatinib	54-60	envoplakin	Mus musculus	82-86
14654084-3	2004	Here, we showed that the apoptotic death triggered by STI571, an inhibitor of the p210 bcr-abl tyrosine kinase, in murine myeloid progenitors transducing the p210 bcr-abl tyrosine kinase of Chronic Myeloid Leukemia (CML) proceeds from ER stress.	imatinib	54-60	envoplakin	Mus musculus	158-162
14654084-4	2004	The Bcl-2 dowmodulation and inactivation induced by the binding to its antagonist: Bad, the release of caspase 12 from the ER membranes in its active form and of Ca(2+) from the ER pool addressed towards ER a sensor of STI571-induced pro-apoptotic signal.	imatinib	219-225	B cell leukemia/lymphoma 2	Mus musculus	4-9
15018431-12	2004	These results suggest that such drugs as imatinib mesylate, which inhibit the c-kit tyrosine kinase, should be investigated for these mesenchymal neoplasms.	imatinib	41-58	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	78-83
15027317-1	2004	Imatinib mesylate is a new drug that can inhibit the tyrosine kinase activity of Bcr-Abl, the receptors for platelet-derived growth factor receptor(PDGF) and stem cell factor, or c-kit.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
14737178-4	2004	One such example is imatinib mesylate, which targets the BCR-ABL kinase as well as a few structurally related kinases.	imatinib	20-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
14757533-2	2004	Beginning with the observation that imatinib mesylate (Gleevec) could elicit rapid and complete hematologic remissions in a proportion of patients with HES, a reverse bedside-to-bench translational research effort led to the discovery of FIP1L1-PDGFRA, a novel fusion gene on chromosome 4q12 whose product is an imatinib-sensitive protein tyrosine kinase.	imatinib	36-53	factor interacting with PAPOLA and CPSF1	Homo sapiens	238-244
14757533-2	2004	Beginning with the observation that imatinib mesylate (Gleevec) could elicit rapid and complete hematologic remissions in a proportion of patients with HES, a reverse bedside-to-bench translational research effort led to the discovery of FIP1L1-PDGFRA, a novel fusion gene on chromosome 4q12 whose product is an imatinib-sensitive protein tyrosine kinase.	imatinib	36-44	factor interacting with PAPOLA and CPSF1	Homo sapiens	238-244
15027317-1	2004	Imatinib mesylate is a new drug that can inhibit the tyrosine kinase activity of Bcr-Abl, the receptors for platelet-derived growth factor receptor(PDGF) and stem cell factor, or c-kit.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	179-184
15027317-5	2004	Imatinib can block the kinase activity of Bcr-Abl, thus inhibiting the proliferation of Ph-positive progenitors, and has shown activity against all phases of CML, though responses are most substantial and durable in patients in the chronic phase.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
14744784-0	2004	Imatinib mesylate resistance through BCR-ABL independence in chronic myelogenous leukemia.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
12969987-4	2004	A dose-dependent decrease in proliferation potential was found when CD34+ cells were expanded in serum-free medium supplemented with 6 growth factors and imatinib.	imatinib	154-162	CD34 molecule	Homo sapiens	68-72
12969987-8	2004	These data suggest a significant inhibitory effect of imatinib on normal CD34+ progenitor (but not stem) cells that is largely independent of c-kit signaling.	imatinib	54-62	CD34 molecule	Homo sapiens	73-77
14735360-5	2004	Imatinib is a small-molecule inhibitor that selectively blocks the activity of the PDGF-R, ABL and KIT receptor tyrosine kinases by competitive binding to the adenosine triphosphate binding site of their catalytic domains.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	83-89
14735360-5	2004	Imatinib is a small-molecule inhibitor that selectively blocks the activity of the PDGF-R, ABL and KIT receptor tyrosine kinases by competitive binding to the adenosine triphosphate binding site of their catalytic domains.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-94
14735360-5	2004	Imatinib is a small-molecule inhibitor that selectively blocks the activity of the PDGF-R, ABL and KIT receptor tyrosine kinases by competitive binding to the adenosine triphosphate binding site of their catalytic domains.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	99-102
14504105-0	2004	Imatinib mesylate affects the development and function of dendritic cells generated from CD34+ peripheral blood progenitor cells.	imatinib	0-17	CD34 molecule	Homo sapiens	89-93
14504105-1	2004	Imatinib mesylate (STI571) is a competitive Bcr-Abl tyrosine kinase inhibitor and has yielded encouraging results in treatment of chronic myelogenous leukemia (CML) and gastrointestinal stroma tumors (GISTs).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
14504105-1	2004	Imatinib mesylate (STI571) is a competitive Bcr-Abl tyrosine kinase inhibitor and has yielded encouraging results in treatment of chronic myelogenous leukemia (CML) and gastrointestinal stroma tumors (GISTs).	imatinib	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
14504105-3	2004	In vitro studies have revealed that imatinib mesylate can inhibit growth of cell lines and primitive malignant progenitor cells in CML expressing Bcr-Abl.	imatinib	36-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	146-153
14504105-5	2004	In the current study we demonstrate that in vitro exposure of mobilized human CD34+ progenitors to therapeutic concentrations of imatinib mesylate (1-5 microM) inhibits their differentiation into dendritic cells (DCs).	imatinib	129-146	CD34 molecule	Homo sapiens	78-82
14504105-6	2004	DCs obtained after 10 to 16 days of culture in the presence of imatinib mesylate showed concentration-dependent reduced expression levels of CD1a and costimulatory molecules such as CD80 and CD40.	imatinib	63-80	CD1a molecule	Homo sapiens	141-145
14504105-6	2004	DCs obtained after 10 to 16 days of culture in the presence of imatinib mesylate showed concentration-dependent reduced expression levels of CD1a and costimulatory molecules such as CD80 and CD40.	imatinib	63-80	CD80 molecule	Homo sapiens	182-186
14504105-6	2004	DCs obtained after 10 to 16 days of culture in the presence of imatinib mesylate showed concentration-dependent reduced expression levels of CD1a and costimulatory molecules such as CD80 and CD40.	imatinib	63-80	CD40 molecule	Homo sapiens	191-195
14504105-8	2004	The inhibitory effects of imatinib mesylate were accompanied by down-regulation of nuclear localized RelB protein.	imatinib	26-43	RELB proto-oncogene, NF-kB subunit	Homo sapiens	101-105
14760091-0	2004	Imatinib mesylate (Gleevec) inhibits ovarian cancer cell growth through a mechanism dependent on platelet-derived growth factor receptor alpha and Akt inactivation.	imatinib	0-17	platelet derived growth factor receptor alpha	Homo sapiens	97-142
14760098-0	2004	Imatinib inhibits proliferation of Ewing tumor cells mediated by the stem cell factor/KIT receptor pathway, and sensitizes cells to vincristine and doxorubicin-induced apoptosis.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	86-89
14760098-2	2004	We analyzed the in vitro impact of KIT blockade by imatinib in Ewing tumor cell lines.	imatinib	51-59	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	35-38
14760098-6	2004	Treatment with KIT tyrosine kinase inhibitor imatinib (0.5-20 micro M) induced down-regulation of KIT phosphorylation and dose response inhibition of cell proliferation (IC(50), 12-15 micro M).	imatinib	45-53	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	15-18
14760098-6	2004	Treatment with KIT tyrosine kinase inhibitor imatinib (0.5-20 micro M) induced down-regulation of KIT phosphorylation and dose response inhibition of cell proliferation (IC(50), 12-15 micro M).	imatinib	45-53	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	98-101
14744784-1	2004	Imatinib mesylate (IM) binds to the BCR-ABL protein, inhibiting its kinase activity and effectively controlling diseases driven by this kinase.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
14760098-8	2004	We then analyzed if blockade of KIT loop through imatinib (10 micro M) was able to increase the antitumor in vitro effect of doxorubicin (DXR) and vincristine (VCR), drugs usually used in Ewing tumor treatment.	imatinib	49-57	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	32-35
14760098-10	2004	CONCLUSIONS: Inhibition of Ewing tumor cell proliferation by imatinib is mediated through blockade of KIT receptor signaling.	imatinib	61-69	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	102-105
14760091-0	2004	Imatinib mesylate (Gleevec) inhibits ovarian cancer cell growth through a mechanism dependent on platelet-derived growth factor receptor alpha and Akt inactivation.	imatinib	0-17	AKT serine/threonine kinase 1	Homo sapiens	147-150
14710199-2	2004	The leading drug in this area is imatinib mesylate, which targets ABL, KIT and PDGFR.	imatinib	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-69
14760091-0	2004	Imatinib mesylate (Gleevec) inhibits ovarian cancer cell growth through a mechanism dependent on platelet-derived growth factor receptor alpha and Akt inactivation.	imatinib	19-26	platelet derived growth factor receptor alpha	Homo sapiens	97-142
14760091-0	2004	Imatinib mesylate (Gleevec) inhibits ovarian cancer cell growth through a mechanism dependent on platelet-derived growth factor receptor alpha and Akt inactivation.	imatinib	19-26	AKT serine/threonine kinase 1	Homo sapiens	147-150
14760091-2	2004	The purpose of this study is to evaluate whether disruption of the platelet-derived growth factor-regulated growth pathway by Imatinib mesylate (Gleevec), a partially selective PDGFR inhibitor, inhibits growth of ovarian cancer cells expressing PDGFR.	imatinib	126-143	platelet derived growth factor receptor beta	Homo sapiens	177-182
14760091-2	2004	The purpose of this study is to evaluate whether disruption of the platelet-derived growth factor-regulated growth pathway by Imatinib mesylate (Gleevec), a partially selective PDGFR inhibitor, inhibits growth of ovarian cancer cells expressing PDGFR.	imatinib	126-143	platelet derived growth factor receptor beta	Homo sapiens	245-250
14760091-4	2004	In addition, we investigated the involvement of Akt in mediating Imatinib-inhibited cell growth inhibition.	imatinib	65-73	AKT serine/threonine kinase 1	Homo sapiens	48-51
14760091-6	2004	We showed that Imatinib inhibits the growth of ovarian cancer cells in a PDGFR-specific manner, at clinically relevant concentrations (IC(50) < 1 micro M).	imatinib	15-23	platelet derived growth factor receptor beta	Homo sapiens	73-78
14760091-7	2004	Imatinib inhibits the growth of three primary ovarian cultures and two immortalized cultures (PDGFR positive), but has no effects on SkOv3 and CaOv3 cell lines (PDGFR negative).	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	94-99
14760091-9	2004	Imatinib inhibits both PDGFRalpha and Akt phosphorylation at a concentration of 1 micro M. Stable expression of constitutively active Akt induces partial resistance to PDGFR inhibition in ovarian cancer cells, as demonstrated by cell proliferation assay and cell cycle analysis.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	23-33
14760091-9	2004	Imatinib inhibits both PDGFRalpha and Akt phosphorylation at a concentration of 1 micro M. Stable expression of constitutively active Akt induces partial resistance to PDGFR inhibition in ovarian cancer cells, as demonstrated by cell proliferation assay and cell cycle analysis.	imatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	38-41
14760091-9	2004	Imatinib inhibits both PDGFRalpha and Akt phosphorylation at a concentration of 1 micro M. Stable expression of constitutively active Akt induces partial resistance to PDGFR inhibition in ovarian cancer cells, as demonstrated by cell proliferation assay and cell cycle analysis.	imatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	134-137
14760091-9	2004	Imatinib inhibits both PDGFRalpha and Akt phosphorylation at a concentration of 1 micro M. Stable expression of constitutively active Akt induces partial resistance to PDGFR inhibition in ovarian cancer cells, as demonstrated by cell proliferation assay and cell cycle analysis.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	23-28
14760091-10	2004	CONCLUSIONS: Our data indicate that Imatinib mesylate inhibits the growth of ovarian cancer cells through PDGFR inactivation.	imatinib	36-53	platelet derived growth factor receptor beta	Homo sapiens	106-111
14760091-11	2004	In addition, our results suggest that constitutive Akt activation modulates sensitivity to Imatinib in ovarian cancer cells.	imatinib	91-99	AKT serine/threonine kinase 1	Homo sapiens	51-54
14709738-3	2004	We therefore evaluated the effects of imatinib mesylate (imatinib), a selective inhibitor of the tyrosine kinase activities of c-Kit and PDGFR, on the growth of neuroblastoma cells in vivo and in vitro.	imatinib	38-55	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	127-132
14709738-3	2004	We therefore evaluated the effects of imatinib mesylate (imatinib), a selective inhibitor of the tyrosine kinase activities of c-Kit and PDGFR, on the growth of neuroblastoma cells in vivo and in vitro.	imatinib	38-55	platelet derived growth factor receptor, beta polypeptide	Mus musculus	137-142
14709738-11	2004	RESULTS: All seven neuroblastoma cell lines treated with imatinib displayed concentration-dependent decreases in cell viability, which coincided with an induction of apoptosis, and with ligand-stimulated phosphorylation of c-Kit and PDGFR.	imatinib	57-65	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	223-228
14709738-11	2004	RESULTS: All seven neuroblastoma cell lines treated with imatinib displayed concentration-dependent decreases in cell viability, which coincided with an induction of apoptosis, and with ligand-stimulated phosphorylation of c-Kit and PDGFR.	imatinib	57-65	platelet derived growth factor receptor, beta polypeptide	Mus musculus	233-238
14709738-13	2004	Expression of VEGF, but not phosphorylation of Flk-1, its receptor, was reduced in neuroblastoma cells treated with imatinib at 10 microM or higher.	imatinib	116-124	vascular endothelial growth factor A	Mus musculus	14-18
15179008-5	2004	Quantitative RT-PCR (Q-PCR) assays enable to monitor the kinetics of residual BCR-ABL transcripts over time in patients with a good response to imatinib.	imatinib	144-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
15327887-4	2004	As imatinib also inhibits the tyrosine kinase activity of KIT and the platelet-derived growth factor receptors, the extension of imatinib to malignancies driven by these kinases will be described.	imatinib	3-11	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	58-61
15327887-4	2004	As imatinib also inhibits the tyrosine kinase activity of KIT and the platelet-derived growth factor receptors, the extension of imatinib to malignancies driven by these kinases will be described.	imatinib	129-137	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	58-61
15032571-4	2004	Imatinib mesylate (Gleevec, STI571, or CP57148B) is a direct inhibitor of ABL (ABL1), ARG (ABL2), KIT, and PDGFR tyrosine kinases.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-77
15032571-4	2004	Imatinib mesylate (Gleevec, STI571, or CP57148B) is a direct inhibitor of ABL (ABL1), ARG (ABL2), KIT, and PDGFR tyrosine kinases.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-83
15032571-4	2004	Imatinib mesylate (Gleevec, STI571, or CP57148B) is a direct inhibitor of ABL (ABL1), ARG (ABL2), KIT, and PDGFR tyrosine kinases.	imatinib	0-17	ABL proto-oncogene 2, non-receptor tyrosine kinase	Homo sapiens	91-95
15032571-4	2004	Imatinib mesylate (Gleevec, STI571, or CP57148B) is a direct inhibitor of ABL (ABL1), ARG (ABL2), KIT, and PDGFR tyrosine kinases.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	98-101
15032571-4	2004	Imatinib mesylate (Gleevec, STI571, or CP57148B) is a direct inhibitor of ABL (ABL1), ARG (ABL2), KIT, and PDGFR tyrosine kinases.	imatinib	28-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-77
15032571-4	2004	Imatinib mesylate (Gleevec, STI571, or CP57148B) is a direct inhibitor of ABL (ABL1), ARG (ABL2), KIT, and PDGFR tyrosine kinases.	imatinib	28-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-83
15032571-4	2004	Imatinib mesylate (Gleevec, STI571, or CP57148B) is a direct inhibitor of ABL (ABL1), ARG (ABL2), KIT, and PDGFR tyrosine kinases.	imatinib	28-34	ABL proto-oncogene 2, non-receptor tyrosine kinase	Homo sapiens	91-95
15032571-4	2004	Imatinib mesylate (Gleevec, STI571, or CP57148B) is a direct inhibitor of ABL (ABL1), ARG (ABL2), KIT, and PDGFR tyrosine kinases.	imatinib	28-34	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	98-101
15032571-6	2004	Analysis of CML patients resistant to BCR-ABL suppression by Imatinib mesylate coupled with the crystallographic structure of ABL complexed to this inhibitor have shown how structural mutations in ABL can circumvent an otherwise potent anticancer drug.	imatinib	61-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
15032571-6	2004	Analysis of CML patients resistant to BCR-ABL suppression by Imatinib mesylate coupled with the crystallographic structure of ABL complexed to this inhibitor have shown how structural mutations in ABL can circumvent an otherwise potent anticancer drug.	imatinib	61-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-45
15161340-4	2004	Imatinib mesylate was also effective in patients with chronic-phase CML refractory to or intolerant of treatment with IFNalpha (as 400 mg/day) and in those with blast-crisis or accelerated-phase CML (600 mg/day).	imatinib	0-17	interferon alpha 1	Homo sapiens	118-126
15322333-4	2004	The inhibitory effect of STI-571 suggests a role for c-kit tyrosine kinase on glucose transport activation not only by SCF, but also by H2O2.	imatinib	25-32	KIT ligand	Homo sapiens	119-122
14646349-2	2004	Imatinib mesylate (STI571) targets the tyrosine kinase activity of the BCR-ABL fusion protein in CML, and was superior to IFN-alpha plus low-dose cytarabine in newly diagnosed chronic-phase CML in a phase III randomized study.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
14646349-2	2004	Imatinib mesylate (STI571) targets the tyrosine kinase activity of the BCR-ABL fusion protein in CML, and was superior to IFN-alpha plus low-dose cytarabine in newly diagnosed chronic-phase CML in a phase III randomized study.	imatinib	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
14646349-3	2004	Imatinib induced apoptosis in BCR-ABL-positive cells in vitro, and activates several signaling pathways such as PI3K/Akt, STAT5 and Ras/MAPK.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
14646349-3	2004	Imatinib induced apoptosis in BCR-ABL-positive cells in vitro, and activates several signaling pathways such as PI3K/Akt, STAT5 and Ras/MAPK.	imatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	117-120
14646349-3	2004	Imatinib induced apoptosis in BCR-ABL-positive cells in vitro, and activates several signaling pathways such as PI3K/Akt, STAT5 and Ras/MAPK.	imatinib	0-8	signal transducer and activator of transcription 5A	Homo sapiens	122-127
15124675-0	2004	Imatinib mesylate selectively influences the cellular metabolism of cytarabine in BCR/ABL negative leukemia cell lines and normal CD34+ progenitor cells.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
15124675-0	2004	Imatinib mesylate selectively influences the cellular metabolism of cytarabine in BCR/ABL negative leukemia cell lines and normal CD34+ progenitor cells.	imatinib	0-17	CD34 molecule	Homo sapiens	130-134
15124675-1	2004	STI-571 (Imatinib/Glivec) has been shown to have synergism with various chemotherapeutic agents including cytosine arabinoside (Ara-C) in BCR/ABL positive leukemia cells.	imatinib	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
15124675-1	2004	STI-571 (Imatinib/Glivec) has been shown to have synergism with various chemotherapeutic agents including cytosine arabinoside (Ara-C) in BCR/ABL positive leukemia cells.	imatinib	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
15124675-1	2004	STI-571 (Imatinib/Glivec) has been shown to have synergism with various chemotherapeutic agents including cytosine arabinoside (Ara-C) in BCR/ABL positive leukemia cells.	imatinib	18-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
15124675-3	2004	We investigated the effects of STI-571 in combination with Ara-C on BCR/ABL negative leukemia cell lines and CD34+ hematopoietic progenitor cells in-vitro.	imatinib	31-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
15124675-7	2004	A linear increase of Ara-CTP could be induced by increasing the incubation time with STI-571 from 2-6 h with a ceiling effect after 8 h. In contrast coincubation of mononuclear cells or purified CD34+ cells with STI-571 at therapeutic concentrations lead to decreased intracellular levels of Ara-CTP.	imatinib	212-219	CD34 molecule	Homo sapiens	195-199
15124675-8	2004	The synergism between Ara-C and STI-571 was even more pronounced in Raji and HL-60 cells when 300 ng/ml G-CSF were added at the beginning of the culture period.	imatinib	32-39	colony stimulating factor 3	Homo sapiens	104-109
15243647-0	2004	Two different point mutations in ABL gene ATP-binding domain conferring Primary Imatinib resistance in a Chronic Myeloid Leukemia (CML) patient: A case report.	imatinib	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-36
15243647-1	2004	Imatinib (Gleevec) is the effective therapy for BCR-ABL positive CML patients.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
12933582-0	2004	In vitro efficacy of combined treatment depends on the underlying mechanism of resistance in imatinib-resistant Bcr-Abl-positive cell lines.	imatinib	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
12933582-5	2004	Our results indicate that resistance to imatinib induced by Bcr-Abl overexpression or by engineered expression of clinically relevant Bcr-Abl mutants does not induce cross-resistance to As2O3 or decitabine.	imatinib	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
12933582-5	2004	Our results indicate that resistance to imatinib induced by Bcr-Abl overexpression or by engineered expression of clinically relevant Bcr-Abl mutants does not induce cross-resistance to As2O3 or decitabine.	imatinib	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
14687026-0	2004	Apicidin potentiates the imatinib-induced apoptosis of Bcr-Abl-positive human leukaemia cells by enhancing the activation of mitochondria-dependent caspase cascades.	imatinib	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
14687026-2	2004	We examined whether apicidin potentiates the imatinib-induced apoptosis of Bcr-Abl-positive human leukaemia cells.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
14687026-5	2004	Imatinib/apicidin co-treatment for 48 h resulted in a near complete loss of the full-length XIAP (X-linked inhibitor of apoptosis) protein, with a corresponding increase in the 29-kDa XIAP cleavage product.	imatinib	0-8	X-linked inhibitor of apoptosis	Homo sapiens	92-96
14687026-5	2004	Imatinib/apicidin co-treatment for 48 h resulted in a near complete loss of the full-length XIAP (X-linked inhibitor of apoptosis) protein, with a corresponding increase in the 29-kDa XIAP cleavage product.	imatinib	0-8	X-linked inhibitor of apoptosis	Homo sapiens	98-129
14687026-5	2004	Imatinib/apicidin co-treatment for 48 h resulted in a near complete loss of the full-length XIAP (X-linked inhibitor of apoptosis) protein, with a corresponding increase in the 29-kDa XIAP cleavage product.	imatinib	0-8	X-linked inhibitor of apoptosis	Homo sapiens	184-188
14687026-7	2004	Imatinib/apicidin co-treatment for 48 h produced a prominent decrease in Bcr-Abl protein levels in a caspase-dependent manner.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
14687026-8	2004	In summary, these data indicate that apicidin potentiates the imatinib-induced apoptosis of Bcr-Abl-positive leukaemia cells through the enhanced activation of the mitochondria-dependent caspase cascades, accompanied by caspase-dependent downregulation of Bcr-Abl and XIAP.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
14687026-8	2004	In summary, these data indicate that apicidin potentiates the imatinib-induced apoptosis of Bcr-Abl-positive leukaemia cells through the enhanced activation of the mitochondria-dependent caspase cascades, accompanied by caspase-dependent downregulation of Bcr-Abl and XIAP.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	256-263
14687026-8	2004	In summary, these data indicate that apicidin potentiates the imatinib-induced apoptosis of Bcr-Abl-positive leukaemia cells through the enhanced activation of the mitochondria-dependent caspase cascades, accompanied by caspase-dependent downregulation of Bcr-Abl and XIAP.	imatinib	62-70	X-linked inhibitor of apoptosis	Homo sapiens	268-272
14710199-2	2004	The leading drug in this area is imatinib mesylate, which targets ABL, KIT and PDGFR.	imatinib	33-41	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	71-74
14687026-9	2004	These findings generate a rationale for further investigation of apicidin and imatinib as a potential therapeutic strategy in Bcr-Abl-positive leukaemias.	imatinib	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
15250677-0	2004	Use and limitations of imatinib mesylate (Glivec), a selective inhibitor of the tyrosine kinase Abl transcript in the treatment of chronic myeloid leukaemia.	imatinib	23-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-99
14710199-2	2004	The leading drug in this area is imatinib mesylate, which targets ABL, KIT and PDGFR.	imatinib	33-41	platelet derived growth factor receptor beta	Homo sapiens	79-84
15250677-0	2004	Use and limitations of imatinib mesylate (Glivec), a selective inhibitor of the tyrosine kinase Abl transcript in the treatment of chronic myeloid leukaemia.	imatinib	42-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-99
14676625-0	2004	Mechanisms and implications of imatinib resistance mutations in BCR-ABL.	imatinib	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
15250677-3	2004	Imatinib mesylate, an inhibitor of the BCR-Abl transcript modelled on the ATP binding pocket of the Abl oncoprotein, prevents phosphorylation of effector molecules and induces apoptosis.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
15250677-3	2004	Imatinib mesylate, an inhibitor of the BCR-Abl transcript modelled on the ATP binding pocket of the Abl oncoprotein, prevents phosphorylation of effector molecules and induces apoptosis.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-46
15250677-4	2004	Imatinib has limited effectiveness when BCR-Abl cells are in the quiescent cell-cycle state of G0.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
15250677-6	2004	Up-regulation of BCR-Abl expression, ATP binding pocket mutations, up-regulation of MDR1 and over-expression of Pgp are all thought to limit the effectiveness of imatinib.	imatinib	162-170	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
15250677-6	2004	Up-regulation of BCR-Abl expression, ATP binding pocket mutations, up-regulation of MDR1 and over-expression of Pgp are all thought to limit the effectiveness of imatinib.	imatinib	162-170	ATP binding cassette subfamily B member 1	Homo sapiens	84-88
15250677-6	2004	Up-regulation of BCR-Abl expression, ATP binding pocket mutations, up-regulation of MDR1 and over-expression of Pgp are all thought to limit the effectiveness of imatinib.	imatinib	162-170	phosphoglycolate phosphatase	Homo sapiens	112-115
15250677-9	2004	Research studies have identified imatinib as a potential treatment option for a diverse range of malignancies associated with BCR-Abl, platelet-derived growth factor receptor (PDGFr) and c-Kit pathways.	imatinib	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
15250677-9	2004	Research studies have identified imatinib as a potential treatment option for a diverse range of malignancies associated with BCR-Abl, platelet-derived growth factor receptor (PDGFr) and c-Kit pathways.	imatinib	33-41	platelet derived growth factor receptor beta	Homo sapiens	135-174
15250677-9	2004	Research studies have identified imatinib as a potential treatment option for a diverse range of malignancies associated with BCR-Abl, platelet-derived growth factor receptor (PDGFr) and c-Kit pathways.	imatinib	33-41	platelet derived growth factor receptor beta	Homo sapiens	176-181
15250677-9	2004	Research studies have identified imatinib as a potential treatment option for a diverse range of malignancies associated with BCR-Abl, platelet-derived growth factor receptor (PDGFr) and c-Kit pathways.	imatinib	33-41	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	187-192
15069768-7	2004	Recently, a small molecule tyrosine kinase inhibitor (STI571, imatinib mesylate, Gleevec) directed against the enzymatic (kinase) domain of the KIT protein was found to produce dramatic clinical responses as monotherapy for metastatic GISTs.	imatinib	54-60	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	144-147
15069768-7	2004	Recently, a small molecule tyrosine kinase inhibitor (STI571, imatinib mesylate, Gleevec) directed against the enzymatic (kinase) domain of the KIT protein was found to produce dramatic clinical responses as monotherapy for metastatic GISTs.	imatinib	62-79	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	144-147
14734453-0	2004	Survival advantage with imatinib mesylate therapy in chronic-phase chronic myelogenous ;eukemia (CML-CP) after IFN-alpha failure and in late CML-CP, comparison with historical controls.	imatinib	24-41	interferon alpha 1	Homo sapiens	111-120
14734453-1	2004	PURPOSE: The purpose of this research was to compare the survival of patients with Philadelphia chromosome (Ph) -positive chronic myelogenous leukemia (CML) post-IFN-alpha failure treated with imatinib to historical experiences with standards of care or other therapies.	imatinib	193-201	interferon alpha 1	Homo sapiens	162-171
14734453-13	2004	CONCLUSIONS: This analysis provides evidence for a survival advantage with imatinib versus other therapies in chronic-phase CML post-IFN failure, and for a survival advantage with imatinib versus IFN in late chronic-phase CML.	imatinib	75-83	interferon alpha 1	Homo sapiens	133-136
14734467-2	2004	Some KIT-overexpressing solid tumors have responded favorably to STI571, potentially because of the presence of KIT-activating mutations.	imatinib	65-71	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	5-8
14734467-2	2004	Some KIT-overexpressing solid tumors have responded favorably to STI571, potentially because of the presence of KIT-activating mutations.	imatinib	65-71	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	112-115
15532894-2	2004	This review outlines present-day experiences with imatinib (Glivec), a potent inhibitor of the tyrosine kinases bcr-abl, c-kit and platelet-derived growth factor receptor kinase.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
15532894-2	2004	This review outlines present-day experiences with imatinib (Glivec), a potent inhibitor of the tyrosine kinases bcr-abl, c-kit and platelet-derived growth factor receptor kinase.	imatinib	50-58	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	121-126
15532894-2	2004	This review outlines present-day experiences with imatinib (Glivec), a potent inhibitor of the tyrosine kinases bcr-abl, c-kit and platelet-derived growth factor receptor kinase.	imatinib	60-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
15532894-2	2004	This review outlines present-day experiences with imatinib (Glivec), a potent inhibitor of the tyrosine kinases bcr-abl, c-kit and platelet-derived growth factor receptor kinase.	imatinib	60-66	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	121-126
15532894-3	2004	Due to inhibition of bcr-abl tyroxine kinase, imatinib has rapidly become the standard therapy for chronic myelocytic leukemia; inhibition of c-kit receptor explains its effectivity in the treatment of patients with gastrointestinal stromal tumors.	imatinib	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
15532894-4	2004	Another known target of imatinib is tyrosine kinase of PDGFR, which is activated in numerous malignancies, particularly in dermatofibrosarcoma protuberans.	imatinib	24-32	platelet derived growth factor receptor beta	Homo sapiens	55-60
15180525-7	2004	Although highly homologous to other class III RTKs, Flt3 is resistant to the phenylaminopyrimidine STI571 (Gleevec, Imatinib), a potent inhibitor of other RTKs in the family, such as the PDGFbeta-receptor or c-Kit.	imatinib	99-105	fms related receptor tyrosine kinase 3	Homo sapiens	52-56
15180525-7	2004	Although highly homologous to other class III RTKs, Flt3 is resistant to the phenylaminopyrimidine STI571 (Gleevec, Imatinib), a potent inhibitor of other RTKs in the family, such as the PDGFbeta-receptor or c-Kit.	imatinib	116-124	fms related receptor tyrosine kinase 3	Homo sapiens	52-56
15180525-8	2004	STI571 binding to Flt3 is prevented by the phenylalanine 691 side-chain in the ATP binding center and mutating this site to threonine renders the corresponding Flt3 mutant sensitive to STI571.	imatinib	0-6	fms related receptor tyrosine kinase 3	Homo sapiens	18-22
15180525-8	2004	STI571 binding to Flt3 is prevented by the phenylalanine 691 side-chain in the ATP binding center and mutating this site to threonine renders the corresponding Flt3 mutant sensitive to STI571.	imatinib	0-6	fms related receptor tyrosine kinase 3	Homo sapiens	160-164
15180525-8	2004	STI571 binding to Flt3 is prevented by the phenylalanine 691 side-chain in the ATP binding center and mutating this site to threonine renders the corresponding Flt3 mutant sensitive to STI571.	imatinib	185-191	fms related receptor tyrosine kinase 3	Homo sapiens	18-22
15180525-8	2004	STI571 binding to Flt3 is prevented by the phenylalanine 691 side-chain in the ATP binding center and mutating this site to threonine renders the corresponding Flt3 mutant sensitive to STI571.	imatinib	185-191	fms related receptor tyrosine kinase 3	Homo sapiens	160-164
14676625-4	2004	This can result from gene amplification and, more importantly, point mutations that disrupt the bind of imatinib to BCR-ABL itself.	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
14676625-6	2004	RECENT FINDINGS: In light of recent studies and publications, it is now clear that Imatinib exerts its inhibitory action by stabilizing the inactive non ATP-binding conformation of BCR-ABL and that mutations even outside the kinase domain can lead to enhanced autophosphorylation of the kinase, thereby stabilizing the active conformation that resists imatinib binding.	imatinib	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	181-188
14676625-6	2004	RECENT FINDINGS: In light of recent studies and publications, it is now clear that Imatinib exerts its inhibitory action by stabilizing the inactive non ATP-binding conformation of BCR-ABL and that mutations even outside the kinase domain can lead to enhanced autophosphorylation of the kinase, thereby stabilizing the active conformation that resists imatinib binding.	imatinib	352-360	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	181-188
14676625-10	2004	SUMMARY: The most common mechanism of relapse for CML patients treated with Imatinib is the appearance of point mutations in the BCR-ABL oncogene that confer resistance to this drug.	imatinib	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
14676627-3	2004	Successful empiric treatment of patients with the hypereosinophilic syndrome with the selective tyrosine kinase inhibitor imatinib mesylate (Gleevec, Novartis) ultimately led to the discovery of the FIP1L1-PDGFRalpha fusion kinase in about half of the hypereosinophilic syndrome cases.	imatinib	122-139	factor interacting with PAPOLA and CPSF1	Homo sapiens	199-205
14676627-3	2004	Successful empiric treatment of patients with the hypereosinophilic syndrome with the selective tyrosine kinase inhibitor imatinib mesylate (Gleevec, Novartis) ultimately led to the discovery of the FIP1L1-PDGFRalpha fusion kinase in about half of the hypereosinophilic syndrome cases.	imatinib	122-139	platelet derived growth factor receptor alpha	Homo sapiens	206-216
14676627-6	2004	In vitro and in vivo studies confirmed that FIP1L1-PDGFRalpha is a therapeutic target of imatinib, forming a rational basis for the treatment of FIP1L1-PDGFRA positive chronic eosinophilic leukemia and mastocytosis with imatinib.	imatinib	89-97	factor interacting with PAPOLA and CPSF1	Homo sapiens	44-50
14676627-6	2004	In vitro and in vivo studies confirmed that FIP1L1-PDGFRalpha is a therapeutic target of imatinib, forming a rational basis for the treatment of FIP1L1-PDGFRA positive chronic eosinophilic leukemia and mastocytosis with imatinib.	imatinib	89-97	platelet derived growth factor receptor alpha	Homo sapiens	51-61
14676627-6	2004	In vitro and in vivo studies confirmed that FIP1L1-PDGFRalpha is a therapeutic target of imatinib, forming a rational basis for the treatment of FIP1L1-PDGFRA positive chronic eosinophilic leukemia and mastocytosis with imatinib.	imatinib	89-97	factor interacting with PAPOLA and CPSF1	Homo sapiens	145-151
14967957-0	2004	Metastatic gastrointestinal stromal tumor with an exon 11 c-kit mutation responding to the tyrosine kinase inhibitor imatinib.	imatinib	117-125	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	58-63
14676627-6	2004	In vitro and in vivo studies confirmed that FIP1L1-PDGFRalpha is a therapeutic target of imatinib, forming a rational basis for the treatment of FIP1L1-PDGFRA positive chronic eosinophilic leukemia and mastocytosis with imatinib.	imatinib	89-97	platelet derived growth factor receptor alpha	Homo sapiens	152-158
14676627-6	2004	In vitro and in vivo studies confirmed that FIP1L1-PDGFRalpha is a therapeutic target of imatinib, forming a rational basis for the treatment of FIP1L1-PDGFRA positive chronic eosinophilic leukemia and mastocytosis with imatinib.	imatinib	220-228	factor interacting with PAPOLA and CPSF1	Homo sapiens	44-50
14676627-6	2004	In vitro and in vivo studies confirmed that FIP1L1-PDGFRalpha is a therapeutic target of imatinib, forming a rational basis for the treatment of FIP1L1-PDGFRA positive chronic eosinophilic leukemia and mastocytosis with imatinib.	imatinib	220-228	platelet derived growth factor receptor alpha	Homo sapiens	51-61
14676627-6	2004	In vitro and in vivo studies confirmed that FIP1L1-PDGFRalpha is a therapeutic target of imatinib, forming a rational basis for the treatment of FIP1L1-PDGFRA positive chronic eosinophilic leukemia and mastocytosis with imatinib.	imatinib	220-228	factor interacting with PAPOLA and CPSF1	Homo sapiens	145-151
14676627-7	2004	Similar to BCR-ABL-positive leukemias, resistance to imatinib due to point mutations in the PDGFRalpha kinase domain may develop.	imatinib	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-18
15350151-5	2004	Drugs most prominently affected and contraindicated for concomitant use with St John"s wort are metabolised via both CYP3A4 and P-glycoprotein pathways, including HIV protease inhibitors, HIV non-nucleoside reverse transcriptase inhibitors (only CYP3A4), the immunosuppressants ciclosporin and tacrolimus, and the antineoplastic agents irinotecan and imatinib mesylate.	imatinib	351-368	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	117-123
14676627-7	2004	Similar to BCR-ABL-positive leukemias, resistance to imatinib due to point mutations in the PDGFRalpha kinase domain may develop.	imatinib	53-61	platelet derived growth factor receptor alpha	Homo sapiens	92-102
14676628-6	2004	FIP1L1-PDGFRA+ mast cell disease responds completely to imatinib mesylate.	imatinib	56-73	factor interacting with PAPOLA and CPSF1	Homo sapiens	0-6
14676628-6	2004	FIP1L1-PDGFRA+ mast cell disease responds completely to imatinib mesylate.	imatinib	56-73	platelet derived growth factor receptor alpha	Homo sapiens	7-13
14695851-2	2004	Imatinib mesylate, a selective inhibitor of BCR-ABL, has been introduced into clinical trials with favorable toxicity and impressive activity at all disease stages.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
14725895-2	2004	Most recently, knowledge of the central function of the BCR-ABL fusion gene led to the development of a small molecule, imatinib, that has proved remarkably effective at reducing the number of leukemia cells in individual CML patients and promises to prolong life substantially in comparison with earlier treatments.	imatinib	120-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
14962264-0	2004	Ida-FLAG plus imatinib mesylate-induced molecular remission in a patient with chemoresistant Ph1+ acute myeloid leukemia.	imatinib	14-31	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	93-96
14962264-1	2004	Imatinib mesylate is a potent, selective inhibitor of the tyrosine kinase activity of bcr-abl,which is now established as the state-of-the-art treatment for chronic, accelerated or even blastic phase of Philadelphia-positive [Ph(1)(+)] chronic myelogenous leukemia.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
15167915-4	2004	Treatment with imatinib mesylate resulted in a substantial decrease of the BCR-ABL/ABL ratio and in the absence of c-kit mutation.	imatinib	15-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
15048068-0	2004	Chk2 drives late G1/early S phase arrest of clonal myeloid progenitors expressing the p210 BCR-ABL tyrosine kinase in response to STI571.	imatinib	130-136	checkpoint kinase 2	Homo sapiens	0-4
15048068-0	2004	Chk2 drives late G1/early S phase arrest of clonal myeloid progenitors expressing the p210 BCR-ABL tyrosine kinase in response to STI571.	imatinib	130-136	envoplakin	Mus musculus	86-90
14745431-0	2004	High incidence of BCR-ABL kinase domain mutations and absence of mutations of the PDGFR and KIT activation loops in CML patients with secondary resistance to imatinib.	imatinib	158-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
14745431-0	2004	High incidence of BCR-ABL kinase domain mutations and absence of mutations of the PDGFR and KIT activation loops in CML patients with secondary resistance to imatinib.	imatinib	158-166	platelet derived growth factor receptor beta	Homo sapiens	82-87
14745431-0	2004	High incidence of BCR-ABL kinase domain mutations and absence of mutations of the PDGFR and KIT activation loops in CML patients with secondary resistance to imatinib.	imatinib	158-166	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	92-95
14745431-1	2004	Imatinib, a specific inhibitor of the Abl, Kit and platelet-derived growth factor receptor (PDGFR) tyrosine kinases, is effective in all phases of chronic myelogenous leukemia.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-41
14745431-1	2004	Imatinib, a specific inhibitor of the Abl, Kit and platelet-derived growth factor receptor (PDGFR) tyrosine kinases, is effective in all phases of chronic myelogenous leukemia.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	43-46
14745431-1	2004	Imatinib, a specific inhibitor of the Abl, Kit and platelet-derived growth factor receptor (PDGFR) tyrosine kinases, is effective in all phases of chronic myelogenous leukemia.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	51-90
14745431-1	2004	Imatinib, a specific inhibitor of the Abl, Kit and platelet-derived growth factor receptor (PDGFR) tyrosine kinases, is effective in all phases of chronic myelogenous leukemia.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	92-97
14745431-10	2004	Our results confirm the high frequency of BCR-ABL kinase domain mutations in patients with secondary resistance to imatinib and exclude mutations of the activation loops of KIT, PDGFRA and PDGFRB as possible causes of resistance in patients without ABL mutations.	imatinib	115-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
14745431-10	2004	Our results confirm the high frequency of BCR-ABL kinase domain mutations in patients with secondary resistance to imatinib and exclude mutations of the activation loops of KIT, PDGFRA and PDGFRB as possible causes of resistance in patients without ABL mutations.	imatinib	115-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-49
15048068-3	2004	Here, we demonstrated that STI571 also induces growth arrest by activating the Chk2-Cdc25A-Cdk2 axis, a pathway complementary to p53 in the activation of G(1)/S cell cycle checkpoint.	imatinib	27-33	checkpoint kinase 2	Homo sapiens	79-83
15048068-3	2004	Here, we demonstrated that STI571 also induces growth arrest by activating the Chk2-Cdc25A-Cdk2 axis, a pathway complementary to p53 in the activation of G(1)/S cell cycle checkpoint.	imatinib	27-33	cell division cycle 25A	Homo sapiens	84-90
15048068-3	2004	Here, we demonstrated that STI571 also induces growth arrest by activating the Chk2-Cdc25A-Cdk2 axis, a pathway complementary to p53 in the activation of G(1)/S cell cycle checkpoint.	imatinib	27-33	cyclin dependent kinase 2	Homo sapiens	91-95
15048068-3	2004	Here, we demonstrated that STI571 also induces growth arrest by activating the Chk2-Cdc25A-Cdk2 axis, a pathway complementary to p53 in the activation of G(1)/S cell cycle checkpoint.	imatinib	27-33	tumor protein p53	Homo sapiens	129-132
15511212-9	2004	Using STI571 (5 microM, 16 hours) to inhibit the c-Kit pathway following stimulation with SCF (100 ng/mL), an upregulation of topo-I activity was observed in H526 cells but not in H82 cells.	imatinib	6-12	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	49-54
15511212-9	2004	Using STI571 (5 microM, 16 hours) to inhibit the c-Kit pathway following stimulation with SCF (100 ng/mL), an upregulation of topo-I activity was observed in H526 cells but not in H82 cells.	imatinib	6-12	KIT ligand	Homo sapiens	90-93
15167915-4	2004	Treatment with imatinib mesylate resulted in a substantial decrease of the BCR-ABL/ABL ratio and in the absence of c-kit mutation.	imatinib	15-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-82
15015226-2	2004	Imatinib potently inhibits several protein tyrosine kinases, including BCR-ABL, c-Kit, and PDGF receptor.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
14630086-6	2004	At relapse, the BCR-ABL transcripts were undetectable, which suggests that imatinib mesylate could be an effective adjuvant treatment in acute leukemia with a secondary t(9;22)(q34;q11).	imatinib	75-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
14603339-1	2004	Treatment of chronic myelogenous leukemia with a specific inhibitor of the Bcr/Abl tyrosine kinase, imatinib, has shown great promise.	imatinib	100-108	BCR activator of RhoGEF and GTPase	Mus musculus	75-78
14603339-2	2004	However, acute lymphoblastic leukemias that express Bcr/Abl only transiently respond to imatinib.	imatinib	88-96	BCR activator of RhoGEF and GTPase	Mus musculus	52-55
15579919-0	2004	Serial monitoring of BCR-ABL transcripts in chronic myelogenous leukemia (CML) treated with imatinib mesylate.	imatinib	92-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
15579919-3	2004	We have serially monitored peripheral blood and bone marrow BCR-ABL transcripts using qRT-PCR in CML patients commencing imatinib therapy, and compared the results with bone marrow cytogenetics.	imatinib	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
15579919-9	2004	Before start of imatinib therapy there was a considerable variation in BCR-ABL transcripts among the patients, ranging approximately one log (base 10).	imatinib	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
15579919-10	2004	Similarly, patients with a complete cytogenetic response following imatinib therapy had variable BCR-ABL transcript levels, ranging at least three logs (base 10).	imatinib	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
15579919-11	2004	The major decline in BCR-ABL transcripts occurred within 6 mo after start of imatinib therapy.	imatinib	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
15579919-12	2004	The decline in BCR-ABL transcripts, following imatinib therapy, appears to level off at 12-15 mo.	imatinib	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
15579919-15	2004	A plateau in BCR-ABL transcripts seems to have been reached after 12-15 mo of imatinib treatment; however, some "late responders" are seen.	imatinib	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
15169981-2	2004	Imatinib is a potent, specific inhibitor of BCR-ABL, the constitutively active protein tyrosine kinase critical to the pathogenesis of CML.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
15277706-0	2004	Erythropoietin overcomes imatinib-induced apoptosis and induces erythroid differentiation in TF-1/bcr-abl cells.	imatinib	25-33	erythropoietin	Homo sapiens	0-14
15277706-7	2004	However, GM-CSF, a survival factor of the parental TF-1 cells, protected TF-1/bcr-abl cells from imatinib-induced apoptosis in a dose-dependent manner.	imatinib	97-105	colony stimulating factor 2	Homo sapiens	9-15
15277706-8	2004	Concomitantly, constitutive phosphorylation of Stat5 and FKHRL1 was significantly inhibited by imatinib, and the inhibition was canceled by the addition of GM-CSF, accompanied by upregulation of Bcl-xL and downregulation of p27/Kip1.	imatinib	95-103	signal transducer and activator of transcription 5A	Homo sapiens	47-52
15277706-8	2004	Concomitantly, constitutive phosphorylation of Stat5 and FKHRL1 was significantly inhibited by imatinib, and the inhibition was canceled by the addition of GM-CSF, accompanied by upregulation of Bcl-xL and downregulation of p27/Kip1.	imatinib	95-103	forkhead box O3	Homo sapiens	57-63
15277706-10	2004	Importantly, imatinib-treated TF-1/bcr-abl cells differentiated into hemoglobin-positive cells in the presence of EPO, as in the case for the parental TF-1 cells.	imatinib	13-21	erythropoietin	Homo sapiens	114-117
15277706-11	2004	Taken together, imatinib-treated CML cells may differentiate into mature cells in the presence of differentiation-inducing cytokines such as EPO.	imatinib	16-24	erythropoietin	Homo sapiens	141-144
15015226-2	2004	Imatinib potently inhibits several protein tyrosine kinases, including BCR-ABL, c-Kit, and PDGF receptor.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	80-85
12881321-2	2003	Imatinib mesylate (STI-571 or Gleevec) is a potent inhibitor of the BCR/ABL and c-KIT tyrosine kinases.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
12881321-2	2003	Imatinib mesylate (STI-571 or Gleevec) is a potent inhibitor of the BCR/ABL and c-KIT tyrosine kinases.	imatinib	19-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
12881321-6	2003	The imatinib-sensitive human leukemic cell line K562, which is dependent on the activity of BCR/ABL for survival and growth, provides a convenient system for evaluating modulation of drug activity.	imatinib	4-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
14669283-2	2003	This was most likely because approximately 90% of patients receiving IFN-alpha plus ara-C changed to imatinib therapy after a median of 8 months into therapy.	imatinib	101-109	interferon alpha 1	Homo sapiens	69-78
14635084-1	2003	BACKGROUND: Imatinib mesylate is a tyrosine kinase inhibitor that targets the BCR-ABL protein in CML, c-kit (KIT) and platelet-derived growth factor receptors.	imatinib	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
14695158-12	2003	Tumors from mice treated with both STI571 and gemcitabine had decreased expression of activated (phosphorylated) PDGFR-alpha and -beta, decreased mean vessel density, decreased cell proliferation, and increased apoptosis of tumor cells.	imatinib	35-41	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	113-134
14672776-1	2003	BACKGROUND: Imatinib mesylate (Gleevec) is being studied as adjuvant chemotherapy for the treatment of cKIT+ gastrointestinal stromal tumors (GISTs).	imatinib	12-29	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	103-107
14632777-2	2003	We have investigated the effect of imatinib mesylate (STI571), an inhibitor of c-Kit, on MM cells.	imatinib	35-52	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	79-84
14632777-2	2003	We have investigated the effect of imatinib mesylate (STI571), an inhibitor of c-Kit, on MM cells.	imatinib	54-60	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	79-84
14632777-4	2003	Western blotting of cell cycle proteins showed that STI571 increased the levels of p21 and p16.	imatinib	52-58	H3 histone pseudogene 16	Homo sapiens	83-86
14632777-4	2003	Western blotting of cell cycle proteins showed that STI571 increased the levels of p21 and p16.	imatinib	52-58	cyclin dependent kinase inhibitor 2A	Homo sapiens	91-94
14635203-1	2003	Imatinib mesylate targets the adenosine triphosphate (ATP)-binding sites of the protein tyrosine kinase domains associated with Bcr-abl, the platelet-derived growth factor (PDGF) and c-kit.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
14635203-1	2003	Imatinib mesylate targets the adenosine triphosphate (ATP)-binding sites of the protein tyrosine kinase domains associated with Bcr-abl, the platelet-derived growth factor (PDGF) and c-kit.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	183-188
14635203-8	2003	One patient continued IFN when treatment with imatinib was started.	imatinib	46-54	interferon alpha 1	Homo sapiens	22-25
14635203-13	2003	In nine patients imatinib treatment was followed by a rise in leukocyte and platelet counts that required combination with HU or IFN.	imatinib	17-25	interferon alpha 1	Homo sapiens	129-132
12907457-5	2003	Imatinib mesylate has recently been shown to be efficacious in MPDs with PDGFR activation.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	73-78
14635084-1	2003	BACKGROUND: Imatinib mesylate is a tyrosine kinase inhibitor that targets the BCR-ABL protein in CML, c-kit (KIT) and platelet-derived growth factor receptors.	imatinib	12-29	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	102-107
14635084-1	2003	BACKGROUND: Imatinib mesylate is a tyrosine kinase inhibitor that targets the BCR-ABL protein in CML, c-kit (KIT) and platelet-derived growth factor receptors.	imatinib	12-29	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	109-112
14635084-9	2003	Several lines of evidence have previously reported that KIT and its ligand stem cell factor (SCF) have a regulatory role in melanocyte development and survival, suggesting a rational mechanism of action for imatinib mesylate in the pathogenesis of hypopigmentation.	imatinib	207-224	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	56-59
14635084-9	2003	Several lines of evidence have previously reported that KIT and its ligand stem cell factor (SCF) have a regulatory role in melanocyte development and survival, suggesting a rational mechanism of action for imatinib mesylate in the pathogenesis of hypopigmentation.	imatinib	207-224	KIT ligand	Homo sapiens	75-91
14635084-9	2003	Several lines of evidence have previously reported that KIT and its ligand stem cell factor (SCF) have a regulatory role in melanocyte development and survival, suggesting a rational mechanism of action for imatinib mesylate in the pathogenesis of hypopigmentation.	imatinib	207-224	KIT ligand	Homo sapiens	93-96
15025410-6	2003	Imatinib mesylate is an orally available tyrosine kinase inhibitor that specifically blocks Bcr-Abl function.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
14639002-4	2003	STI571 competitively binds to the ATP binding site of Bcr-Abl kinase and inhibits Abl tyrosine kinase activity.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
14676110-14	2003	Further testing of imatinib in patients with SCLC will focus on demonstration of KIT expression in the setting of confirmed SCLC histology.	imatinib	19-27	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	81-84
14686698-4	2003	Imatinib is the first rationally designed selective inhibitor of specific protein tyrosine kinases, including KIT.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	110-113
12960256-2	2003	We thus examined the effects of STI571, an inhibitor of the c-kit tyrosine kinase receptor, on the proliferation and function of human mast cells.	imatinib	32-38	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	60-65
12960256-6	2003	Two-hour exposure to STI571 that failed to influence the total viable cell number suppressed adhesion of the cells to fibronectin in the presence of SCF without altering the expressions of integrin molecules.	imatinib	21-27	fibronectin 1	Homo sapiens	118-129
12960256-6	2003	Two-hour exposure to STI571 that failed to influence the total viable cell number suppressed adhesion of the cells to fibronectin in the presence of SCF without altering the expressions of integrin molecules.	imatinib	21-27	KIT ligand	Homo sapiens	149-152
14562121-5	2003	Although increased levels of FGFR-3 were found in majority of late chronic phase patients treated with interferon alpha or hydroxyurea, the expression of FGFR-3 was always lowered following treatment with BCR-ABL tyrosine kinase inhibitor STI571.	imatinib	239-245	fibroblast growth factor receptor 3	Homo sapiens	154-160
14562121-5	2003	Although increased levels of FGFR-3 were found in majority of late chronic phase patients treated with interferon alpha or hydroxyurea, the expression of FGFR-3 was always lowered following treatment with BCR-ABL tyrosine kinase inhibitor STI571.	imatinib	239-245	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	205-212
14687999-0	2003	Lack of Bcr-Abl point mutations in chronic myeloid leukemia patients in chronic phase before imatinib treatment is not predictive of response.	imatinib	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-15
14645423-1	2003	PURPOSE: Most gastrointestinal stromal tumors (GISTs) express constitutively activated mutant isoforms of KIT or kinase platelet-derived growth factor receptor alpha (PDGFRA) that are potential therapeutic targets for imatinib mesylate.	imatinib	218-235	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	106-109
14645423-1	2003	PURPOSE: Most gastrointestinal stromal tumors (GISTs) express constitutively activated mutant isoforms of KIT or kinase platelet-derived growth factor receptor alpha (PDGFRA) that are potential therapeutic targets for imatinib mesylate.	imatinib	218-235	platelet derived growth factor receptor alpha	Homo sapiens	167-173
14645423-7	2003	All KIT mutant isoforms, but only a subset of PDGFRA mutant isoforms, were sensitive to imatinib, in vitro.	imatinib	88-96	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	4-7
14645423-7	2003	All KIT mutant isoforms, but only a subset of PDGFRA mutant isoforms, were sensitive to imatinib, in vitro.	imatinib	88-96	platelet derived growth factor receptor alpha	Homo sapiens	46-52
14645423-10	2003	CONCLUSION: Activating mutations of KIT or PDGFRA are found in the vast majority of GISTs, and the mutational status of these oncoproteins is predictive of clinical response to imatinib.	imatinib	177-185	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	36-39
14645423-10	2003	CONCLUSION: Activating mutations of KIT or PDGFRA are found in the vast majority of GISTs, and the mutational status of these oncoproteins is predictive of clinical response to imatinib.	imatinib	177-185	platelet derived growth factor receptor alpha	Homo sapiens	43-49
14645423-11	2003	PDGFRA mutations can explain response and sensitivity to imatinib in some GISTs lacking KIT mutations.	imatinib	57-65	platelet derived growth factor receptor alpha	Homo sapiens	0-6
16767900-0	2003	Tyrosine kinase inhibitor imatinib mesylate as anticancer agent for advanced ocular melanoma expressing immunoistochemical C-KIT (CD 117): preliminary results of a compassionate use clinical trial.	imatinib	26-43	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	123-128
16767900-0	2003	Tyrosine kinase inhibitor imatinib mesylate as anticancer agent for advanced ocular melanoma expressing immunoistochemical C-KIT (CD 117): preliminary results of a compassionate use clinical trial.	imatinib	26-43	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	130-136
16767900-1	2003	Imatinib mesylate (IM), is a selective and competitive inhibitor of tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
16767900-1	2003	Imatinib mesylate (IM), is a selective and competitive inhibitor of tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-103
16767900-1	2003	Imatinib mesylate (IM), is a selective and competitive inhibitor of tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	110-113
16767900-1	2003	Imatinib mesylate (IM), is a selective and competitive inhibitor of tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	123-163
16767900-1	2003	Imatinib mesylate (IM), is a selective and competitive inhibitor of tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	165-171
16767900-1	2003	Imatinib mesylate (IM), is a selective and competitive inhibitor of tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	19-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
16767900-1	2003	Imatinib mesylate (IM), is a selective and competitive inhibitor of tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	19-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-103
16767900-1	2003	Imatinib mesylate (IM), is a selective and competitive inhibitor of tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	19-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	110-113
16767900-1	2003	Imatinib mesylate (IM), is a selective and competitive inhibitor of tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	19-21	platelet derived growth factor receptor beta	Homo sapiens	123-163
16767900-1	2003	Imatinib mesylate (IM), is a selective and competitive inhibitor of tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	19-21	platelet derived growth factor receptor beta	Homo sapiens	165-171
14523461-2	2003	BCR-ABL/BCR% levels were measured by real-time quantitative RT-PCR and were significantly lower for the imatinib-treated patients at all time points up to 18 months, P<0.0001.	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
14523461-5	2003	Once imatinib commenced, the median BCR-ABL/BCR% levels in these patients were not significantly different to those on first-line imatinib for the equivalent number of months.	imatinib	5-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
14523461-9	2003	In conclusion, first-line imatinib-treated patients had profound reductions in BCR-ABL/BCR%, which significantly exceeded those of IFN+AraC-treated patients and early measurements were predictive of subsequent response.	imatinib	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
14523462-0	2003	Dynamics of BCR-ABL mRNA expression in first-line therapy of chronic myelogenous leukemia patients with imatinib or interferon alpha/ara-C.	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
14523462-4	2003	Within the first year after CCR, best median ratio BCR-ABL/ABL was 0.087%, (imatinib, n=48) vs 0.27% (IFN/Ara-C, n=9, P=0.025).	imatinib	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
14523462-7	2003	We conclude that (i) treatment with imatinib in newly diagnosed CML patients is associated with a rapid decrease of BCR-ABL transcript levels; (ii) nested PCR may reveal residual BCR-ABL transcripts in samples that are negative by real-time PCR; (iii) BCR-ABL transcript levels parallel cytogenetic response, and (iv) imatinib is superior to IFN/Ara-C in terms of the speed and degree of molecular responses, but residual disease is rarely eliminated.	imatinib	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
14523462-7	2003	We conclude that (i) treatment with imatinib in newly diagnosed CML patients is associated with a rapid decrease of BCR-ABL transcript levels; (ii) nested PCR may reveal residual BCR-ABL transcripts in samples that are negative by real-time PCR; (iii) BCR-ABL transcript levels parallel cytogenetic response, and (iv) imatinib is superior to IFN/Ara-C in terms of the speed and degree of molecular responses, but residual disease is rarely eliminated.	imatinib	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	179-186
14523462-7	2003	We conclude that (i) treatment with imatinib in newly diagnosed CML patients is associated with a rapid decrease of BCR-ABL transcript levels; (ii) nested PCR may reveal residual BCR-ABL transcripts in samples that are negative by real-time PCR; (iii) BCR-ABL transcript levels parallel cytogenetic response, and (iv) imatinib is superior to IFN/Ara-C in terms of the speed and degree of molecular responses, but residual disease is rarely eliminated.	imatinib	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	179-186
14523462-7	2003	We conclude that (i) treatment with imatinib in newly diagnosed CML patients is associated with a rapid decrease of BCR-ABL transcript levels; (ii) nested PCR may reveal residual BCR-ABL transcripts in samples that are negative by real-time PCR; (iii) BCR-ABL transcript levels parallel cytogenetic response, and (iv) imatinib is superior to IFN/Ara-C in terms of the speed and degree of molecular responses, but residual disease is rarely eliminated.	imatinib	36-44	interferon alpha 1	Homo sapiens	342-345
14639002-4	2003	STI571 competitively binds to the ATP binding site of Bcr-Abl kinase and inhibits Abl tyrosine kinase activity.	imatinib	0-6	TXK tyrosine kinase	Homo sapiens	86-101
14639002-7	2003	STI571 is also a potent inhibitor of a receptor-type c-Kit tyrosine kinase.	imatinib	0-6	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	53-58
14639002-7	2003	STI571 is also a potent inhibitor of a receptor-type c-Kit tyrosine kinase.	imatinib	0-6	TXK tyrosine kinase	Homo sapiens	59-74
14706143-1	2003	To explore the possibility of leukemia cell line of both bcr-abl and mdr-1 positive were cross-resistant to tyrosine kinase inhibitor STI571 and its reversal way, the inhibitory effect of STI571 on K562-n/VCR cells was detected with MTT method and reverse effects of CsA, TAM, IFN-alpha and CsA cominated with IFN-alpha were observed.	imatinib	134-140	ATP binding cassette subfamily B member 1	Homo sapiens	69-74
14706143-0	2003	[The reverse effect on drug-resistance against tyrosine kinase inhibitor STI571 in mdr1 and bcr-abl positive leukemic cells].	imatinib	73-79	ATP binding cassette subfamily B member 1	Homo sapiens	83-87
14706143-0	2003	[The reverse effect on drug-resistance against tyrosine kinase inhibitor STI571 in mdr1 and bcr-abl positive leukemic cells].	imatinib	73-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
14986524-4	2003	The rewardable clinical response of tumors that express C-Kit to treatment with the tyrosine kinase inhibitor STI 571 is a triumph of molecular pharmacology.	imatinib	110-117	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	56-61
14706143-1	2003	To explore the possibility of leukemia cell line of both bcr-abl and mdr-1 positive were cross-resistant to tyrosine kinase inhibitor STI571 and its reversal way, the inhibitory effect of STI571 on K562-n/VCR cells was detected with MTT method and reverse effects of CsA, TAM, IFN-alpha and CsA cominated with IFN-alpha were observed.	imatinib	188-194	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
14706143-1	2003	To explore the possibility of leukemia cell line of both bcr-abl and mdr-1 positive were cross-resistant to tyrosine kinase inhibitor STI571 and its reversal way, the inhibitory effect of STI571 on K562-n/VCR cells was detected with MTT method and reverse effects of CsA, TAM, IFN-alpha and CsA cominated with IFN-alpha were observed.	imatinib	134-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
14706143-1	2003	To explore the possibility of leukemia cell line of both bcr-abl and mdr-1 positive were cross-resistant to tyrosine kinase inhibitor STI571 and its reversal way, the inhibitory effect of STI571 on K562-n/VCR cells was detected with MTT method and reverse effects of CsA, TAM, IFN-alpha and CsA cominated with IFN-alpha were observed.	imatinib	188-194	ATP binding cassette subfamily B member 1	Homo sapiens	69-74
14612892-1	2003	The inhibition by imatinib of the cytochrome p450 3A4 isoenzyme may reduce the CYP3A4-mediated metabolic clearance of clinically important coadministered drugs.	imatinib	18-26	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	34-53
14612892-1	2003	The inhibition by imatinib of the cytochrome p450 3A4 isoenzyme may reduce the CYP3A4-mediated metabolic clearance of clinically important coadministered drugs.	imatinib	18-26	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	79-85
14612892-2	2003	The main purpose of this study was to evaluate the effect of the coadministration of imatinib on the pharmacokinetics of simvastatin, a probe CYP3A4 substrate.	imatinib	85-93	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	142-148
14612892-11	2003	Caution is therefore required when administering imatinib with CYP3A4 substrates with a narrow therapeutic window.	imatinib	49-57	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	63-69
12842979-3	2003	Recently, a novel tyrosine kinase that is generated from fusion of the Fip1-like 1 (FIP1L1) and PDGFR alpha (PDGFRA) genes has been identified as a therapeutic target for imatinib mesylate in hypereosinophilic syndrome (HES).	imatinib	171-179	platelet derived growth factor receptor alpha	Homo sapiens	109-115
14599548-7	2003	By using in vitro tests combining various imatinib concentrations (1-10 microM) with purified human AGP (1 and 3 mg/mL), we demonstrate that imatinib-induced apoptosis of K562 or fresh leukemic CML cells is abrogated or reduced.	imatinib	141-149	orosomucoid 1	Homo sapiens	100-112
12893773-6	2003	Lastly, this regimen potently induced apoptosis in STI571 (imatinib mesylate)-resistant K562 cells and CD34+ mononuclear cells obtained from a patient with STI571-resistant disease, as well as in Bcr/Abl- leukemia cells (eg, HL-60, U937, Jurkat).	imatinib	51-57	BCR activator of RhoGEF and GTPase	Homo sapiens	196-199
12893773-6	2003	Lastly, this regimen potently induced apoptosis in STI571 (imatinib mesylate)-resistant K562 cells and CD34+ mononuclear cells obtained from a patient with STI571-resistant disease, as well as in Bcr/Abl- leukemia cells (eg, HL-60, U937, Jurkat).	imatinib	59-76	BCR activator of RhoGEF and GTPase	Homo sapiens	196-199
14614449-7	2003	Inhibition of Bcr/Abl P190 in lymphoma cells from Bcr/Abl transgenic mice using imatinib reduced CKIIalpha activity.	imatinib	80-88	BCR activator of RhoGEF and GTPase	Mus musculus	14-17
14614449-7	2003	Inhibition of Bcr/Abl P190 in lymphoma cells from Bcr/Abl transgenic mice using imatinib reduced CKIIalpha activity.	imatinib	80-88	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	18-21
14614449-7	2003	Inhibition of Bcr/Abl P190 in lymphoma cells from Bcr/Abl transgenic mice using imatinib reduced CKIIalpha activity.	imatinib	80-88	BCR activator of RhoGEF and GTPase	Mus musculus	50-53
14614449-7	2003	Inhibition of Bcr/Abl P190 in lymphoma cells from Bcr/Abl transgenic mice using imatinib reduced CKIIalpha activity.	imatinib	80-88	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	54-57
14614449-7	2003	Inhibition of Bcr/Abl P190 in lymphoma cells from Bcr/Abl transgenic mice using imatinib reduced CKIIalpha activity.	imatinib	80-88	casein kinase 2, alpha 1 polypeptide	Mus musculus	97-106
14686005-3	2003	Imatinib (2-fenilaminopirimidine) is a selective inhibitor of the mutated C-KIT.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	74-79
12829606-3	2003	The inhibition of BCR/ABL tyrosine kinase activity by STI571 in chronic myeloid leukemia (CML) cell lines and CD34+ cells from patients with CML in lymphoid crisis results in induction of BACH2 expression.	imatinib	54-60	BTB domain and CNC homolog 2	Homo sapiens	188-193
12829606-10	2003	These results, coupled with our previous data showing that BACH2 promotes oxidative stress-induced cell death, suggest that combination chemotherapy involving STI571 and anticancer drugs that produce ROS may be of benefit in the treatment of Philadelphia chromosome 1 (Ph1)-positive leukemia.	imatinib	159-165	BTB domain and CNC homolog 2	Homo sapiens	59-64
12842979-0	2003	CHIC2 deletion, a surrogate for FIP1L1-PDGFRA fusion, occurs in systemic mastocytosis associated with eosinophilia and predicts response to imatinib mesylate therapy.	imatinib	140-148	cysteine rich hydrophobic domain 2	Homo sapiens	0-5
12842979-7	2003	While all 3 patients with the FIP1L1-PDGFRA rearrangement achieved a sustained complete response with imatinib mesylate therapy, the other two, both carrying the c-kit Asp816 to Val (Asp816Val) mutation, did not.	imatinib	102-119	factor interacting with PAPOLA and CPSF1	Homo sapiens	30-36
12975485-0	2003	Interaction of imatinib mesilate with human P-glycoprotein.	imatinib	15-32	ATP binding cassette subfamily B member 1	Homo sapiens	44-58
14688462-2	2003	Notable successes include imatinib mesylate (STI571, Gleevec) in Chronic Myelogenous Leukemia (CML), and Gastrointestinal Stromal Tumors (GIST) and trastuzumab (Herceptin) in HER2 amplified breast carcinoma.	imatinib	26-43	erb-b2 receptor tyrosine kinase 2	Homo sapiens	175-179
12842979-1	2003	Imatinib mesylate is effective in the treatment of hematologic malignancies that are characterized by either abl- or PDGFR beta- activating mutations.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	117-127
12842979-3	2003	Recently, a novel tyrosine kinase that is generated from fusion of the Fip1-like 1 (FIP1L1) and PDGFR alpha (PDGFRA) genes has been identified as a therapeutic target for imatinib mesylate in hypereosinophilic syndrome (HES).	imatinib	171-179	factor interacting with PAPOLA and CPSF1	Homo sapiens	71-82
12842979-3	2003	Recently, a novel tyrosine kinase that is generated from fusion of the Fip1-like 1 (FIP1L1) and PDGFR alpha (PDGFRA) genes has been identified as a therapeutic target for imatinib mesylate in hypereosinophilic syndrome (HES).	imatinib	171-179	factor interacting with PAPOLA and CPSF1	Homo sapiens	84-90
12842979-3	2003	Recently, a novel tyrosine kinase that is generated from fusion of the Fip1-like 1 (FIP1L1) and PDGFR alpha (PDGFRA) genes has been identified as a therapeutic target for imatinib mesylate in hypereosinophilic syndrome (HES).	imatinib	171-179	platelet derived growth factor receptor alpha	Homo sapiens	96-107
14585372-5	2003	MATERIALS AND METHODS: We have previously described such innate resistance to imatinib in subclones of a myeloid leukemia cell line, KCL22, in which imatinib exposure inhibits the activity of Bcr-Abl and yet fails to induce apoptosis.	imatinib	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	192-199
14585372-5	2003	MATERIALS AND METHODS: We have previously described such innate resistance to imatinib in subclones of a myeloid leukemia cell line, KCL22, in which imatinib exposure inhibits the activity of Bcr-Abl and yet fails to induce apoptosis.	imatinib	149-157	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	192-199
14585372-9	2003	CONCLUSION: Amongst the differentially-expressed genes correlating with imatinib resistance, several suggest the activation of alternative pathway(s) that maintain viability and growth independently of Bcr-Abl kinase activity.	imatinib	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	202-209
14650975-5	2003	we discuss efficacy of the combined therapy, composed of interferon and imatinib, for chronic myelogenous leukemia and other bcr-abl fusion chromosome positive diseases.	imatinib	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
12975485-1	2003	The interaction of imatinib mesilate with P-glycoprotein (P-gp) was examined using pig kidney epithelial LLC-PK1 cells versus L-MDR1 cells, which overexpress human P-gp on the apical membrane.	imatinib	19-36	ATP binding cassette subfamily B member 1	Homo sapiens	42-56
12975485-1	2003	The interaction of imatinib mesilate with P-glycoprotein (P-gp) was examined using pig kidney epithelial LLC-PK1 cells versus L-MDR1 cells, which overexpress human P-gp on the apical membrane.	imatinib	19-36	ATP binding cassette subfamily B member 1	Homo sapiens	58-62
12975485-6	2003	The rhodamine 123 efflux assay showed that the efflux of rhodamine 123 in K562/DXR cells, which overexpress human P-gp, could be blocked markedly by imatinib mesilate in a dose-dependent fashion.	imatinib	149-166	ATP binding cassette subfamily B member 1	Homo sapiens	114-118
12975485-7	2003	The Ki values for the inhibition of P-gp function by cyclosporin A and imatinib mesilate were estimated to be 6.1 and 18.3 muM, respectively, using a calcein-AM efflux assay.	imatinib	71-88	ATP binding cassette subfamily B member 1	Homo sapiens	36-40
12975485-8	2003	These observations demonstrate that imatinib mesilate is a substrate as well as a modulator of human P-gp, suggesting that imatinib mesilate drug interactions may occur via P-gp.	imatinib	36-53	ATP binding cassette subfamily B member 1	Homo sapiens	101-105
12975485-8	2003	These observations demonstrate that imatinib mesilate is a substrate as well as a modulator of human P-gp, suggesting that imatinib mesilate drug interactions may occur via P-gp.	imatinib	36-53	ATP binding cassette subfamily B member 1	Homo sapiens	173-177
12975485-8	2003	These observations demonstrate that imatinib mesilate is a substrate as well as a modulator of human P-gp, suggesting that imatinib mesilate drug interactions may occur via P-gp.	imatinib	123-140	ATP binding cassette subfamily B member 1	Homo sapiens	101-105
12975485-8	2003	These observations demonstrate that imatinib mesilate is a substrate as well as a modulator of human P-gp, suggesting that imatinib mesilate drug interactions may occur via P-gp.	imatinib	123-140	ATP binding cassette subfamily B member 1	Homo sapiens	173-177
14738154-0	2003	Aminopeptidase inhibitors inhibit proliferation and induce apoptosis of K562 and STI571-resistant K562 cell lines through the MAPK and GSK-3beta pathways.	imatinib	81-87	carboxypeptidase Q	Homo sapiens	0-14
12975485-9	2003	It is necessary to consider the pharmacokinetic and pharmacodynamic interactions of imatinib mesilate with other drugs via P-gp.	imatinib	84-101	ATP binding cassette subfamily B member 1	Homo sapiens	123-127
14738154-0	2003	Aminopeptidase inhibitors inhibit proliferation and induce apoptosis of K562 and STI571-resistant K562 cell lines through the MAPK and GSK-3beta pathways.	imatinib	81-87	glycogen synthase kinase 3 beta	Homo sapiens	135-144
14682111-4	2003	Imatinib mesylate (Gleevec) is a specific inhibitor of KIT kinase activation, and in phase II clinical trials has proven to be remarkably efficacious in heavily pretreated GIST patients with advanced disease.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	55-58
14738154-2	2003	STI571 inhibits tyrosine kinase activity of ABL and induces apoptosis of CML cells.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-47
14638869-0	2003	Erythropoietin promotes resistance against the Abl tyrosine kinase inhibitor imatinib (STI571) in K562 human leukemia cells.	imatinib	77-85	erythropoietin	Homo sapiens	0-14
14638869-0	2003	Erythropoietin promotes resistance against the Abl tyrosine kinase inhibitor imatinib (STI571) in K562 human leukemia cells.	imatinib	87-93	erythropoietin	Homo sapiens	0-14
14638869-2	2003	Imatinib mesylate (STI571, Gleevec), a therapeutically used inhibitor of Bcr-Abl, causes apoptosis of Bcr-Abl-positive cells.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
14638869-2	2003	Imatinib mesylate (STI571, Gleevec), a therapeutically used inhibitor of Bcr-Abl, causes apoptosis of Bcr-Abl-positive cells.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
14638869-2	2003	Imatinib mesylate (STI571, Gleevec), a therapeutically used inhibitor of Bcr-Abl, causes apoptosis of Bcr-Abl-positive cells.	imatinib	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
14638869-2	2003	Imatinib mesylate (STI571, Gleevec), a therapeutically used inhibitor of Bcr-Abl, causes apoptosis of Bcr-Abl-positive cells.	imatinib	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
14638869-4	2003	Surprisingly, in the presence of erythropoietin (Epo), K562 cells were temporarily able to sustain proliferation in the presence of imatinib, and imatinib-resistant clones could be isolated with high frequencies.	imatinib	132-140	erythropoietin	Homo sapiens	33-47
14638869-4	2003	Surprisingly, in the presence of erythropoietin (Epo), K562 cells were temporarily able to sustain proliferation in the presence of imatinib, and imatinib-resistant clones could be isolated with high frequencies.	imatinib	132-140	erythropoietin	Homo sapiens	49-52
14638869-4	2003	Surprisingly, in the presence of erythropoietin (Epo), K562 cells were temporarily able to sustain proliferation in the presence of imatinib, and imatinib-resistant clones could be isolated with high frequencies.	imatinib	146-154	erythropoietin	Homo sapiens	33-47
14638869-4	2003	Surprisingly, in the presence of erythropoietin (Epo), K562 cells were temporarily able to sustain proliferation in the presence of imatinib, and imatinib-resistant clones could be isolated with high frequencies.	imatinib	146-154	erythropoietin	Homo sapiens	49-52
14638869-5	2003	From such imatinib-resistant, Epo-dependent clones, sublines could be established that were resistant to imatinib in the absence of Epo.	imatinib	10-18	erythropoietin	Homo sapiens	30-33
14638869-5	2003	From such imatinib-resistant, Epo-dependent clones, sublines could be established that were resistant to imatinib in the absence of Epo.	imatinib	105-113	erythropoietin	Homo sapiens	30-33
14638869-8	2003	The data suggest that K562 cells acquire factor dependency under imatinib/Epo treatment, allowing them to escape from imatinib-induced, immediate cell death.	imatinib	65-73	erythropoietin	Homo sapiens	74-77
14638869-8	2003	The data suggest that K562 cells acquire factor dependency under imatinib/Epo treatment, allowing them to escape from imatinib-induced, immediate cell death.	imatinib	118-126	erythropoietin	Homo sapiens	74-77
14638869-10	2003	Thus, Epo, an endogenous regulator of hematopoiesis, promotes the development of resistance to imatinib.	imatinib	95-103	erythropoietin	Homo sapiens	6-9
14682111-4	2003	Imatinib mesylate (Gleevec) is a specific inhibitor of KIT kinase activation, and in phase II clinical trials has proven to be remarkably efficacious in heavily pretreated GIST patients with advanced disease.	imatinib	19-26	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	55-58
14624253-7	2003	Inhibition of Abl by the drug STI-571 or inhibition of signaling events upstream of Erk increases RAG-1 expression.	imatinib	30-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-17
14523244-4	2003	In addition, the Abl kinase inhibitor imatinib mesylate (Gleevec, or STI571), which targets the ATP-binding site of Abl and several other tyrosine kinases, potently reduces Abeta production in the N2a cell-free system and in intact N2a cells.	imatinib	38-55	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	17-20
14606348-1	2003	One of the undoubted major breakthroughs in the recent treatment of cancer is imatinib, a tyrosine-kinase inhibitor of the bcr-abl fusion protein, the stem-cell factor receptor c-kit (KIT) and the platelet-derived growth-factor receptor.	imatinib	78-86	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	177-182
14606348-1	2003	One of the undoubted major breakthroughs in the recent treatment of cancer is imatinib, a tyrosine-kinase inhibitor of the bcr-abl fusion protein, the stem-cell factor receptor c-kit (KIT) and the platelet-derived growth-factor receptor.	imatinib	78-86	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	184-187
14606348-3	2003	However, experience so far with imatinib in KIT-positive tumours indicates that imatinib seems only to be effective in those tumours with a gain-of-function mutation in c-kit.	imatinib	32-40	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	44-47
14606348-3	2003	However, experience so far with imatinib in KIT-positive tumours indicates that imatinib seems only to be effective in those tumours with a gain-of-function mutation in c-kit.	imatinib	80-88	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	44-47
14606348-3	2003	However, experience so far with imatinib in KIT-positive tumours indicates that imatinib seems only to be effective in those tumours with a gain-of-function mutation in c-kit.	imatinib	80-88	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	169-174
14606351-4	2003	The correct diagnosis of GISTs is crucial for the new treatment option with imatinib, the tyrosine-kinase inhibitor specifically targeted against KIT.	imatinib	76-84	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	146-149
12829585-2	2003	The ABL kinase activity is blocked by the ABL kinase inhibitor STI571 which abrogates transformation by X-ABL.	imatinib	63-69	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	4-7
12829585-2	2003	The ABL kinase activity is blocked by the ABL kinase inhibitor STI571 which abrogates transformation by X-ABL.	imatinib	63-69	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	42-45
12829585-2	2003	The ABL kinase activity is blocked by the ABL kinase inhibitor STI571 which abrogates transformation by X-ABL.	imatinib	63-69	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	42-45
12829585-7	2003	Our results indicate that targeting of the oligomerization interfaces of the X-ABL enhances the effects of STI571 in the treatment of leukemia caused by X-ABL.	imatinib	107-113	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	79-82
12829585-7	2003	Our results indicate that targeting of the oligomerization interfaces of the X-ABL enhances the effects of STI571 in the treatment of leukemia caused by X-ABL.	imatinib	107-113	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	155-158
12842984-4	2003	After the first imatinib cycle, 11 patients remained in sustained CHR with a decrease in the BCR-ABL/ABL ratios (0.89 logs), and one refractory patient achieved CHR.	imatinib	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
12842984-4	2003	After the first imatinib cycle, 11 patients remained in sustained CHR with a decrease in the BCR-ABL/ABL ratios (0.89 logs), and one refractory patient achieved CHR.	imatinib	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-100
12842984-6	2003	Ten patients receiving a second imatinib cycle following consolidation showed sustained CHR, including 2 molecular CR, with a further decrease in the BCR-ABL/ABL ratios (0.19 logs).	imatinib	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
12842984-6	2003	Ten patients receiving a second imatinib cycle following consolidation showed sustained CHR, including 2 molecular CR, with a further decrease in the BCR-ABL/ABL ratios (0.19 logs).	imatinib	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-157
14523244-4	2003	In addition, the Abl kinase inhibitor imatinib mesylate (Gleevec, or STI571), which targets the ATP-binding site of Abl and several other tyrosine kinases, potently reduces Abeta production in the N2a cell-free system and in intact N2a cells.	imatinib	38-55	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	116-119
14523244-4	2003	In addition, the Abl kinase inhibitor imatinib mesylate (Gleevec, or STI571), which targets the ATP-binding site of Abl and several other tyrosine kinases, potently reduces Abeta production in the N2a cell-free system and in intact N2a cells.	imatinib	38-55	amyloid beta (A4) precursor protein	Mus musculus	173-178
14523244-4	2003	In addition, the Abl kinase inhibitor imatinib mesylate (Gleevec, or STI571), which targets the ATP-binding site of Abl and several other tyrosine kinases, potently reduces Abeta production in the N2a cell-free system and in intact N2a cells.	imatinib	69-75	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	17-20
14523244-4	2003	In addition, the Abl kinase inhibitor imatinib mesylate (Gleevec, or STI571), which targets the ATP-binding site of Abl and several other tyrosine kinases, potently reduces Abeta production in the N2a cell-free system and in intact N2a cells.	imatinib	69-75	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	116-119
14523244-4	2003	In addition, the Abl kinase inhibitor imatinib mesylate (Gleevec, or STI571), which targets the ATP-binding site of Abl and several other tyrosine kinases, potently reduces Abeta production in the N2a cell-free system and in intact N2a cells.	imatinib	69-75	amyloid beta (A4) precursor protein	Mus musculus	173-178
14523244-5	2003	Both STI571 and a related compound, inhibitor 2, also reduce Abeta production in rat primary neuronal cultures and in vivo in guinea pig brain.	imatinib	5-11	amyloid beta (A4) precursor protein	Mus musculus	61-66
14523244-7	2003	Furthermore, production of Abeta and its inhibition by STI571 were demonstrated to occur to similar extents in both Abl-/- and WT mouse fibroblasts, indicating that the effect of STI571 on Abeta production does not involve Abl kinase.	imatinib	55-61	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	116-119
14523244-7	2003	Furthermore, production of Abeta and its inhibition by STI571 were demonstrated to occur to similar extents in both Abl-/- and WT mouse fibroblasts, indicating that the effect of STI571 on Abeta production does not involve Abl kinase.	imatinib	179-185	amyloid beta (A4) precursor protein	Mus musculus	27-32
14523244-7	2003	Furthermore, production of Abeta and its inhibition by STI571 were demonstrated to occur to similar extents in both Abl-/- and WT mouse fibroblasts, indicating that the effect of STI571 on Abeta production does not involve Abl kinase.	imatinib	179-185	amyloid beta (A4) precursor protein	Mus musculus	189-194
14523244-8	2003	The efficacy of STI571 in reducing Abeta without affecting Notch-1 cleavage may prove useful as a basis for developing novel therapies for Alzheimer"s disease.	imatinib	16-22	amyloid beta (A4) precursor protein	Mus musculus	35-40
13679030-1	2003	STI-571 (imatinib, Gleevec, Glivec, CGP 57148) is an inhibitor of the Abl group of protein-tyrosine kinases.	imatinib	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-73
14534335-5	2003	RESULTS: In patients who had a complete cytogenetic remission, levels of BCR-ABL transcripts after 12 months of treatment had fallen by at least 3 log in 57 percent of those in the imatinib group and 24 percent of those in the group given interferon plus cytarabine (P=0.003).	imatinib	181-189	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
14534335-8	2003	CONCLUSIONS: The proportion of patients with CML who had a reduction in BCR-ABL transcript levels of at least 3 log by 12 months of therapy was far greater with imatinib treatment than with treatment with interferon plus cytarabine.	imatinib	161-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
13679030-1	2003	STI-571 (imatinib, Gleevec, Glivec, CGP 57148) is an inhibitor of the Abl group of protein-tyrosine kinases.	imatinib	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-73
13679030-10	2003	STI-571 is a competitive inhibitor of Abl kinase with respect to ATP.	imatinib	0-7	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	38-41
14555991-5	2003	In K562 cells, Phorbol 12-myristate 13-acetate activates Erk1/2 and consequently increases Bim-EL phosphorylation and degradation by the proteasome, resulting in cell survival, while the Bcr-Abl inhibitor imatinib abrogates Bim-EL phosphorylation and degradation and induces caspase activation and apoptosis.	imatinib	205-213	mitogen-activated protein kinase 3	Homo sapiens	57-63
14551510-8	2003	Imatinib (10 and 20 micromol/l) alone inhibited cell growth significantly higher in c-kit+ cell lines (p<0.02) and inhibition was independent of PDGFR status.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	84-89
14555991-5	2003	In K562 cells, Phorbol 12-myristate 13-acetate activates Erk1/2 and consequently increases Bim-EL phosphorylation and degradation by the proteasome, resulting in cell survival, while the Bcr-Abl inhibitor imatinib abrogates Bim-EL phosphorylation and degradation and induces caspase activation and apoptosis.	imatinib	205-213	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	187-194
14551510-11	2003	We conclude that imatinib alone exerts marked effects on c-kit+ biliary tract cancer cell lines only at intermediate and high concentrations, but there is a potential role of low-dose imatinib in combination with 5-FU for the treatment of biliary tract cancers.	imatinib	17-25	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	57-62
14510940-9	2003	In Bcr-Abl-expressing cells, p21WAF-1 rapidly diminishes as the cells are sensitized to apoptosis, using the inhibitor STI571.	imatinib	119-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	3-10
14504072-0	2003	Imatinib mesylate elicits positive clinical response in atypical chronic myeloid leukemia involving the platelet-derived growth factor receptor beta.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	104-148
12829601-5	2003	The ABL tyrosine kinase inhibitor STI571 reversed these effects, showing that p210 BCR/ABL tyrosine kinase activity is responsible for deregulation of NER.	imatinib	34-40	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	4-7
12829601-5	2003	The ABL tyrosine kinase inhibitor STI571 reversed these effects, showing that p210 BCR/ABL tyrosine kinase activity is responsible for deregulation of NER.	imatinib	34-40	envoplakin	Mus musculus	78-82
12829601-5	2003	The ABL tyrosine kinase inhibitor STI571 reversed these effects, showing that p210 BCR/ABL tyrosine kinase activity is responsible for deregulation of NER.	imatinib	34-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
14515284-4	2003	GISTs are notoriously unresponsive to chemotherapy and, until the recent introduction of the KIT inhibitor imatinib, there has been no effective therapy for advanced, metastatic disease.	imatinib	107-115	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	93-96
14508830-2	2003	The objective of the current study was to evaluate the benefit of adding imatinib to the treatment sequence of patients with early chronic phase Ph-positive CML who received interferon alpha (IFN)-based regimens as frontline therapy.	imatinib	73-81	interferon alpha 1	Homo sapiens	192-195
14555307-0	2003	Imatinib mesylate therapy of chronic phase chronic myeloid leukemia resistant or intolerant to interferon: results and prognostic factors for response and progression-free survival in 150 patients.	imatinib	0-17	interferon alpha 1	Homo sapiens	95-105
14559829-3	2003	Point mutations within the BCR-ABL kinase domain emerged as a major mechanism of resistance toward imatinib.	imatinib	99-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
14559829-13	2003	We conclude that pyrido-pyrimidine-type kinase inhibitors are active against different frequently observed kinase domain mutations of BCR-ABL that cause resistance toward imatinib.	imatinib	171-179	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
14559829-14	2003	Resistance as a consequence of selection of mutant BCR-ABL by imatinib may be overcome using second-generation kinase inhibitors because of their higher potency and their ability to bind Bcr-Abl irrespective of the conformation of the activation loop.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
14559829-14	2003	Resistance as a consequence of selection of mutant BCR-ABL by imatinib may be overcome using second-generation kinase inhibitors because of their higher potency and their ability to bind Bcr-Abl irrespective of the conformation of the activation loop.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	187-194
14555307-2	2003	The results of imatinib treatment in chronic-phase CML patients resistant or intolerant to interferon (IFN) and the factors predicting therapeutic response and progression-free survival were analyzed.	imatinib	15-23	interferon alpha 1	Homo sapiens	91-107
14555307-3	2003	DESIGN AND METHODS: One hundred and fifty patients with chronic-phase CML resistant (n=111) or intolerant (n=39) to IFN were treated with imatinib.	imatinib	138-146	interferon alpha 1	Homo sapiens	116-119
14555307-13	2003	INTERPRETATION AND CONCLUSIONS: Imatinib is highly effective in chronic-phase CML patients resistant or intolerant to IFN, especially in those with normal platelet counts and in those not requiring prolonged treatment discontinuation due to neutropenia.	imatinib	32-40	interferon alpha 1	Homo sapiens	118-121
14560786-2	2003	More probable is the likelihood that the molecular basis of the various chronic MPD gradually will be elucidated such that specific inhibitory molecules analogous to imatinib may be designed for each disease or each subtype of disease.	imatinib	166-174	mevalonate diphosphate decarboxylase	Homo sapiens	80-83
14604282-2	2003	We investigated the effects of a Bcr-Abl tyrosine kinase inhibitor, imatinib mesylate, on the proliferation, adhesive properties, and morphology of a Bcr-Abl-transferred cell line, TF-1 Bcr-Abl, in comparison with parental TF-1.	imatinib	68-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
14604282-3	2003	First, the factor-independent growth of TF-1 Bcr-Abl was inhibited in the presence of imatinib mesylate, but this inhibition was overcome by addition of exogenous granulocyte-macrophage colony-stimulating factor.	imatinib	86-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
14604282-0	2003	Effects of the tyrosine kinase inhibitor imatinib mesylate on a Bcr-Abl-positive cell line: suppression of autonomous cell growth but no effect on decreased adhesive property and morphological changes.	imatinib	41-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
14604282-2	2003	We investigated the effects of a Bcr-Abl tyrosine kinase inhibitor, imatinib mesylate, on the proliferation, adhesive properties, and morphology of a Bcr-Abl-transferred cell line, TF-1 Bcr-Abl, in comparison with parental TF-1.	imatinib	68-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
14604282-4	2003	Imatinib mesylate remarkably reduced tyrosine phosphorylation of Bcr-Abl, Cbl, and Crkl in a time-dependent manner, and their complex formation also was affected.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
14604282-4	2003	Imatinib mesylate remarkably reduced tyrosine phosphorylation of Bcr-Abl, Cbl, and Crkl in a time-dependent manner, and their complex formation also was affected.	imatinib	0-17	Cbl proto-oncogene	Homo sapiens	74-77
14604282-4	2003	Imatinib mesylate remarkably reduced tyrosine phosphorylation of Bcr-Abl, Cbl, and Crkl in a time-dependent manner, and their complex formation also was affected.	imatinib	0-17	CRK like proto-oncogene, adaptor protein	Homo sapiens	83-87
14604282-5	2003	Imatinib mesylate inhibited activation of Stat5 rather than the MEK-ERK1/2 pathway.	imatinib	0-17	signal transducer and activator of transcription 5A	Homo sapiens	42-47
14604282-7	2003	Although the Bcr-Abl oncoprotein may be involved negatively in cell adhesion, the decreased adhesion and altered morphology of TF-1 Bcr-Abl cells were minimally affected by imatinib mesylate and seemed independent of Bcr-Abl kinase activity.	imatinib	173-190	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
14604282-7	2003	Although the Bcr-Abl oncoprotein may be involved negatively in cell adhesion, the decreased adhesion and altered morphology of TF-1 Bcr-Abl cells were minimally affected by imatinib mesylate and seemed independent of Bcr-Abl kinase activity.	imatinib	173-190	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
14507401-10	2003	Since malignant melanoma expresses PTK, it may be a candidate for treatment with anti-PTK, such as STI-571 (Gleevec).	imatinib	99-106	protein tyrosine kinase 2 beta	Homo sapiens	35-38
14507401-10	2003	Since malignant melanoma expresses PTK, it may be a candidate for treatment with anti-PTK, such as STI-571 (Gleevec).	imatinib	99-106	protein tyrosine kinase 2 beta	Homo sapiens	86-89
19774741-4	2003	These agents will be used soon in different combinations, most likely including imatinib, with the hope of obtaining a complete blockade of the intracellular pathways that are triggered by Bcr-Abl.	imatinib	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	189-196
14513038-2	2003	Experimental data suggest that interferon-alpha (IFN-alpha) enhances the antileukemic activity of imatinib.	imatinib	98-106	interferon alpha 1	Homo sapiens	49-58
14513039-0	2003	FISH for BCR-ABL on interphases of peripheral blood neutrophils but not of unselected white cells correlates with bone marrow cytogenetics in CML patients treated with imatinib.	imatinib	168-176	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
14613030-2	2003	This quest has taken a major leap forward with the demonstration that STI-571 (imatinib mesylate) induces clinical and molecular remissions in the majority of patients with interferon-refractory chronic myelogenous leukemia and gastrointestinal stromal tumors through inhibition of the Bcr/Abl fusion protein required for the initiation and progression of chronic myelogenous leukemia and inhibition of a mutant, activated c-kit present in gastrointestinal stromal tumors.	imatinib	70-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	286-293
14613030-2	2003	This quest has taken a major leap forward with the demonstration that STI-571 (imatinib mesylate) induces clinical and molecular remissions in the majority of patients with interferon-refractory chronic myelogenous leukemia and gastrointestinal stromal tumors through inhibition of the Bcr/Abl fusion protein required for the initiation and progression of chronic myelogenous leukemia and inhibition of a mutant, activated c-kit present in gastrointestinal stromal tumors.	imatinib	70-77	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	423-428
14613030-2	2003	This quest has taken a major leap forward with the demonstration that STI-571 (imatinib mesylate) induces clinical and molecular remissions in the majority of patients with interferon-refractory chronic myelogenous leukemia and gastrointestinal stromal tumors through inhibition of the Bcr/Abl fusion protein required for the initiation and progression of chronic myelogenous leukemia and inhibition of a mutant, activated c-kit present in gastrointestinal stromal tumors.	imatinib	79-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	286-293
14613030-2	2003	This quest has taken a major leap forward with the demonstration that STI-571 (imatinib mesylate) induces clinical and molecular remissions in the majority of patients with interferon-refractory chronic myelogenous leukemia and gastrointestinal stromal tumors through inhibition of the Bcr/Abl fusion protein required for the initiation and progression of chronic myelogenous leukemia and inhibition of a mutant, activated c-kit present in gastrointestinal stromal tumors.	imatinib	79-96	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	423-428
14653203-0	2003	[The monitoring of residual disease for chronic myelogenous leukemia patients treated with imatinib mesylate: detection of T315I mutation in ATP binding site of BCR/ABL gene].	imatinib	91-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-168
14653203-1	2003	Imatinib Mesylate, a specific inhibitor of BCR/ABL tyrosine kinase, was developed as a molecularly targeted drug for the treatment of patients with chronic myelogenous leukemia.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
12866022-2	2003	Previous studies have demonstrated that imatinib mesylate also inhibits the survival and functions of normal mast cells by interfering with the receptor tyrosine kinase for stem cell factor (SCF), c-kit, which is expressed by mast cells.	imatinib	40-57	TYRO3 protein tyrosine kinase 3	Mus musculus	144-168
12866022-2	2003	Previous studies have demonstrated that imatinib mesylate also inhibits the survival and functions of normal mast cells by interfering with the receptor tyrosine kinase for stem cell factor (SCF), c-kit, which is expressed by mast cells.	imatinib	40-57	kit ligand	Mus musculus	173-189
12866022-2	2003	Previous studies have demonstrated that imatinib mesylate also inhibits the survival and functions of normal mast cells by interfering with the receptor tyrosine kinase for stem cell factor (SCF), c-kit, which is expressed by mast cells.	imatinib	40-57	kit ligand	Mus musculus	191-194
12866022-2	2003	Previous studies have demonstrated that imatinib mesylate also inhibits the survival and functions of normal mast cells by interfering with the receptor tyrosine kinase for stem cell factor (SCF), c-kit, which is expressed by mast cells.	imatinib	40-57	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	197-202
14519654-0	2003	BCL-2 antisense oligonucleotide genasense is active against imatinib-resistant BCR-ABL-positive cells.	imatinib	60-68	B cell leukemia/lymphoma 2	Mus musculus	0-5
12750174-7	2003	Furthermore, bcr-abl-homologous siRNA increased sensitivity to imatinib in Bcr-Abl-overexpressing cells and in a cell line expressing the imatinib-resistant Bcr-Abl kinase domain mutation His396Pro, thereby antagonizing 2 of the major mechanisms of resistance to imatinib.	imatinib	138-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
12750174-7	2003	Furthermore, bcr-abl-homologous siRNA increased sensitivity to imatinib in Bcr-Abl-overexpressing cells and in a cell line expressing the imatinib-resistant Bcr-Abl kinase domain mutation His396Pro, thereby antagonizing 2 of the major mechanisms of resistance to imatinib.	imatinib	138-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-164
12750153-2	2003	However, it is currently unknown if the presence of deletions influences the response to imatinib, an Abl-specific tyrosine kinase inhibitor, that has recently shown excellent hematologic and cytogenetic responses in patients with CML.	imatinib	89-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-105
12750174-0	2003	Inhibition of bcr-abl gene expression by small interfering RNA sensitizes for imatinib mesylate (STI571).	imatinib	78-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
12750174-0	2003	Inhibition of bcr-abl gene expression by small interfering RNA sensitizes for imatinib mesylate (STI571).	imatinib	97-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
12750174-2	2003	Targeting bcr-abl by treatment with the selective tyrosine kinase inhibitor imatinib has proved to be highly efficient for controlling leukemic growth.	imatinib	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
12750174-7	2003	Furthermore, bcr-abl-homologous siRNA increased sensitivity to imatinib in Bcr-Abl-overexpressing cells and in a cell line expressing the imatinib-resistant Bcr-Abl kinase domain mutation His396Pro, thereby antagonizing 2 of the major mechanisms of resistance to imatinib.	imatinib	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
12750174-7	2003	Furthermore, bcr-abl-homologous siRNA increased sensitivity to imatinib in Bcr-Abl-overexpressing cells and in a cell line expressing the imatinib-resistant Bcr-Abl kinase domain mutation His396Pro, thereby antagonizing 2 of the major mechanisms of resistance to imatinib.	imatinib	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
12750174-7	2003	Furthermore, bcr-abl-homologous siRNA increased sensitivity to imatinib in Bcr-Abl-overexpressing cells and in a cell line expressing the imatinib-resistant Bcr-Abl kinase domain mutation His396Pro, thereby antagonizing 2 of the major mechanisms of resistance to imatinib.	imatinib	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-164
12750174-7	2003	Furthermore, bcr-abl-homologous siRNA increased sensitivity to imatinib in Bcr-Abl-overexpressing cells and in a cell line expressing the imatinib-resistant Bcr-Abl kinase domain mutation His396Pro, thereby antagonizing 2 of the major mechanisms of resistance to imatinib.	imatinib	138-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
12750174-7	2003	Furthermore, bcr-abl-homologous siRNA increased sensitivity to imatinib in Bcr-Abl-overexpressing cells and in a cell line expressing the imatinib-resistant Bcr-Abl kinase domain mutation His396Pro, thereby antagonizing 2 of the major mechanisms of resistance to imatinib.	imatinib	138-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-164
14519654-0	2003	BCL-2 antisense oligonucleotide genasense is active against imatinib-resistant BCR-ABL-positive cells.	imatinib	60-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
14519654-4	2003	EXPERIMENTAL DESIGN: Nude mice (n = 5/group) were transplanted s.c. with imatinib-resistant BCR-ABL-transformed TF-1 cells (BCR-ABL-TF-1-R cells).	imatinib	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
14519654-4	2003	EXPERIMENTAL DESIGN: Nude mice (n = 5/group) were transplanted s.c. with imatinib-resistant BCR-ABL-transformed TF-1 cells (BCR-ABL-TF-1-R cells).	imatinib	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
14522890-5	2003	They also provide a rationale for testing the combination of mTOR inhibitors with the Abl kinase inhibitor imatinib in patients with CML.	imatinib	107-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-89
14522890-6	2003	The mTOR inhibitor rapamycin enhanced imatinib-mediated killing of CML cell lines in vitro, and it overcame imatinib resistance in cells with Bcr-Abl gene amplification.	imatinib	38-46	mechanistic target of rapamycin kinase	Homo sapiens	4-8
14522890-6	2003	The mTOR inhibitor rapamycin enhanced imatinib-mediated killing of CML cell lines in vitro, and it overcame imatinib resistance in cells with Bcr-Abl gene amplification.	imatinib	108-116	mechanistic target of rapamycin kinase	Homo sapiens	4-8
14522890-6	2003	The mTOR inhibitor rapamycin enhanced imatinib-mediated killing of CML cell lines in vitro, and it overcame imatinib resistance in cells with Bcr-Abl gene amplification.	imatinib	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
14531349-2	2003	A new drug, Imatinib, is a potent inhibitor of a subgroup of the tyrosine kinase family comprising BCR-ABL, platelet-derived growth factor, and c-kit.	imatinib	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
12928501-7	2003	Sensitivity to the Abl inhibitor STI571 suggests differential utilization of the p53 and c-Abl/p73 pathways by different tumor cell lines.	imatinib	33-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-22
12928501-7	2003	Sensitivity to the Abl inhibitor STI571 suggests differential utilization of the p53 and c-Abl/p73 pathways by different tumor cell lines.	imatinib	33-39	tumor protein p53	Homo sapiens	81-84
12928501-7	2003	Sensitivity to the Abl inhibitor STI571 suggests differential utilization of the p53 and c-Abl/p73 pathways by different tumor cell lines.	imatinib	33-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-94
12963124-0	2003	Anti-proliferative effect of the abl tyrosine kinase inhibitor STI571 on the P-glycoprotein positive K562/ADM cell line.	imatinib	63-69	ATP binding cassette subfamily B member 1	Homo sapiens	77-91
12963124-2	2003	We addressed whether STI571 is effective for the CML blastic crisis cell line K562 and the P-glycoprotein (P-gp) positive, multidrug resistance cell line K562/ADM.	imatinib	21-27	ATP binding cassette subfamily B member 1	Homo sapiens	91-105
12963124-3	2003	The present results demonstrate that P-gp positive K562/ADM cells were more resistant than K562 cells to the anti-proliferative and apoptotic effect of STI571, but the co-addition of a P-gp modulator augmented the sensitivity of K562/ADM cells to STI571.	imatinib	152-158	ATP binding cassette subfamily B member 1	Homo sapiens	37-41
12963124-4	2003	For patients in CML blastic crisis, simultaneous use of a P-gp modulator may increase the efficacy of STI571.	imatinib	102-108	ATP binding cassette subfamily B member 1	Homo sapiens	58-62
12824179-6	2003	Moreover, STI-571, a specific c-Abl kinase inhibitor, is sufficient to block significantly p73 alpha nuclear matrix association.	imatinib	10-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-35
12824179-6	2003	Moreover, STI-571, a specific c-Abl kinase inhibitor, is sufficient to block significantly p73 alpha nuclear matrix association.	imatinib	10-17	tumor protein p73	Homo sapiens	91-94
12928501-7	2003	Sensitivity to the Abl inhibitor STI571 suggests differential utilization of the p53 and c-Abl/p73 pathways by different tumor cell lines.	imatinib	33-39	tumor protein p73	Homo sapiens	95-98
14531349-2	2003	A new drug, Imatinib, is a potent inhibitor of a subgroup of the tyrosine kinase family comprising BCR-ABL, platelet-derived growth factor, and c-kit.	imatinib	12-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	144-149
12942553-1	2003	BACKGROUND: Before the discovery of imatinib mesylate, a Bcr-Abl selective tyrosine kinase inhibitor, three agents, interferon-alpha (IFN-alpha), cytarabine (ara-C), and homoharringtonine (HHT), had demonstrated activity against Philadelphia chromosome (Ph)-positive chronic myelogenous leukemia (CML) as single agents and in couplet combinations.	imatinib	36-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
14666655-2	2003	We hypothesized that STI571 (Gleevec) would inhibit RET kinase and be a useful agent in the treatment of MTC.	imatinib	21-27	ret proto-oncogene	Homo sapiens	52-55
14666655-3	2003	MATERIALS AND METHODS: We determined the IC50 of STI571 for RET using an in vitro kinase assay and also examined the effects of STI571 on cellular proliferation and viability in TT cells, a human MTC cell line.	imatinib	49-55	ret proto-oncogene	Homo sapiens	60-63
14666655-7	2003	CONCLUSION: The concentrations of STI571 required to significantly inhibit RET and to inhibit TT cell proliferation are not clinically achievable.	imatinib	34-40	ret proto-oncogene	Homo sapiens	75-78
12783207-1	2003	PURPOSE: The tyrosine kinase inhibitor imatinib mesylate inhibits the function of the Bcr-Abl oncoprotein associated with Philadelphia-positive chronic myelogenous leukemia (CML).	imatinib	39-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
14565659-3	2003	In this study we have tried to answer the question if the combination of STI571 with purine nucleoside analogues (PNAs)- cladribine (2-CdA) and fludarabine (F-ara-A) intensifies the antiproliferative effect on granulocyte-macrophage progenitor cells (CFU-GM) from patients with CML as well as from normal persons.	imatinib	73-79	cytidine deaminase	Homo sapiens	135-138
12949711-8	2003	Inhibitory effect of Imatinib mesylate on activated PDGFR alpha was examined.	imatinib	21-38	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	52-63
12949711-12	2003	The constitutive activation of PDGFR alpha with Val-561 to Asp was inhibited effectively by Imatinib mesylate but that of PDGFR alpha with Asp-842 to Val was inhibited only weakly, even at the concentration of 10 micromol/L.	imatinib	92-109	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	31-42
12804638-4	2003	Phosphorylated STAT5 was found to measure 2.22+/-0.09 relative fluorescence units (RFU) falling to 0.925+/-0.005RFU in the presence of STI571.	imatinib	135-141	signal transducer and activator of transcription 5A	Homo sapiens	15-20
14565659-7	2003	We also observed that STI571 used together with 2-CdA (5,10 and 20 microM) or F-ara-A (0.2, 0.4 and 0.8 microM) at all the combinations significantly inhibited the colony growth of CML CFU-GM, as compared either to the control or to STI571 used alone (p < 0.05).	imatinib	22-28	cytidine deaminase	Homo sapiens	50-53
12970765-2	2003	A significant proportion of chronic myeloid leukemia (CML) patients achieve a major cytogenetic remission (MCR) to imatinib therapy after failing interferon (IFN) alpha-based protocols.	imatinib	115-123	interferon alpha 1	Homo sapiens	146-168
14565659-8	2003	In addition, the differences between CML and normal CFU-GM colony growth inhibition after the use of the combination of the highest concentrations of STI571 either with 2-CdA or F-ara-A were statistically significant (p = 0.03 and p = 0.01, respectively).	imatinib	150-156	cytidine deaminase	Homo sapiens	171-174
12970769-1	2003	The antileukaemic tyrosine kinase inhibitor, imatinib, has been reported to inhibit specifically the growth of bcr-abl expressing CML progenitors at levels of 0.1-5.0 microM, by blocking the ATP-binding site of the kinase domain of bcr-abl.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
12970769-1	2003	The antileukaemic tyrosine kinase inhibitor, imatinib, has been reported to inhibit specifically the growth of bcr-abl expressing CML progenitors at levels of 0.1-5.0 microM, by blocking the ATP-binding site of the kinase domain of bcr-abl.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	232-239
12869662-3	2003	Imatinib, an ATP-competitive selective inhibitor of Bcr-Abl, has unprecedented efficacy for the treatment of CML.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
12970769-2	2003	Inhibition of the c-abl, platelet-derived growth factor receptor and stem cell factor receptor (c-kit) tyrosine kinases by imatinib has also been reported.	imatinib	123-131	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	96-101
12970769-6	2003	Imatinib blocked monocyte/macrophage development in cultures stimulated with and without M-CSF, suggesting that inhibition of the M-CSF receptor, c-fms, by imatinib was unlikely to be responsible.	imatinib	0-8	colony stimulating factor 1	Homo sapiens	89-94
12944467-6	2003	WRN is tyrosine phosphorylated either transiently by treatment of HeLa cells with bleomycin or constitutively in cells from chronic myeloid leukemia (CML) patients, and these phosphorylations are prevented by treatment with the Abl kinase inhibitor STI-571.	imatinib	249-256	WRN RecQ like helicase	Homo sapiens	0-3
12944919-4	2003	The involvement of PDGFRA led us to treat the patient with the small organic compound imatinib mesylate/STI571 (Glivec) that blocks the ATP binding site of tyrosine kinases such as Abelson, KIT and platelet-derived growth factor receptors.	imatinib	86-103	platelet derived growth factor receptor alpha	Homo sapiens	19-25
12951180-6	2003	At least, tyrosine kinase inhibitors, a new family of molecules, are able of inhibiting some types of the mutated c-kit protein and one of them, imatinib mesylate, has shown a great efficacy in the treatment of gastro intestinal stromal tumors (GIST) which also involves the c-kit mutation.	imatinib	145-153	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	114-119
12951180-6	2003	At least, tyrosine kinase inhibitors, a new family of molecules, are able of inhibiting some types of the mutated c-kit protein and one of them, imatinib mesylate, has shown a great efficacy in the treatment of gastro intestinal stromal tumors (GIST) which also involves the c-kit mutation.	imatinib	145-153	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	275-280
12944919-4	2003	The involvement of PDGFRA led us to treat the patient with the small organic compound imatinib mesylate/STI571 (Glivec) that blocks the ATP binding site of tyrosine kinases such as Abelson, KIT and platelet-derived growth factor receptors.	imatinib	86-103	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	190-193
12944919-4	2003	The involvement of PDGFRA led us to treat the patient with the small organic compound imatinib mesylate/STI571 (Glivec) that blocks the ATP binding site of tyrosine kinases such as Abelson, KIT and platelet-derived growth factor receptors.	imatinib	104-110	platelet derived growth factor receptor alpha	Homo sapiens	19-25
12944919-4	2003	The involvement of PDGFRA led us to treat the patient with the small organic compound imatinib mesylate/STI571 (Glivec) that blocks the ATP binding site of tyrosine kinases such as Abelson, KIT and platelet-derived growth factor receptors.	imatinib	104-110	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	190-193
12941812-7	2003	We observed an increased frequency of insertions and deletions in the tissues of preleukemic animals, which could be partially reversed with the c-Abl specific inhibitor STI571.	imatinib	170-176	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	147-150
12800187-10	2003	These data demonstrate that both c-Kit and SCF are preferentially expressed in vivo in the most aggressive neuroblastic tumors and that their signaling is active in promoting in vitro NB cell proliferation that can be selectively inhibited by treatment with STI-571.	imatinib	258-265	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	33-38
12800187-10	2003	These data demonstrate that both c-Kit and SCF are preferentially expressed in vivo in the most aggressive neuroblastic tumors and that their signaling is active in promoting in vitro NB cell proliferation that can be selectively inhibited by treatment with STI-571.	imatinib	258-265	KIT ligand	Homo sapiens	43-46
12869489-0	2003	Functional consequence of MDR1 expression on imatinib intracellular concentrations.	imatinib	45-53	ATP binding cassette subfamily B member 1	Homo sapiens	26-30
12888812-4	2003	Imatinib, a KIT tyrosine kinase inhibitor, has recently been found to have a dramatic antitumour effect on GIST.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	12-15
12938259-1	2003	Imatinib mesylate is a 2-phenylaminopyrimidine tyrosine kinase inhibitor with specific activity for ABL, platelet-derived growth factor receptor, and c-kit receptor.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-103
12912938-5	2003	Success of inhibition of KIT in malignant gastrointestinal stromal tumors with imatinib mesylate seems mutation-dependent, with a favorable response in the presence of exon 11 mutations.	imatinib	79-87	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	25-28
12912938-25	2003	Still, without the availability of effective therapies, treatment with the KIT inhibitor imatinib mesylate might be considered for patients with postradiation sarcomas.	imatinib	89-106	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	75-78
12901973-1	2003	OBJECTIVE: STI571 is a tyrosine kinase inhibitor which inhibits the kinase activity of kit, the receptor for stem cell factor (SCF).	imatinib	11-17	KIT ligand	Homo sapiens	109-125
12901973-1	2003	OBJECTIVE: STI571 is a tyrosine kinase inhibitor which inhibits the kinase activity of kit, the receptor for stem cell factor (SCF).	imatinib	11-17	KIT ligand	Homo sapiens	127-130
12901973-4	2003	RESULTS: STI571 failed to inhibit the growth of HMC-1(560,816) cells bearing a codon 816 mutation but effectively suppressed the proliferation of HMC-1(560) carrying c-kit with the wild-type codon 816.	imatinib	9-15	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	166-171
12935973-1	2003	BACKGROUND AND OBJECTIVES: Imatinib mesylate (IM) is the choice treatment for Bcr/Abl-positive malignancies.	imatinib	27-44	BCR activator of RhoGEF and GTPase	Homo sapiens	78-81
12935973-1	2003	BACKGROUND AND OBJECTIVES: Imatinib mesylate (IM) is the choice treatment for Bcr/Abl-positive malignancies.	imatinib	46-48	BCR activator of RhoGEF and GTPase	Homo sapiens	78-81
12938259-3	2003	Imatinib mesylate binds to the amino acids of the BCR-ABL tyrosine kinase ATP binding site and stabilizes the inactive, non-ATP-binding form of BCR-ABL, thereby preventing tyrosine autophosphorylation, and in turn, phosphorylation of its substrates.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
12938259-3	2003	Imatinib mesylate binds to the amino acids of the BCR-ABL tyrosine kinase ATP binding site and stabilizes the inactive, non-ATP-binding form of BCR-ABL, thereby preventing tyrosine autophosphorylation, and in turn, phosphorylation of its substrates.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
12938280-3	2003	Because imatinib also inhibits c-kit and platelet-derived growth-factor (PDGF) receptor, it may be efficacious against some tumors which possess c-kit or PDGF receptors.	imatinib	8-16	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	31-36
12938280-3	2003	Because imatinib also inhibits c-kit and platelet-derived growth-factor (PDGF) receptor, it may be efficacious against some tumors which possess c-kit or PDGF receptors.	imatinib	8-16	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	145-150
12902920-8	2003	The authors suggest that the PDGFR-signaling pathway postulated to contribute to the development of gliomas in adults might not contribute to pilocytic astrocytomas in children, and that treatment with imatinib mesylate should be considered in patients with refractory pilocytic astrocytoma.	imatinib	202-219	platelet derived growth factor receptor beta	Homo sapiens	29-34
12663457-0	2003	Presence of the BCR-ABL mutation Glu255Lys prior to STI571 (imatinib) treatment in patients with Ph+ acute lymphoblastic leukemia.	imatinib	52-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
12939459-8	2003	On a functional level, we demonstrated that imatinib inhibited phosphorylation of KIT, AKT, and extracellular signal-regulated kinase 1/2 without affecting the total level of these proteins and that differential expression of these response genes involved activation of mitogen-activated protein kinase-dependent and -independent pathways.	imatinib	44-52	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	82-85
12939459-8	2003	On a functional level, we demonstrated that imatinib inhibited phosphorylation of KIT, AKT, and extracellular signal-regulated kinase 1/2 without affecting the total level of these proteins and that differential expression of these response genes involved activation of mitogen-activated protein kinase-dependent and -independent pathways.	imatinib	44-52	AKT serine/threonine kinase 1	Homo sapiens	87-90
12939459-8	2003	On a functional level, we demonstrated that imatinib inhibited phosphorylation of KIT, AKT, and extracellular signal-regulated kinase 1/2 without affecting the total level of these proteins and that differential expression of these response genes involved activation of mitogen-activated protein kinase-dependent and -independent pathways.	imatinib	44-52	mitogen-activated protein kinase 3	Homo sapiens	96-137
12663457-0	2003	Presence of the BCR-ABL mutation Glu255Lys prior to STI571 (imatinib) treatment in patients with Ph+ acute lymphoblastic leukemia.	imatinib	60-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
12663457-1	2003	The tyrosine kinase inhibitor STI571 (imatinib) binds competitively to the adenosine triphosphate (ATP) binding site of the ABL kinase, thereby inhibiting auto- and substrate phosphorylation of the oncogenic protein BCR-ABL and preventing the activation of downstream signaling pathways.	imatinib	30-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	216-223
12663457-1	2003	The tyrosine kinase inhibitor STI571 (imatinib) binds competitively to the adenosine triphosphate (ATP) binding site of the ABL kinase, thereby inhibiting auto- and substrate phosphorylation of the oncogenic protein BCR-ABL and preventing the activation of downstream signaling pathways.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	216-223
12798163-1	2003	Imatinib mesylate (Gleevec, Glivec, STI571) is a targeted, small molecule inhibitor of the oncogenes, BCR/ABL and c-KIT, and has striking antitumor activity in patients with chronic myelogenous leukemia or gastrointestinal stromal tumors.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
12798163-1	2003	Imatinib mesylate (Gleevec, Glivec, STI571) is a targeted, small molecule inhibitor of the oncogenes, BCR/ABL and c-KIT, and has striking antitumor activity in patients with chronic myelogenous leukemia or gastrointestinal stromal tumors.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	114-119
12798163-1	2003	Imatinib mesylate (Gleevec, Glivec, STI571) is a targeted, small molecule inhibitor of the oncogenes, BCR/ABL and c-KIT, and has striking antitumor activity in patients with chronic myelogenous leukemia or gastrointestinal stromal tumors.	imatinib	36-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
12798163-1	2003	Imatinib mesylate (Gleevec, Glivec, STI571) is a targeted, small molecule inhibitor of the oncogenes, BCR/ABL and c-KIT, and has striking antitumor activity in patients with chronic myelogenous leukemia or gastrointestinal stromal tumors.	imatinib	36-42	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	114-119
12623848-0	2003	Detection of BCR-ABL mutations in patients with CML treated with imatinib is virtually always accompanied by clinical resistance, and mutations in the ATP phosphate-binding loop (P-loop) are associated with a poor prognosis.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
12623848-1	2003	Imatinib-treated chronic myeloid leukemia (CML) patients with acquired resistance commonly have detectable BCR-ABL kinase domain mutations.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
12623848-3	2003	We evaluated 144 patients treated with imatinib for BCR-ABL kinase domain mutations by direct sequencing of 40 accelerated phase (AP), 64 late chronic phase (> or = 12 months from diagnosis, late-CP), and 40 early-CP patients.	imatinib	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
12823349-0	2003	Clinical and genetic studies of ETV6/ABL1-positive chronic myeloid leukaemia in blast crisis treated with imatinib mesylate.	imatinib	106-123	ETS variant transcription factor 6	Homo sapiens	32-36
12823349-0	2003	Clinical and genetic studies of ETV6/ABL1-positive chronic myeloid leukaemia in blast crisis treated with imatinib mesylate.	imatinib	106-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-41
12857554-1	2003	BACKGROUND AND OBJECTIVES: Imatinib mesylate inhibits ABL tyrosine kinase.	imatinib	27-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-57
12823349-3	2003	Here we describe the clinical and genetic response to imatinib mesylate treatment of an ETV6/ABL1-positive CML patient diagnosed in blast crisis (BC).	imatinib	54-71	ETS variant transcription factor 6	Homo sapiens	88-92
12823349-3	2003	Here we describe the clinical and genetic response to imatinib mesylate treatment of an ETV6/ABL1-positive CML patient diagnosed in blast crisis (BC).	imatinib	54-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-97
12823349-6	2003	Until d 71 of imatinib mesylate therapy, stable improvements in the clinical and laboratory features were noted, and the frequency of ABL1-rearranged peripheral blood cells decreased from 56% to 11%.	imatinib	14-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-138
12850478-1	2003	To elucidate the role of mitogen-activated protein kinases (MAPKs) and Akt kinase in leukemogenesis caused by the breakpoint cluster region (BCR)-Abelson (ABL) tyrosine kinase oncoprotein, we examined the activities of MAPKs and Akt kinase and their roles in the action of STI571, a specific inhibitor of BCR-ABL tyrosine kinase, in chronic myelogenous leukemia (CML) cells.	imatinib	273-279	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-158
12850478-3	2003	Both interferon-alpha and STI571 suppressed ERK1/2 activity in K562 cells.	imatinib	26-32	mitogen-activated protein kinase 3	Homo sapiens	44-50
12850478-6	2003	In addition, caspase-3 was activated by treatment of cells with STI571 and LY294002 but not with PD98059.	imatinib	64-70	caspase 3	Homo sapiens	13-22
12857554-3	2003	We describe the immunologic findings in patients with chronic myeloid leukemia resistant to or intolerant of interferon (IFN) a who were treated with imatinib.	imatinib	150-158	interferon alpha 1	Homo sapiens	109-127
12857554-14	2003	The reduction of Ig is greater in patients with a better cytogenetic response, perhaps reflecting that the efficacy of imatinib in blocking BCR-ABL kinase activity runs in parallel with ABL inhibition, leading to a dysregulation of B-lymphocyte function.	imatinib	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
12857554-14	2003	The reduction of Ig is greater in patients with a better cytogenetic response, perhaps reflecting that the efficacy of imatinib in blocking BCR-ABL kinase activity runs in parallel with ABL inhibition, leading to a dysregulation of B-lymphocyte function.	imatinib	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-147
12850478-8	2003	Primary leukemia cells from patients with CML blast crisis did not show inhibition of ERK1/2 or Akt kinase activity and were resistant to caspase-3-associated apoptosis after treatment with STI571.	imatinib	190-196	caspase 3	Homo sapiens	138-147
12887890-5	2003	These results suggest that Bcr-Abl has a monomeric, unphosphorylated state with the SH3 domain engaged intramolecularly to Pro1124 in the SH2-CD linker, the form that is sensitive to the inhibitor imatinib (STI-571).	imatinib	197-205	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
12916883-2	2003	The decision to try Imatinib was guided by bright expression of c-kit on the patient"s blasts.	imatinib	20-28	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	64-69
12916883-9	2003	This is the first report demonstrating that Imatinib can induce complete remission in relapsed c-kit positive AML in an elderly patient.	imatinib	44-52	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	95-100
12595307-0	2003	The CNS is a sanctuary for leukemic cells in mice receiving imatinib mesylate for Bcr/Abl-induced leukemia.	imatinib	60-77	BCR activator of RhoGEF and GTPase	Mus musculus	82-85
12808148-8	2003	Proliferation and viability of EOL-1 and BaF3 cells expressing Rhe-PDGFRalpha are ablated by the PDGFRalpha inhibitors imatinib, vatalanib, and THRX-165724.	imatinib	119-127	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	67-77
12808148-8	2003	Proliferation and viability of EOL-1 and BaF3 cells expressing Rhe-PDGFRalpha are ablated by the PDGFRalpha inhibitors imatinib, vatalanib, and THRX-165724.	imatinib	119-127	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	97-107
12576334-1	2003	The BCR/ABL tyrosine kinase inhibitor imatinib mesylate (Gleevec, STI571; Novartis, Basel, Switzerland) has shown remarkable efficacy in the treatment of chronic myelogenous leukemia (CML), with a high proportion of patients achieving complete cytogenetic responses (CCRs).	imatinib	38-55	BCR activator of RhoGEF and GTPase	Homo sapiens	4-7
12576334-1	2003	The BCR/ABL tyrosine kinase inhibitor imatinib mesylate (Gleevec, STI571; Novartis, Basel, Switzerland) has shown remarkable efficacy in the treatment of chronic myelogenous leukemia (CML), with a high proportion of patients achieving complete cytogenetic responses (CCRs).	imatinib	38-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-11
12576334-1	2003	The BCR/ABL tyrosine kinase inhibitor imatinib mesylate (Gleevec, STI571; Novartis, Basel, Switzerland) has shown remarkable efficacy in the treatment of chronic myelogenous leukemia (CML), with a high proportion of patients achieving complete cytogenetic responses (CCRs).	imatinib	66-72	BCR activator of RhoGEF and GTPase	Homo sapiens	4-7
12576334-1	2003	The BCR/ABL tyrosine kinase inhibitor imatinib mesylate (Gleevec, STI571; Novartis, Basel, Switzerland) has shown remarkable efficacy in the treatment of chronic myelogenous leukemia (CML), with a high proportion of patients achieving complete cytogenetic responses (CCRs).	imatinib	66-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-11
12595307-1	2003	The chronic myelogenous leukemia (CML)-like myeloproliferative disorder observed in the BCR/ABL murine bone marrow transduction and transplantation model shares several features with the human disease, including a high response rate to the tyrosine kinase inhibitor imatinib mesylate (STI571).	imatinib	266-283	BCR activator of RhoGEF and GTPase	Mus musculus	88-91
12576334-3	2003	We investigated whether residual BCR/ABL+ hematopoietic progenitors were present in patients who achieved CCRs with imatinib mesylate treatment.	imatinib	116-133	BCR activator of RhoGEF and GTPase	Homo sapiens	33-36
12576334-9	2003	Our results indicate that inhibition of BCR/ABL tyrosine kinase activity by imatinib mesylate does not eliminate malignant primitive progenitors in CML patients.	imatinib	76-93	BCR activator of RhoGEF and GTPase	Homo sapiens	40-43
12576334-9	2003	Our results indicate that inhibition of BCR/ABL tyrosine kinase activity by imatinib mesylate does not eliminate malignant primitive progenitors in CML patients.	imatinib	76-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-47
12595307-1	2003	The chronic myelogenous leukemia (CML)-like myeloproliferative disorder observed in the BCR/ABL murine bone marrow transduction and transplantation model shares several features with the human disease, including a high response rate to the tyrosine kinase inhibitor imatinib mesylate (STI571).	imatinib	285-291	BCR activator of RhoGEF and GTPase	Mus musculus	88-91
12595307-5	2003	Thus, in the mouse, the limited ability of imatinib mesylate to cross the blood-brain barrier allowed the CNS to become a sanctuary for Bcr/Abl-induced leukemia.	imatinib	43-51	BCR activator of RhoGEF and GTPase	Mus musculus	136-139
12801741-1	2003	cKit and platelet-derived growth-factor receptor (PDGFR) are receptor tyrosine kinases expressed in the testis, are involved in testosterone production, and are inhibited by imatinib.	imatinib	174-182	platelet derived growth factor receptor beta	Homo sapiens	9-48
12801741-1	2003	cKit and platelet-derived growth-factor receptor (PDGFR) are receptor tyrosine kinases expressed in the testis, are involved in testosterone production, and are inhibited by imatinib.	imatinib	174-182	platelet derived growth factor receptor beta	Homo sapiens	50-55
12734675-0	2003	Prolonged treatment with imatinib mesylate in patients with advanced chronic myeloid leukemia causes a reduction of bcr/abl mRNA levels independent of cytogenetic response.	imatinib	25-42	BCR activator of RhoGEF and GTPase	Homo sapiens	116-119
12734675-4	2003	These results suggest that bcr/abl mRNA levels may reflect cytogenetic response only during the early phases of imatinib therapy.	imatinib	112-120	BCR activator of RhoGEF and GTPase	Homo sapiens	27-30
12767088-1	2003	BACKGROUND: Imatinib mesylate is a selective tyrosine kinase inhibitor of c-abl, bcr/abl, c-kit, and platelet-derived growth factor-receptor (PDGF-R).	imatinib	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-79
12576318-0	2003	Several Bcr-Abl kinase domain mutants associated with imatinib mesylate resistance remain sensitive to imatinib.	imatinib	54-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-15
12576318-0	2003	Several Bcr-Abl kinase domain mutants associated with imatinib mesylate resistance remain sensitive to imatinib.	imatinib	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-15
12576318-1	2003	Imatinib mesylate is a selective Bcr-Abl kinase inhibitor, effective in the treatment of chronic myelogenous leukemia.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-40
12576318-4	2003	Many of these mutations decrease the sensitivity of the Abl kinase to imatinib, thus accounting for resistance to imatinib.	imatinib	70-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-59
12576318-4	2003	Many of these mutations decrease the sensitivity of the Abl kinase to imatinib, thus accounting for resistance to imatinib.	imatinib	114-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-59
12576318-7	2003	While some Abl mutations lead to imatinib resistance, many others are significantly, and some fully, inhibited.	imatinib	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-14
12576338-6	2003	It is abolished on exposure of the cells to STI571 and by mutation in the adenosine triphosphate (ATP) pocket of p210 and thus seems to require the tyrosine kinase activity of BCR-ABL.	imatinib	44-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	176-183
12767088-1	2003	BACKGROUND: Imatinib mesylate is a selective tyrosine kinase inhibitor of c-abl, bcr/abl, c-kit, and platelet-derived growth factor-receptor (PDGF-R).	imatinib	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
12767088-1	2003	BACKGROUND: Imatinib mesylate is a selective tyrosine kinase inhibitor of c-abl, bcr/abl, c-kit, and platelet-derived growth factor-receptor (PDGF-R).	imatinib	12-29	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	90-95
12824882-1	2003	STI571, an Abl-specific tyrosine kinase inhibitor, selectively kills Bcr-Abl-containing cells in vitro and in vivo.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-14
12767088-1	2003	BACKGROUND: Imatinib mesylate is a selective tyrosine kinase inhibitor of c-abl, bcr/abl, c-kit, and platelet-derived growth factor-receptor (PDGF-R).	imatinib	12-29	platelet derived growth factor receptor beta	Homo sapiens	101-140
12824882-1	2003	STI571, an Abl-specific tyrosine kinase inhibitor, selectively kills Bcr-Abl-containing cells in vitro and in vivo.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-76
12824882-4	2003	STI571 inhibited the [(125)I]azidoagosterol A-photolabeling of P-gp, but not that of MRP1.	imatinib	0-6	ATP binding cassette subfamily B member 1	Homo sapiens	63-67
12824882-5	2003	K562/MDR cells that overexpress P-gp were 3.67 times more resistant to STI571 than the parental Philadelphia-chromosome-positive (Ph +) CML K562 cells, and this resistance was most effectively reversed by cepharanthine among the tested reversing agents.	imatinib	71-77	ATP binding cassette subfamily B member 1	Homo sapiens	32-36
12824882-7	2003	In KB-G2 cells that overexpress P-gp, but not Bcr-Abl, 2.5 micro M STI571 partly reversed the resistance to vincristine (VCR), paclitaxel, etoposide (VP-16) and actinomycin D (ACD) but not to Adriamycin (ADM) or colchicine.	imatinib	67-73	ATP binding cassette subfamily B member 1	Homo sapiens	32-36
12824882-10	2003	These findings suggest that STI571 is a substrate for P-gp, but is less efficiently transported by P-gp than VCR, and STI571 is not a substrate for MRP1.	imatinib	28-34	ATP binding cassette subfamily B member 1	Homo sapiens	99-103
12824882-11	2003	Among the tested reversing agents that interact with P-gp, cepharanthine was the most effective agent for the reversal of the resistance to STI571 in K562/MDR cells.	imatinib	140-146	ATP binding cassette subfamily B member 1	Homo sapiens	53-57
12824882-12	2003	Furthermore, STI571 itself was a potent reversing agent for MDR in P-gp-expressing KB-G2 cells.	imatinib	13-19	ATP binding cassette subfamily B member 1	Homo sapiens	67-71
12824882-7	2003	In KB-G2 cells that overexpress P-gp, but not Bcr-Abl, 2.5 micro M STI571 partly reversed the resistance to vincristine (VCR), paclitaxel, etoposide (VP-16) and actinomycin D (ACD) but not to Adriamycin (ADM) or colchicine.	imatinib	67-73	host cell factor C1	Homo sapiens	150-155
12767088-1	2003	BACKGROUND: Imatinib mesylate is a selective tyrosine kinase inhibitor of c-abl, bcr/abl, c-kit, and platelet-derived growth factor-receptor (PDGF-R).	imatinib	12-29	platelet derived growth factor receptor beta	Homo sapiens	142-148
12824882-10	2003	These findings suggest that STI571 is a substrate for P-gp, but is less efficiently transported by P-gp than VCR, and STI571 is not a substrate for MRP1.	imatinib	28-34	ATP binding cassette subfamily B member 1	Homo sapiens	54-58
12796373-1	2003	PURPOSE: Imatinib mesylate is a tyrosine kinase inhibitor with high affinity for the BCR-ABL fusion protein expressed by the hematopoietic cells in chronic myelogenous leukemia (CML).	imatinib	9-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
12901289-4	2003	In preclinical studies, STI571 (Gleevec, imatinib mesylate), a Bcr-Abl tyrosine kinase inhibitor, specifically inhibited the proliferation of Bcr-Abl-expressing cells in vitro and in vivo.	imatinib	24-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
12901289-4	2003	In preclinical studies, STI571 (Gleevec, imatinib mesylate), a Bcr-Abl tyrosine kinase inhibitor, specifically inhibited the proliferation of Bcr-Abl-expressing cells in vitro and in vivo.	imatinib	24-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
12901289-4	2003	In preclinical studies, STI571 (Gleevec, imatinib mesylate), a Bcr-Abl tyrosine kinase inhibitor, specifically inhibited the proliferation of Bcr-Abl-expressing cells in vitro and in vivo.	imatinib	41-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
12901289-4	2003	In preclinical studies, STI571 (Gleevec, imatinib mesylate), a Bcr-Abl tyrosine kinase inhibitor, specifically inhibited the proliferation of Bcr-Abl-expressing cells in vitro and in vivo.	imatinib	41-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
12844407-0	2003	[In vitro effect of STI571 on expression of c-kit in bone marrow cells from patients with acute non-lymphocytic leukemia].	imatinib	20-26	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	44-49
12783584-4	2003	Imatinib mesylate (Gleevec), Glivec, Novartis) is a specific inhibitor of Kit kinase activation and in Phase II clinical trials, it has proven to be remarkably effective in heavily pre-treated patients with advanced GIST.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	74-77
12783584-4	2003	Imatinib mesylate (Gleevec), Glivec, Novartis) is a specific inhibitor of Kit kinase activation and in Phase II clinical trials, it has proven to be remarkably effective in heavily pre-treated patients with advanced GIST.	imatinib	19-26	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	74-77
12764361-0	2003	In BCR-ABL-positive cells, STAT-5 tyrosine-phosphorylation integrates signals induced by imatinib mesylate and Ara-C.	imatinib	89-106	signal transducer and activator of transcription 5A	Homo sapiens	27-33
12764361-3	2003	Here, we investigated the effects of imatinib mesylate and cytosine arabinoside (Ara-C) on STAT-5 tyrosine-phosphorylation, cellular proliferation and induction of apoptosis in cell lines and primary hematopoietic cells.	imatinib	37-54	signal transducer and activator of transcription 5A	Homo sapiens	91-97
12764361-4	2003	Imatinib mesylate treatment strongly suppressed STAT-5 tyrosine-phosphorylation in K562 and primary CML blasts.	imatinib	0-17	signal transducer and activator of transcription 5A	Homo sapiens	48-54
12764361-9	2003	Treatment of K562 cells with Ara-C in combination with imatinib mesylate revealed synergistic effects at the level of STAT-5 tyrosine-phosphorylation and DNA binding, Hck tyrosine-phosphorylation, cell growth and induction of apoptosis.	imatinib	55-72	signal transducer and activator of transcription 5A	Homo sapiens	118-124
12764361-9	2003	Treatment of K562 cells with Ara-C in combination with imatinib mesylate revealed synergistic effects at the level of STAT-5 tyrosine-phosphorylation and DNA binding, Hck tyrosine-phosphorylation, cell growth and induction of apoptosis.	imatinib	55-72	HCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	167-170
12764361-10	2003	Overall, in this report we demonstrate that STAT-5 tyrosine-phosphorylation is a specific target of imatinib mesylate and Ara-C.	imatinib	100-117	signal transducer and activator of transcription 5A	Homo sapiens	44-50
12844407-1	2003	This study was designed to explore the influence of STI571, a tyrosine kinase inhibitor, on the expression of c-kit in the bone marrow cells from patients with acute non-lymphocytic leukemia (ANLL).	imatinib	52-58	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	110-115
12844407-3	2003	The results showed that STI571 treatment induced concentration-dependent decrease of c-kit and CD117 expression, which was significant lower than that in group before treatment and untreated control groups (P < 0.05) and 0.1 micro mol/L STI571 group was significantly higher than that in 10 micro mol/L group (P < 0.05).	imatinib	24-30	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	85-90
12844407-3	2003	The results showed that STI571 treatment induced concentration-dependent decrease of c-kit and CD117 expression, which was significant lower than that in group before treatment and untreated control groups (P < 0.05) and 0.1 micro mol/L STI571 group was significantly higher than that in 10 micro mol/L group (P < 0.05).	imatinib	24-30	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	95-100
12743148-11	2003	Accordingly, the dose of STI-571 required to give a significant ES growth inhibition is much higher than for those tumors in which mutations of c-kit constitute a relevant pathogenetic event.	imatinib	25-32	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	144-149
12672043-7	2003	Imatinib could inhibit the KIT, MAP and Akt phosphorylation of all the transfectants but had a weaker effect on KIT(820Tyr).	imatinib	0-8	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	27-30
12672043-7	2003	Imatinib could inhibit the KIT, MAP and Akt phosphorylation of all the transfectants but had a weaker effect on KIT(820Tyr).	imatinib	0-8	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	112-115
12672043-8	2003	Imatinib potently inhibited the proliferation of cells transfected with KIT(820Tyr) at the concentration of 10 microM whereas it inhibited the other 3 types at 1 microM.	imatinib	0-8	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	72-75
12672043-10	2003	In various types of activating mutant KIT, Imatinib could inhibit the constitutive activation of KIT signal transduction and cell proliferation both in vitro and in vivo although the effect of Imatinib on KIT(820Tyr) was weaker than that on KIT(del559-560) or KIT(642Glu).	imatinib	43-51	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	38-41
12672043-10	2003	In various types of activating mutant KIT, Imatinib could inhibit the constitutive activation of KIT signal transduction and cell proliferation both in vitro and in vivo although the effect of Imatinib on KIT(820Tyr) was weaker than that on KIT(del559-560) or KIT(642Glu).	imatinib	43-51	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	97-100
12672043-10	2003	In various types of activating mutant KIT, Imatinib could inhibit the constitutive activation of KIT signal transduction and cell proliferation both in vitro and in vivo although the effect of Imatinib on KIT(820Tyr) was weaker than that on KIT(del559-560) or KIT(642Glu).	imatinib	43-51	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	97-100
12672043-10	2003	In various types of activating mutant KIT, Imatinib could inhibit the constitutive activation of KIT signal transduction and cell proliferation both in vitro and in vivo although the effect of Imatinib on KIT(820Tyr) was weaker than that on KIT(del559-560) or KIT(642Glu).	imatinib	43-51	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	97-100
12672043-10	2003	In various types of activating mutant KIT, Imatinib could inhibit the constitutive activation of KIT signal transduction and cell proliferation both in vitro and in vivo although the effect of Imatinib on KIT(820Tyr) was weaker than that on KIT(del559-560) or KIT(642Glu).	imatinib	43-51	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	97-100
12743148-7	2003	In vitro growth of ES cell lines showing high levels of c-kit demonstrated limited inhibition by exposure to STI-571 (10 micromol/L is required to obtain 40% to 50% of growth inhibition).	imatinib	109-116	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	56-61
12672043-0	2003	Imatinib inhibits various types of activating mutant kit found in gastrointestinal stromal tumors.	imatinib	0-8	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	53-56
12672043-2	2003	Imatinib has therapeutic potential for GISTs because of its inhibitory effect on KIT kinase activity.	imatinib	0-8	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	81-84
12702540-0	2003	Potential use of imatinib mesylate in ocular melanoma and liposarcoma expressing immunohistochemical c-KIT (CD117).	imatinib	17-34	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	101-106
12702540-0	2003	Potential use of imatinib mesylate in ocular melanoma and liposarcoma expressing immunohistochemical c-KIT (CD117).	imatinib	17-34	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	108-113
12692682-1	2003	Recently, various mutations within the Abl sequence have been described that negatively affect imatinib binding to Bcr/Abl resulting in cellular resistance of chronic myeloid leukemia (CML) cells.	imatinib	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-42
12692682-1	2003	Recently, various mutations within the Abl sequence have been described that negatively affect imatinib binding to Bcr/Abl resulting in cellular resistance of chronic myeloid leukemia (CML) cells.	imatinib	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
12506022-1	2003	Imatinib mesylate (Gleevec), a small molecule inhibitor of abl, kit, and platelet-derived growth factor receptor (PDGFR) tyrosine kinases, has been reported to be effective in the treatment of hypereosinophilic syndrome (HES) and a rare eosinophilia-associated chronic myeloid disorder (eos-CMD) characterized by the t(5;12)(q33;p13) cytogenetic abnormality.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	73-112
12506022-1	2003	Imatinib mesylate (Gleevec), a small molecule inhibitor of abl, kit, and platelet-derived growth factor receptor (PDGFR) tyrosine kinases, has been reported to be effective in the treatment of hypereosinophilic syndrome (HES) and a rare eosinophilia-associated chronic myeloid disorder (eos-CMD) characterized by the t(5;12)(q33;p13) cytogenetic abnormality.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	114-119
12511422-5	2003	Although the ABL-specific tyrosine kinase inhibitor imatinib mesylate (STI-571) had no effect on parental NK92 cells, it markedly decreased the growth and survival of IL-2-independent p210(+) NK92 cells.	imatinib	52-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
12506022-1	2003	Imatinib mesylate (Gleevec), a small molecule inhibitor of abl, kit, and platelet-derived growth factor receptor (PDGFR) tyrosine kinases, has been reported to be effective in the treatment of hypereosinophilic syndrome (HES) and a rare eosinophilia-associated chronic myeloid disorder (eos-CMD) characterized by the t(5;12)(q33;p13) cytogenetic abnormality.	imatinib	19-26	platelet derived growth factor receptor beta	Homo sapiens	73-112
12511422-5	2003	Although the ABL-specific tyrosine kinase inhibitor imatinib mesylate (STI-571) had no effect on parental NK92 cells, it markedly decreased the growth and survival of IL-2-independent p210(+) NK92 cells.	imatinib	52-69	interleukin 2	Homo sapiens	167-171
12511422-5	2003	Although the ABL-specific tyrosine kinase inhibitor imatinib mesylate (STI-571) had no effect on parental NK92 cells, it markedly decreased the growth and survival of IL-2-independent p210(+) NK92 cells.	imatinib	71-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
12506022-1	2003	Imatinib mesylate (Gleevec), a small molecule inhibitor of abl, kit, and platelet-derived growth factor receptor (PDGFR) tyrosine kinases, has been reported to be effective in the treatment of hypereosinophilic syndrome (HES) and a rare eosinophilia-associated chronic myeloid disorder (eos-CMD) characterized by the t(5;12)(q33;p13) cytogenetic abnormality.	imatinib	19-26	platelet derived growth factor receptor beta	Homo sapiens	114-119
12511422-5	2003	Although the ABL-specific tyrosine kinase inhibitor imatinib mesylate (STI-571) had no effect on parental NK92 cells, it markedly decreased the growth and survival of IL-2-independent p210(+) NK92 cells.	imatinib	71-78	interleukin 2	Homo sapiens	167-171
12752093-0	2003	Fluorescence in situ hybridization for the BCR-ABL fusion gene in a patient with imatinib mesylate-resistant chronic myelogenous leukaemia in extramedullary blast crisis.	imatinib	81-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
12727828-0	2003	Histone deacetylase inhibitors promote STI571-mediated apoptosis in STI571-sensitive and -resistant Bcr/Abl+ human myeloid leukemia cells.	imatinib	39-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
12752112-0	2003	Cross-resistance of imatinib mesylate and 17-AAG in imatinib-resistant cells that overexpress BCR-ABL.	imatinib	20-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
12752112-0	2003	Cross-resistance of imatinib mesylate and 17-AAG in imatinib-resistant cells that overexpress BCR-ABL.	imatinib	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
12727828-0	2003	Histone deacetylase inhibitors promote STI571-mediated apoptosis in STI571-sensitive and -resistant Bcr/Abl+ human myeloid leukemia cells.	imatinib	68-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
12727828-2	2003	Cotreatment of K562 cells with 250 nM imatinib mesylate and 2.0 micro M suberoylanilide hydroxamic acid (SAHA) for 24 h, exposures that were minimally toxic alone, resulted in a marked increase in mitochondrial damage (e.g., cytochrome c, Smac/DIABLO, and apoptosis-inducing factor release), caspase activation, and apoptosis.	imatinib	38-55	cytochrome c, somatic	Homo sapiens	225-237
12727828-2	2003	Cotreatment of K562 cells with 250 nM imatinib mesylate and 2.0 micro M suberoylanilide hydroxamic acid (SAHA) for 24 h, exposures that were minimally toxic alone, resulted in a marked increase in mitochondrial damage (e.g., cytochrome c, Smac/DIABLO, and apoptosis-inducing factor release), caspase activation, and apoptosis.	imatinib	38-55	diablo IAP-binding mitochondrial protein	Homo sapiens	239-243
12781364-0	2003	PKC412 overcomes resistance to imatinib in a murine model of FIP1L1-PDGFRalpha-induced myeloproliferative disease.	imatinib	31-39	FIP1 like 1 (S. cerevisiae)	Mus musculus	61-67
12781364-1	2003	FIP1L1-PDGFRalpha causes hypereosinophilic syndrome (HES) and is inhibited by the tyrosine kinase inhibitor imatinib (Gleevec).	imatinib	108-116	FIP1 like 1 (S. cerevisiae)	Mus musculus	0-6
12727828-2	2003	Cotreatment of K562 cells with 250 nM imatinib mesylate and 2.0 micro M suberoylanilide hydroxamic acid (SAHA) for 24 h, exposures that were minimally toxic alone, resulted in a marked increase in mitochondrial damage (e.g., cytochrome c, Smac/DIABLO, and apoptosis-inducing factor release), caspase activation, and apoptosis.	imatinib	38-55	diablo IAP-binding mitochondrial protein	Homo sapiens	244-250
12781364-1	2003	FIP1L1-PDGFRalpha causes hypereosinophilic syndrome (HES) and is inhibited by the tyrosine kinase inhibitor imatinib (Gleevec).	imatinib	108-116	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	7-17
12781364-1	2003	FIP1L1-PDGFRalpha causes hypereosinophilic syndrome (HES) and is inhibited by the tyrosine kinase inhibitor imatinib (Gleevec).	imatinib	118-125	FIP1 like 1 (S. cerevisiae)	Mus musculus	0-6
12727828-6	2003	STI571 and SAHA also interacted synergistically to induce apoptosis in STI571-resistant K562 and LAMA 84 cells that display increased Bcr/Abl protein expression.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
12781364-1	2003	FIP1L1-PDGFRalpha causes hypereosinophilic syndrome (HES) and is inhibited by the tyrosine kinase inhibitor imatinib (Gleevec).	imatinib	118-125	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	7-17
12781364-2	2003	Imatinib is a potent inhibitor of ABL, ARG, PDGFRalpha, PDGFRbeta, and KIT and induces durable hematologic responses in HES patients.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-37
12728257-3	2003	A rational drug development produced a specific inhibitor of the catalytic activity of Bcr-Abl called STI571.	imatinib	102-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
12781364-2	2003	Imatinib is a potent inhibitor of ABL, ARG, PDGFRalpha, PDGFRbeta, and KIT and induces durable hematologic responses in HES patients.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	44-54
12727828-6	2003	STI571 and SAHA also interacted synergistically to induce apoptosis in STI571-resistant K562 and LAMA 84 cells that display increased Bcr/Abl protein expression.	imatinib	71-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
12781364-2	2003	Imatinib is a potent inhibitor of ABL, ARG, PDGFRalpha, PDGFRbeta, and KIT and induces durable hematologic responses in HES patients.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	56-65
12781364-2	2003	Imatinib is a potent inhibitor of ABL, ARG, PDGFRalpha, PDGFRbeta, and KIT and induces durable hematologic responses in HES patients.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	71-74
12728257-5	2003	In the study described here, Bcr-Abl-positive cells treated with tyrosine-kinase inhibitors such as herbimycin A, genistein or STI571 lost their phosphotyrosine-containing proteins, but were still extremely resistant to apoptosis.	imatinib	127-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
12727828-7	2003	Lastly, inducible expression of a constitutively active MEK1/2 construct significantly attenuated SAHA/STI571-mediated apoptosis in K562 cells, implicating disruption of the Raf/MEK/ERK axis in synergistic antileukemic effects of this drug combination.	imatinib	103-109	mitogen-activated protein kinase kinase 1	Homo sapiens	56-62
12781364-3	2003	However, we observed relapse with resistance to imatinib as consequence of a T674I mutation in FIP1L1-PDGFRalpha, analogous to the imatinib-resistant T315I mutation in BCR-ABL.	imatinib	48-56	FIP1 like 1 (S. cerevisiae)	Mus musculus	95-101
12781364-3	2003	However, we observed relapse with resistance to imatinib as consequence of a T674I mutation in FIP1L1-PDGFRalpha, analogous to the imatinib-resistant T315I mutation in BCR-ABL.	imatinib	48-56	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	102-112
12781364-3	2003	However, we observed relapse with resistance to imatinib as consequence of a T674I mutation in FIP1L1-PDGFRalpha, analogous to the imatinib-resistant T315I mutation in BCR-ABL.	imatinib	131-139	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	102-112
12727828-7	2003	Lastly, inducible expression of a constitutively active MEK1/2 construct significantly attenuated SAHA/STI571-mediated apoptosis in K562 cells, implicating disruption of the Raf/MEK/ERK axis in synergistic antileukemic effects of this drug combination.	imatinib	103-109	zinc fingers and homeoboxes 2	Homo sapiens	174-177
12727828-7	2003	Lastly, inducible expression of a constitutively active MEK1/2 construct significantly attenuated SAHA/STI571-mediated apoptosis in K562 cells, implicating disruption of the Raf/MEK/ERK axis in synergistic antileukemic effects of this drug combination.	imatinib	103-109	mitogen-activated protein kinase kinase 7	Homo sapiens	56-59
12727828-8	2003	Together, these findings indicate that combined exposure of Bcr/Abl(+) cells to the kinase inhibitor STI571 and HDIs leads to diverse perturbations in signaling and cell cycle-regulatory proteins, associated with a marked increase in mitochondrial damage and cell death.	imatinib	101-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
12706873-0	2003	Tyrosine kinase inhibitor STI-571/Gleevec down-regulates the beta-catenin signaling activity.	imatinib	26-33	catenin beta 1	Homo sapiens	61-73
12714574-0	2003	Imatinib restores expression of CD62L in BCR-ABL-positive cells.	imatinib	0-8	selectin L	Homo sapiens	32-37
12714574-0	2003	Imatinib restores expression of CD62L in BCR-ABL-positive cells.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
12714574-4	2003	Following addition of the Abelson (ABL) tyrosine kinase inhibitor imatinib (formerly STI571) to two BCR-ABL-positive cell lines (BV173, SD-1), we observed a dose-dependent increase in CD62L RNA levels of up to 45-fold by a quantitative, real-time polymerase chain reaction and an increase in the amount of cell surface-bound CD62L of up to 18-fold by quantitative flow cytometry, respectively.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
12714574-4	2003	Following addition of the Abelson (ABL) tyrosine kinase inhibitor imatinib (formerly STI571) to two BCR-ABL-positive cell lines (BV173, SD-1), we observed a dose-dependent increase in CD62L RNA levels of up to 45-fold by a quantitative, real-time polymerase chain reaction and an increase in the amount of cell surface-bound CD62L of up to 18-fold by quantitative flow cytometry, respectively.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
12714574-4	2003	Following addition of the Abelson (ABL) tyrosine kinase inhibitor imatinib (formerly STI571) to two BCR-ABL-positive cell lines (BV173, SD-1), we observed a dose-dependent increase in CD62L RNA levels of up to 45-fold by a quantitative, real-time polymerase chain reaction and an increase in the amount of cell surface-bound CD62L of up to 18-fold by quantitative flow cytometry, respectively.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
12714574-4	2003	Following addition of the Abelson (ABL) tyrosine kinase inhibitor imatinib (formerly STI571) to two BCR-ABL-positive cell lines (BV173, SD-1), we observed a dose-dependent increase in CD62L RNA levels of up to 45-fold by a quantitative, real-time polymerase chain reaction and an increase in the amount of cell surface-bound CD62L of up to 18-fold by quantitative flow cytometry, respectively.	imatinib	66-74	selectin L	Homo sapiens	184-189
12714574-4	2003	Following addition of the Abelson (ABL) tyrosine kinase inhibitor imatinib (formerly STI571) to two BCR-ABL-positive cell lines (BV173, SD-1), we observed a dose-dependent increase in CD62L RNA levels of up to 45-fold by a quantitative, real-time polymerase chain reaction and an increase in the amount of cell surface-bound CD62L of up to 18-fold by quantitative flow cytometry, respectively.	imatinib	66-74	selectin L	Homo sapiens	325-330
12714574-4	2003	Following addition of the Abelson (ABL) tyrosine kinase inhibitor imatinib (formerly STI571) to two BCR-ABL-positive cell lines (BV173, SD-1), we observed a dose-dependent increase in CD62L RNA levels of up to 45-fold by a quantitative, real-time polymerase chain reaction and an increase in the amount of cell surface-bound CD62L of up to 18-fold by quantitative flow cytometry, respectively.	imatinib	85-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
12714574-4	2003	Following addition of the Abelson (ABL) tyrosine kinase inhibitor imatinib (formerly STI571) to two BCR-ABL-positive cell lines (BV173, SD-1), we observed a dose-dependent increase in CD62L RNA levels of up to 45-fold by a quantitative, real-time polymerase chain reaction and an increase in the amount of cell surface-bound CD62L of up to 18-fold by quantitative flow cytometry, respectively.	imatinib	85-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
12714574-4	2003	Following addition of the Abelson (ABL) tyrosine kinase inhibitor imatinib (formerly STI571) to two BCR-ABL-positive cell lines (BV173, SD-1), we observed a dose-dependent increase in CD62L RNA levels of up to 45-fold by a quantitative, real-time polymerase chain reaction and an increase in the amount of cell surface-bound CD62L of up to 18-fold by quantitative flow cytometry, respectively.	imatinib	85-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
12714574-4	2003	Following addition of the Abelson (ABL) tyrosine kinase inhibitor imatinib (formerly STI571) to two BCR-ABL-positive cell lines (BV173, SD-1), we observed a dose-dependent increase in CD62L RNA levels of up to 45-fold by a quantitative, real-time polymerase chain reaction and an increase in the amount of cell surface-bound CD62L of up to 18-fold by quantitative flow cytometry, respectively.	imatinib	85-91	selectin L	Homo sapiens	184-189
12714574-4	2003	Following addition of the Abelson (ABL) tyrosine kinase inhibitor imatinib (formerly STI571) to two BCR-ABL-positive cell lines (BV173, SD-1), we observed a dose-dependent increase in CD62L RNA levels of up to 45-fold by a quantitative, real-time polymerase chain reaction and an increase in the amount of cell surface-bound CD62L of up to 18-fold by quantitative flow cytometry, respectively.	imatinib	85-91	selectin L	Homo sapiens	325-330
12714574-5	2003	These data are validated by an increased CD62L expression in the bone marrow of patients (n=6) with advanced CML who received imatinib.	imatinib	126-134	selectin L	Homo sapiens	41-46
12714574-6	2003	Restoration of defective cell adhesion mediated via the CD62L pathway may be one mechanism of action of imatinib in BCR-ABL-positive leukemias.	imatinib	104-112	selectin L	Homo sapiens	56-61
12714574-6	2003	Restoration of defective cell adhesion mediated via the CD62L pathway may be one mechanism of action of imatinib in BCR-ABL-positive leukemias.	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
12739051-8	2003	Imatinib (STI571/Glivec) is a selective inhibitor of BCR/ABL, PDGFR and KIT receptor-tyrosine kinases.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	62-67
12739051-8	2003	Imatinib (STI571/Glivec) is a selective inhibitor of BCR/ABL, PDGFR and KIT receptor-tyrosine kinases.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	72-75
12759750-7	2003	STI-571 (imatinib mesylate) is a molecule that inhibits the function of various receptors with tyrosine kinase activity, such as abl, the bcr-abl chimeric product, platelet-derived growth factor receptor, and KIT.	imatinib	9-26	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	209-212
12594213-2	2003	Clinical resistance formation to the BCR-ABL inhibitor STI571 has been observed in patients with advanced chronic myeloid leukemia and was frequently caused by a C to T single nucleotide change in the Abl kinase domain, which substituted Thr-315 with isoleucine and rendered BCR-ABL resistant to STI571 inhibition.	imatinib	55-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
12594213-2	2003	Clinical resistance formation to the BCR-ABL inhibitor STI571 has been observed in patients with advanced chronic myeloid leukemia and was frequently caused by a C to T single nucleotide change in the Abl kinase domain, which substituted Thr-315 with isoleucine and rendered BCR-ABL resistant to STI571 inhibition.	imatinib	55-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	275-282
12594213-2	2003	Clinical resistance formation to the BCR-ABL inhibitor STI571 has been observed in patients with advanced chronic myeloid leukemia and was frequently caused by a C to T single nucleotide change in the Abl kinase domain, which substituted Thr-315 with isoleucine and rendered BCR-ABL resistant to STI571 inhibition.	imatinib	296-302	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
12750693-6	2003	Alternatively, leukemia cells that harbor secondary genetic alterations resulting in Bcr-Abl-independent proliferation are selected for their growth advantage in the presence of imatinib.	imatinib	178-186	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
12750693-7	2003	Point mutations in the BCR-ABL kinase domain prevent binding of imatinib but still allow binding of ATP, thus retaining Bcr-Abl kinase activity.	imatinib	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
12750693-8	2003	Mutated BCR-ABL is frequently detected in cases of imatinib-resistant Ph+ leukemia and therefore represents the main challenge for the investigation of alternative strategies to either overcome resistance or to prevent the emergence of a resistant leukemic clone.	imatinib	51-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-15
12748309-4	2003	The biological significance of KIT inhibition was evaluated in vivo by treating mice bearing s.c. NCI-H526 tumors with SU11248 or another structurally unrelated KIT inhibitor, STI571 (Gleevec), which is also known to inhibit Bcr-Abl and PDGFRbeta.	imatinib	176-182	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	31-34
12748309-7	2003	Likewise, phospho-PDGFRbeta levels contributed by tumor stroma and with known involvement in angiogenesis were strongly inhibited by SU11248 and less so by STI571.	imatinib	156-162	platelet derived growth factor receptor beta	Homo sapiens	18-27
12739051-8	2003	Imatinib (STI571/Glivec) is a selective inhibitor of BCR/ABL, PDGFR and KIT receptor-tyrosine kinases.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
12759750-7	2003	STI-571 (imatinib mesylate) is a molecule that inhibits the function of various receptors with tyrosine kinase activity, such as abl, the bcr-abl chimeric product, platelet-derived growth factor receptor, and KIT.	imatinib	0-7	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	209-212
12706873-3	2003	In this report, we investigated whether tyrosine kinase inhibitor STI-571 could inhibit the beta-catenin signaling activity and hence suppress cell proliferation.	imatinib	66-73	catenin beta 1	Homo sapiens	92-104
12706873-4	2003	Our results demonstrated that STI-571 effectively inhibited the constitutive activity of beta-catenin signaling in human colon cancer cells as well as the Wnt1-induced activation of beta-catenin signaling in HOS, HTB-94, and HEK 293 cells.	imatinib	30-37	catenin beta 1	Homo sapiens	89-101
12706873-4	2003	Our results demonstrated that STI-571 effectively inhibited the constitutive activity of beta-catenin signaling in human colon cancer cells as well as the Wnt1-induced activation of beta-catenin signaling in HOS, HTB-94, and HEK 293 cells.	imatinib	30-37	Wnt family member 1	Homo sapiens	155-159
12679736-9	2003	As c-KIT was expressed in 78% of the pancreatic IDCs, it suggests that STI571 may be a beneficial agent for chemotherapy against human pancreatic IDCs.	imatinib	71-77	steroid sulfatase	Homo sapiens	0-4
12446442-0	2003	Cotreatment with the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) enhances imatinib-induced apoptosis of Bcr-Abl-positive human acute leukemia cells.	imatinib	99-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
12446442-2	2003	Cotreatment with SAHA and imatinib (Gleevec) caused more down-regulation of the levels and auto-tyrosine phosphorylation of Bcr-Abl and apoptosis of these cell types, as compared with treatment with either agent alone (P <.05).	imatinib	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
12480706-1	2003	Imatinib mesylate, a tyrosine kinase inhibitor targeting bcr-abl, platelet-derived growth factor receptor (PDGF-R), and c-Kit, effectively induces hematologic and cytogenetic remissions in bcr-abl(+) chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL) with only mild to moderate side effects.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	66-105
12480706-1	2003	Imatinib mesylate, a tyrosine kinase inhibitor targeting bcr-abl, platelet-derived growth factor receptor (PDGF-R), and c-Kit, effectively induces hematologic and cytogenetic remissions in bcr-abl(+) chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL) with only mild to moderate side effects.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	107-113
12480706-1	2003	Imatinib mesylate, a tyrosine kinase inhibitor targeting bcr-abl, platelet-derived growth factor receptor (PDGF-R), and c-Kit, effectively induces hematologic and cytogenetic remissions in bcr-abl(+) chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL) with only mild to moderate side effects.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	120-125
12679736-9	2003	As c-KIT was expressed in 78% of the pancreatic IDCs, it suggests that STI571 may be a beneficial agent for chemotherapy against human pancreatic IDCs.	imatinib	71-77	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	5-8
12651205-1	2003	Previous studies have shown that STI571, a selective tyrosine kinase inhibitor of c-KIT, is highly effective in c-KIT/CD117-positive gastrointestinal stromal tumours (GIST), especially those that have activating mutations in the c-kit exon 11 that encodes the juxtamembrane (JM) domain of the c-KIT oncoprotein.	imatinib	33-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	82-87
12824897-6	2003	Imatinib mesylate inhibits BCR-ABL fused tyrosine kinase that causes CML.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
12824897-7	2003	Imatinib mesylate also inhibits the mutated KIT observed in most GISTs, and this explains the effectiveness of Imatinib mesylate on GISTs.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	44-47
12824897-7	2003	Imatinib mesylate also inhibits the mutated KIT observed in most GISTs, and this explains the effectiveness of Imatinib mesylate on GISTs.	imatinib	111-128	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	44-47
12684394-1	2003	Inhibition of the constitutively active Bcr-abl tyrosine kinase(TK) by STI571 has proven to be a highly effective treatment for chronic myelogenous leukemia (CML).	imatinib	71-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
12651205-1	2003	Previous studies have shown that STI571, a selective tyrosine kinase inhibitor of c-KIT, is highly effective in c-KIT/CD117-positive gastrointestinal stromal tumours (GIST), especially those that have activating mutations in the c-kit exon 11 that encodes the juxtamembrane (JM) domain of the c-KIT oncoprotein.	imatinib	33-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	112-117
12656746-1	2003	Imatinib (glivec), formerly known as STI571) effectively blocks the ATP-binding site of the bcr/abl fusion protein thereby inactivating selectively the tyrosine kinase activity of bcr/abl.	imatinib	0-8	BCR activator of RhoGEF and GTPase	Homo sapiens	92-95
12651205-1	2003	Previous studies have shown that STI571, a selective tyrosine kinase inhibitor of c-KIT, is highly effective in c-KIT/CD117-positive gastrointestinal stromal tumours (GIST), especially those that have activating mutations in the c-kit exon 11 that encodes the juxtamembrane (JM) domain of the c-KIT oncoprotein.	imatinib	33-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	118-123
12656746-1	2003	Imatinib (glivec), formerly known as STI571) effectively blocks the ATP-binding site of the bcr/abl fusion protein thereby inactivating selectively the tyrosine kinase activity of bcr/abl.	imatinib	0-8	BCR activator of RhoGEF and GTPase	Homo sapiens	180-183
12656746-1	2003	Imatinib (glivec), formerly known as STI571) effectively blocks the ATP-binding site of the bcr/abl fusion protein thereby inactivating selectively the tyrosine kinase activity of bcr/abl.	imatinib	37-43	BCR activator of RhoGEF and GTPase	Homo sapiens	92-95
12651205-1	2003	Previous studies have shown that STI571, a selective tyrosine kinase inhibitor of c-KIT, is highly effective in c-KIT/CD117-positive gastrointestinal stromal tumours (GIST), especially those that have activating mutations in the c-kit exon 11 that encodes the juxtamembrane (JM) domain of the c-KIT oncoprotein.	imatinib	33-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	229-234
12656746-1	2003	Imatinib (glivec), formerly known as STI571) effectively blocks the ATP-binding site of the bcr/abl fusion protein thereby inactivating selectively the tyrosine kinase activity of bcr/abl.	imatinib	37-43	BCR activator of RhoGEF and GTPase	Homo sapiens	180-183
12651205-1	2003	Previous studies have shown that STI571, a selective tyrosine kinase inhibitor of c-KIT, is highly effective in c-KIT/CD117-positive gastrointestinal stromal tumours (GIST), especially those that have activating mutations in the c-kit exon 11 that encodes the juxtamembrane (JM) domain of the c-KIT oncoprotein.	imatinib	33-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	112-117
12656747-0	2003	Double minutes containing amplified bcr-abl fusion gene in a case of chronic myeloid leukemia treated by imatinib.	imatinib	105-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
12656747-1	2003	Amplification of the bcr-abl fusion gene has recently been associated with resistance to imatinib therapy in chronic myeloid leukemia (CML).	imatinib	89-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
12681968-3	2003	The expression of PDGFRbeta fusions in CMML could have therapeutic relevance, as PDGFRb is inhibited by the selective tyrosine kinase inhibitor, imatinib.	imatinib	145-153	platelet derived growth factor receptor beta	Homo sapiens	18-27
12681968-3	2003	The expression of PDGFRbeta fusions in CMML could have therapeutic relevance, as PDGFRb is inhibited by the selective tyrosine kinase inhibitor, imatinib.	imatinib	145-153	platelet derived growth factor receptor beta	Homo sapiens	18-24
12681968-5	2003	DESIGN AND METHODS: We assessed the effect of imatinib on TEL/PDGFRbeta transformed cells in terms of proliferation, by trypan blue exclusion and 3H-thymidine uptake, and TEL/PDGFRbeta autophosphorylation by anti-phosphotyrosine immunoblotting.	imatinib	46-54	ETS variant transcription factor 6	Homo sapiens	58-61
12681968-5	2003	DESIGN AND METHODS: We assessed the effect of imatinib on TEL/PDGFRbeta transformed cells in terms of proliferation, by trypan blue exclusion and 3H-thymidine uptake, and TEL/PDGFRbeta autophosphorylation by anti-phosphotyrosine immunoblotting.	imatinib	46-54	platelet derived growth factor receptor beta	Homo sapiens	62-71
12681968-7	2003	RESULTS: Imatinib potently inhibited the proliferation of TEL/PDGFRbeta transformed cells (IC50=7.5 nM), and TEL/PDGFRbeta kinase activity.	imatinib	9-17	ETS variant transcription factor 6	Homo sapiens	58-61
12681968-7	2003	RESULTS: Imatinib potently inhibited the proliferation of TEL/PDGFRbeta transformed cells (IC50=7.5 nM), and TEL/PDGFRbeta kinase activity.	imatinib	9-17	platelet derived growth factor receptor beta	Homo sapiens	62-71
12681968-7	2003	RESULTS: Imatinib potently inhibited the proliferation of TEL/PDGFRbeta transformed cells (IC50=7.5 nM), and TEL/PDGFRbeta kinase activity.	imatinib	9-17	ETS variant transcription factor 6	Homo sapiens	109-112
12681968-10	2003	INTERPRETATION AND CONCLUSIONS: Although imatinib represents an attractive therapeutic agent for neoplasias associated with abnormal PDGFRbeta signaling, the low frequency of the TEL/PDGFRbeta and Hip1/PDGFRbeta fusion proteins in CMML suggests that its application to this disease maybe limited.	imatinib	41-49	platelet derived growth factor receptor beta	Homo sapiens	133-142
12679488-8	2003	Taken together, these results suggest that selective suppression of c-ABL activity by STI571 may represent a potential anticancer strategy for p53-mutated undifferentiated thyroid carcinomas.	imatinib	86-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-73
12679488-8	2003	Taken together, these results suggest that selective suppression of c-ABL activity by STI571 may represent a potential anticancer strategy for p53-mutated undifferentiated thyroid carcinomas.	imatinib	86-92	tumor protein p53	Homo sapiens	143-146
12682643-0	2003	G-CSF for imatinib-induced neutropenia.	imatinib	10-18	colony stimulating factor 3	Homo sapiens	0-5
12660384-3	2003	Recent reports of responses to imatinib in patients with the syndrome suggested that an activated kinase such as ABL, platelet-derived growth factor receptor (PDGFR), or KIT, all of which are inhibited by imatinib, might be the cause.	imatinib	205-213	platelet derived growth factor receptor beta	Homo sapiens	159-164
12669727-4	2003	(2) Imatinib inhibits tyrosine kinase, an enzyme encoded by the pathological gene BCR-ABL, which is created during a reverse translocation between chromosomes 9 and 22 (characteristic of chronic myeloid leukaemia).	imatinib	4-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
12669727-11	2003	Some patients developed relapses resistant to imatinib, owing to mutations in the BCR-ABL gene.	imatinib	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
12654249-0	2003	Mechanisms of autoinhibition and STI-571/imatinib resistance revealed by mutagenesis of BCR-ABL.	imatinib	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
12660384-0	2003	A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome.	imatinib	94-102	platelet derived growth factor receptor alpha	Homo sapiens	43-49
12660384-0	2003	A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome.	imatinib	94-102	factor interacting with PAPOLA and CPSF1	Homo sapiens	54-60
12660384-3	2003	Recent reports of responses to imatinib in patients with the syndrome suggested that an activated kinase such as ABL, platelet-derived growth factor receptor (PDGFR), or KIT, all of which are inhibited by imatinib, might be the cause.	imatinib	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-116
12660384-3	2003	Recent reports of responses to imatinib in patients with the syndrome suggested that an activated kinase such as ABL, platelet-derived growth factor receptor (PDGFR), or KIT, all of which are inhibited by imatinib, might be the cause.	imatinib	31-39	platelet derived growth factor receptor beta	Homo sapiens	118-157
12660384-3	2003	Recent reports of responses to imatinib in patients with the syndrome suggested that an activated kinase such as ABL, platelet-derived growth factor receptor (PDGFR), or KIT, all of which are inhibited by imatinib, might be the cause.	imatinib	31-39	platelet derived growth factor receptor beta	Homo sapiens	159-164
12660384-3	2003	Recent reports of responses to imatinib in patients with the syndrome suggested that an activated kinase such as ABL, platelet-derived growth factor receptor (PDGFR), or KIT, all of which are inhibited by imatinib, might be the cause.	imatinib	31-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	170-173
12660384-3	2003	Recent reports of responses to imatinib in patients with the syndrome suggested that an activated kinase such as ABL, platelet-derived growth factor receptor (PDGFR), or KIT, all of which are inhibited by imatinib, might be the cause.	imatinib	205-213	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-116
12660384-3	2003	Recent reports of responses to imatinib in patients with the syndrome suggested that an activated kinase such as ABL, platelet-derived growth factor receptor (PDGFR), or KIT, all of which are inhibited by imatinib, might be the cause.	imatinib	205-213	platelet derived growth factor receptor beta	Homo sapiens	118-157
12660384-3	2003	Recent reports of responses to imatinib in patients with the syndrome suggested that an activated kinase such as ABL, platelet-derived growth factor receptor (PDGFR), or KIT, all of which are inhibited by imatinib, might be the cause.	imatinib	205-213	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	170-173
12660384-7	2003	FIP1L1-PDGFRalpha is a constitutively activated tyrosine kinase that transforms hematopoietic cells and is inhibited by imatinib (50 percent inhibitory concentration, 3.2 nM).	imatinib	120-128	factor interacting with PAPOLA and CPSF1	Homo sapiens	0-6
12660384-7	2003	FIP1L1-PDGFRalpha is a constitutively activated tyrosine kinase that transforms hematopoietic cells and is inhibited by imatinib (50 percent inhibitory concentration, 3.2 nM).	imatinib	120-128	platelet derived growth factor receptor alpha	Homo sapiens	7-17
12660384-8	2003	The FIP1L1-PDGFRA fusion gene was subsequently detected in 9 of 16 patients with the syndrome and in 5 of the 9 patients with responses to imatinib that lasted more than three months.	imatinib	139-147	factor interacting with PAPOLA and CPSF1	Homo sapiens	4-10
12660384-8	2003	The FIP1L1-PDGFRA fusion gene was subsequently detected in 9 of 16 patients with the syndrome and in 5 of the 9 patients with responses to imatinib that lasted more than three months.	imatinib	139-147	platelet derived growth factor receptor alpha	Homo sapiens	11-17
12660384-9	2003	Relapse in one patient correlated with the appearance of a T674I mutation in PDGFRA that confers resistance to imatinib.	imatinib	111-119	platelet derived growth factor receptor alpha	Homo sapiens	77-83
12660384-11	2003	The acquisition of a T674I resistance mutation at the time of relapse demonstrates that FIP1L1-PDGFRalpha is the target of imatinib.	imatinib	123-131	factor interacting with PAPOLA and CPSF1	Homo sapiens	88-94
12660384-11	2003	The acquisition of a T674I resistance mutation at the time of relapse demonstrates that FIP1L1-PDGFRalpha is the target of imatinib.	imatinib	123-131	platelet derived growth factor receptor alpha	Homo sapiens	95-105
12654249-1	2003	The Bcr-Abl fusion protein kinase causes chronic myeloid leukemia and is targeted by the signal transduction inhibitor STI-571/Gleevec/imatinib (STI-571).	imatinib	119-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
12654249-1	2003	The Bcr-Abl fusion protein kinase causes chronic myeloid leukemia and is targeted by the signal transduction inhibitor STI-571/Gleevec/imatinib (STI-571).	imatinib	127-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
12654249-1	2003	The Bcr-Abl fusion protein kinase causes chronic myeloid leukemia and is targeted by the signal transduction inhibitor STI-571/Gleevec/imatinib (STI-571).	imatinib	135-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
12654249-1	2003	The Bcr-Abl fusion protein kinase causes chronic myeloid leukemia and is targeted by the signal transduction inhibitor STI-571/Gleevec/imatinib (STI-571).	imatinib	145-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
12654250-4	2003	Ligand-activated c-Abl is particularly sensitive to the anti-cancer drug STI-571/Gleevec/imatinib (STI-571).	imatinib	89-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-22
12654251-4	2003	Autoinhibited c-Abl forms an assembly that is strikingly similar to that of inactive Src kinases but with specific differences that explain the differential ability of the drug STI-571/Gleevec/imatinib (STI-571) to inhibit the catalytic activity of Abl, but not that of c-Src.	imatinib	177-184	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
12654251-4	2003	Autoinhibited c-Abl forms an assembly that is strikingly similar to that of inactive Src kinases but with specific differences that explain the differential ability of the drug STI-571/Gleevec/imatinib (STI-571) to inhibit the catalytic activity of Abl, but not that of c-Src.	imatinib	177-184	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-19
12644539-2	2003	The tyrosine kinase inhibitor STI571 blocks the PDGF signaling pathway by inhibiting PDGF-R autophosphorylation.	imatinib	30-36	platelet derived growth factor receptor, beta polypeptide	Mus musculus	85-91
12654251-4	2003	Autoinhibited c-Abl forms an assembly that is strikingly similar to that of inactive Src kinases but with specific differences that explain the differential ability of the drug STI-571/Gleevec/imatinib (STI-571) to inhibit the catalytic activity of Abl, but not that of c-Src.	imatinib	177-184	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	270-275
12644539-10	2003	RESULTS: PC-3MM2 cells cultured from bone lesions and treated in vitro with STI571 had less phosphorylated PDGF-R than untreated cells.	imatinib	76-82	platelet derived growth factor receptor, beta polypeptide	Mus musculus	107-113
12644539-14	2003	Mice treated with STI571 or STI571 plus paclitaxel had less phosphorylated PDGF-R on tumor cells and tumor-associated endothelial cells, less tumor cell proliferation, statistically significantly more apoptotic tumor cells (all P<.001), and fewer tumor-associated endothelial cells (P<.001) than control mice.	imatinib	18-24	platelet derived growth factor receptor, beta polypeptide	Mus musculus	75-81
12654251-4	2003	Autoinhibited c-Abl forms an assembly that is strikingly similar to that of inactive Src kinases but with specific differences that explain the differential ability of the drug STI-571/Gleevec/imatinib (STI-571) to inhibit the catalytic activity of Abl, but not that of c-Src.	imatinib	193-201	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
12644539-14	2003	Mice treated with STI571 or STI571 plus paclitaxel had less phosphorylated PDGF-R on tumor cells and tumor-associated endothelial cells, less tumor cell proliferation, statistically significantly more apoptotic tumor cells (all P<.001), and fewer tumor-associated endothelial cells (P<.001) than control mice.	imatinib	28-34	platelet derived growth factor receptor, beta polypeptide	Mus musculus	75-81
12644539-16	2003	Using STI571 to inhibit PDGF-R phosphorylation may, especially in combination with paclitaxel, produce substantial therapeutic effects against prostate cancer bone metastasis.	imatinib	6-12	platelet derived growth factor receptor, beta polypeptide	Mus musculus	24-30
12654251-4	2003	Autoinhibited c-Abl forms an assembly that is strikingly similar to that of inactive Src kinases but with specific differences that explain the differential ability of the drug STI-571/Gleevec/imatinib (STI-571) to inhibit the catalytic activity of Abl, but not that of c-Src.	imatinib	193-201	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-19
12783370-1	2003	Imatinib (Gleevec) (formerly STI571) is an orally bioavailable rationally developed inhibitor of the tyrosine kinases Bcr-Abl, Kit, and platelet-derived growth factor receptor (PDGFR).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
12654251-4	2003	Autoinhibited c-Abl forms an assembly that is strikingly similar to that of inactive Src kinases but with specific differences that explain the differential ability of the drug STI-571/Gleevec/imatinib (STI-571) to inhibit the catalytic activity of Abl, but not that of c-Src.	imatinib	193-201	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	270-275
12783370-1	2003	Imatinib (Gleevec) (formerly STI571) is an orally bioavailable rationally developed inhibitor of the tyrosine kinases Bcr-Abl, Kit, and platelet-derived growth factor receptor (PDGFR).	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	136-175
12654251-4	2003	Autoinhibited c-Abl forms an assembly that is strikingly similar to that of inactive Src kinases but with specific differences that explain the differential ability of the drug STI-571/Gleevec/imatinib (STI-571) to inhibit the catalytic activity of Abl, but not that of c-Src.	imatinib	203-210	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
12783370-1	2003	Imatinib (Gleevec) (formerly STI571) is an orally bioavailable rationally developed inhibitor of the tyrosine kinases Bcr-Abl, Kit, and platelet-derived growth factor receptor (PDGFR).	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	177-182
12783370-1	2003	Imatinib (Gleevec) (formerly STI571) is an orally bioavailable rationally developed inhibitor of the tyrosine kinases Bcr-Abl, Kit, and platelet-derived growth factor receptor (PDGFR).	imatinib	29-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
12654251-4	2003	Autoinhibited c-Abl forms an assembly that is strikingly similar to that of inactive Src kinases but with specific differences that explain the differential ability of the drug STI-571/Gleevec/imatinib (STI-571) to inhibit the catalytic activity of Abl, but not that of c-Src.	imatinib	203-210	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-19
12783370-1	2003	Imatinib (Gleevec) (formerly STI571) is an orally bioavailable rationally developed inhibitor of the tyrosine kinases Bcr-Abl, Kit, and platelet-derived growth factor receptor (PDGFR).	imatinib	29-35	platelet derived growth factor receptor beta	Homo sapiens	136-175
12783370-1	2003	Imatinib (Gleevec) (formerly STI571) is an orally bioavailable rationally developed inhibitor of the tyrosine kinases Bcr-Abl, Kit, and platelet-derived growth factor receptor (PDGFR).	imatinib	29-35	platelet derived growth factor receptor beta	Homo sapiens	177-182
12406906-0	2003	High levels of BAX, low levels of MRP-1, and high platelets are independent predictors of response to imatinib in myeloid blast crisis of CML.	imatinib	102-110	BCL2 associated X, apoptosis regulator	Homo sapiens	15-18
12654251-4	2003	Autoinhibited c-Abl forms an assembly that is strikingly similar to that of inactive Src kinases but with specific differences that explain the differential ability of the drug STI-571/Gleevec/imatinib (STI-571) to inhibit the catalytic activity of Abl, but not that of c-Src.	imatinib	203-210	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	270-275
12406906-0	2003	High levels of BAX, low levels of MRP-1, and high platelets are independent predictors of response to imatinib in myeloid blast crisis of CML.	imatinib	102-110	ATP binding cassette subfamily C member 1	Homo sapiens	34-39
12406906-6	2003	We show that high levels of BAX, low levels of MRP-1, and a high platelet count are independently predictive of response to imatinib.	imatinib	124-132	BCL2 associated X, apoptosis regulator	Homo sapiens	28-31
12609962-0	2003	MDR1 gene overexpression confers resistance to imatinib mesylate in leukemia cell line models.	imatinib	47-64	ATP binding cassette subfamily B member 1	Homo sapiens	0-4
12406906-6	2003	We show that high levels of BAX, low levels of MRP-1, and a high platelet count are independently predictive of response to imatinib.	imatinib	124-132	ATP binding cassette subfamily C member 1	Homo sapiens	47-52
12783374-3	2003	In fact, the use of real-time polymerase chaine reaction (PCR) to quantitatively measure the WT1 transcript amount may be a predictor of patient response to imatinib therapy.	imatinib	157-165	WT1 transcription factor	Homo sapiens	93-96
12783377-2	2003	Imatinib (Gleevec) (formerly STI571), a potent inhibitor of BCR-ABL, is very effective in inducing CgRs in chronic-phase CML patients, even in late chronic-phase patients in whom interferon (IFN) was unsuccessful.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
12783377-2	2003	Imatinib (Gleevec) (formerly STI571), a potent inhibitor of BCR-ABL, is very effective in inducing CgRs in chronic-phase CML patients, even in late chronic-phase patients in whom interferon (IFN) was unsuccessful.	imatinib	0-8	interferon alpha 1	Homo sapiens	179-195
12783379-1	2003	Selective inhibition of the BCR-ABL tyrosine kinase by imatinib (Gleevec) (formerly STI571) is a promising new therapeutic strategy in patients with chronic myelogenous leukemia (CML).	imatinib	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
12783379-1	2003	Selective inhibition of the BCR-ABL tyrosine kinase by imatinib (Gleevec) (formerly STI571) is a promising new therapeutic strategy in patients with chronic myelogenous leukemia (CML).	imatinib	84-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
12783379-9	2003	Clonal selection of resistant cells harboring a BCR-ABL mutation might be reversed by stopping imatinib therapy and switching to chemotherapy.	imatinib	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
12783380-0	2003	Mutations in the ABL kinase domain pre-exist the onset of imatinib treatment.	imatinib	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-20
12783380-1	2003	Imatinib (Gleevec) (formerly STI571) competitively targets the adenosine 5-triphosphate (ATP) binding site of the kinase domain of ABL and was recently approved for the treatment of chronic myeloid leukemia (CML).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-134
12783380-1	2003	Imatinib (Gleevec) (formerly STI571) competitively targets the adenosine 5-triphosphate (ATP) binding site of the kinase domain of ABL and was recently approved for the treatment of chronic myeloid leukemia (CML).	imatinib	29-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-134
12783380-2	2003	Point mutations occurring in the kinase domain of BCR-ABL have been identified as a cause of imatinib resistance.	imatinib	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
12783380-4	2003	Functional analysis of mutant BCR-ABL alleles in vitro has demonstrated four mutations (Q252H, F317L,M351T, E355G) to confer moderate resistance to imatinib, while T315I-, E255K-, Y253F-, and G250E-expressing cells are markedly resistant.	imatinib	148-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
12783380-6	2003	Another possible explanation for imatinib resistance is that mutated BCR-ABL-expressing cells might pre-exist the onset of treatment at levels below threshold detection (<20%), then expand under selective pressure of imatinib treatment.	imatinib	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
12609962-7	2003	Retroviral-mediated transfection of the BCR-ABL(+) AR230 cell line with the MDR1 gene decreased its sensitivity to imatinib, an effect that was also reversed by verapamil.	imatinib	115-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
12783380-6	2003	Another possible explanation for imatinib resistance is that mutated BCR-ABL-expressing cells might pre-exist the onset of treatment at levels below threshold detection (<20%), then expand under selective pressure of imatinib treatment.	imatinib	220-228	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
12783382-1	2003	Imatinib (Gleevec) (formerly STI571) has been shown to selectively inhibit the tyrosine kinase domain of the oncogenic BCR-ABL fusion protein of chronic myelogenous leukemia (CML) cells.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-126
12609962-7	2003	Retroviral-mediated transfection of the BCR-ABL(+) AR230 cell line with the MDR1 gene decreased its sensitivity to imatinib, an effect that was also reversed by verapamil.	imatinib	115-123	ATP binding cassette subfamily B member 1	Homo sapiens	76-80
12688234-4	2003	A novel promising treatment modality is the selective inhibition of the BCR-ABL tyrosine kinase, by the Signal Transduction inhibitor (STI 571) imatinib mesylate which may cause a high response rate of clinical and cytogenetic remission and raise hope for a possible cure of disease by drug therapy alone.	imatinib	135-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
12784659-4	2003	He was therefore treated with imatinib mesylate, a specific inhibitor of BCR/ABL tyrosine kinase, at a dose of 600 mg/day.	imatinib	30-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-80
12688234-4	2003	A novel promising treatment modality is the selective inhibition of the BCR-ABL tyrosine kinase, by the Signal Transduction inhibitor (STI 571) imatinib mesylate which may cause a high response rate of clinical and cytogenetic remission and raise hope for a possible cure of disease by drug therapy alone.	imatinib	144-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
12475982-5	2003	SCF-induced c-Kit phosphorylation was also inhibited by the related inhibitor 4-amino-5- (4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]-pyrimidine (PP2) and by STI571 but not by the Src inhibitor SU6656.	imatinib	157-163	KIT ligand	Homo sapiens	0-3
12640290-2	2003	This effect is consistent with the inhibitory effect of imatinib mesylate on c-kit"s tyrosine kinase activity as demonstrated by its effectiveness in patients with gastrointestinal stromal tumors.	imatinib	56-73	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	77-82
12610357-1	2003	The presence of c-Kit immunoreactivity in gastrointestinal stromal tumor (GIST), currently guides treatment with the selective c-Kit inhibitor STI571 (or Gleevec) in clinical trials and establishes a precedent of immunohistochemistry-guided treatment decisions.	imatinib	143-149	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	16-21
12610357-1	2003	The presence of c-Kit immunoreactivity in gastrointestinal stromal tumor (GIST), currently guides treatment with the selective c-Kit inhibitor STI571 (or Gleevec) in clinical trials and establishes a precedent of immunohistochemistry-guided treatment decisions.	imatinib	143-149	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	127-132
12648069-2	2003	The peripheral blood BCR-ABL/ABL ratio, as assessed by Q-RT-PCR, has been shown to correlate with the contemporary cytogenetic response in patients receiving imatinib (Glivec, Gleevec).	imatinib	158-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
12648069-2	2003	The peripheral blood BCR-ABL/ABL ratio, as assessed by Q-RT-PCR, has been shown to correlate with the contemporary cytogenetic response in patients receiving imatinib (Glivec, Gleevec).	imatinib	158-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-28
12648069-4	2003	After 4 weeks of imatinib therapy, patients whose BCR-ABL/ABL ratio had fallen to less than 50% that of baseline had a significantly higher probability of achieving a major cytogenetic response after 6 months of therapy, when compared with those whose ratio did not fall by this amount (P < 0.001).	imatinib	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
12648069-4	2003	After 4 weeks of imatinib therapy, patients whose BCR-ABL/ABL ratio had fallen to less than 50% that of baseline had a significantly higher probability of achieving a major cytogenetic response after 6 months of therapy, when compared with those whose ratio did not fall by this amount (P < 0.001).	imatinib	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-57
12648069-9	2003	In conclusion, the data suggest that the early trend in the BCR-ABL/ABL ratio may be clinically useful for the early identification of patients destined to fare poorly on imatinib.	imatinib	171-179	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
12648069-9	2003	In conclusion, the data suggest that the early trend in the BCR-ABL/ABL ratio may be clinically useful for the early identification of patients destined to fare poorly on imatinib.	imatinib	171-179	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-67
12657715-0	2003	Efficacy of SCH66336, a farnesyl transferase inhibitor, in conjunction with imatinib against BCR-ABL-positive cells.	imatinib	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
12657715-3	2003	Imatinib (Novartis, Basel, Switzerland) is a potent and selective inhibitor of the tyrosine kinase activity of BCR-ABL.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
12657715-9	2003	SCH66336 combined with imatinib was shown to induce apoptosis in imatinib-resistant BCR-ABL cells by flow cytometric analysis with an APO2.7 monoclonal antibody.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
12657715-9	2003	SCH66336 combined with imatinib was shown to induce apoptosis in imatinib-resistant BCR-ABL cells by flow cytometric analysis with an APO2.7 monoclonal antibody.	imatinib	23-31	TNF receptor superfamily member 10a	Homo sapiens	134-138
12657715-9	2003	SCH66336 combined with imatinib was shown to induce apoptosis in imatinib-resistant BCR-ABL cells by flow cytometric analysis with an APO2.7 monoclonal antibody.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
12657715-9	2003	SCH66336 combined with imatinib was shown to induce apoptosis in imatinib-resistant BCR-ABL cells by flow cytometric analysis with an APO2.7 monoclonal antibody.	imatinib	65-73	TNF receptor superfamily member 10a	Homo sapiens	134-138
12435730-1	2003	The tyrosine kinase inhibitor STI-571 potently blocks BCR-Abl, platelet-derived growth factor (PDGF) alpha- and beta-receptors, and c-Kit kinase activity.	imatinib	30-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
12435730-1	2003	The tyrosine kinase inhibitor STI-571 potently blocks BCR-Abl, platelet-derived growth factor (PDGF) alpha- and beta-receptors, and c-Kit kinase activity.	imatinib	30-37	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	101-137
12435730-6	2003	Docking of STI-571 into computer models of the PDGFbeta-receptor and Flt3 kinase domains and comparison with the crystal structure of the STI-571 Abl kinase complex indicated very similar binding sites among the three nonphosphorylated kinases, suggesting corresponding courses of their Asp-Phe-Gly motifs and activation loops.	imatinib	11-18	fms related receptor tyrosine kinase 3	Homo sapiens	69-73
12435730-7	2003	Accordingly, we observed reduced sensitivity of preactivated compared with nonactivated PDGFR-beta for the inhibition by STI-571.	imatinib	121-128	platelet derived growth factor receptor beta	Homo sapiens	88-98
12435730-8	2003	Courses of the activation loop that collide with STI-571 binding explain its inactivity at other kinases as the insulin receptor.	imatinib	49-56	insulin receptor	Homo sapiens	112-128
12411298-2	2003	Imatinib, a selective inhibitor of Bcr-Abl, induces major cytogenetic remission (MCR) or complete cytogenetic remission (CCR) in the majority of patients with CML in first chronic phase.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
12655446-0	2003	Response to imatinib mesylate of a gastrointestinal stromal tumor with very low expression of KIT.	imatinib	12-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	94-97
12655446-2	2003	Imatinib mesylate (formerly STI571) is a potent inhibitor of KIT kinase activity and has been proven to be highly active in patients with unresectable or metastatic GIST expressing immunohistochemically detectable KIT protein.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	61-64
12655446-2	2003	Imatinib mesylate (formerly STI571) is a potent inhibitor of KIT kinase activity and has been proven to be highly active in patients with unresectable or metastatic GIST expressing immunohistochemically detectable KIT protein.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	214-217
12655446-2	2003	Imatinib mesylate (formerly STI571) is a potent inhibitor of KIT kinase activity and has been proven to be highly active in patients with unresectable or metastatic GIST expressing immunohistochemically detectable KIT protein.	imatinib	28-34	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	61-64
12655446-2	2003	Imatinib mesylate (formerly STI571) is a potent inhibitor of KIT kinase activity and has been proven to be highly active in patients with unresectable or metastatic GIST expressing immunohistochemically detectable KIT protein.	imatinib	28-34	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	214-217
12655446-5	2003	Our experience with this patient suggests that even GISTs with very low levels of KIT expression may respond to imatinib mesylate therapy.	imatinib	112-129	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	82-85
12626632-5	2003	Furthermore, treatment of wild-type slices with the specific Abl family kinase inhibitor STI571 also reduced PPF.	imatinib	89-95	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	61-64
12537980-9	2003	Inhibition of BCR/ABL kinase activity by STI571 (Gleevec, inatinib mesylate) abrogated the resistance to genotoxic treatment and inhibited DNA repair mechanisms.	imatinib	41-47	BCR activator of RhoGEF and GTPase	Mus musculus	14-17
12537980-9	2003	Inhibition of BCR/ABL kinase activity by STI571 (Gleevec, inatinib mesylate) abrogated the resistance to genotoxic treatment and inhibited DNA repair mechanisms.	imatinib	41-47	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	18-21
12646934-5	2003	The median duration of imatinib treatment before the identification of cytogenetic abnormalities in BCR-ABL-negative cells was 13 months.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
12456669-0	2003	A member of Forkhead transcription factor FKHRL1 is a downstream effector of STI571-induced cell cycle arrest in BCR-ABL-expressing cells.	imatinib	77-83	forkhead box O3	Homo sapiens	42-48
12456669-0	2003	A member of Forkhead transcription factor FKHRL1 is a downstream effector of STI571-induced cell cycle arrest in BCR-ABL-expressing cells.	imatinib	77-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
12456669-3	2003	FKHRL1 was constitutively phosphorylated in BCR-ABL-expressing cell lines KCL22 and KU812, and its phosphorylation was inhibited by treatment with STI571, a specific inhibitor of BCR-ABL tyrosine kinase.	imatinib	147-153	forkhead box O3	Homo sapiens	0-6
12456669-3	2003	FKHRL1 was constitutively phosphorylated in BCR-ABL-expressing cell lines KCL22 and KU812, and its phosphorylation was inhibited by treatment with STI571, a specific inhibitor of BCR-ABL tyrosine kinase.	imatinib	147-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
12456669-3	2003	FKHRL1 was constitutively phosphorylated in BCR-ABL-expressing cell lines KCL22 and KU812, and its phosphorylation was inhibited by treatment with STI571, a specific inhibitor of BCR-ABL tyrosine kinase.	imatinib	147-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	179-186
12456669-4	2003	Concomitantly, STI571 induced cell cycle arrest at the G(0)/G(1) phase, accompanied by up-regulation of a cyclin-dependent kinase inhibitor p27/Kip1 in KCL22 cells.	imatinib	15-21	zinc ribbon domain containing 2	Homo sapiens	140-143
12456669-4	2003	Concomitantly, STI571 induced cell cycle arrest at the G(0)/G(1) phase, accompanied by up-regulation of a cyclin-dependent kinase inhibitor p27/Kip1 in KCL22 cells.	imatinib	15-21	cyclin dependent kinase inhibitor 1B	Homo sapiens	144-148
12475982-5	2003	SCF-induced c-Kit phosphorylation was also inhibited by the related inhibitor 4-amino-5- (4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]-pyrimidine (PP2) and by STI571 but not by the Src inhibitor SU6656.	imatinib	157-163	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	12-17
12591277-5	2003	Expression of LTC(4)S was investigated in CD16(+) neutrophils from CML patients before and after 1 month of medication with imatinib mesylate (STI571), which is a specific inhibitor of p210 BCR-ABL.	imatinib	124-141	leukotriene C4 synthase	Homo sapiens	14-21
12591277-12	2003	Interestingly, treatment of five CML patients with imatinib mesylate down-regulated the abnormal neutrophil LTC(4)S expression and activity.	imatinib	51-68	leukotriene C4 synthase	Homo sapiens	108-115
12569358-0	2003	Effect of tyrosine kinase inhibitor STI571 on the kinase activity of wild-type and various mutated c-kit receptors found in mast cell neoplasms.	imatinib	36-42	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	99-104
12569358-5	2003	Here, we show that STI571 inhibits both wild-type and juxtamembrane mutant c-kit kinase activity, but has no effect on the activity of the D816 V mutant.	imatinib	19-25	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	75-80
12569358-6	2003	Accordingly, STI571 selectively decreases the survival of normal mast cell and of mast cell lines either with juxtamembrane c-kit mutations, but not that of tumoral mast cell from patient with SM or of mast cell lines with the D816 V mutation.	imatinib	13-19	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	124-129
12591277-5	2003	Expression of LTC(4)S was investigated in CD16(+) neutrophils from CML patients before and after 1 month of medication with imatinib mesylate (STI571), which is a specific inhibitor of p210 BCR-ABL.	imatinib	143-149	leukotriene C4 synthase	Homo sapiens	14-21
12573349-1	2003	Imatinib (STI571 or CGP57148B) is an innovative treatment for tumours with a constitutively activated form of c-ABL, c-KIT, or PDGFR.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-115
12678420-5	2003	Lately reports of efficacy of a specific anticancer drug with imatinib (ST1571) based on specific molecular abnormalities of proto-oncogene c-kit present in gastrointestinal stromal tumors induced us to identify the c-kit phenotype also in uterine leiomyosarcomas.	imatinib	62-70	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	125-145
12678420-5	2003	Lately reports of efficacy of a specific anticancer drug with imatinib (ST1571) based on specific molecular abnormalities of proto-oncogene c-kit present in gastrointestinal stromal tumors induced us to identify the c-kit phenotype also in uterine leiomyosarcomas.	imatinib	62-70	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	140-145
12592326-3	2003	Imatinib is a tyrosine kinase inhibitor with high affinity for c-Abl, PDGFR and c-kit.	imatinib	0-8	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	63-68
12592326-3	2003	Imatinib is a tyrosine kinase inhibitor with high affinity for c-Abl, PDGFR and c-kit.	imatinib	0-8	platelet derived growth factor receptor, beta polypeptide	Mus musculus	70-75
12592326-3	2003	Imatinib is a tyrosine kinase inhibitor with high affinity for c-Abl, PDGFR and c-kit.	imatinib	0-8	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	80-85
12604417-0	2003	Granulocyte colony-stimulating factor reverses cytopenia and may permit cytogenetic responses in patients with chronic myeloid leukemia treated with imatinib mesylate.	imatinib	149-166	colony stimulating factor 3	Homo sapiens	0-37
12573349-1	2003	Imatinib (STI571 or CGP57148B) is an innovative treatment for tumours with a constitutively activated form of c-ABL, c-KIT, or PDGFR.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	117-122
12592326-9	2003	In vitro culture of murine bone marrow cells in the presence of imatinib inhibited SCF-induced proliferation and recovery from treatment with idarubicin.	imatinib	64-72	kit ligand	Mus musculus	83-86
12573349-1	2003	Imatinib (STI571 or CGP57148B) is an innovative treatment for tumours with a constitutively activated form of c-ABL, c-KIT, or PDGFR.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	127-132
12573349-4	2003	Clinical trials assessing the therapeutic effects of imatinib have shown that the drug is highly effective with few associated side-effects, achieving durable cytogenetic responses in many patients with chronic-phase BCR-ABL-positive leukaemias.	imatinib	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	217-224
12594232-11	2003	The expression of smooth muscle alpha-actin protein in cultured peribiliary myofibroblasts was stimulated by PDGF-BB and inhibited by STI571, a PDGF receptor tyrosine kinase inhibitor, whereas in bile duct-ligated rats, the administration of STI571 caused a significant decrease in peribiliary smooth muscle alpha-actin immunoreactivity, and to a lesser extent, a decrease in peribiliary fibrosis.	imatinib	134-140	actin alpha 2, smooth muscle	Rattus norvegicus	18-43
12573349-7	2003	Two cellular mechanisms for resistance to imatinib have been identified: amplification of BCR-ABL gene and mutations in the catalytic domain of the protein.	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
12594232-11	2003	The expression of smooth muscle alpha-actin protein in cultured peribiliary myofibroblasts was stimulated by PDGF-BB and inhibited by STI571, a PDGF receptor tyrosine kinase inhibitor, whereas in bile duct-ligated rats, the administration of STI571 caused a significant decrease in peribiliary smooth muscle alpha-actin immunoreactivity, and to a lesser extent, a decrease in peribiliary fibrosis.	imatinib	134-140	actin alpha 2, smooth muscle	Rattus norvegicus	294-319
12594232-11	2003	The expression of smooth muscle alpha-actin protein in cultured peribiliary myofibroblasts was stimulated by PDGF-BB and inhibited by STI571, a PDGF receptor tyrosine kinase inhibitor, whereas in bile duct-ligated rats, the administration of STI571 caused a significant decrease in peribiliary smooth muscle alpha-actin immunoreactivity, and to a lesser extent, a decrease in peribiliary fibrosis.	imatinib	242-248	actin alpha 2, smooth muscle	Rattus norvegicus	18-43
12527798-0	2003	Abrogation of the cell death response to oxidative stress by the c-Abl tyrosine kinase inhibitor STI571.	imatinib	97-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-70
12527798-4	2003	Herein, we show that STI571, an inhibitor of Bcr-Abl in chronic myelogenous leukemia, blocks activation of c-Abl in the response of mouse embryo fibroblasts and human U-937 myeloid leukemia cells to hydrogen peroxide (H(2)O(2)).	imatinib	21-27	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	107-112
12527798-5	2003	Immunofluorescence microscopy and subcellular fractionation studies demonstrate that STI571 decreases H(2)O(2)-induced targeting of c-Abl to mitochondria in the two cell types by 59 to 85%.	imatinib	85-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-137
12616857-1	2003	Imatinib mesilate (Glivec) is a protein-tyrosine kinase inhibitor that potently inhibits the Bcr-Abl tyrosine kinase as well as the receptors for platelet-derived growth factor (PDGF) and stem cell factor (SCF), c-Kit, at in vitro and cellular kinase assay levels.	imatinib	0-17	KIT ligand	Homo sapiens	188-204
12527798-8	2003	These findings indicate that inhibition of c-Abl signaling by STI571 attenuates mitochondrial dysfunction and cell death in the cellular response to oxidative stress.	imatinib	62-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-48
12589034-9	2003	Treatment of BCR/ABL(+) cells with the Abl-specific tyrosine kinase inhibitor STI571 decreased expression at the mRNA as well as protein level of some but not all of the gene products.	imatinib	78-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
12589034-9	2003	Treatment of BCR/ABL(+) cells with the Abl-specific tyrosine kinase inhibitor STI571 decreased expression at the mRNA as well as protein level of some but not all of the gene products.	imatinib	78-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-42
12616857-1	2003	Imatinib mesilate (Glivec) is a protein-tyrosine kinase inhibitor that potently inhibits the Bcr-Abl tyrosine kinase as well as the receptors for platelet-derived growth factor (PDGF) and stem cell factor (SCF), c-Kit, at in vitro and cellular kinase assay levels.	imatinib	0-17	KIT ligand	Homo sapiens	206-209
12616857-1	2003	Imatinib mesilate (Glivec) is a protein-tyrosine kinase inhibitor that potently inhibits the Bcr-Abl tyrosine kinase as well as the receptors for platelet-derived growth factor (PDGF) and stem cell factor (SCF), c-Kit, at in vitro and cellular kinase assay levels.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	212-217
12616857-1	2003	Imatinib mesilate (Glivec) is a protein-tyrosine kinase inhibitor that potently inhibits the Bcr-Abl tyrosine kinase as well as the receptors for platelet-derived growth factor (PDGF) and stem cell factor (SCF), c-Kit, at in vitro and cellular kinase assay levels.	imatinib	19-25	KIT ligand	Homo sapiens	188-204
12616857-1	2003	Imatinib mesilate (Glivec) is a protein-tyrosine kinase inhibitor that potently inhibits the Bcr-Abl tyrosine kinase as well as the receptors for platelet-derived growth factor (PDGF) and stem cell factor (SCF), c-Kit, at in vitro and cellular kinase assay levels.	imatinib	19-25	KIT ligand	Homo sapiens	206-209
12616857-1	2003	Imatinib mesilate (Glivec) is a protein-tyrosine kinase inhibitor that potently inhibits the Bcr-Abl tyrosine kinase as well as the receptors for platelet-derived growth factor (PDGF) and stem cell factor (SCF), c-Kit, at in vitro and cellular kinase assay levels.	imatinib	19-25	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	212-217
12522257-1	2003	Most gastrointestinal stromal tumors (GISTs) have activating mutations in the KIT receptor tyrosine kinase, and most patients with GISTs respond well to Gleevec, which inhibits KIT kinase activity.	imatinib	153-160	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	78-81
12522257-1	2003	Most gastrointestinal stromal tumors (GISTs) have activating mutations in the KIT receptor tyrosine kinase, and most patients with GISTs respond well to Gleevec, which inhibits KIT kinase activity.	imatinib	153-160	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	177-180
12393636-1	2003	The leukemogenic tyrosine kinase Bcr-Abl contains a highly conserved inhibitor-binding pocket (IBP), which serves as a binding site for imatinib mesylate.	imatinib	136-153	trafficking protein particle complex subunit 9	Homo sapiens	95-98
12560071-0	2003	BCR-ABL binds to IRS-1 and IRS-1 phosphorylation is inhibited by imatinib in K562 cells.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
12560071-0	2003	BCR-ABL binds to IRS-1 and IRS-1 phosphorylation is inhibited by imatinib in K562 cells.	imatinib	65-73	insulin receptor substrate 1	Homo sapiens	27-32
12560071-3	2003	Our findings demonstrate that imatinib treatment resulted in marked attenuation of BCR-ABL/IRS-1 association and of IRS-1-stimulated PI3-kinase activity in K562 cells.	imatinib	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
12560071-3	2003	Our findings demonstrate that imatinib treatment resulted in marked attenuation of BCR-ABL/IRS-1 association and of IRS-1-stimulated PI3-kinase activity in K562 cells.	imatinib	30-38	insulin receptor substrate 1	Homo sapiens	91-96
12560071-3	2003	Our findings demonstrate that imatinib treatment resulted in marked attenuation of BCR-ABL/IRS-1 association and of IRS-1-stimulated PI3-kinase activity in K562 cells.	imatinib	30-38	insulin receptor substrate 1	Homo sapiens	116-121
12393636-0	2003	Dual-specific Src and Abl kinase inhibitors, PP1 and CGP76030, inhibit growth and survival of cells expressing imatinib mesylate-resistant Bcr-Abl kinases.	imatinib	111-119	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	14-17
12393636-0	2003	Dual-specific Src and Abl kinase inhibitors, PP1 and CGP76030, inhibit growth and survival of cells expressing imatinib mesylate-resistant Bcr-Abl kinases.	imatinib	111-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-25
12393636-2	2003	Mutations at the IBP may lead to resistance of the Abl kinase against imatinib mesylate.	imatinib	70-78	trafficking protein particle complex subunit 9	Homo sapiens	17-20
12393636-0	2003	Dual-specific Src and Abl kinase inhibitors, PP1 and CGP76030, inhibit growth and survival of cells expressing imatinib mesylate-resistant Bcr-Abl kinases.	imatinib	111-119	inorganic pyrophosphatase 1	Homo sapiens	45-48
12393636-2	2003	Mutations at the IBP may lead to resistance of the Abl kinase against imatinib mesylate.	imatinib	70-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-54
12393636-0	2003	Dual-specific Src and Abl kinase inhibitors, PP1 and CGP76030, inhibit growth and survival of cells expressing imatinib mesylate-resistant Bcr-Abl kinases.	imatinib	111-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-146
12393636-1	2003	The leukemogenic tyrosine kinase Bcr-Abl contains a highly conserved inhibitor-binding pocket (IBP), which serves as a binding site for imatinib mesylate.	imatinib	136-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
12393636-1	2003	The leukemogenic tyrosine kinase Bcr-Abl contains a highly conserved inhibitor-binding pocket (IBP), which serves as a binding site for imatinib mesylate.	imatinib	136-153	trafficking protein particle complex subunit 9	Homo sapiens	69-93
12393636-3	2003	To examine the mechanisms of imatinib mesylate binding and resistance in more detail, we created several point mutations at amino acid positions 315 and 380 of Abl, blocking the access to the IBP and rendering Bcr-Abl imatinib mesylate-resistant.	imatinib	29-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-163
12393636-3	2003	To examine the mechanisms of imatinib mesylate binding and resistance in more detail, we created several point mutations at amino acid positions 315 and 380 of Abl, blocking the access to the IBP and rendering Bcr-Abl imatinib mesylate-resistant.	imatinib	218-235	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-163
12393636-3	2003	To examine the mechanisms of imatinib mesylate binding and resistance in more detail, we created several point mutations at amino acid positions 315 and 380 of Abl, blocking the access to the IBP and rendering Bcr-Abl imatinib mesylate-resistant.	imatinib	218-235	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	210-217
12393636-4	2003	Moreover, introduction of a mutation destabilizing the inactive conformation of Abl (Asp276Ser/Glu279Ser) also led to imatinib mesylate resistance, suggesting that the inhibitor required inactivation of the kinase prior to binding.	imatinib	118-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
12393636-9	2003	The results suggest that the use of Src kinase inhibitors is a potential strategy to prevent or overcome clonal evolution of imatinib mesylate resistance in Bcr-Abl(+) leukemia.	imatinib	125-142	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	36-39
12393636-9	2003	The results suggest that the use of Src kinase inhibitors is a potential strategy to prevent or overcome clonal evolution of imatinib mesylate resistance in Bcr-Abl(+) leukemia.	imatinib	125-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-164
12509383-1	2003	Clinical studies have shown that the tyrosine kinase inhibitor STI571 effectively controls BCR-ABL-positive chronic myelogenous leukemia (CML).	imatinib	63-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
12393654-0	2003	The effects of Bcr-Abl on C/EBP transcription-factor regulation and neutrophilic differentiation are reversed by the Abl kinase inhibitor imatinib mesylate.	imatinib	138-155	CCAAT/enhancer binding protein (C/EBP), alpha	Mus musculus	26-31
12393654-2	2003	This study was undertaken to investigate the influence of Bcr-Abl and of the small molecule Abl tyrosine-kinase inhibitor imatinib mesylate on granulocyte colony-stimulating factor (G-CSF)-induced neutrophilic differentiation.	imatinib	122-139	colony stimulating factor 3 (granulocyte)	Mus musculus	143-180
12393654-2	2003	This study was undertaken to investigate the influence of Bcr-Abl and of the small molecule Abl tyrosine-kinase inhibitor imatinib mesylate on granulocyte colony-stimulating factor (G-CSF)-induced neutrophilic differentiation.	imatinib	122-139	colony stimulating factor 3 (granulocyte)	Mus musculus	182-187
12393654-7	2003	Importantly, incubation of 32D(Bcr-Ablwt) cells with the kinase inhibitor imatinib mesylate prior to G-CSF stimulation completely neutralized the effects of Bcr-Abl on granulocytic differentiation and on C/EBPalpha and C/EBPepsilon expression.	imatinib	74-91	CCAAT/enhancer binding protein (C/EBP), alpha	Mus musculus	204-214
12393654-7	2003	Importantly, incubation of 32D(Bcr-Ablwt) cells with the kinase inhibitor imatinib mesylate prior to G-CSF stimulation completely neutralized the effects of Bcr-Abl on granulocytic differentiation and on C/EBPalpha and C/EBPepsilon expression.	imatinib	74-91	CCAAT/enhancer binding protein (C/EBP), epsilon	Mus musculus	219-231
12543778-5	2003	Addition of the Abl kinase inhibitor STI-571 to ABL SH2-transformed Rat-1 cells inhibited tyrosine phosphorylation of p145 ABL.	imatinib	37-44	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	16-19
12543778-5	2003	Addition of the Abl kinase inhibitor STI-571 to ABL SH2-transformed Rat-1 cells inhibited tyrosine phosphorylation of p145 ABL.	imatinib	37-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Rattus norvegicus	48-51
12543790-3	2003	The selective Abl kinase inhibitor, STI-571 (marketed as Gleevec), is toxic to CML cells in culture, causes regression of CML tumors in nude mice, and is currently used to treat CML patients.	imatinib	36-43	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	14-17
12543778-5	2003	Addition of the Abl kinase inhibitor STI-571 to ABL SH2-transformed Rat-1 cells inhibited tyrosine phosphorylation of p145 ABL.	imatinib	37-44	sperm hammerhead 2	Mus musculus	52-55
12543778-5	2003	Addition of the Abl kinase inhibitor STI-571 to ABL SH2-transformed Rat-1 cells inhibited tyrosine phosphorylation of p145 ABL.	imatinib	37-44	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	123-126
12908555-4	2003	The tyrosine kinase inhibitor imatinib mesylate (formerly STI571, Gleevec, Novartis Pharmaceuticals Corp, East Hanover, NJ) blocks activity of the Bcr-Abl oncoprotein and the cell surface tyrosine kinase receptor c-Kit, and as such was recently approved for several indications in the treatment on chronic myeloid leukemia and gastrointestinal stromal tumors.	imatinib	30-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-154
14677715-1	2003	The publication provides an up-to-date review of the significance of cytogenetic abnormalities in chronic myelogenous leukemia (CML) and the development of a promising agent with specific molecular target against tyrosine kinase, product of the BCR-ABL fusion gene, namely imatinib mesylate (STI 571, Glivec).	imatinib	273-290	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	245-252
12908555-6	2003	Imatinib mesylate is also a potent inhibitor of PDGFR kinase and is currently being evaluated for the treatment of chronic myelomonocytic leukemia and glioblastoma multiforme, based upon evidence in these diseases of activating mutations in PDGFR.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	48-53
12908555-6	2003	Imatinib mesylate is also a potent inhibitor of PDGFR kinase and is currently being evaluated for the treatment of chronic myelomonocytic leukemia and glioblastoma multiforme, based upon evidence in these diseases of activating mutations in PDGFR.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	241-246
12393581-1	2003	The Abl kinase inhibitor imatinib mesylate (STI571) has significant and rapid antileukemic activity in Philadelphia chromosome/Bcr-Abl-positive acute lymphoblastic leukemia (Ph(+) ALL) but such activity is usually of short duration except for a small proportion of patients.	imatinib	25-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
12393722-5	2003	Expression of MBN was found to be down-regulated in remission under imatinib therapy (0 of 7 MBN(+) patients).	imatinib	68-76	proteinase 3	Homo sapiens	14-17
12393722-5	2003	Expression of MBN was found to be down-regulated in remission under imatinib therapy (0 of 7 MBN(+) patients).	imatinib	68-76	proteinase 3	Homo sapiens	93-96
12952023-1	2003	BACKGROUND: Imatinib mesylate is an inhibitor of a few tyrosine kinases including KIT, which is an important growth factor receptor of mast cells.	imatinib	12-29	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	82-85
12952023-11	2003	The mechanism of action is not known, but one possible target for the action of imatinib is inhibition of the KIT receptor on mast cells.	imatinib	80-88	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	110-113
14615817-2	2003	As exemplified by imatinib (Gleevec), a specific inhibitor of the Chronic Myeloid Leukemia (CML)-associated Bcr-Abl kinase, these agents promise impressive activity in clinical trials, with low levels of clinical toxicity.	imatinib	18-26	BCR activator of RhoGEF and GTPase	Homo sapiens	108-111
14615817-2	2003	As exemplified by imatinib (Gleevec), a specific inhibitor of the Chronic Myeloid Leukemia (CML)-associated Bcr-Abl kinase, these agents promise impressive activity in clinical trials, with low levels of clinical toxicity.	imatinib	18-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-115
14615817-2	2003	As exemplified by imatinib (Gleevec), a specific inhibitor of the Chronic Myeloid Leukemia (CML)-associated Bcr-Abl kinase, these agents promise impressive activity in clinical trials, with low levels of clinical toxicity.	imatinib	28-35	BCR activator of RhoGEF and GTPase	Homo sapiens	108-111
14615817-2	2003	As exemplified by imatinib (Gleevec), a specific inhibitor of the Chronic Myeloid Leukemia (CML)-associated Bcr-Abl kinase, these agents promise impressive activity in clinical trials, with low levels of clinical toxicity.	imatinib	28-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-115
12393581-1	2003	The Abl kinase inhibitor imatinib mesylate (STI571) has significant and rapid antileukemic activity in Philadelphia chromosome/Bcr-Abl-positive acute lymphoblastic leukemia (Ph(+) ALL) but such activity is usually of short duration except for a small proportion of patients.	imatinib	44-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
12393581-9	2003	The data show that Bcr-Abl levels in PB and BM after 2 weeks of imatinib treatment and in BM after 4 weeks have predictive relevance and may guide the application of additional therapies.	imatinib	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
12817876-2	2003	The specific identification of GIST has become more important after the availability of KIT-selective tyrosine kinase inhibitor Imatinib mesylate, STI571, commercially known as Gleevec/Glivec (Novartis Pharma, Basel, Switzerland) in the treatment of unresectable and metastatic tumors.	imatinib	128-145	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	88-91
12673129-0	2003	Imatinib (ST1571) provides only limited selectivity for CML cells and treatment might be complicated by silent BCR-ABL genes.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
12538464-0	2003	Quantitative polymerase chain reaction monitoring of BCR-ABL during therapy with imatinib mesylate (STI571; gleevec) in chronic-phase chronic myelogenous leukemia.	imatinib	81-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
12538464-0	2003	Quantitative polymerase chain reaction monitoring of BCR-ABL during therapy with imatinib mesylate (STI571; gleevec) in chronic-phase chronic myelogenous leukemia.	imatinib	100-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
14689066-0	2003	The clinical characteristics and the role of surgery and imatinib treatment in patients with liver metastases from c-Kit positive gastrointestinal stromal tumors (GIST).	imatinib	57-65	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	115-120
12542482-3	2003	An accurate molecular diagnosis of PDGFRB-rearranged patients has become increasingly important since recent data have indicated that they respond very well to imatinib mesylate therapy.	imatinib	160-177	platelet derived growth factor receptor beta	Homo sapiens	35-41
12483110-3	2003	Although the tyrosine kinase inhibitor imatinib mesylate (Gleevec) targeting the ABL protein tyrosine kinase has revolutionized current chronic myeloid leukemia therapy, it became rapidly evident that overcoming the multiple cellular resistance mechanisms will be very challenging.	imatinib	39-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-84
12600228-1	2003	Imatinib mesylate (imatinib) is an orally administered competitive inhibitor of the tyrosine kinases associated with the KIT protein (stem cell factor receptor), ABL protein and platelet-derived growth factor receptors.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	121-124
12600228-1	2003	Imatinib mesylate (imatinib) is an orally administered competitive inhibitor of the tyrosine kinases associated with the KIT protein (stem cell factor receptor), ABL protein and platelet-derived growth factor receptors.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-165
12600228-1	2003	Imatinib mesylate (imatinib) is an orally administered competitive inhibitor of the tyrosine kinases associated with the KIT protein (stem cell factor receptor), ABL protein and platelet-derived growth factor receptors.	imatinib	19-27	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	121-124
12600228-1	2003	Imatinib mesylate (imatinib) is an orally administered competitive inhibitor of the tyrosine kinases associated with the KIT protein (stem cell factor receptor), ABL protein and platelet-derived growth factor receptors.	imatinib	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-165
12600228-11	2003	One such drug is imatinib mesylate (imatinib, Glivic/Gleevec), an orally administered 2-phenylaminopyrimidine derivative that is a competitive inhibitor of the tyrosine kinases associated with platelet-derived growth factor (PDGF) receptors, the Abelson (ABL) protein and the KIT protein (also known as stem cell factor [SCF] receptor).	imatinib	17-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	246-253
12600228-11	2003	One such drug is imatinib mesylate (imatinib, Glivic/Gleevec), an orally administered 2-phenylaminopyrimidine derivative that is a competitive inhibitor of the tyrosine kinases associated with platelet-derived growth factor (PDGF) receptors, the Abelson (ABL) protein and the KIT protein (also known as stem cell factor [SCF] receptor).	imatinib	17-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	255-258
12600228-11	2003	One such drug is imatinib mesylate (imatinib, Glivic/Gleevec), an orally administered 2-phenylaminopyrimidine derivative that is a competitive inhibitor of the tyrosine kinases associated with platelet-derived growth factor (PDGF) receptors, the Abelson (ABL) protein and the KIT protein (also known as stem cell factor [SCF] receptor).	imatinib	17-34	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	276-279
12600228-11	2003	One such drug is imatinib mesylate (imatinib, Glivic/Gleevec), an orally administered 2-phenylaminopyrimidine derivative that is a competitive inhibitor of the tyrosine kinases associated with platelet-derived growth factor (PDGF) receptors, the Abelson (ABL) protein and the KIT protein (also known as stem cell factor [SCF] receptor).	imatinib	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	246-253
12600228-11	2003	One such drug is imatinib mesylate (imatinib, Glivic/Gleevec), an orally administered 2-phenylaminopyrimidine derivative that is a competitive inhibitor of the tyrosine kinases associated with platelet-derived growth factor (PDGF) receptors, the Abelson (ABL) protein and the KIT protein (also known as stem cell factor [SCF] receptor).	imatinib	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	255-258
12600228-11	2003	One such drug is imatinib mesylate (imatinib, Glivic/Gleevec), an orally administered 2-phenylaminopyrimidine derivative that is a competitive inhibitor of the tyrosine kinases associated with platelet-derived growth factor (PDGF) receptors, the Abelson (ABL) protein and the KIT protein (also known as stem cell factor [SCF] receptor).	imatinib	17-25	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	276-279
12600228-13	2003	More recently, imatinib has been approved for the treatment of patients with advanced gastrointestinal stromal tumour (GIST), in which KIT, a tyrosine kinase receptor, is abnormally expressed.	imatinib	15-23	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	135-138
12600228-24	2003	Imatinib selectively inhibits the tyrosine kinase activity associated with KIT, which forms the rationale for evaluating its effects in GIST.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	75-78
12600228-25	2003	Subsequent to initial evidence of the clinical efficacy of imatinib in a single patient with progressive, metastatic, CD117-positive GIST, formal studies of imatinib in this new indication were initiated.	imatinib	59-67	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	118-123
12898363-4	2003	STI571 selectively inhibits c-Kit, BCR-ABL, and PDGFR tyrosine kinases.	imatinib	0-6	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	28-33
12898363-4	2003	STI571 selectively inhibits c-Kit, BCR-ABL, and PDGFR tyrosine kinases.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
12898363-5	2003	Based on this potential to inhibit critical c-Kit function in GISTs, case studies have reported effective outcomes following treatment with STI571.	imatinib	140-146	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	44-49
12691137-11	2003	The tyrosine-kinase inhibitor STI 571 offers new perspectives for patients with the Phl/bcr/abl translocation.	imatinib	30-37	BCR activator of RhoGEF and GTPase	Homo sapiens	84-87
14657531-6	2003	STI571 (imatinib mesylate) inhibits the Bcr-Abl TK, blocks the growth of these leukemia cells, and induces apoptosis.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
14657531-6	2003	STI571 (imatinib mesylate) inhibits the Bcr-Abl TK, blocks the growth of these leukemia cells, and induces apoptosis.	imatinib	8-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
14657531-7	2003	STI571 also inhibits other TKs, including the receptor TK c-kit, which is expressed in gastrointestinal stromal tumors.	imatinib	0-6	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	58-63
12817876-2	2003	The specific identification of GIST has become more important after the availability of KIT-selective tyrosine kinase inhibitor Imatinib mesylate, STI571, commercially known as Gleevec/Glivec (Novartis Pharma, Basel, Switzerland) in the treatment of unresectable and metastatic tumors.	imatinib	147-153	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	88-91
12436445-5	2002	Imatinib mesylate appears to demonstrate inhibitory activity against multiple class 3 receptor tyrosine kinases, including platelet-derived growth factor receptor (PDGFR)-alpha and PDGFR-beta, as well as c-kit.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	123-162
12743326-1	2003	The BCR/ABL tyrosine kinase inhibitor, imatinib, has shown substantial effects in blast crises of chronic myelogenous leukemia.	imatinib	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
12743326-3	2003	In this study, we generated a new imatinib-resistant BCR/ABL-positive cell line, KCL22/SR.	imatinib	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
12743326-6	2003	Furthermore, the level of phosphorylated BCR/ABL protein was suppressed by imatinib treatment, suggesting that mechanisms independent of BCR/ABL signaling are involved in the imatinib resistance in KCL22/SR cells.	imatinib	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
12743326-6	2003	Furthermore, the level of phosphorylated BCR/ABL protein was suppressed by imatinib treatment, suggesting that mechanisms independent of BCR/ABL signaling are involved in the imatinib resistance in KCL22/SR cells.	imatinib	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-144
12743326-6	2003	Furthermore, the level of phosphorylated BCR/ABL protein was suppressed by imatinib treatment, suggesting that mechanisms independent of BCR/ABL signaling are involved in the imatinib resistance in KCL22/SR cells.	imatinib	175-183	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
12743326-8	2003	Furthermore, imatinib treatment significantly suppressed the level of phosphorylated p44/42 in KCL22 cells but not in KCL22/SR cells, even when BCR/ABL was inhibited by imatinib.	imatinib	13-21	interferon induced protein 44	Homo sapiens	85-88
12743326-8	2003	Furthermore, imatinib treatment significantly suppressed the level of phosphorylated p44/42 in KCL22 cells but not in KCL22/SR cells, even when BCR/ABL was inhibited by imatinib.	imatinib	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
12743326-8	2003	Furthermore, imatinib treatment significantly suppressed the level of phosphorylated p44/42 in KCL22 cells but not in KCL22/SR cells, even when BCR/ABL was inhibited by imatinib.	imatinib	169-177	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
12499247-0	2002	Activity of the Bcr-Abl kinase inhibitor PD180970 against clinically relevant Bcr-Abl isoforms that cause resistance to imatinib mesylate (Gleevec, STI571).	imatinib	120-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
12499247-0	2002	Activity of the Bcr-Abl kinase inhibitor PD180970 against clinically relevant Bcr-Abl isoforms that cause resistance to imatinib mesylate (Gleevec, STI571).	imatinib	120-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
12483533-10	2002	Moreover, PD180970 blocked Stat5 signaling and induced apoptosis of STI-571 (Gleevec, Imatinib)-resistant Bcr-Abl-positive cells.	imatinib	77-84	signal transducer and activator of transcription 5A	Homo sapiens	27-32
12483533-10	2002	Moreover, PD180970 blocked Stat5 signaling and induced apoptosis of STI-571 (Gleevec, Imatinib)-resistant Bcr-Abl-positive cells.	imatinib	77-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
12483533-10	2002	Moreover, PD180970 blocked Stat5 signaling and induced apoptosis of STI-571 (Gleevec, Imatinib)-resistant Bcr-Abl-positive cells.	imatinib	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
12476293-2	2002	Treatment with the ABL-specific tyrosine kinase inhibitor STI571 (Glivec, Gleevec, imatinib mesylate) resulted in a complete haematologic and cytogenetic remission.	imatinib	58-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-22
12476293-2	2002	Treatment with the ABL-specific tyrosine kinase inhibitor STI571 (Glivec, Gleevec, imatinib mesylate) resulted in a complete haematologic and cytogenetic remission.	imatinib	83-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-22
12682876-3	2003	Recently, three phase II studies of imatinib mesylate (STI571), a new inhibitor specific for tyrosine kinase of the Bcr-Abl oncoprotein, have been reported.	imatinib	36-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
12682876-3	2003	Recently, three phase II studies of imatinib mesylate (STI571), a new inhibitor specific for tyrosine kinase of the Bcr-Abl oncoprotein, have been reported.	imatinib	55-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
12499247-6	2002	Our data indicate that PD180970 is active against several Bcr-Abl mutations that are resistant to imatinib and support the notion that developing additional Abl kinase inhibitors would be useful as a treatment strategy for chronic myelogenous leukemia.	imatinib	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
12476305-4	2002	Support for this has only been strengthened by the observations that resistance to imatinib mesylate (imatinib) commonly involves a breakthrough and the persistent activity of Bcr-Abl TK.	imatinib	83-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	176-183
12476305-4	2002	Support for this has only been strengthened by the observations that resistance to imatinib mesylate (imatinib) commonly involves a breakthrough and the persistent activity of Bcr-Abl TK.	imatinib	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	176-183
12476305-5	2002	This is due to either mutations that inhibit imatinib action on Bcr-Abl TK or amplification of the bcr-abl gene.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
12476306-6	2002	Inhibition of BCR/ABL kinase activity by STI571 (Gleevec, imatinib mesylate) reverses drug resistance and, in combination with standard chemotherapeutics can exert strong anti-leukemia effect.	imatinib	41-47	BCR activator of RhoGEF and GTPase	Homo sapiens	14-17
12476306-6	2002	Inhibition of BCR/ABL kinase activity by STI571 (Gleevec, imatinib mesylate) reverses drug resistance and, in combination with standard chemotherapeutics can exert strong anti-leukemia effect.	imatinib	41-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-21
12476306-6	2002	Inhibition of BCR/ABL kinase activity by STI571 (Gleevec, imatinib mesylate) reverses drug resistance and, in combination with standard chemotherapeutics can exert strong anti-leukemia effect.	imatinib	58-75	BCR activator of RhoGEF and GTPase	Homo sapiens	14-17
12476306-6	2002	Inhibition of BCR/ABL kinase activity by STI571 (Gleevec, imatinib mesylate) reverses drug resistance and, in combination with standard chemotherapeutics can exert strong anti-leukemia effect.	imatinib	58-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-21
12538164-8	2002	Inhibition of c-Kit activity with the pharmacological inhibitor of c-Kit signaling STI571 reversed the KSHV-induced morphological transformation of DMVEC.	imatinib	83-89	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-19
12538164-8	2002	Inhibition of c-Kit activity with the pharmacological inhibitor of c-Kit signaling STI571 reversed the KSHV-induced morphological transformation of DMVEC.	imatinib	83-89	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	67-72
12617875-3	2002	With the advent of the ABL-selective tyrosine kinase inhibitor STI571 (imatinib mesylate, Glivec), it has become apparent that the understanding of crucial leukaemogenic pathways at the molecular level can lead to the development of specific and selective agents.	imatinib	63-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-26
12617875-3	2002	With the advent of the ABL-selective tyrosine kinase inhibitor STI571 (imatinib mesylate, Glivec), it has become apparent that the understanding of crucial leukaemogenic pathways at the molecular level can lead to the development of specific and selective agents.	imatinib	71-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-26
12617875-3	2002	With the advent of the ABL-selective tyrosine kinase inhibitor STI571 (imatinib mesylate, Glivec), it has become apparent that the understanding of crucial leukaemogenic pathways at the molecular level can lead to the development of specific and selective agents.	imatinib	90-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-26
12436445-5	2002	Imatinib mesylate appears to demonstrate inhibitory activity against multiple class 3 receptor tyrosine kinases, including platelet-derived growth factor receptor (PDGFR)-alpha and PDGFR-beta, as well as c-kit.	imatinib	0-17	platelet derived growth factor receptor alpha	Homo sapiens	164-176
12436445-5	2002	Imatinib mesylate appears to demonstrate inhibitory activity against multiple class 3 receptor tyrosine kinases, including platelet-derived growth factor receptor (PDGFR)-alpha and PDGFR-beta, as well as c-kit.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	181-191
12436445-5	2002	Imatinib mesylate appears to demonstrate inhibitory activity against multiple class 3 receptor tyrosine kinases, including platelet-derived growth factor receptor (PDGFR)-alpha and PDGFR-beta, as well as c-kit.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	204-209
12436445-9	2002	CONCLUSIONS: Imatinib mesylate has been reported to have activity against desmoid tumor, most likely because of c-kit and PDGFR receptor tyrosine kinase activity inhibition, and warrants further study.	imatinib	13-30	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	112-117
12436445-9	2002	CONCLUSIONS: Imatinib mesylate has been reported to have activity against desmoid tumor, most likely because of c-kit and PDGFR receptor tyrosine kinase activity inhibition, and warrants further study.	imatinib	13-30	platelet derived growth factor receptor beta	Homo sapiens	122-127
12504677-5	2002	Structural studies of the Abl tyrosine kinase domain in complex with the small-molecule inhibitor STI571 provide a molecular basis for understanding the specificity determinants of this highly successful drug used in the treatment of chronic myeloid leukemia.	imatinib	98-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-29
12490842-7	2002	RESULTS: RET phosphorylation was inhibited at 24 hours of exposure to 5 to 20 micromol/L STI571 and 48 hours of exposure to genistein (200 micromol/L) and allyl-geldanamycin (6 micromol/L).	imatinib	89-95	ret proto-oncogene	Homo sapiens	9-12
12495909-0	2002	Combination of imatinib and established antileukemic treatment modalities for otherwise refractory BCR-ABL positive lymphoblastic leukemia.	imatinib	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
12514786-2	2002	Studies have shown that the tyrosine kinase inhibitor STI-571 (Gleevec) is used successfully against tumors expressing the c-kit oncogene, such as gastrointestinal stromal tumors (GISTs).	imatinib	54-61	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	123-128
12613514-2	2002	We sought to determine if quantitative PCR measurement of peripheral blood BCR/ABL transcript can be used to monitor response in CML patients with clinically evident disease while receiving the protein tyrosine kinase inhibitor STI-571.	imatinib	228-235	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
12512837-0	2002	Constitutive activation of c-kit by the juxtamembrane but not the catalytic domain mutations is inhibited selectively by tyrosine kinase inhibitors STI571 and AG1296.	imatinib	148-154	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	27-32
12454739-1	2002	Imatinib mesylate (STI571, Glivec, Gleevec) is a powerful inhibitor of the tyrosine kinase activity of Bcr-Abl, the oncoprotein responsible for chronic myeloid leukemia (CML).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
12454739-1	2002	Imatinib mesylate (STI571, Glivec, Gleevec) is a powerful inhibitor of the tyrosine kinase activity of Bcr-Abl, the oncoprotein responsible for chronic myeloid leukemia (CML).	imatinib	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
12496355-0	2002	Imatinib mesylate (STI-571) reduces Bcr-Abl-mediated vascular endothelial growth factor secretion in chronic myelogenous leukemia.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-43
12496355-0	2002	Imatinib mesylate (STI-571) reduces Bcr-Abl-mediated vascular endothelial growth factor secretion in chronic myelogenous leukemia.	imatinib	0-17	vascular endothelial growth factor A	Homo sapiens	53-87
12496355-3	2002	We found that levels of VEGF expression in BCR-ABL-positive K562 cells were reduced in vitro by treatment with STI-571 in a dose-dependent fashion.	imatinib	111-118	vascular endothelial growth factor A	Homo sapiens	24-28
12496355-3	2002	We found that levels of VEGF expression in BCR-ABL-positive K562 cells were reduced in vitro by treatment with STI-571 in a dose-dependent fashion.	imatinib	111-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
12439339-0	2002	DNA damage and repair in BCR/ABL-expressing cells after combined action of idarubicin, STI571 and amifostine.	imatinib	87-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
12441322-3	2002	METHODS: The effect of imatinib on c-kit expression and phosphorylation in Ewing"s sarcoma cells was examined by immunoblotting.	imatinib	23-31	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	35-40
12441322-4	2002	The effect of imatinib on cell growth and apoptosis was examined with an MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] assay and with a morphologic test and Annexin V staining, respectively.	imatinib	14-22	annexin A5	Mus musculus	179-188
12441322-6	2002	RESULTS: All Ewing"s sarcoma cell lines tested were sensitive to imatinib-mediated apoptosis with a concentration inhibiting growth by 50% (IC50) of 10-12 micro M. Imatinib inhibited SCF-mediated c-kit phosphorylation (IC50 = 0.1-0.5 microM).	imatinib	65-73	kit ligand	Mus musculus	183-186
12441322-6	2002	RESULTS: All Ewing"s sarcoma cell lines tested were sensitive to imatinib-mediated apoptosis with a concentration inhibiting growth by 50% (IC50) of 10-12 micro M. Imatinib inhibited SCF-mediated c-kit phosphorylation (IC50 = 0.1-0.5 microM).	imatinib	65-73	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	196-201
12441322-6	2002	RESULTS: All Ewing"s sarcoma cell lines tested were sensitive to imatinib-mediated apoptosis with a concentration inhibiting growth by 50% (IC50) of 10-12 micro M. Imatinib inhibited SCF-mediated c-kit phosphorylation (IC50 = 0.1-0.5 microM).	imatinib	164-172	kit ligand	Mus musculus	183-186
12441322-6	2002	RESULTS: All Ewing"s sarcoma cell lines tested were sensitive to imatinib-mediated apoptosis with a concentration inhibiting growth by 50% (IC50) of 10-12 micro M. Imatinib inhibited SCF-mediated c-kit phosphorylation (IC50 = 0.1-0.5 microM).	imatinib	164-172	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	196-201
12417503-5	2002	STI571 is an oral agent that selectively inhibits Kit.	imatinib	0-6	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	50-53
12439339-1	2002	STI571 is a specific ABL family tyrosine kinases inhibitor approved for treatment of leukemias.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-24
12414661-3	2002	In vitro, the inhibition of c-Kit tyrosine kinase activity by the small molecule tyrosine kinase inhibitor STI571 (Gleevec) abrogates cell growth.	imatinib	107-113	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	28-33
12414661-11	2002	Treatment of NCI-H69 cells with STI571 specifically inhibited the c-Kit signaling events of Akt and p70 S6 kinase, whereas SDF-1alpha-mediated activation of Akt or p70 S6 kinase was normal.	imatinib	32-38	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	66-71
12414617-1	2002	The major mechanism of action of STI571 is a competitive interference with the ATP-binding site of the Bcr/Abl tyrosine kinase.	imatinib	33-39	BCR activator of RhoGEF and GTPase	Homo sapiens	103-106
12414661-11	2002	Treatment of NCI-H69 cells with STI571 specifically inhibited the c-Kit signaling events of Akt and p70 S6 kinase, whereas SDF-1alpha-mediated activation of Akt or p70 S6 kinase was normal.	imatinib	32-38	AKT serine/threonine kinase 1	Homo sapiens	92-95
12414617-1	2002	The major mechanism of action of STI571 is a competitive interference with the ATP-binding site of the Bcr/Abl tyrosine kinase.	imatinib	33-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-110
12429650-3	2002	It has been reported previously that STI571 has specific activity in inhibiting select tyrosine kinase receptors, including PDGF and c-Kit.	imatinib	37-43	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	133-138
12414617-4	2002	The activity of the Bcr/Abl kinase (level of autophosphorylation) in resistant cells was, however, incompletely inhibited by STI571, and the acquisition of the high degree of resistance was associated with a single-point mutation leading to a substitution of a threonine-to-isoleucine at position 315 of Abl.	imatinib	125-131	BCR activator of RhoGEF and GTPase	Homo sapiens	20-23
12414617-4	2002	The activity of the Bcr/Abl kinase (level of autophosphorylation) in resistant cells was, however, incompletely inhibited by STI571, and the acquisition of the high degree of resistance was associated with a single-point mutation leading to a substitution of a threonine-to-isoleucine at position 315 of Abl.	imatinib	125-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-27
12414617-6	2002	The mutation was present in all 10 STI571-resistant clones derived from low density clonogenic assay, confirming its presence in all colony-forming cells but only in a fraction of the BCR/ABL gene copies in each cell.	imatinib	35-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	184-191
12429620-0	2002	Inhibition of human telomerase enhances the effect of the tyrosine kinase inhibitor, imatinib, in BCR-ABL-positive leukemia cells.	imatinib	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
12429620-10	2002	CONCLUSIONS: These results demonstrate that disruption of telomere maintenance limits the cellular life span of leukemia cells and show that the combined use of imatinib and telomere maintenance inhibition may be effective in the treatment of BCR-ABL-positive leukemia.	imatinib	161-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	243-250
12547154-0	2002	BCR/ABL amplification in chronic myelocytic leukemia blast crisis following imatinib mesylate administration.	imatinib	76-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
12547154-2	2002	We describe the cytogenetic and molecular genetic findings in two cases of myelocytic blast crisis of CML, one occurring 6 months after commencing treatment with the ABL-specific tyrosine kinase inhibitor imatinib mesylate (STI571, Glivec, or Gleevec) and the second treated with imatinib mesylate for established blast crisis.	imatinib	205-222	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-169
12547154-2	2002	We describe the cytogenetic and molecular genetic findings in two cases of myelocytic blast crisis of CML, one occurring 6 months after commencing treatment with the ABL-specific tyrosine kinase inhibitor imatinib mesylate (STI571, Glivec, or Gleevec) and the second treated with imatinib mesylate for established blast crisis.	imatinib	224-230	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-169
12547154-3	2002	In both cases, multiple secondary cytogenetic abnormalities were observed at transformation, with homogeneously staining regions that were shown to contain BCR/ABL amplification by fluorescence in situ hybridization appearing after imatinib mesylate administration.	imatinib	232-249	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
12547154-4	2002	BCR/ABL amplification is emerging as an important mechanism of acquired resistance to imatinib mesylate.	imatinib	86-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
12429650-7	2002	STI571 (1.0 micro M) inhibited both PDGFR-alpha and PDGFR-beta phosphorylation and the downstream phosphorylation targets extracellular signal-regulated kinase and Akt.	imatinib	0-6	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	36-47
12429650-7	2002	STI571 (1.0 micro M) inhibited both PDGFR-alpha and PDGFR-beta phosphorylation and the downstream phosphorylation targets extracellular signal-regulated kinase and Akt.	imatinib	0-6	platelet derived growth factor receptor, beta polypeptide	Mus musculus	52-62
12390311-6	2002	This response was inhibited totally by the addition of STI-571, demonstrating that IL-10 mitogenic activity has an absolute requirement for signalling through the PDGF receptor.	imatinib	55-62	interleukin 10	Rattus norvegicus	83-88
12429650-7	2002	STI571 (1.0 micro M) inhibited both PDGFR-alpha and PDGFR-beta phosphorylation and the downstream phosphorylation targets extracellular signal-regulated kinase and Akt.	imatinib	0-6	thymoma viral proto-oncogene 1	Mus musculus	164-167
12429650-15	2002	CONCLUSIONS: Our data demonstrate that STI571 inhibits PDGF-mediated growth and leads to apoptosis of osteosarcoma cells in vitro by selective inhibition of the PDGFR tyrosine kinase.	imatinib	39-45	platelet derived growth factor receptor beta	Homo sapiens	161-166
12399961-1	2002	Selective inhibition of the BCR-ABL tyrosine kinase by imatinib (STI571, Glivec/Gleevec) is a promising new therapeutic strategy in patients with chronic myelogenous leukemia (CML).	imatinib	65-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
12409651-0	2002	Mechanisms of resistance to imatinib mesylate in Bcr-Abl-positive leukemias.	imatinib	28-45	BCR activator of RhoGEF and GTPase	Homo sapiens	49-52
12409651-4	2002	This resistance has been shown to be caused by specific ATP binding site mutations or amplification of Bcr-Abl gene, resulting in a Bcr-Abl tyrosine kinase that is resistant to further inhibition by imatinib.	imatinib	199-207	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
12409651-4	2002	This resistance has been shown to be caused by specific ATP binding site mutations or amplification of Bcr-Abl gene, resulting in a Bcr-Abl tyrosine kinase that is resistant to further inhibition by imatinib.	imatinib	199-207	BCR activator of RhoGEF and GTPase	Homo sapiens	103-106
12409651-5	2002	Alternative (Bcr-Abl-independent) mechanisms driving the growth and survival of the malignant clone may also be responsible for imatinib resistance.	imatinib	128-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
12354363-4	2002	Promising preclinical results have provided the driving force for the rapid clinical development of imatinib mesylate, a selective tyrosine kinase inhibitor of c-Kit.	imatinib	100-117	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	160-165
12399961-1	2002	Selective inhibition of the BCR-ABL tyrosine kinase by imatinib (STI571, Glivec/Gleevec) is a promising new therapeutic strategy in patients with chronic myelogenous leukemia (CML).	imatinib	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
12424067-9	2002	Imatinib mesylate is an orally administered selective inhibitor of certain tyrosine kinases including KIT.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	102-105
12429808-9	2002	Nonetheless, the growth of TAKA-1 cells and pancreatic cancer cells was inhibited by the c-kit tyrosine kinase inhibitor STI571.	imatinib	121-127	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	89-94
12397549-7	2002	Sequencing of the ATP binding site of the BCR-ABL gene, which - at protein level - is the target for imatinib, revealed the clonal selection of cells harboring a point mutation leading to the exchange of amino acid 253 from tyrosine to histidine.	imatinib	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
12384536-0	2002	Molecular characterization and sensitivity of STI-571 (imatinib mesylate, Gleevec)-resistant, Bcr-Abl-positive, human acute leukemia cells to SRC kinase inhibitor PD180970 and 17-allylamino-17-demethoxygeldanamycin.	imatinib	46-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
12370803-6	2002	We treated the 32Dp210 Bcr-Abl cells with the Jak2 specific tyrosine kinase inhibitor, AG490, and found that this drug, like the Abl tyrosine kinase inhibitor STI-571, inhibited c-Myc protein induction by Bcr-Abl.	imatinib	159-166	Janus kinase 2	Homo sapiens	46-50
12370803-6	2002	We treated the 32Dp210 Bcr-Abl cells with the Jak2 specific tyrosine kinase inhibitor, AG490, and found that this drug, like the Abl tyrosine kinase inhibitor STI-571, inhibited c-Myc protein induction by Bcr-Abl.	imatinib	159-166	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	178-183
12370803-15	2002	Of interest, IL-3 containing medium reversed the STI-571 induced apoptosis of 32Dp210 cells but did not reverse the induction of apoptosis by AG490, which strongly supports the specificity of the inhibitory effects of AG490 on the Jak2 tyrosine kinase.	imatinib	49-56	interleukin 3	Homo sapiens	13-17
12440260-0	2002	[Tyrosine kinase inhibitor STI571: new possibility in the treatment of chronic myeloid leukemia].	imatinib	27-33	TXK tyrosine kinase	Homo sapiens	1-16
12440260-5	2002	The specific inhibitor of BCR-ABL TK, STI571 was developed by Brian Druker and his co-workers in 1996.	imatinib	38-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
12440260-5	2002	The specific inhibitor of BCR-ABL TK, STI571 was developed by Brian Druker and his co-workers in 1996.	imatinib	38-44	TXK tyrosine kinase	Homo sapiens	34-36
12440260-6	2002	STI571 (Signal Transduction Inhibitor) occupies the kinase pocket of the BCR-ABL protein, and blocks ATP binding, thereby preventing phosphorylation of any substrate.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
12351420-0	2002	BCR-ABL point mutants isolated from patients with imatinib mesylate-resistant chronic myeloid leukemia remain sensitive to inhibitors of the BCR-ABL chaperone heat shock protein 90.	imatinib	50-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
12351420-0	2002	BCR-ABL point mutants isolated from patients with imatinib mesylate-resistant chronic myeloid leukemia remain sensitive to inhibitors of the BCR-ABL chaperone heat shock protein 90.	imatinib	50-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-148
12351420-0	2002	BCR-ABL point mutants isolated from patients with imatinib mesylate-resistant chronic myeloid leukemia remain sensitive to inhibitors of the BCR-ABL chaperone heat shock protein 90.	imatinib	50-67	heat shock protein 90 alpha family class A member 1	Homo sapiens	159-180
12358910-2	2002	We describe a patient in whom progressive resistance to STI571 correlated with the appearance of a mutation in the Bcr-Abl kinase domain.	imatinib	56-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
12360044-2	2002	In the STI571 (Gleevec, Imatinib) era, the problem may be further compounded when protocol-driven staining for CD117 (c-kit) is performed on spindle cell proliferations presenting in the bowel wall and mesentery using an antibody known to react with the majority of mesenteric fibromatoses when other antibodies are more specific.	imatinib	24-32	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	111-116
12360044-2	2002	In the STI571 (Gleevec, Imatinib) era, the problem may be further compounded when protocol-driven staining for CD117 (c-kit) is performed on spindle cell proliferations presenting in the bowel wall and mesentery using an antibody known to react with the majority of mesenteric fibromatoses when other antibodies are more specific.	imatinib	24-32	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	118-123
12374669-1	2002	PURPOSE: Imatinib mesylate (Gleevec; Novartis, East Hanover, NJ)is a receptor tyrosine kinase inhibitor approved previously in 2001 by the United States Food and Drug Administration for the treatment of chronic myelogenous leukemia in blast crisis, accelerated phase, or in chronic phase after failure of IFN-alpha therapy.	imatinib	9-26	interferon alpha 1	Homo sapiens	305-314
12368958-0	2002	Tyrosine kinase inhibitor STI571 in the treatment of Philadelphia chromosome-positive leukaemia failing myeloablative stem cell transplantation.	imatinib	26-32	TXK tyrosine kinase	Homo sapiens	0-15
12368958-1	2002	Eight patients with Philadelphia chromosome-positive (Ph(+)) leukaemia relapsing from stem cell transplantation (SCT) (one syngeneic and seven allogeneic) were treated with the tyrosine kinase inhibitor STI571.	imatinib	203-209	TXK tyrosine kinase	Homo sapiens	177-192
12359756-4	2002	Inhibitory PDGF aptamers and the PDGF receptor tyrosine kinase inhibitor STI571 enhanced the antitumor effect of Taxol on s.c. KAT-4 tumors in SCID mice.	imatinib	73-79	TATA-box binding protein associated factor 1	Mus musculus	127-132
12357372-0	2002	Efficacy of imatinib mesylate (STI571) in conjunction with alpha-interferon: long-term quantitative molecular remission in relapsed P-190(BCR-ABL)-positive acute lymphoblastic leukemia.	imatinib	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
12512386-7	2002	The improved understanding of the molecular pathophysiology of GIST, a disease that was previously untreatable with any available systemic therapy, has led to the development of imatinib, a well-tolerated agent that can inhibit the dysregulated KIT signaling pathways in GIST.	imatinib	178-186	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	245-248
12357372-0	2002	Efficacy of imatinib mesylate (STI571) in conjunction with alpha-interferon: long-term quantitative molecular remission in relapsed P-190(BCR-ABL)-positive acute lymphoblastic leukemia.	imatinib	31-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
12481435-1	2002	Imatinib (Glivec; STI571) is an ATP-competitive kinase inhibitor of c-Abl, BCR/ABL, c-Kit, and platelet-derived growth factor receptor.	imatinib	0-8	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	68-73
12481435-1	2002	Imatinib (Glivec; STI571) is an ATP-competitive kinase inhibitor of c-Abl, BCR/ABL, c-Kit, and platelet-derived growth factor receptor.	imatinib	0-8	BCR activator of RhoGEF and GTPase	Mus musculus	75-82
12481435-9	2002	In signaling studies, addition of stem cell factor (SCF) induced phosphorylation of ERK and Akt by WTKit, and ERK, Akt and STAT3 by V560GKit, which were all blocked by Imatinib.	imatinib	168-176	thymoma viral proto-oncogene 1	Mus musculus	115-118
12481435-1	2002	Imatinib (Glivec; STI571) is an ATP-competitive kinase inhibitor of c-Abl, BCR/ABL, c-Kit, and platelet-derived growth factor receptor.	imatinib	0-8	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	84-89
12481435-9	2002	In signaling studies, addition of stem cell factor (SCF) induced phosphorylation of ERK and Akt by WTKit, and ERK, Akt and STAT3 by V560GKit, which were all blocked by Imatinib.	imatinib	168-176	signal transducer and activator of transcription 3	Mus musculus	123-128
12481435-10	2002	Imatinib also blocked the constitutive activation of Akt and STAT3 by V560GKit but had no affect on the constitutive activation of ERK, Akt, and STAT3 by D816VKit.	imatinib	0-8	thymoma viral proto-oncogene 1	Mus musculus	53-56
12481435-1	2002	Imatinib (Glivec; STI571) is an ATP-competitive kinase inhibitor of c-Abl, BCR/ABL, c-Kit, and platelet-derived growth factor receptor.	imatinib	10-16	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	68-73
12481435-10	2002	Imatinib also blocked the constitutive activation of Akt and STAT3 by V560GKit but had no affect on the constitutive activation of ERK, Akt, and STAT3 by D816VKit.	imatinib	0-8	signal transducer and activator of transcription 3	Mus musculus	61-66
12481435-1	2002	Imatinib (Glivec; STI571) is an ATP-competitive kinase inhibitor of c-Abl, BCR/ABL, c-Kit, and platelet-derived growth factor receptor.	imatinib	10-16	BCR activator of RhoGEF and GTPase	Mus musculus	75-82
12481435-1	2002	Imatinib (Glivec; STI571) is an ATP-competitive kinase inhibitor of c-Abl, BCR/ABL, c-Kit, and platelet-derived growth factor receptor.	imatinib	10-16	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	84-89
12481435-1	2002	Imatinib (Glivec; STI571) is an ATP-competitive kinase inhibitor of c-Abl, BCR/ABL, c-Kit, and platelet-derived growth factor receptor.	imatinib	18-24	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	68-73
12481435-1	2002	Imatinib (Glivec; STI571) is an ATP-competitive kinase inhibitor of c-Abl, BCR/ABL, c-Kit, and platelet-derived growth factor receptor.	imatinib	18-24	BCR activator of RhoGEF and GTPase	Mus musculus	75-82
12481435-1	2002	Imatinib (Glivec; STI571) is an ATP-competitive kinase inhibitor of c-Abl, BCR/ABL, c-Kit, and platelet-derived growth factor receptor.	imatinib	18-24	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	84-89
12481435-6	2002	Growth of FDC(WTKit) was inhibited by Imatinib with GI50 (a concentration of drug at which 50% inhibition of growth occurs) of 0.1-0.2 microM but FDC(V560GKit) were more sensitive to Imatinib with a GI50 of 0.01-0.025 microM and FDC(D816VKit) were resistant to Imatinib with a GI50 greater than 5 microM.	imatinib	38-46	icos ligand	Mus musculus	52-56
12481435-9	2002	In signaling studies, addition of stem cell factor (SCF) induced phosphorylation of ERK and Akt by WTKit, and ERK, Akt and STAT3 by V560GKit, which were all blocked by Imatinib.	imatinib	168-176	kit ligand	Mus musculus	34-50
12481435-9	2002	In signaling studies, addition of stem cell factor (SCF) induced phosphorylation of ERK and Akt by WTKit, and ERK, Akt and STAT3 by V560GKit, which were all blocked by Imatinib.	imatinib	168-176	kit ligand	Mus musculus	52-55
12481435-9	2002	In signaling studies, addition of stem cell factor (SCF) induced phosphorylation of ERK and Akt by WTKit, and ERK, Akt and STAT3 by V560GKit, which were all blocked by Imatinib.	imatinib	168-176	mitogen-activated protein kinase 1	Mus musculus	84-87
12481435-9	2002	In signaling studies, addition of stem cell factor (SCF) induced phosphorylation of ERK and Akt by WTKit, and ERK, Akt and STAT3 by V560GKit, which were all blocked by Imatinib.	imatinib	168-176	thymoma viral proto-oncogene 1	Mus musculus	92-95
12481435-9	2002	In signaling studies, addition of stem cell factor (SCF) induced phosphorylation of ERK and Akt by WTKit, and ERK, Akt and STAT3 by V560GKit, which were all blocked by Imatinib.	imatinib	168-176	mitogen-activated protein kinase 1	Mus musculus	110-113
12447850-1	2002	Imatinib mesylate (Gleevec, Novartis Pharmaceuticals Corp, East Hanover, NJ; Glivec, Novartis Pharma AG, Basel, Switzerland), a signal transduction inhibitor with preferential effects against the tyrosine kinase activity of the protein product of the ABL proto-oncogene, induced hematologic responses in >or=90% of patients with chronic-phase chronic myeloid leukemia (CML).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	251-254
12389876-5	2002	Imatinib is indicated for the treatment of patients with CML who failed interferon (IFN)-alpha therapy and for the treatment of patients with gastrointestinal stromal tumors (GISTs) expressing the tyrosine kinase receptor c-kit.	imatinib	0-8	interferon alpha 1	Homo sapiens	72-94
12389876-12	2002	In cases of CML, imatinib should be further limited to patients who have tried and failed IFN-alpha therapy or who are not candidates for an allogeneic stem cell transplant.	imatinib	17-25	interferon alpha 1	Homo sapiens	90-99
12176881-2	2002	Imatinib mesylate (STI571), a selective inhibitor of the Bcr-Abl tyrosine kinase, has significant activity in AP CML.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
12447845-5	2002	Imatinib mesylate, a signal transduction inhibitor that inhibits tyrosine kinase activity, the protein product of the ABL proto-oncogene, has remarkable activity in patients with chronic myeloid leukemia (CML) and Philadelphia chromosome-positive (Ph(+)) acute lymphoblastic leukemia (ALL).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-121
12208881-6	2002	Inhibition of BCR/ABL tyrosine kinase with STI571 restores Lyn responsiveness to SDF-1 signaling.	imatinib	43-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
12208881-6	2002	Inhibition of BCR/ABL tyrosine kinase with STI571 restores Lyn responsiveness to SDF-1 signaling.	imatinib	43-49	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	59-62
12208881-6	2002	Inhibition of BCR/ABL tyrosine kinase with STI571 restores Lyn responsiveness to SDF-1 signaling.	imatinib	43-49	C-X-C motif chemokine ligand 12	Homo sapiens	81-86
12200353-3	2002	Imatinib is an orally administered, potent inhibitor of the Bcr-Abl tyrosine kinase.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
12181044-0	2002	Serial monitoring of BCR-ABL by peripheral blood real-time polymerase chain reaction predicts the marrow cytogenetic response to imatinib mesylate in chronic myeloid leukaemia.	imatinib	129-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
12176881-2	2002	Imatinib mesylate (STI571), a selective inhibitor of the Bcr-Abl tyrosine kinase, has significant activity in AP CML.	imatinib	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
12231544-0	2002	Flavopiridol potentiates STI571-induced mitochondrial damage and apoptosis in BCR-ABL-positive human leukemia cells.	imatinib	25-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
12208734-0	2002	The c-kit tyrosine kinase inhibitor STI571 for colorectal cancer therapy.	imatinib	36-42	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	4-9
12208734-1	2002	The c-kit tyrosine kinase inhibitor STI571 exhibits a substantial therapeutic activity in patients with chronic myeloid leukemia and gastrointestinal stromal tumors respectively associated with constitutive activation of the BCR-ABL and c-kit tyrosine kinases.	imatinib	36-42	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	4-9
12208734-1	2002	The c-kit tyrosine kinase inhibitor STI571 exhibits a substantial therapeutic activity in patients with chronic myeloid leukemia and gastrointestinal stromal tumors respectively associated with constitutive activation of the BCR-ABL and c-kit tyrosine kinases.	imatinib	36-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	225-232
12208734-1	2002	The c-kit tyrosine kinase inhibitor STI571 exhibits a substantial therapeutic activity in patients with chronic myeloid leukemia and gastrointestinal stromal tumors respectively associated with constitutive activation of the BCR-ABL and c-kit tyrosine kinases.	imatinib	36-42	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	237-242
12208734-9	2002	These encouraging results warrant further preclinical investigations and clinical trials on the use of the c-kit inhibitor STI571 as a chemotherapeutic agent in colon cancer prevention and in treatment of advanced colorectal cancers associated with liver metastases.	imatinib	123-129	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	107-112
12231544-5	2002	STI571/flavopiridol-mediated apoptosis was associated with the caspase-independent down-regulation of Bcl-x(L) and Mcl-1, activation of extracellular signal-regulated kinase and c-Jun NH(2)-terminal kinase, and the caspase-dependent release of Smac/DIABLO and loss of deltapsi(m).	imatinib	0-6	BCL2 like 1	Homo sapiens	102-110
12231544-1	2002	PURPOSE: The goal of this study was to characterize interactions between the Bcr/Abl kinase inhibitor STI571 and the cyclin-dependent kinase inhibitor flavopiridol in Bcr/Abl(+) human leukemia cells.	imatinib	102-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
12231544-5	2002	STI571/flavopiridol-mediated apoptosis was associated with the caspase-independent down-regulation of Bcl-x(L) and Mcl-1, activation of extracellular signal-regulated kinase and c-Jun NH(2)-terminal kinase, and the caspase-dependent release of Smac/DIABLO and loss of deltapsi(m).	imatinib	0-6	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	115-120
12231544-1	2002	PURPOSE: The goal of this study was to characterize interactions between the Bcr/Abl kinase inhibitor STI571 and the cyclin-dependent kinase inhibitor flavopiridol in Bcr/Abl(+) human leukemia cells.	imatinib	102-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-174
12231544-5	2002	STI571/flavopiridol-mediated apoptosis was associated with the caspase-independent down-regulation of Bcl-x(L) and Mcl-1, activation of extracellular signal-regulated kinase and c-Jun NH(2)-terminal kinase, and the caspase-dependent release of Smac/DIABLO and loss of deltapsi(m).	imatinib	0-6	diablo IAP-binding mitochondrial protein	Homo sapiens	244-248
12231544-5	2002	STI571/flavopiridol-mediated apoptosis was associated with the caspase-independent down-regulation of Bcl-x(L) and Mcl-1, activation of extracellular signal-regulated kinase and c-Jun NH(2)-terminal kinase, and the caspase-dependent release of Smac/DIABLO and loss of deltapsi(m).	imatinib	0-6	diablo IAP-binding mitochondrial protein	Homo sapiens	249-255
12231544-3	2002	RESULTS: In K562 cells, coadministration of marginally toxic concentrations of STI571 (200 nM) and flavopiridol (150 nM) for 48 h resulted in a marked increase in mitochondrial damage (e.g., cytochrome c release), activation of caspase-3, caspase-8, and Bid, and apoptosis.	imatinib	79-85	cytochrome c, somatic	Homo sapiens	191-203
12231544-7	2002	Finally, STI571/flavopiridol effectively induced apoptosis in STI571-resistant K562 cells displaying amplification of the Bcr/Abl protein.	imatinib	9-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
12231544-7	2002	Finally, STI571/flavopiridol effectively induced apoptosis in STI571-resistant K562 cells displaying amplification of the Bcr/Abl protein.	imatinib	62-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
12231544-3	2002	RESULTS: In K562 cells, coadministration of marginally toxic concentrations of STI571 (200 nM) and flavopiridol (150 nM) for 48 h resulted in a marked increase in mitochondrial damage (e.g., cytochrome c release), activation of caspase-3, caspase-8, and Bid, and apoptosis.	imatinib	79-85	caspase 3	Homo sapiens	228-237
12231544-8	2002	CONCLUSIONS: Together, these findings indicate that the cyclin-dependent kinase inhibitor flavopiridol induces multiple perturbations in signaling pathways in STI571-treated Bcr/Abl(+) human leukemia cells that culminate in mitochondrial injury, caspase activation, and apoptosis.	imatinib	159-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-181
12231544-3	2002	RESULTS: In K562 cells, coadministration of marginally toxic concentrations of STI571 (200 nM) and flavopiridol (150 nM) for 48 h resulted in a marked increase in mitochondrial damage (e.g., cytochrome c release), activation of caspase-3, caspase-8, and Bid, and apoptosis.	imatinib	79-85	caspase 8	Homo sapiens	239-248
12231544-3	2002	RESULTS: In K562 cells, coadministration of marginally toxic concentrations of STI571 (200 nM) and flavopiridol (150 nM) for 48 h resulted in a marked increase in mitochondrial damage (e.g., cytochrome c release), activation of caspase-3, caspase-8, and Bid, and apoptosis.	imatinib	79-85	BH3 interacting domain death agonist	Homo sapiens	254-257
12582448-1	2002	Imatinib mesylate (STI571, Gleevec, Glivec, a selective inhibitor of the BCR-ABL tyrosine kinase causative of chronic myeloid leukemia (CML), represents the paradigm of how a better understanding of the pathogenetic mechanisms of a neoplastic disease can lead to the development of a targeted molecular therapy.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
12582448-1	2002	Imatinib mesylate (STI571, Gleevec, Glivec, a selective inhibitor of the BCR-ABL tyrosine kinase causative of chronic myeloid leukemia (CML), represents the paradigm of how a better understanding of the pathogenetic mechanisms of a neoplastic disease can lead to the development of a targeted molecular therapy.	imatinib	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
12217801-5	2002	RESULTS: We show that treatment of K562 with STI571 blocks the binding of DREAM to the Hrk gene and allows the expression of Hrk, which correlates with the induction of apoptosis.	imatinib	45-51	potassium voltage-gated channel interacting protein 3	Homo sapiens	74-79
12528770-3	2002	Based on these observations, imatinib was developed as a specific inhibitor for the Bcr-Abl protein tyrosine kinase.	imatinib	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
12528772-2	2002	The specific identification of GIST has become increasingly important because a Kit-selective tyrosine kinase inhibitor, imatinib (Glivec, formerly known as STI571, Novartis Pharma AG, Basel, Switzerland), has shown promise as an effective adjuvant therapy treatment.	imatinib	131-137	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	80-83
12528772-2	2002	The specific identification of GIST has become increasingly important because a Kit-selective tyrosine kinase inhibitor, imatinib (Glivec, formerly known as STI571, Novartis Pharma AG, Basel, Switzerland), has shown promise as an effective adjuvant therapy treatment.	imatinib	157-163	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	80-83
12528773-9	2002	Signal transduction inhibition as cancer therapy was first tested successfully with imatinib mesylate (formerly known as STI571), a selective small-molecule tyrosine kinase inhibitor, with the initial target being blockade of Bcr-Abl, the oncogene with tyrosine kinase activity responsible for the pathogenesis of chronic myelogenous leukemia (CML).	imatinib	84-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	226-233
12528773-9	2002	Signal transduction inhibition as cancer therapy was first tested successfully with imatinib mesylate (formerly known as STI571), a selective small-molecule tyrosine kinase inhibitor, with the initial target being blockade of Bcr-Abl, the oncogene with tyrosine kinase activity responsible for the pathogenesis of chronic myelogenous leukemia (CML).	imatinib	121-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	226-233
12528773-10	2002	Imatinib was subsequently shown to block activity of the KIT tyrosine kinase as well, and in laboratory studies this led to apoptotic death of GIST cells.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	57-60
12528777-1	2002	Imatinib (Glivec, formerly STI571, Novartis Pharma AG, Basel, Switzerland) potently inhibits several protein tyrosine kinases, including Bcr-Abl, Kit, and the platelet-derived growth factor receptor.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-144
12217811-1	2002	BACKGROUND AND OBJECTIVES: The new Abl tyrosine kinase inhibitor imatinib (imatinib mesylate, STI571) is very effective in the treatment of patients with chronic myeloid leukemia (CML).	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
12217811-1	2002	BACKGROUND AND OBJECTIVES: The new Abl tyrosine kinase inhibitor imatinib (imatinib mesylate, STI571) is very effective in the treatment of patients with chronic myeloid leukemia (CML).	imatinib	75-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
12217811-1	2002	BACKGROUND AND OBJECTIVES: The new Abl tyrosine kinase inhibitor imatinib (imatinib mesylate, STI571) is very effective in the treatment of patients with chronic myeloid leukemia (CML).	imatinib	94-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
12217801-5	2002	RESULTS: We show that treatment of K562 with STI571 blocks the binding of DREAM to the Hrk gene and allows the expression of Hrk, which correlates with the induction of apoptosis.	imatinib	45-51	harakiri, BCL2 interacting protein	Homo sapiens	87-90
12217801-5	2002	RESULTS: We show that treatment of K562 with STI571 blocks the binding of DREAM to the Hrk gene and allows the expression of Hrk, which correlates with the induction of apoptosis.	imatinib	45-51	harakiri, BCL2 interacting protein	Homo sapiens	125-128
12412295-7	2002	Imatinib mesylate, an agent targeting BCR-ABL, is expected to be useful as an effective therapeutic agent for chronic myeloid leukemia.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
12200668-2	2002	More recently, it has been reported that CML patients could develop resistance to the Bcr-Abl tyrosine kinase inhibitor, imatinib (STI571, Gleevec), pointing to the need for development of additional Bcr-Abl tyrosine kinase inhibitors or other therapeutic strategies.	imatinib	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
12200668-2	2002	More recently, it has been reported that CML patients could develop resistance to the Bcr-Abl tyrosine kinase inhibitor, imatinib (STI571, Gleevec), pointing to the need for development of additional Bcr-Abl tyrosine kinase inhibitors or other therapeutic strategies.	imatinib	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	200-207
12200668-2	2002	More recently, it has been reported that CML patients could develop resistance to the Bcr-Abl tyrosine kinase inhibitor, imatinib (STI571, Gleevec), pointing to the need for development of additional Bcr-Abl tyrosine kinase inhibitors or other therapeutic strategies.	imatinib	131-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
12202658-0	2002	Molecular targeting of platelet-derived growth factor B by imatinib mesylate in a patient with metastatic dermatofibrosarcoma protuberans.	imatinib	59-76	platelet derived growth factor subunit B	Homo sapiens	23-55
12202658-3	2002	PATIENTS AND METHODS: A patient with unresectable, metastatic dermatofibrosarcoma protuberans received imatinib mesylate (400 mg bid).	imatinib	103-120	BH3 interacting domain death agonist	Homo sapiens	129-132
12200666-0	2002	Early reduction of BCR-ABL mRNA transcript levels predicts cytogenetic response in chronic phase CML patients treated with imatinib after failure of interferon alpha.	imatinib	123-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
12200666-11	2002	The probability for a major cytogenetic response was significantly higher in patients with a BCR-ABL/ABL ratio <20% after 2 months of imatinib therapy.	imatinib	137-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
12200666-11	2002	The probability for a major cytogenetic response was significantly higher in patients with a BCR-ABL/ABL ratio <20% after 2 months of imatinib therapy.	imatinib	137-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-100
12200666-12	2002	We conclude that: (1) quantitative determination of residual disease with real time RT-PCR is a reliable and sensitive method to monitor CML patients on imatinib therapy; (2) BCR-ABL/ABL ratios correlate well with cytogenetic response; (3) in IFN-pretreated patients all complete responders to imatinib have evidence of residual disease with the limited follow-up available; and (4) cytogenetic response at 6 months of therapy in CP patients is predictable with real time RT-PCR at 2 months.	imatinib	294-302	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-182
12077114-0	2002	Analysis of the structural basis of specificity of inhibition of the Abl kinase by STI571.	imatinib	83-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-72
12231066-2	2002	The success of imatinib mesylate (Gleevec; Novartis Pharmaceuticals, East Hanover, NJ), a small molecule that inhibits the activation of the BCR-Abl oncogene in the treatment of chronic myelogenous leukemia, has demonstrated how effective targeted strategies can be when properly applied.	imatinib	15-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-148
12077114-1	2002	STI571, a selective inhibitor of Bcr-Abl, has been a successful therapeutic agent in clinical trials for chronic myelogenous leukemia.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
12077114-3	2002	Co-crystallization studies of Abl kinase and an STI571-related compound identify specific amino acid residues as critical to STI571 binding, one of which, T315, has been characterized as an acquired Thr to Ile mutation in relapsed patients.	imatinib	125-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-33
12077114-5	2002	Using a variety of models of STI571 binding to the Abl kinase, we have performed an extensive mutational analysis of sites that might alter the sensitivity of the Abl kinase to STI571.	imatinib	29-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-54
12077114-5	2002	Using a variety of models of STI571 binding to the Abl kinase, we have performed an extensive mutational analysis of sites that might alter the sensitivity of the Abl kinase to STI571.	imatinib	29-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-166
12077114-5	2002	Using a variety of models of STI571 binding to the Abl kinase, we have performed an extensive mutational analysis of sites that might alter the sensitivity of the Abl kinase to STI571.	imatinib	177-183	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-54
12077114-5	2002	Using a variety of models of STI571 binding to the Abl kinase, we have performed an extensive mutational analysis of sites that might alter the sensitivity of the Abl kinase to STI571.	imatinib	177-183	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-166
12209733-1	2002	STI571 (imatinib mesylate; Gleevec) is a selective inhibitor of the bcr-abl, c-kit, and platelet-derived growth factor receptor tyrosine kinases.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
12185586-0	2002	Phosphatidylinositol-3 kinase inhibitors enhance the anti-leukemia effect of STI571.	imatinib	77-83	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	0-29
12185586-2	2002	STI571 (Gleevec), a novel anti-leukemia drug targeting BCR/ABL kinase can induce remissions of the Ph(1)-positive leukemias.	imatinib	0-6	BCR activator of RhoGEF and GTPase	Homo sapiens	55-58
12185586-2	2002	STI571 (Gleevec), a novel anti-leukemia drug targeting BCR/ABL kinase can induce remissions of the Ph(1)-positive leukemias.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-62
12181402-0	2002	Response to imatinib mesylate in patients with chronic myeloproliferative diseases with rearrangements of the platelet-derived growth factor receptor beta.	imatinib	12-29	platelet derived growth factor receptor beta	Homo sapiens	110-154
12181402-3	2002	The tyrosine kinase inhibitor imatinib mesylate specifically inhibits ABL, PDGFR, and KIT kinases and has impressive clinical efficacy in BCR-ABL-positive chronic myeloid leukemia.	imatinib	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-73
12181402-3	2002	The tyrosine kinase inhibitor imatinib mesylate specifically inhibits ABL, PDGFR, and KIT kinases and has impressive clinical efficacy in BCR-ABL-positive chronic myeloid leukemia.	imatinib	30-38	platelet derived growth factor receptor beta	Homo sapiens	75-80
12181402-3	2002	The tyrosine kinase inhibitor imatinib mesylate specifically inhibits ABL, PDGFR, and KIT kinases and has impressive clinical efficacy in BCR-ABL-positive chronic myeloid leukemia.	imatinib	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-145
12181402-12	2002	CONCLUSIONS: Imatinib mesylate induces durable responses in patients with chronic myeloproliferative diseases associated with activation of PDGFRB.	imatinib	13-30	platelet derived growth factor receptor beta	Homo sapiens	140-146
12173041-10	2002	Finally, we compared leukemic cell killing by RNAi to that caused by the ABL kinase tyrosine inhibitor, STI 571, Imatinib.	imatinib	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-76
12209733-1	2002	STI571 (imatinib mesylate; Gleevec) is a selective inhibitor of the bcr-abl, c-kit, and platelet-derived growth factor receptor tyrosine kinases.	imatinib	0-6	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	77-82
12209733-1	2002	STI571 (imatinib mesylate; Gleevec) is a selective inhibitor of the bcr-abl, c-kit, and platelet-derived growth factor receptor tyrosine kinases.	imatinib	8-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
12209733-1	2002	STI571 (imatinib mesylate; Gleevec) is a selective inhibitor of the bcr-abl, c-kit, and platelet-derived growth factor receptor tyrosine kinases.	imatinib	8-25	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	77-82
12130526-4	2002	In the current study we show that the farnesyl transferase inhibitor (FTI) SCH66336 (lonafarnib) inhibits the proliferation of STI571-resistant BCR-ABL-positive cell lines and hematopoietic colony formation from peripheral blood samples of STI571-resistant patients with CML.	imatinib	127-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
12149456-0	2002	Clinical resistance to the kinase inhibitor STI-571 in chronic myeloid leukemia by mutation of Tyr-253 in the Abl kinase domain P-loop.	imatinib	44-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-113
12149456-1	2002	The Abl tyrosine kinase inhibitor STI-571 is effective therapy for stable phase chronic myeloid leukemia (CML) patients, but the majority of CML blast-crisis patients that respond to STI-571 relapse because of reactivation of Bcr-Abl signaling.	imatinib	34-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
12149456-1	2002	The Abl tyrosine kinase inhibitor STI-571 is effective therapy for stable phase chronic myeloid leukemia (CML) patients, but the majority of CML blast-crisis patients that respond to STI-571 relapse because of reactivation of Bcr-Abl signaling.	imatinib	34-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	226-233
12149456-1	2002	The Abl tyrosine kinase inhibitor STI-571 is effective therapy for stable phase chronic myeloid leukemia (CML) patients, but the majority of CML blast-crisis patients that respond to STI-571 relapse because of reactivation of Bcr-Abl signaling.	imatinib	183-190	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
12149456-8	2002	The Abl P-loop is a second target for mutations that confer resistance to STI-571 in advanced CML, and the Y253F mutation may impair the induced-fit interaction of STI-571 with the Abl catalytic domain rather than sterically blocking binding of the drug.	imatinib	74-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
12130516-3	2002	We investigated in this study the mechanism of resistance to STI571 through point mutations in the tyrosine kinase domain and/or BCR-ABL gene amplification in 24 patients (16 in chronic phase and 8 in accelerated phase of the disease) who obtained no cytogenetic response to STI571 treatment.	imatinib	61-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
12172985-4	2002	RESULTS: Flow cytometric and RT-PCR analyses in a panel of eight Ewing tumour cell lines demonstrated expression of several imatinib mesylate-sensitive tyrosine kinases, including c-KIT, platelet-derived growth factor receptor, c-ABL and c-ARG.	imatinib	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	228-233
12154025-0	2002	Crystal structures of the kinase domain of c-Abl in complex with the small molecule inhibitors PD173955 and imatinib (STI-571).	imatinib	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-48
12154025-0	2002	Crystal structures of the kinase domain of c-Abl in complex with the small molecule inhibitors PD173955 and imatinib (STI-571).	imatinib	118-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-48
12154025-3	2002	We report crystal structures of the kinase domain of Abl in complex with two such inhibitors, imatinib (also known as STI-571 and Gleevec) and PD173955 (Parke-Davis).	imatinib	94-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
12154025-3	2002	We report crystal structures of the kinase domain of Abl in complex with two such inhibitors, imatinib (also known as STI-571 and Gleevec) and PD173955 (Parke-Davis).	imatinib	118-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
12154026-6	2002	We have compared the potency of these two compounds and four other analogues with imatinib on Bcr-Abl-dependent cell growth, cytokine-dependent cell growth, and tyrosine kinase inhibition.	imatinib	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
12204532-0	2002	Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia.	imatinib	113-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
12204532-1	2002	Through sequencing analysis of blood or bone marrow samples from patients with chronic myeloid leukemia, we identified BCR-ABL kinase domain mutations in 29 of 32 patients whose disease relapsed after an initial response to the tyrosine kinase inhibitor imatinib.	imatinib	254-262	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-126
12204529-2	2002	Imatinib, a potent inhibitor of Bcr-Abl, has shown impressive clinical activity in CML patients.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
12204529-4	2002	Studies reported over the past year have begun to elucidate the molecular basis of imatinib resistance, which may involve amplification of BCR-ABL or, more commonly, mutations that introduce amino acid substitutions into the Bcr-Abl kinase.	imatinib	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-146
12204529-4	2002	Studies reported over the past year have begun to elucidate the molecular basis of imatinib resistance, which may involve amplification of BCR-ABL or, more commonly, mutations that introduce amino acid substitutions into the Bcr-Abl kinase.	imatinib	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	225-232
12204532-0	2002	Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia.	imatinib	103-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
12134042-7	2002	Inhibition of c-Kit activity with either a pharmacological inhibitor of c-Kit (STI 571) or a dominant-negative c-Kit protein reversed SCF-dependent proliferation.	imatinib	79-86	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-19
12134042-7	2002	Inhibition of c-Kit activity with either a pharmacological inhibitor of c-Kit (STI 571) or a dominant-negative c-Kit protein reversed SCF-dependent proliferation.	imatinib	79-86	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	72-77
12134042-7	2002	Inhibition of c-Kit activity with either a pharmacological inhibitor of c-Kit (STI 571) or a dominant-negative c-Kit protein reversed SCF-dependent proliferation.	imatinib	79-86	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	72-77
12134042-7	2002	Inhibition of c-Kit activity with either a pharmacological inhibitor of c-Kit (STI 571) or a dominant-negative c-Kit protein reversed SCF-dependent proliferation.	imatinib	79-86	KIT ligand	Homo sapiens	134-137
12204532-7	2002	Our data support a clonal selection model of preexisting BCR-ABL mutations that confer imatinib resistance.	imatinib	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
12114418-10	2002	In a subset analysis, survival rates among 161 patients with Ph-positive CML after hematological or cytogenetic failure after IFN-alpha who had been treated with imatinib mesylate were better than those for similar patients treated previously with other regimens.	imatinib	162-179	interferon alpha 1	Homo sapiens	126-135
12114418-11	2002	In summary, imatinib mesylate is highly effective in chronic-phase CML after IFN-alpha failure.	imatinib	12-29	interferon alpha 1	Homo sapiens	77-86
12135670-13	2002	CONCLUSIONS: Favorable cytotoxicity and proapoptotic activity of imatinib in conjunction with As2O3 and specific down-regulation of Bcr-Abl protein levels by As2O3 in K562 cells indicate that As2O3 in combination with imatinib might be useful for circumventing resistance to imatinib monotherapy.	imatinib	218-226	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
12042704-2	2002	STI571 is a small molecule inhibitor with activity against BCR-ABL, the deregulated tyrosine kinase responsible for initiation and maintenance of the disease in the chronic phase of chronic myeloid leukemia (CML).	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
12135670-13	2002	CONCLUSIONS: Favorable cytotoxicity and proapoptotic activity of imatinib in conjunction with As2O3 and specific down-regulation of Bcr-Abl protein levels by As2O3 in K562 cells indicate that As2O3 in combination with imatinib might be useful for circumventing resistance to imatinib monotherapy.	imatinib	218-226	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
12094266-0	2002	ABL-specific tyrosine kinase inhibitor imatinib as salvage therapy in a child with Philadelphia chromosome-positive acute mixed lineage leukemia (AMLL).	imatinib	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
12028032-1	2002	We report a 53-year-old man with lymphoid blast crisis of Ph+ chronic myeloid leukaemia who was treated with STI571, a selective inhibitor of the enzymatic activity of BCR-ABL.	imatinib	109-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	168-175
12094244-5	2002	Currently, patients with PDGFRB or ABL fusion genes are candidates for treatment with Imatinib (STI571), but it is likely that alternative strategies will be necessary for the treatment of most other patients.	imatinib	86-94	platelet derived growth factor receptor beta	Homo sapiens	25-31
12094244-5	2002	Currently, patients with PDGFRB or ABL fusion genes are candidates for treatment with Imatinib (STI571), but it is likely that alternative strategies will be necessary for the treatment of most other patients.	imatinib	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
12094244-5	2002	Currently, patients with PDGFRB or ABL fusion genes are candidates for treatment with Imatinib (STI571), but it is likely that alternative strategies will be necessary for the treatment of most other patients.	imatinib	96-102	platelet derived growth factor receptor beta	Homo sapiens	25-31
12094244-5	2002	Currently, patients with PDGFRB or ABL fusion genes are candidates for treatment with Imatinib (STI571), but it is likely that alternative strategies will be necessary for the treatment of most other patients.	imatinib	96-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
12040447-3	2002	In this study, we report the apoptotic effect of STI571 in combination with daunorubicin (DNR) on peripheral blood mononuclear cells from 11 CML patients and four BCR-ABL-positive cell lines: AR230, LAMA84, K562 and KCL22.	imatinib	49-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
12049868-3	2002	Clinical trials have confirmed the efficacy of imatinib, which has toxic effects in cells that express BCR-ABL.	imatinib	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
12411057-1	2002	OBJECTIVE: To investigate the mechanism of STI571 inducing apoptosis of K562 cells which express P210(BCR/ABL).	imatinib	43-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
12411057-6	2002	Caspase-3 was activated and there was an cytosolic accumulation of cyto C. CONCLUSION: STI571 could rapidly decrease the tyrosine phosphorylation level of P210(BCR/ABL).	imatinib	87-93	caspase 3	Homo sapiens	0-9
12411057-6	2002	Caspase-3 was activated and there was an cytosolic accumulation of cyto C. CONCLUSION: STI571 could rapidly decrease the tyrosine phosphorylation level of P210(BCR/ABL).	imatinib	87-93	BCR activator of RhoGEF and GTPase	Homo sapiens	155-167
12021410-0	2002	Inhibition of c-Abl with STI571 attenuates stress-activated protein kinase activation and apoptosis in the cellular response to 1-beta-D-arabinofuranosylcytosine.	imatinib	25-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
12021410-3	2002	STI571 (imatinib mesylate), an inhibitor of c-Abl, blocked both activation and mitochondrial targeting of SAPK in the ara-C response.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-49
12021410-3	2002	STI571 (imatinib mesylate), an inhibitor of c-Abl, blocked both activation and mitochondrial targeting of SAPK in the ara-C response.	imatinib	0-6	mitogen-activated protein kinase 9	Homo sapiens	106-110
12021410-3	2002	STI571 (imatinib mesylate), an inhibitor of c-Abl, blocked both activation and mitochondrial targeting of SAPK in the ara-C response.	imatinib	8-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-49
12021410-3	2002	STI571 (imatinib mesylate), an inhibitor of c-Abl, blocked both activation and mitochondrial targeting of SAPK in the ara-C response.	imatinib	8-25	mitogen-activated protein kinase 9	Homo sapiens	106-110
12021410-4	2002	In concert with these effects of STI571, similar findings were obtained in c-Abl-deficient cells.	imatinib	33-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-80
12021410-5	2002	The results further show that STI571 inhibits ara-C-induced loss of mitochondrial transmembrane potential, caspase-3 activation, and apoptosis.	imatinib	30-36	caspase 3	Homo sapiens	107-116
12021410-6	2002	These findings demonstrate that STI571 down-regulates c-Abl-mediated signals that target the mitochondria in the apoptotic response to ara-C.	imatinib	32-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-59
12009895-7	2002	276, 28984-28990], the Abl inhibitor STI571 did not substantially affect its EGF-dependent phosphorylation, suggesting PLSCR1 is a substrate of the EGF receptor kinase, or another EGF-activated kinase.	imatinib	37-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-26
12173333-2	2002	In vitro, inhibition of BCR-ABL protein tyrosine kinase activity by a tyrosine kinase inhibitor, Imatinib mesylate (STI571; formerly CGP57148B), successfully suppressed proliferation/survival of the BCR-ABL positive clones.	imatinib	97-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
11986250-2	2002	Imatinib mesylate (STI571) is a specific inhibitor of BCR-ABL tyrosine kinase that can induce hematologic and cytogenetic remissions in patients with CML.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
11986250-2	2002	Imatinib mesylate (STI571) is a specific inhibitor of BCR-ABL tyrosine kinase that can induce hematologic and cytogenetic remissions in patients with CML.	imatinib	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
11986206-2	2002	Imatinib mesylate (STI571), a specific Bcr-Abl tyrosine-kinase signal-transduction inhibitor, has shown encouraging activity in phase I and II studies of CML.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
11986206-2	2002	Imatinib mesylate (STI571), a specific Bcr-Abl tyrosine-kinase signal-transduction inhibitor, has shown encouraging activity in phase I and II studies of CML.	imatinib	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
11986238-6	2002	Analysis of cell division using the fluorescent dye carboxyfluorescein diacetate succinimidyl ester indicated that imatinib mesylate (1-2 microM) inhibits cycling of CML primitive (CD34(+)CD38(-)) and committed (CD34(+)CD38(+)) progenitors to a much greater extent than normal cells.	imatinib	115-132	CD34 molecule	Homo sapiens	181-185
11986238-6	2002	Analysis of cell division using the fluorescent dye carboxyfluorescein diacetate succinimidyl ester indicated that imatinib mesylate (1-2 microM) inhibits cycling of CML primitive (CD34(+)CD38(-)) and committed (CD34(+)CD38(+)) progenitors to a much greater extent than normal cells.	imatinib	115-132	CD38 molecule	Homo sapiens	188-192
11986238-6	2002	Analysis of cell division using the fluorescent dye carboxyfluorescein diacetate succinimidyl ester indicated that imatinib mesylate (1-2 microM) inhibits cycling of CML primitive (CD34(+)CD38(-)) and committed (CD34(+)CD38(+)) progenitors to a much greater extent than normal cells.	imatinib	115-132	CD34 molecule	Homo sapiens	212-216
11986238-6	2002	Analysis of cell division using the fluorescent dye carboxyfluorescein diacetate succinimidyl ester indicated that imatinib mesylate (1-2 microM) inhibits cycling of CML primitive (CD34(+)CD38(-)) and committed (CD34(+)CD38(+)) progenitors to a much greater extent than normal cells.	imatinib	115-132	CD38 molecule	Homo sapiens	219-223
12173333-2	2002	In vitro, inhibition of BCR-ABL protein tyrosine kinase activity by a tyrosine kinase inhibitor, Imatinib mesylate (STI571; formerly CGP57148B), successfully suppressed proliferation/survival of the BCR-ABL positive clones.	imatinib	97-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	199-206
12173333-2	2002	In vitro, inhibition of BCR-ABL protein tyrosine kinase activity by a tyrosine kinase inhibitor, Imatinib mesylate (STI571; formerly CGP57148B), successfully suppressed proliferation/survival of the BCR-ABL positive clones.	imatinib	116-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
12173333-2	2002	In vitro, inhibition of BCR-ABL protein tyrosine kinase activity by a tyrosine kinase inhibitor, Imatinib mesylate (STI571; formerly CGP57148B), successfully suppressed proliferation/survival of the BCR-ABL positive clones.	imatinib	116-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	199-206
11986785-10	2002	The combination imatinib + gamma-irradiation proved to be significantly synergistic over a broad range of cell growth inhibition levels in both BCR-ABL-positive cell lines and produced the strongest reduction in primary chronic myelogenous leukaemia colony-forming progenitor cells.	imatinib	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
11964283-5	2002	Additional experiments showed that this erythroid differentiation response was largely prevented when the cells were transduced and maintained in the presence of the BCR-ABL-specific tyrosine kinase inhibitor, STI-571.	imatinib	210-217	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-173
11986783-0	2002	The in vitro activity of the tyrosine kinase inhibitor STI571 in BCR-ABL positive chronic myeloid leukaemia cells: synergistic interactions with anti-leukaemic agents.	imatinib	55-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
11986785-2	2002	The tyrosine kinase inhibitor imatinib (formerly STI571) was reported to selectively suppress the proliferation of BCR-ABL-positive cells.	imatinib	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
11986785-2	2002	The tyrosine kinase inhibitor imatinib (formerly STI571) was reported to selectively suppress the proliferation of BCR-ABL-positive cells.	imatinib	49-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
12082538-4	2002	This was not observed in the absence of Bcr-Abl kinase activity or presence of the BCR-ABL inhibitor STI571, which also inhibits c-kit.	imatinib	101-107	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	129-134
12075749-8	2002	Setting residual BCR/abl < 0.01 as an early goal of molecular response, we observed that STI-571 induced a better response than interferon: 49% (20 of 41 patients) versus 35% (15 of 62 patients) at 6 months (P = 0.025) and 52% (32 of 61 patients) versus 34% (35 of 103 patients) at 12 months (P = 0.01), respectively.	imatinib	92-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
11964320-0	2002	Transient response to imatinib mesylate (STI571) in a patient with the ETV6-ABL t(9;12) translocation.	imatinib	22-39	ETS variant transcription factor 6	Homo sapiens	71-75
11964320-0	2002	Transient response to imatinib mesylate (STI571) in a patient with the ETV6-ABL t(9;12) translocation.	imatinib	22-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-79
11964320-1	2002	We report the transient response of a patient with the ETV6-ABL fusion gene to imatinib mesylate (STI571).	imatinib	79-96	ETS variant transcription factor 6	Homo sapiens	55-59
11964320-1	2002	We report the transient response of a patient with the ETV6-ABL fusion gene to imatinib mesylate (STI571).	imatinib	79-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-63
11964320-2	2002	A 38-year-old man was referred with an erroneous diagnosis of Philadelphia-positive chronic myeloid leukemia in blastic transformation for treatment with the ABL tyrosine kinase inhibitor, STI571.	imatinib	189-195	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-161
12367580-0	2002	Differences between in vivo and in vitro sensitivity to imatinib of Bcr/Abl+ cells obtained from leukemic patients.	imatinib	56-64	BCR activator of RhoGEF and GTPase	Homo sapiens	68-71
11964322-0	2002	High frequency of point mutations clustered within the adenosine triphosphate-binding region of BCR/ABL in patients with chronic myeloid leukemia or Ph-positive acute lymphoblastic leukemia who develop imatinib (STI571) resistance.	imatinib	202-210	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
11964322-0	2002	High frequency of point mutations clustered within the adenosine triphosphate-binding region of BCR/ABL in patients with chronic myeloid leukemia or Ph-positive acute lymphoblastic leukemia who develop imatinib (STI571) resistance.	imatinib	212-218	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
11964322-1	2002	Point mutations were found in the adenosine triphosphate (ATP) binding region of BCR/ABL in 12 of 18 patients with chronic myeloid leukemia (CML) or Ph-positive acute lymphoblastic leukemia (Ph(+) ALL) and imatinib resistance (defined as loss of established hematologic response), but they were found in only 1 of 10 patients with CML with imatinib refractoriness (failure to achieve cytogenetic response).	imatinib	206-214	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
11964322-1	2002	Point mutations were found in the adenosine triphosphate (ATP) binding region of BCR/ABL in 12 of 18 patients with chronic myeloid leukemia (CML) or Ph-positive acute lymphoblastic leukemia (Ph(+) ALL) and imatinib resistance (defined as loss of established hematologic response), but they were found in only 1 of 10 patients with CML with imatinib refractoriness (failure to achieve cytogenetic response).	imatinib	340-348	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
11964322-3	2002	Three mutations (T315I, Y253H, and F317L present in 3, 1, and 1 patients, respectively) have a predicted role in abrogating imatinib binding to BCR/ABL, whereas 3 other mutations (E255K, G250E, and M351T, present in 4, 2, and 2 patients, respectively) do not.	imatinib	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
12367580-1	2002	Imatinib mesylate (imatinib) inhibits Bcr/Abl, an oncogenic fusion protein.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
12367580-1	2002	Imatinib mesylate (imatinib) inhibits Bcr/Abl, an oncogenic fusion protein.	imatinib	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
12367580-2	2002	The in vitro effects of imatinib on BCR/ABL+ leukemic cells include inhibition of Bcr/Abl tyrosine phosphorylation, block of proliferation, and induction of apoptosis.	imatinib	24-32	BCR activator of RhoGEF and GTPase	Homo sapiens	36-39
12367580-2	2002	The in vitro effects of imatinib on BCR/ABL+ leukemic cells include inhibition of Bcr/Abl tyrosine phosphorylation, block of proliferation, and induction of apoptosis.	imatinib	24-32	BCR activator of RhoGEF and GTPase	Homo sapiens	82-85
12367580-5	2002	Imatinib also caused an inhibition of Bcr/Abl autophosphorylation; however, the degree of inhibition obtained in vivo was substantially lower than that achieved in vitro with similar concentrations of imatinib.	imatinib	0-8	BCR activator of RhoGEF and GTPase	Homo sapiens	38-41
12367580-8	2002	Leukemic cells obtained at relapse maintained in vitro sensitivity (Bcr/Abl autophosphorylation and proliferation inhibition) to imatinib concentration measured in vivo (3 microM or higher), although a partial resistance to the antiproliferative effects of imatinib was present at low (0.01-0.3 microM) concentrations.	imatinib	129-137	BCR activator of RhoGEF and GTPase	Homo sapiens	68-71
11914627-2	2002	Studies using the oral agent STI-571 (Gleevec, Novartis), an inhibitor of the tyrosine kinases bcr-abl, c-kit, and PDGFR, have shown significant responses in patients with chronic myelogenous leukemia and gastrointestinal stromal tumor.	imatinib	29-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
12006504-2	2002	Imatinib, an orally administered inhibitor of the breakpoint cluster region-Abl tyrosine kinase, is capable of blocking proliferation and inducing apoptosis in CML cell lines.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-79
12006504-11	2002	Cytochrome P-450 3A4 is the main enzyme responsible for imatinib metabolism.	imatinib	56-64	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-20
12094371-7	2002	STI-571 is a small molecule that selectively inhibits the enzymatic activity of the ABL, platelet-derived growth factor receptor, and KIT tyrosine kinases and the BCR-ABL fusion protein and is a landmark development in cancer therapy.	imatinib	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-87
12094371-7	2002	STI-571 is a small molecule that selectively inhibits the enzymatic activity of the ABL, platelet-derived growth factor receptor, and KIT tyrosine kinases and the BCR-ABL fusion protein and is a landmark development in cancer therapy.	imatinib	0-7	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	134-137
12094371-7	2002	STI-571 is a small molecule that selectively inhibits the enzymatic activity of the ABL, platelet-derived growth factor receptor, and KIT tyrosine kinases and the BCR-ABL fusion protein and is a landmark development in cancer therapy.	imatinib	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
12094372-5	2002	A KIT tyrosine kinase inhibitor, STI-571 (imatinib [Gleevec]; Novartis, Basel, Switzerland), has recently shown promise in the treatment of metastatic GISTs.	imatinib	33-40	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	2-5
12094372-5	2002	A KIT tyrosine kinase inhibitor, STI-571 (imatinib [Gleevec]; Novartis, Basel, Switzerland), has recently shown promise in the treatment of metastatic GISTs.	imatinib	42-50	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	2-5
12094372-5	2002	A KIT tyrosine kinase inhibitor, STI-571 (imatinib [Gleevec]; Novartis, Basel, Switzerland), has recently shown promise in the treatment of metastatic GISTs.	imatinib	52-59	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	2-5
11953894-1	2002	STI571 is a selective tyrosine kinase inhibitor with proven therapeutic potential in malignancies expressing c-kit.	imatinib	0-6	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	109-114
11914627-2	2002	Studies using the oral agent STI-571 (Gleevec, Novartis), an inhibitor of the tyrosine kinases bcr-abl, c-kit, and PDGFR, have shown significant responses in patients with chronic myelogenous leukemia and gastrointestinal stromal tumor.	imatinib	29-36	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	104-109
11914627-2	2002	Studies using the oral agent STI-571 (Gleevec, Novartis), an inhibitor of the tyrosine kinases bcr-abl, c-kit, and PDGFR, have shown significant responses in patients with chronic myelogenous leukemia and gastrointestinal stromal tumor.	imatinib	29-36	platelet derived growth factor receptor beta	Homo sapiens	115-120
11877286-8	2002	Treatment of UT-7/9 cells by STI571 (a specific inhibitor of the abl kinase) resulted in a decrease in NK susceptibility to lysis and ICAM-1 down-regulation in target cells.	imatinib	29-35	intercellular adhesion molecule 1	Homo sapiens	134-140
11993784-6	2002	In particular imatinib mesylate (ST1571, Gleevec) an oral Bcr-Abl kinase inhibitor, has demonstrated activity in all phases of CML, and may replace interferon and alloSCT as the initial therapy for this disease.	imatinib	14-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
11976731-6	2002	We also discuss the development of imatinib mesylate, a selective inhibitor of Bcr-Abl which has shown promise in clinical trials with CML.	imatinib	35-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
12054102-2	2002	Novartis has launched imatinib, an inhibitor of tyrosine kinases, including Bcr-Abl, for the treatment of chronic myeloid leukemia (CML).	imatinib	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
11861291-0	2002	The c-KIT mutation causing human mastocytosis is resistant to STI571 and other KIT kinase inhibitors; kinases with enzymatic site mutations show different inhibitor sensitivity profiles than wild-type kinases and those with regulatory-type mutations.	imatinib	62-68	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	4-9
11861291-0	2002	The c-KIT mutation causing human mastocytosis is resistant to STI571 and other KIT kinase inhibitors; kinases with enzymatic site mutations show different inhibitor sensitivity profiles than wild-type kinases and those with regulatory-type mutations.	imatinib	62-68	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	6-9
11861293-6	2002	Activation of this pathway requires the kinase activity of TEL/PDGF beta R and is inhibited by the PDGF beta R inhibitor, STI571.	imatinib	122-128	ets variant 6	Mus musculus	59-62
11861293-10	2002	Both STI571 and LY294002 lead to a decrease in the activity of cdk4 kinase activity and a decrease in expression of both Cyclin D2 and Cyclin E within several hours.	imatinib	5-11	cyclin-dependent kinase 4	Mus musculus	63-67
11861293-10	2002	Both STI571 and LY294002 lead to a decrease in the activity of cdk4 kinase activity and a decrease in expression of both Cyclin D2 and Cyclin E within several hours.	imatinib	5-11	cyclin D2	Mus musculus	121-130
11861294-9	2002	Ectopic overexpression of SOCS-2 in 32Dp210 cells slowed growth, inhibited clonogenicity, and increased their motility and sensitivity to STI571.	imatinib	138-144	suppressor of cytokine signaling 2	Homo sapiens	26-32
11861307-0	2002	Ph(+) acute lymphoblastic leukemia resistant to the tyrosine kinase inhibitor STI571 has a unique BCR-ABL gene mutation.	imatinib	78-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
12054102-6	2002	Futhermore, Bcr-Abl-expressing cells treated with imatinib undergo apoptosis.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
11891774-4	2002	STI571, an Abl family kinase inhibitor, further accentuates these stimulatory effects.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Rattus norvegicus	11-14
11790564-3	2002	STI-571, a small molecule inhibitor of the Bcr-Abl, c-kit and platelet derived growth factor receptor tyrosine kinases, produced dramatic clinical responses in patients with Bcr-Abl positive chronic myeloid leukemia and c-kit positive gastrointestinal stromal tumors.	imatinib	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
11853795-2	2002	STI571, a competitive inhibitor at the ATP-binding site of BCR-ABL, has been shown to have high activity in this type of leukaemia.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
11790564-3	2002	STI-571, a small molecule inhibitor of the Bcr-Abl, c-kit and platelet derived growth factor receptor tyrosine kinases, produced dramatic clinical responses in patients with Bcr-Abl positive chronic myeloid leukemia and c-kit positive gastrointestinal stromal tumors.	imatinib	0-7	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	52-57
11790564-3	2002	STI-571, a small molecule inhibitor of the Bcr-Abl, c-kit and platelet derived growth factor receptor tyrosine kinases, produced dramatic clinical responses in patients with Bcr-Abl positive chronic myeloid leukemia and c-kit positive gastrointestinal stromal tumors.	imatinib	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-181
11790564-3	2002	STI-571, a small molecule inhibitor of the Bcr-Abl, c-kit and platelet derived growth factor receptor tyrosine kinases, produced dramatic clinical responses in patients with Bcr-Abl positive chronic myeloid leukemia and c-kit positive gastrointestinal stromal tumors.	imatinib	0-7	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	220-225
11831067-6	2002	STI571 was shown to be a competitive inhibitor at the ATP-binding site of the Bcr-Abl tyrosine kinase, the platelet-derived growth factor receptor and c-kit tyrosine kinases.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
12191602-9	2002	In a preclinical model, STI571 (Glivec(R), Gleevec) showed potent in vitro and in vivo antitumor activity that was selective for Abl, c-Kit, and the platelet-derived growth factor-receptor.	imatinib	24-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-132
12191602-9	2002	In a preclinical model, STI571 (Glivec(R), Gleevec) showed potent in vitro and in vivo antitumor activity that was selective for Abl, c-Kit, and the platelet-derived growth factor-receptor.	imatinib	24-30	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	134-139
12191602-10	2002	Phase I/II studies demonstrated that STI571 is well tolerated, and that it showed promising hematological and cytogenetic responses in CML and clinical responses in the c-Kit-driven gastrointestinal tumors.	imatinib	37-43	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	169-174
11707430-9	2002	Rottlerin blocked c-Abl activation, but the c-Abl inhibitor STI-571 increased MGO and cisplatin-induced apoptosis by 50%.	imatinib	60-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-49
11831067-6	2002	STI571 was shown to be a competitive inhibitor at the ATP-binding site of the Bcr-Abl tyrosine kinase, the platelet-derived growth factor receptor and c-kit tyrosine kinases.	imatinib	0-6	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	151-156
11831067-14	2002	According to its pharmacological profile, STI571 could also be useful in the treatment of tumors with deregulated PDGF receptor or c-kit signaling, e.g., in chronic myelomonocytic leukemia with a t(5;12) chromosomal translocation or in cases with gastrointestinal stromal tumors (GIST).	imatinib	42-48	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	131-136
11831069-1	2002	BACKGROUND: Imatinib (STI571 or Glivec, Novartis) is a new type of tyrosine kinase inhibitor that selectively inhibits various tyrosine kinases including ABL, BCR-ABL, KIT and PDGF receptors.	imatinib	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-157
11831069-1	2002	BACKGROUND: Imatinib (STI571 or Glivec, Novartis) is a new type of tyrosine kinase inhibitor that selectively inhibits various tyrosine kinases including ABL, BCR-ABL, KIT and PDGF receptors.	imatinib	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-166
11831069-1	2002	BACKGROUND: Imatinib (STI571 or Glivec, Novartis) is a new type of tyrosine kinase inhibitor that selectively inhibits various tyrosine kinases including ABL, BCR-ABL, KIT and PDGF receptors.	imatinib	12-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	168-171
11831069-1	2002	BACKGROUND: Imatinib (STI571 or Glivec, Novartis) is a new type of tyrosine kinase inhibitor that selectively inhibits various tyrosine kinases including ABL, BCR-ABL, KIT and PDGF receptors.	imatinib	22-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-166
11831069-1	2002	BACKGROUND: Imatinib (STI571 or Glivec, Novartis) is a new type of tyrosine kinase inhibitor that selectively inhibits various tyrosine kinases including ABL, BCR-ABL, KIT and PDGF receptors.	imatinib	22-28	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	168-171
11831069-5	2002	IMATINIB IN GIST: Gastrointestinal stromal tumors (GIST) are also suitable indications for treatment with Imatinib, the prerequisite being overexpression by the tumor of c-KIT (CD117).	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	170-175
11831069-5	2002	IMATINIB IN GIST: Gastrointestinal stromal tumors (GIST) are also suitable indications for treatment with Imatinib, the prerequisite being overexpression by the tumor of c-KIT (CD117).	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	177-182
11831069-5	2002	IMATINIB IN GIST: Gastrointestinal stromal tumors (GIST) are also suitable indications for treatment with Imatinib, the prerequisite being overexpression by the tumor of c-KIT (CD117).	imatinib	106-114	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	170-175
11831069-5	2002	IMATINIB IN GIST: Gastrointestinal stromal tumors (GIST) are also suitable indications for treatment with Imatinib, the prerequisite being overexpression by the tumor of c-KIT (CD117).	imatinib	106-114	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	177-182
11782377-8	2002	Significantly, coexposure to PD184352 strikingly increased the lethality of a pharmacologically achievable concentration of STI571 (i.e., 1-2 microM) in resistant K562 cells expressing marked increases in Bcr-Abl protein levels.	imatinib	124-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	205-212
12611069-0	2002	Imatinib for relapsed BCR/ABL positive leukemias.	imatinib	0-8	BCR activator of RhoGEF and GTPase	Homo sapiens	22-25
11987244-2	2002	The tyrosine kinase inhibitor STI571 inhibits the BCR/ABL and ABL kinase activity and consequently inhibits growth of BCR/ABL-positive cells.	imatinib	30-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
11987244-2	2002	The tyrosine kinase inhibitor STI571 inhibits the BCR/ABL and ABL kinase activity and consequently inhibits growth of BCR/ABL-positive cells.	imatinib	30-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-57
11987244-2	2002	The tyrosine kinase inhibitor STI571 inhibits the BCR/ABL and ABL kinase activity and consequently inhibits growth of BCR/ABL-positive cells.	imatinib	30-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
11782377-0	2002	Pharmacologic mitogen-activated protein/extracellular signal-regulated kinase kinase/mitogen-activated protein kinase inhibitors interact synergistically with STI571 to induce apoptosis in Bcr/Abl-expressing human leukemia cells.	imatinib	159-165	mitogen-activated protein kinase kinase 7	Homo sapiens	14-84
11782377-9	2002	Together, these findings raise the possibility that treatment of Bcr-Abl-expressing cells with STI571 elicits a cytoprotective MAPK activation response and that interruption of the latter pathway (e.g., by pharmacological MEK1/2 inhibitors) is associated with a highly synergistic induction of mitochondrial damage and apoptosis.	imatinib	95-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
11782377-0	2002	Pharmacologic mitogen-activated protein/extracellular signal-regulated kinase kinase/mitogen-activated protein kinase inhibitors interact synergistically with STI571 to induce apoptosis in Bcr/Abl-expressing human leukemia cells.	imatinib	159-165	BCR activator of RhoGEF and GTPase	Homo sapiens	189-192
11782377-1	2002	Interactions between the kinase inhibitor STI571 and pharmacological antagonists of the mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK)/mitogen-activated protein kinase (MAPK) cascade have been examined in human myeloid leukemia cells (K562 and LAMA 84) that express the Bcr-Abl kinase.	imatinib	42-48	mitogen-activated protein kinase kinase 7	Homo sapiens	88-158
11782377-9	2002	Together, these findings raise the possibility that treatment of Bcr-Abl-expressing cells with STI571 elicits a cytoprotective MAPK activation response and that interruption of the latter pathway (e.g., by pharmacological MEK1/2 inhibitors) is associated with a highly synergistic induction of mitochondrial damage and apoptosis.	imatinib	95-101	mitogen-activated protein kinase kinase 1	Homo sapiens	222-228
11782377-1	2002	Interactions between the kinase inhibitor STI571 and pharmacological antagonists of the mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK)/mitogen-activated protein kinase (MAPK) cascade have been examined in human myeloid leukemia cells (K562 and LAMA 84) that express the Bcr-Abl kinase.	imatinib	42-48	mitogen-activated protein kinase kinase 7	Homo sapiens	160-163
11782377-2	2002	Exposure of K562 cells to concentrations of STI571 that minimally induced apoptosis (e.g., approximately 200 nM) resulted in early suppression (i.e., at 6 h) of p42/44 MAPK phosphorylation followed at later intervals (i.e., > or =24 h) by a marked increase in p42/44 MAPK phosphorylation/activation.	imatinib	44-50	cyclin dependent kinase like 1	Homo sapiens	161-164
11741179-5	2002	CONCLUSION: Evidence is presented that demonstrates opposite changes in metabolic phenotypes induced by TGF-beta, a cell-transforming agent, and tumor growth-inhibiting phytochemicals such as genistein and Avemar, or novel synthetic anti-leukemic drugs such as STI571 (Gleevec).	imatinib	261-267	transforming growth factor beta 1	Homo sapiens	104-112
11782377-2	2002	Exposure of K562 cells to concentrations of STI571 that minimally induced apoptosis (e.g., approximately 200 nM) resulted in early suppression (i.e., at 6 h) of p42/44 MAPK phosphorylation followed at later intervals (i.e., > or =24 h) by a marked increase in p42/44 MAPK phosphorylation/activation.	imatinib	44-50	cyclin dependent kinase like 1	Homo sapiens	263-266
11782377-3	2002	Coadministration of a nontoxic concentration of the MEK1/2 inhibitor PD184352 (5 microM) prevented STI571-mediated activation of p42/44 MAPK.	imatinib	99-105	mitogen-activated protein kinase kinase 1	Homo sapiens	52-58
11782377-3	2002	Coadministration of a nontoxic concentration of the MEK1/2 inhibitor PD184352 (5 microM) prevented STI571-mediated activation of p42/44 MAPK.	imatinib	99-105	cyclin dependent kinase like 1	Homo sapiens	129-132
11782377-4	2002	Cells exposed to STI571 in combination with PD184352 for 48 h demonstrated a very dramatic increase in mitochondrial dysfunction (e.g., loss of DeltaPsim and cytosolic cytochrome c release) associated with procaspase-3 activation, poly(ADP-ribose) polymerase cleavage, and the appearance of the characteristic morphological features of apoptosis.	imatinib	17-23	cytochrome c, somatic	Homo sapiens	168-180
11782377-4	2002	Cells exposed to STI571 in combination with PD184352 for 48 h demonstrated a very dramatic increase in mitochondrial dysfunction (e.g., loss of DeltaPsim and cytosolic cytochrome c release) associated with procaspase-3 activation, poly(ADP-ribose) polymerase cleavage, and the appearance of the characteristic morphological features of apoptosis.	imatinib	17-23	caspase 3	Homo sapiens	206-218
11782377-7	2002	Synergistic potentiation of STI571-mediated lethality by PD184352 was associated with multiple perturbations in signaling and apoptotic regulatory pathways, including caspase-dependent down-regulation of Bcr-Abl and Bcl-2; caspase-independent down-regulation of Bcl-x(L) and Mcl-1; activation of JNK, p38 MAPK, and p34(cdc2); and diminished phosphorylation of Stat5 and CREB.	imatinib	28-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	204-211
11782377-7	2002	Synergistic potentiation of STI571-mediated lethality by PD184352 was associated with multiple perturbations in signaling and apoptotic regulatory pathways, including caspase-dependent down-regulation of Bcr-Abl and Bcl-2; caspase-independent down-regulation of Bcl-x(L) and Mcl-1; activation of JNK, p38 MAPK, and p34(cdc2); and diminished phosphorylation of Stat5 and CREB.	imatinib	28-34	BCL2 apoptosis regulator	Homo sapiens	216-221
11782377-7	2002	Synergistic potentiation of STI571-mediated lethality by PD184352 was associated with multiple perturbations in signaling and apoptotic regulatory pathways, including caspase-dependent down-regulation of Bcr-Abl and Bcl-2; caspase-independent down-regulation of Bcl-x(L) and Mcl-1; activation of JNK, p38 MAPK, and p34(cdc2); and diminished phosphorylation of Stat5 and CREB.	imatinib	28-34	BCL2 like 1	Homo sapiens	262-270
11782377-7	2002	Synergistic potentiation of STI571-mediated lethality by PD184352 was associated with multiple perturbations in signaling and apoptotic regulatory pathways, including caspase-dependent down-regulation of Bcr-Abl and Bcl-2; caspase-independent down-regulation of Bcl-x(L) and Mcl-1; activation of JNK, p38 MAPK, and p34(cdc2); and diminished phosphorylation of Stat5 and CREB.	imatinib	28-34	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	275-280
11782377-7	2002	Synergistic potentiation of STI571-mediated lethality by PD184352 was associated with multiple perturbations in signaling and apoptotic regulatory pathways, including caspase-dependent down-regulation of Bcr-Abl and Bcl-2; caspase-independent down-regulation of Bcl-x(L) and Mcl-1; activation of JNK, p38 MAPK, and p34(cdc2); and diminished phosphorylation of Stat5 and CREB.	imatinib	28-34	leucine rich repeat containing 59	Homo sapiens	315-318
11782377-7	2002	Synergistic potentiation of STI571-mediated lethality by PD184352 was associated with multiple perturbations in signaling and apoptotic regulatory pathways, including caspase-dependent down-regulation of Bcr-Abl and Bcl-2; caspase-independent down-regulation of Bcl-x(L) and Mcl-1; activation of JNK, p38 MAPK, and p34(cdc2); and diminished phosphorylation of Stat5 and CREB.	imatinib	28-34	cyclin dependent kinase 1	Homo sapiens	319-323
11782377-7	2002	Synergistic potentiation of STI571-mediated lethality by PD184352 was associated with multiple perturbations in signaling and apoptotic regulatory pathways, including caspase-dependent down-regulation of Bcr-Abl and Bcl-2; caspase-independent down-regulation of Bcl-x(L) and Mcl-1; activation of JNK, p38 MAPK, and p34(cdc2); and diminished phosphorylation of Stat5 and CREB.	imatinib	28-34	signal transducer and activator of transcription 5A	Homo sapiens	360-365
11782377-7	2002	Synergistic potentiation of STI571-mediated lethality by PD184352 was associated with multiple perturbations in signaling and apoptotic regulatory pathways, including caspase-dependent down-regulation of Bcr-Abl and Bcl-2; caspase-independent down-regulation of Bcl-x(L) and Mcl-1; activation of JNK, p38 MAPK, and p34(cdc2); and diminished phosphorylation of Stat5 and CREB.	imatinib	28-34	cAMP responsive element binding protein 1	Homo sapiens	370-374
14660054-0	2002	Increased IFN-gamma synthesis by T cells from patients on imatinib therapy for chronic myeloid leukemia.	imatinib	58-66	interferon gamma	Homo sapiens	10-19
14660054-12	2002	In conclusion, treatment with imatinib achieves a significant increase in Type 1 (IFN-gamma) cytokine-producing T cells in patients with CML.	imatinib	30-38	interferon gamma	Homo sapiens	82-91
12122963-3	2002	Imatinib mesylate is indicated for the treatment of patients with Kit (CD117)-positive unresectable and/or metastatic malignant gastrointestinal stromal tumors and patients with Philadelphia chromosome-positive chronic myeloid leukemia in blast crisis, accelerated phase, or in chronic phase after failure of interferon-alfa.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	71-76
11751374-3	2001	The tyrosine kinase inhibitor STI571, active against the BCR-ABL fusion protein in chronic myeloid leukemia, was recently shown to be highly effective in GISTs.	imatinib	30-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
11739186-9	2001	As expected, growth of BaF3/BCR-ABL was inhibited by STI571 but not by SU5402.	imatinib	53-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
11781820-7	2001	In the recent structure of the Abl catalytic domain bound to the STI-571 inhibitor, unphosphorylated Tyr412 in the activation loop points inward and appears to interfere with catalysis.	imatinib	65-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-34
11691826-4	2001	Inhibition of Bcr-Abl with STI571 resulted in down-regulation of cyclin D2 and reduction of the number of cells in S phase, although complete G1 arrest was not induced.	imatinib	27-33	BCR activator of RhoGEF and GTPase	Mus musculus	14-17
11751479-1	2001	STI571 is a 2-phenylalaminopyrimidine derivative that inhibits c-abl, Bcr-Abl, and platelet-derived growth factor receptor tyrosine kinases.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-68
11751479-1	2001	STI571 is a 2-phenylalaminopyrimidine derivative that inhibits c-abl, Bcr-Abl, and platelet-derived growth factor receptor tyrosine kinases.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
11751479-9	2001	SCF-induced phosphorylation of c-kit in MO7e cells was inhibited by STI571.	imatinib	68-74	KIT ligand	Homo sapiens	0-3
11751479-9	2001	SCF-induced phosphorylation of c-kit in MO7e cells was inhibited by STI571.	imatinib	68-74	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	31-36
11675355-2	2001	In this report, mice reconstituted with P210(BCR/ABL)-transduced bone marrow cells received posttransplantation therapy with either the tyrosine kinase inhibitor STI571 or placebo.	imatinib	162-168	BCR activator of RhoGEF and GTPase	Mus musculus	40-52
11675355-4	2001	There was decreased tyrosine phosphorylation of STAT5, Shc, and Crk-L in leukemic cells from STI571-treated animals, consistent with STI571-mediated inhibition of the Bcr/Abl tyrosine kinase in vivo.	imatinib	93-99	signal transducer and activator of transcription 5A	Mus musculus	48-53
11675355-4	2001	There was decreased tyrosine phosphorylation of STAT5, Shc, and Crk-L in leukemic cells from STI571-treated animals, consistent with STI571-mediated inhibition of the Bcr/Abl tyrosine kinase in vivo.	imatinib	93-99	src homology 2 domain-containing transforming protein C1	Mus musculus	55-58
11675355-4	2001	There was decreased tyrosine phosphorylation of STAT5, Shc, and Crk-L in leukemic cells from STI571-treated animals, consistent with STI571-mediated inhibition of the Bcr/Abl tyrosine kinase in vivo.	imatinib	93-99	v-crk avian sarcoma virus CT10 oncogene homolog	Mus musculus	64-67
11675355-4	2001	There was decreased tyrosine phosphorylation of STAT5, Shc, and Crk-L in leukemic cells from STI571-treated animals, consistent with STI571-mediated inhibition of the Bcr/Abl tyrosine kinase in vivo.	imatinib	93-99	BCR activator of RhoGEF and GTPase	Mus musculus	167-170
11675355-4	2001	There was decreased tyrosine phosphorylation of STAT5, Shc, and Crk-L in leukemic cells from STI571-treated animals, consistent with STI571-mediated inhibition of the Bcr/Abl tyrosine kinase in vivo.	imatinib	93-99	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	171-174
11675355-4	2001	There was decreased tyrosine phosphorylation of STAT5, Shc, and Crk-L in leukemic cells from STI571-treated animals, consistent with STI571-mediated inhibition of the Bcr/Abl tyrosine kinase in vivo.	imatinib	133-139	signal transducer and activator of transcription 5A	Mus musculus	48-53
11675355-4	2001	There was decreased tyrosine phosphorylation of STAT5, Shc, and Crk-L in leukemic cells from STI571-treated animals, consistent with STI571-mediated inhibition of the Bcr/Abl tyrosine kinase in vivo.	imatinib	133-139	v-crk avian sarcoma virus CT10 oncogene homolog	Mus musculus	64-67
11675355-4	2001	There was decreased tyrosine phosphorylation of STAT5, Shc, and Crk-L in leukemic cells from STI571-treated animals, consistent with STI571-mediated inhibition of the Bcr/Abl tyrosine kinase in vivo.	imatinib	133-139	BCR activator of RhoGEF and GTPase	Mus musculus	167-170
11675355-4	2001	There was decreased tyrosine phosphorylation of STAT5, Shc, and Crk-L in leukemic cells from STI571-treated animals, consistent with STI571-mediated inhibition of the Bcr/Abl tyrosine kinase in vivo.	imatinib	133-139	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	171-174
11746976-2	2001	Inhibition of the BCR/ABL kinase activity in the BV173 CML cell line with STI571 resulted in a significant overexpression of a 10-kb novel mRNA, found to be the human ortholog of the murine Bach2, a B-cell-specific transcription factor.	imatinib	74-80	BCR activator of RhoGEF and GTPase	Homo sapiens	18-21
11746976-2	2001	Inhibition of the BCR/ABL kinase activity in the BV173 CML cell line with STI571 resulted in a significant overexpression of a 10-kb novel mRNA, found to be the human ortholog of the murine Bach2, a B-cell-specific transcription factor.	imatinib	74-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-25
11746976-2	2001	Inhibition of the BCR/ABL kinase activity in the BV173 CML cell line with STI571 resulted in a significant overexpression of a 10-kb novel mRNA, found to be the human ortholog of the murine Bach2, a B-cell-specific transcription factor.	imatinib	74-80	BTB and CNC homology, basic leucine zipper transcription factor 2	Mus musculus	190-195
11746976-7	2001	Moreover, CD34+ cells treated in vitro with STI571 exhibited a consistent upregulation of BACH2 in 8 of 10 CMLs but in none of the 9 normal individuals tested.	imatinib	44-50	CD34 molecule	Homo sapiens	10-14
11746976-7	2001	Moreover, CD34+ cells treated in vitro with STI571 exhibited a consistent upregulation of BACH2 in 8 of 10 CMLs but in none of the 9 normal individuals tested.	imatinib	44-50	BTB domain and CNC homolog 2	Homo sapiens	90-95
11691826-4	2001	Inhibition of Bcr-Abl with STI571 resulted in down-regulation of cyclin D2 and reduction of the number of cells in S phase, although complete G1 arrest was not induced.	imatinib	27-33	cyclin D2	Mus musculus	65-74
11691826-7	2001	In contrast to the human cell lines, murine Baf/BCR-ABL cells exposed to STI571 inhibitor were all arrested in G1.	imatinib	73-79	b-associated fitness	Mus musculus	44-47
11691826-7	2001	In contrast to the human cell lines, murine Baf/BCR-ABL cells exposed to STI571 inhibitor were all arrested in G1.	imatinib	73-79	BCR activator of RhoGEF and GTPase	Mus musculus	48-51
11705489-3	2001	Imatinib (STI571) inhibits a similar tyrosine kinase, BCR-ABL, leading to responses in chronic myeloid leukaemia, and has also been shown to inhibit KIT.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
11718431-6	2001	Now, the advent of imatinib mesylate, a specific inhibitor of BCR/ABL tyrosine kinase, promises to change existing treatment paradigms	imatinib	19-36	BCR activator of RhoGEF and GTPase	Homo sapiens	62-85
11681425-0	2001	Marked ploidy and BCR-ABL gene amplification in vivo in a patient treated with STI571.	imatinib	79-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
11705489-3	2001	Imatinib (STI571) inhibits a similar tyrosine kinase, BCR-ABL, leading to responses in chronic myeloid leukaemia, and has also been shown to inhibit KIT.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	149-152
11705489-3	2001	Imatinib (STI571) inhibits a similar tyrosine kinase, BCR-ABL, leading to responses in chronic myeloid leukaemia, and has also been shown to inhibit KIT.	imatinib	10-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
11705489-3	2001	Imatinib (STI571) inhibits a similar tyrosine kinase, BCR-ABL, leading to responses in chronic myeloid leukaemia, and has also been shown to inhibit KIT.	imatinib	10-16	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	149-152
11489902-8	2001	The administration of specific hexokinase/glucose-6-phosphate 1-dehydrogenase inhibitor anti-metabolite substrates or competitive enzyme inhibitor compounds, alone or in combination, should be explored for the treatment of STI571-resistant advanced leukemias as well as that of Bcr-Abl-negative human malignancies.	imatinib	223-229	hexokinase 1	Homo sapiens	31-41
11606405-5	2001	Apoptotic cell death induced by STI571 is partially dependent on p53.	imatinib	32-38	tumor protein p53	Homo sapiens	65-68
11489902-8	2001	The administration of specific hexokinase/glucose-6-phosphate 1-dehydrogenase inhibitor anti-metabolite substrates or competitive enzyme inhibitor compounds, alone or in combination, should be explored for the treatment of STI571-resistant advanced leukemias as well as that of Bcr-Abl-negative human malignancies.	imatinib	223-229	glucose-6-phosphate dehydrogenase	Homo sapiens	42-77
11680792-1	2001	Imatinib mesylate, also known as STI571 or CGP57148, is a competitive inhibitor of a few tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
11680792-1	2001	Imatinib mesylate, also known as STI571 or CGP57148, is a competitive inhibitor of a few tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-124
11587211-6	2001	Like GA, STI 571 (an inhibitor of the Abl kinase) sensitized Bcr-Abl-expressing cells to DOX.	imatinib	9-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-41
11680792-1	2001	Imatinib mesylate, also known as STI571 or CGP57148, is a competitive inhibitor of a few tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	131-134
11680792-1	2001	Imatinib mesylate, also known as STI571 or CGP57148, is a competitive inhibitor of a few tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	144-184
11680792-1	2001	Imatinib mesylate, also known as STI571 or CGP57148, is a competitive inhibitor of a few tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	186-192
11680792-1	2001	Imatinib mesylate, also known as STI571 or CGP57148, is a competitive inhibitor of a few tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	33-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
11680792-1	2001	Imatinib mesylate, also known as STI571 or CGP57148, is a competitive inhibitor of a few tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	33-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-124
11680792-1	2001	Imatinib mesylate, also known as STI571 or CGP57148, is a competitive inhibitor of a few tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	33-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	131-134
11680792-1	2001	Imatinib mesylate, also known as STI571 or CGP57148, is a competitive inhibitor of a few tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	33-39	platelet derived growth factor receptor beta	Homo sapiens	144-184
11680792-1	2001	Imatinib mesylate, also known as STI571 or CGP57148, is a competitive inhibitor of a few tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	33-39	platelet derived growth factor receptor beta	Homo sapiens	186-192
11680792-1	2001	Imatinib mesylate, also known as STI571 or CGP57148, is a competitive inhibitor of a few tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
11680792-1	2001	Imatinib mesylate, also known as STI571 or CGP57148, is a competitive inhibitor of a few tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-124
11680792-1	2001	Imatinib mesylate, also known as STI571 or CGP57148, is a competitive inhibitor of a few tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	43-51	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	131-134
11680792-1	2001	Imatinib mesylate, also known as STI571 or CGP57148, is a competitive inhibitor of a few tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	43-51	platelet derived growth factor receptor beta	Homo sapiens	144-184
11680792-1	2001	Imatinib mesylate, also known as STI571 or CGP57148, is a competitive inhibitor of a few tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R).	imatinib	43-51	platelet derived growth factor receptor beta	Homo sapiens	186-192
11680792-4	2001	Imatinib also has substantial activity in Philadelphia chromosome-positive acute lymphoblastic leukaemia expressing the BCR-ABL fusion protein.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
11587211-6	2001	Like GA, STI 571 (an inhibitor of the Abl kinase) sensitized Bcr-Abl-expressing cells to DOX.	imatinib	9-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
11600816-4	2001	The 2-phenylpyrimidine derivative STI571 was rationally designed to inhibit ABL and BCR-ABL tyrosine kinase activities through competitive ATP-binding pocket interactions.	imatinib	34-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-79
11593427-5	2001	Moreover, tyrosine phosphorylation of Jak2 by Bcr-Abl was inhibited by the Abl tyrosine kinase inhibitor, STI 571, in a dose-dependent manner.	imatinib	106-113	Janus kinase 2	Homo sapiens	38-42
11593427-5	2001	Moreover, tyrosine phosphorylation of Jak2 by Bcr-Abl was inhibited by the Abl tyrosine kinase inhibitor, STI 571, in a dose-dependent manner.	imatinib	106-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
11593427-5	2001	Moreover, tyrosine phosphorylation of Jak2 by Bcr-Abl was inhibited by the Abl tyrosine kinase inhibitor, STI 571, in a dose-dependent manner.	imatinib	106-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-53
11740801-7	2001	The success of imatinib mesylate in CML led rapidly to clinical trials in other cancers associated with activation of two other tyrosine kinases known to be sensitive to imatinib mesylate, c-Kit and the platelet-derived growth factor receptor.	imatinib	15-32	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	189-194
11740802-9	2001	Additional trials are planned to investigate the efficacy of imatinib mesylate to treat a variety of solid tumors whose pathogenesis is driven by the other tyrosine kinase targets, c-Kit and platelet-derived growth factor receptor.	imatinib	61-78	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	181-186
11740803-8	2001	This hypothesis became testable with the identification of the signal transduction inhibitor imatinib mesylate (formerly STI571, [Gleevec]; Novartis Pharmaceuticals Corp, East Hanover, NJ), which blocks the tyrosine kinase activity of KIT as well as the kinase activity of the normal c-abl gene product, the oncogenic Bcr-Abl chimeric fusion protein of chronic myeloid leukemia, and the platelet-derived growth factor receptor.	imatinib	93-110	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	235-238
11740803-8	2001	This hypothesis became testable with the identification of the signal transduction inhibitor imatinib mesylate (formerly STI571, [Gleevec]; Novartis Pharmaceuticals Corp, East Hanover, NJ), which blocks the tyrosine kinase activity of KIT as well as the kinase activity of the normal c-abl gene product, the oncogenic Bcr-Abl chimeric fusion protein of chronic myeloid leukemia, and the platelet-derived growth factor receptor.	imatinib	93-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	284-289
11740803-8	2001	This hypothesis became testable with the identification of the signal transduction inhibitor imatinib mesylate (formerly STI571, [Gleevec]; Novartis Pharmaceuticals Corp, East Hanover, NJ), which blocks the tyrosine kinase activity of KIT as well as the kinase activity of the normal c-abl gene product, the oncogenic Bcr-Abl chimeric fusion protein of chronic myeloid leukemia, and the platelet-derived growth factor receptor.	imatinib	93-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	318-325
11740803-8	2001	This hypothesis became testable with the identification of the signal transduction inhibitor imatinib mesylate (formerly STI571, [Gleevec]; Novartis Pharmaceuticals Corp, East Hanover, NJ), which blocks the tyrosine kinase activity of KIT as well as the kinase activity of the normal c-abl gene product, the oncogenic Bcr-Abl chimeric fusion protein of chronic myeloid leukemia, and the platelet-derived growth factor receptor.	imatinib	121-127	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	235-238
11740803-8	2001	This hypothesis became testable with the identification of the signal transduction inhibitor imatinib mesylate (formerly STI571, [Gleevec]; Novartis Pharmaceuticals Corp, East Hanover, NJ), which blocks the tyrosine kinase activity of KIT as well as the kinase activity of the normal c-abl gene product, the oncogenic Bcr-Abl chimeric fusion protein of chronic myeloid leukemia, and the platelet-derived growth factor receptor.	imatinib	121-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	284-289
11740803-8	2001	This hypothesis became testable with the identification of the signal transduction inhibitor imatinib mesylate (formerly STI571, [Gleevec]; Novartis Pharmaceuticals Corp, East Hanover, NJ), which blocks the tyrosine kinase activity of KIT as well as the kinase activity of the normal c-abl gene product, the oncogenic Bcr-Abl chimeric fusion protein of chronic myeloid leukemia, and the platelet-derived growth factor receptor.	imatinib	121-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	318-325
11740803-9	2001	Preclinical experiments showed rapid inhibition of ligand-independent KIT phosphorylation, decreased cellular proliferation, and induction of apoptosis after exposure of GIST cells to imatinib mesylate in vitro.	imatinib	184-201	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	70-73
11740804-5	2001	The tyrosine kinase inhibitor imatinib mesylate (formerly STI571, [Gleevec]; Novartis Pharmaceuticals Corp, East Hanover, NJ) blocks activity of the Bcr-Abl oncoprotein, and was recently approved for several indications in the treatment of chronic myeloid leukemia.	imatinib	30-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
11600816-4	2001	The 2-phenylpyrimidine derivative STI571 was rationally designed to inhibit ABL and BCR-ABL tyrosine kinase activities through competitive ATP-binding pocket interactions.	imatinib	34-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
11600816-10	2001	Since c-kit overexpression is inhibited in small-cell lung cancer cell lines, a study with STI571 as second-line therapy of c-kit-positive small-cell lung cancer is in progress.	imatinib	91-97	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	124-129
11587372-3	2001	ST1571 (formerly CGP57148B), is an Abl-specific tyrosine kinase inhibitor that in preclinical studies selectively kills Bcr-Abl-containing cells in vitro and in vivo.	imatinib	17-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
11526490-5	2001	GIST882 c-KIT protein is constitutively tyrosine phosphorylated, but tyrosine phosphorylation was rapidly and completely abolished after incubating the cells with the selective tyrosine kinase inhibitor STI571.	imatinib	203-209	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	8-13
11526490-7	2001	Similar results were obtained after administering STI571 to a primary GIST cell culture that expressed a c-KIT exon 11 juxtamembrane mutation (K558NP).	imatinib	50-56	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	105-110
11390389-9	2001	The Tyr phosphorylation of PLSCR1 was increased upon overexpression of c-Abl and significantly reduced either upon cell treatment with the Abl kinase inhibitor STI571, or in Abl-/- mouse fibroblasts, suggesting that cellular PLSCR1 is a normal substrate of c-Abl.	imatinib	160-166	phospholipid scramblase 1	Mus musculus	27-33
11390389-9	2001	The Tyr phosphorylation of PLSCR1 was increased upon overexpression of c-Abl and significantly reduced either upon cell treatment with the Abl kinase inhibitor STI571, or in Abl-/- mouse fibroblasts, suggesting that cellular PLSCR1 is a normal substrate of c-Abl.	imatinib	160-166	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	139-142
12578590-0	2001	[Low Concentrations of STI571 Enhances beta1 Integrin Mediated Inhibitory Effect on Proliferation of Myeloid Progenitors in Ph(+)Chronic Myeloid Leukemia] To investigate whether ABL specific tyrosine kinase specific inhibitor STI571 can restore beta1 integrin mediated negative effect on Ph(+) chronic myeloid leukemia(CML), the inhibitory effect of beta 1 integrin activator (beta1 integrin activating antibody 8A2, cytokines such as GM-CSF, G-CSF and SCF) and/or FN on the granulocyte-macrophage colony forming unit (CFU-GM) from 16 patients with Ph(+)CML and 13 normal individuals were examined; the bone marrow mononuclear cells (BMMNC) before and after ABL kinase specific inhibitor STI571 pretreatment (0.1 micro mol/L for 30-60 minutes) were target cells in this study.	imatinib	23-29	integrin subunit beta 1	Homo sapiens	39-53
12578590-0	2001	[Low Concentrations of STI571 Enhances beta1 Integrin Mediated Inhibitory Effect on Proliferation of Myeloid Progenitors in Ph(+)Chronic Myeloid Leukemia] To investigate whether ABL specific tyrosine kinase specific inhibitor STI571 can restore beta1 integrin mediated negative effect on Ph(+) chronic myeloid leukemia(CML), the inhibitory effect of beta 1 integrin activator (beta1 integrin activating antibody 8A2, cytokines such as GM-CSF, G-CSF and SCF) and/or FN on the granulocyte-macrophage colony forming unit (CFU-GM) from 16 patients with Ph(+)CML and 13 normal individuals were examined; the bone marrow mononuclear cells (BMMNC) before and after ABL kinase specific inhibitor STI571 pretreatment (0.1 micro mol/L for 30-60 minutes) were target cells in this study.	imatinib	23-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-181
12578590-0	2001	[Low Concentrations of STI571 Enhances beta1 Integrin Mediated Inhibitory Effect on Proliferation of Myeloid Progenitors in Ph(+)Chronic Myeloid Leukemia] To investigate whether ABL specific tyrosine kinase specific inhibitor STI571 can restore beta1 integrin mediated negative effect on Ph(+) chronic myeloid leukemia(CML), the inhibitory effect of beta 1 integrin activator (beta1 integrin activating antibody 8A2, cytokines such as GM-CSF, G-CSF and SCF) and/or FN on the granulocyte-macrophage colony forming unit (CFU-GM) from 16 patients with Ph(+)CML and 13 normal individuals were examined; the bone marrow mononuclear cells (BMMNC) before and after ABL kinase specific inhibitor STI571 pretreatment (0.1 micro mol/L for 30-60 minutes) were target cells in this study.	imatinib	23-29	integrin subunit beta 1	Homo sapiens	245-259
12578590-0	2001	[Low Concentrations of STI571 Enhances beta1 Integrin Mediated Inhibitory Effect on Proliferation of Myeloid Progenitors in Ph(+)Chronic Myeloid Leukemia] To investigate whether ABL specific tyrosine kinase specific inhibitor STI571 can restore beta1 integrin mediated negative effect on Ph(+) chronic myeloid leukemia(CML), the inhibitory effect of beta 1 integrin activator (beta1 integrin activating antibody 8A2, cytokines such as GM-CSF, G-CSF and SCF) and/or FN on the granulocyte-macrophage colony forming unit (CFU-GM) from 16 patients with Ph(+)CML and 13 normal individuals were examined; the bone marrow mononuclear cells (BMMNC) before and after ABL kinase specific inhibitor STI571 pretreatment (0.1 micro mol/L for 30-60 minutes) were target cells in this study.	imatinib	23-29	integrin subunit beta 1	Homo sapiens	377-391
12578590-0	2001	[Low Concentrations of STI571 Enhances beta1 Integrin Mediated Inhibitory Effect on Proliferation of Myeloid Progenitors in Ph(+)Chronic Myeloid Leukemia] To investigate whether ABL specific tyrosine kinase specific inhibitor STI571 can restore beta1 integrin mediated negative effect on Ph(+) chronic myeloid leukemia(CML), the inhibitory effect of beta 1 integrin activator (beta1 integrin activating antibody 8A2, cytokines such as GM-CSF, G-CSF and SCF) and/or FN on the granulocyte-macrophage colony forming unit (CFU-GM) from 16 patients with Ph(+)CML and 13 normal individuals were examined; the bone marrow mononuclear cells (BMMNC) before and after ABL kinase specific inhibitor STI571 pretreatment (0.1 micro mol/L for 30-60 minutes) were target cells in this study.	imatinib	23-29	colony stimulating factor 2	Homo sapiens	435-441
12578590-0	2001	[Low Concentrations of STI571 Enhances beta1 Integrin Mediated Inhibitory Effect on Proliferation of Myeloid Progenitors in Ph(+)Chronic Myeloid Leukemia] To investigate whether ABL specific tyrosine kinase specific inhibitor STI571 can restore beta1 integrin mediated negative effect on Ph(+) chronic myeloid leukemia(CML), the inhibitory effect of beta 1 integrin activator (beta1 integrin activating antibody 8A2, cytokines such as GM-CSF, G-CSF and SCF) and/or FN on the granulocyte-macrophage colony forming unit (CFU-GM) from 16 patients with Ph(+)CML and 13 normal individuals were examined; the bone marrow mononuclear cells (BMMNC) before and after ABL kinase specific inhibitor STI571 pretreatment (0.1 micro mol/L for 30-60 minutes) were target cells in this study.	imatinib	23-29	colony stimulating factor 3	Homo sapiens	443-448
12578590-0	2001	[Low Concentrations of STI571 Enhances beta1 Integrin Mediated Inhibitory Effect on Proliferation of Myeloid Progenitors in Ph(+)Chronic Myeloid Leukemia] To investigate whether ABL specific tyrosine kinase specific inhibitor STI571 can restore beta1 integrin mediated negative effect on Ph(+) chronic myeloid leukemia(CML), the inhibitory effect of beta 1 integrin activator (beta1 integrin activating antibody 8A2, cytokines such as GM-CSF, G-CSF and SCF) and/or FN on the granulocyte-macrophage colony forming unit (CFU-GM) from 16 patients with Ph(+)CML and 13 normal individuals were examined; the bone marrow mononuclear cells (BMMNC) before and after ABL kinase specific inhibitor STI571 pretreatment (0.1 micro mol/L for 30-60 minutes) were target cells in this study.	imatinib	23-29	KIT ligand	Homo sapiens	453-456
12578590-0	2001	[Low Concentrations of STI571 Enhances beta1 Integrin Mediated Inhibitory Effect on Proliferation of Myeloid Progenitors in Ph(+)Chronic Myeloid Leukemia] To investigate whether ABL specific tyrosine kinase specific inhibitor STI571 can restore beta1 integrin mediated negative effect on Ph(+) chronic myeloid leukemia(CML), the inhibitory effect of beta 1 integrin activator (beta1 integrin activating antibody 8A2, cytokines such as GM-CSF, G-CSF and SCF) and/or FN on the granulocyte-macrophage colony forming unit (CFU-GM) from 16 patients with Ph(+)CML and 13 normal individuals were examined; the bone marrow mononuclear cells (BMMNC) before and after ABL kinase specific inhibitor STI571 pretreatment (0.1 micro mol/L for 30-60 minutes) were target cells in this study.	imatinib	23-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	658-661
12578590-4	2001	(3) The inhibitory effect of beta1 integrin activator(s) plus FN on CML CFU-GM after STI571 pretreatment is comparable to that on normal CFU-GM.	imatinib	85-91	integrin subunit beta 1	Homo sapiens	29-43
12578590-5	2001	(4) Monoclonal antibody to VLA4 and VLA5 or to total beta1 integrins almost completely abrogate the above effect of STI571.	imatinib	116-122	integrin subunit alpha 5	Homo sapiens	36-40
12578590-5	2001	(4) Monoclonal antibody to VLA4 and VLA5 or to total beta1 integrins almost completely abrogate the above effect of STI571.	imatinib	116-122	potassium calcium-activated channel subfamily M regulatory beta subunit 1	Homo sapiens	53-58
11587372-3	2001	ST1571 (formerly CGP57148B), is an Abl-specific tyrosine kinase inhibitor that in preclinical studies selectively kills Bcr-Abl-containing cells in vitro and in vivo.	imatinib	17-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
11526597-1	2001	The tyrosine kinase inhibitor imatinib mesylate (Gleevec, Novartis Pharmaceuticals Corp, East Hanover, NJ) (formerly STI571) blocks the constitutively activated Bcr-Abl tyrosine kinase that is characteristic of chronic myeloid leukemia (CML).	imatinib	30-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-168
11480565-2	2001	Here, we demonstrate that when K562 chronic myelogenous leukemia (CML) cells are adhered to fibronectin (FN), they become resistant to apoptosis induced by the BCR/ABL inhibitors AG957 and STI-571, as well as DNA damaging agents and gamma-irradiation.	imatinib	189-196	fibronectin 1	Homo sapiens	92-103
11480565-2	2001	Here, we demonstrate that when K562 chronic myelogenous leukemia (CML) cells are adhered to fibronectin (FN), they become resistant to apoptosis induced by the BCR/ABL inhibitors AG957 and STI-571, as well as DNA damaging agents and gamma-irradiation.	imatinib	189-196	fibronectin 1	Homo sapiens	105-107
11495816-4	2001	Produced from the 2-phenylaminopyrimidine class, a novel synthetic inhibitor, identified as CGP57148 (STI571), inhibits tyrosine kinase activity of c-ABL, BCR-ABL, PDGF-R and c-kit at micromolar concentrations.	imatinib	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	148-153
11495816-4	2001	Produced from the 2-phenylaminopyrimidine class, a novel synthetic inhibitor, identified as CGP57148 (STI571), inhibits tyrosine kinase activity of c-ABL, BCR-ABL, PDGF-R and c-kit at micromolar concentrations.	imatinib	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-162
11495816-4	2001	Produced from the 2-phenylaminopyrimidine class, a novel synthetic inhibitor, identified as CGP57148 (STI571), inhibits tyrosine kinase activity of c-ABL, BCR-ABL, PDGF-R and c-kit at micromolar concentrations.	imatinib	92-100	platelet derived growth factor receptor beta	Homo sapiens	164-170
11495816-4	2001	Produced from the 2-phenylaminopyrimidine class, a novel synthetic inhibitor, identified as CGP57148 (STI571), inhibits tyrosine kinase activity of c-ABL, BCR-ABL, PDGF-R and c-kit at micromolar concentrations.	imatinib	92-100	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	175-180
11454136-2	2001	Signal transduction inhibitor (STI571) (formerly CGP57 148B), is an ABL specific, tyrosine kinase inhibitor.	imatinib	31-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-71
11504279-5	2001	STI571, an Abl-specific tyrosine kinase inhibitor, has shown remarkable activity in all phases of CML.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-14
11526597-2	2001	Molecular analysis for the presence of residual Bcr-Abl-positive cells in patients with a cytogenetic response following treatment with imatinib mesylate reveals that some patients have undetectable disease using quantitative reverse-transcriptase polymerase chain reaction (RT-PCR) assays capable of detecting 1 in 10(5) Philadelphia chromosome-positive (Ph(+)) cells.	imatinib	136-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
11526597-3	2001	To examine whether the leukemia is still Bcr-Abl-dependent in patients who have responded to imatinib mesylate but have relapsed, a quantitative assay that directly measures enzymatic activity of Bcr-Abl toward one of its major signaling substrates has been developed.	imatinib	93-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
11526597-3	2001	To examine whether the leukemia is still Bcr-Abl-dependent in patients who have responded to imatinib mesylate but have relapsed, a quantitative assay that directly measures enzymatic activity of Bcr-Abl toward one of its major signaling substrates has been developed.	imatinib	93-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	196-203
11526597-4	2001	This assay allows monitoring both of the imatinib mesylate sensitivity of patient cells in vitro, and of the endogenous inhibition of Bcr-Abl kinase activity during imatinib mesylate treatment and relapse.	imatinib	165-182	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
11526597-5	2001	Studies show that imatinib mesylate resistance is associated with restored activation of the Bcr-Abl signal transduction pathway in the majority of cases, indicating that Bcr-Abl remains a valid target for therapeutic intervention.	imatinib	18-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
11526597-5	2001	Studies show that imatinib mesylate resistance is associated with restored activation of the Bcr-Abl signal transduction pathway in the majority of cases, indicating that Bcr-Abl remains a valid target for therapeutic intervention.	imatinib	18-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-178
11526598-9	2001	Low-dose IFN-alpha may be given after imatinib mesylate-induced remission as a specific immune stimulant to consolidate the remission.	imatinib	38-55	interferon alpha 1	Homo sapiens	9-18
11526598-10	2001	Recent data showing a possible additive effect of imatinib mesylate and IFN-alpha suggest that concurrent use of these agents may also be more effective than single use, particularly in advanced stages of CML where imatinib mesylate has activity but resistance develops.	imatinib	215-232	interferon alpha 1	Homo sapiens	72-81
11439348-0	2001	Tyrosine kinase inhibitor STI571 enhances thyroid cancer cell motile response to Hepatocyte Growth Factor.	imatinib	26-32	TXK tyrosine kinase	Homo sapiens	0-15
11439348-0	2001	Tyrosine kinase inhibitor STI571 enhances thyroid cancer cell motile response to Hepatocyte Growth Factor.	imatinib	26-32	hepatocyte growth factor	Homo sapiens	81-105
11439348-3	2001	We show here that the tyrosine kinase inhibitor STI571 has a stimulatory effect on HGF-induced migration and branching morphogenesis in thyroid cancer but not in primary or immortalized thyroid epithelial cells.	imatinib	48-54	TXK tyrosine kinase	Homo sapiens	22-37
11439348-3	2001	We show here that the tyrosine kinase inhibitor STI571 has a stimulatory effect on HGF-induced migration and branching morphogenesis in thyroid cancer but not in primary or immortalized thyroid epithelial cells.	imatinib	48-54	hepatocyte growth factor	Homo sapiens	83-86
11439348-5	2001	The STI571-enhanced motile response can be correlated with an increase in the Met receptor tyrosine phosphorylation as well as ERK and Akt activation by HGF.	imatinib	4-10	AKT serine/threonine kinase 1	Homo sapiens	135-138
11439348-5	2001	The STI571-enhanced motile response can be correlated with an increase in the Met receptor tyrosine phosphorylation as well as ERK and Akt activation by HGF.	imatinib	4-10	hepatocyte growth factor	Homo sapiens	153-156
11785454-4	2001	Many rationally designed drugs are now in clinical trials and exciting results were presented for the Bcr-Abl inhibitor STI-571.	imatinib	120-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
11417489-0	2001	ABL-specific tyrosine kinase inhibitor, STI571 in vitro, affects Ph-positive acute lymphoblastic leukemia and chronic myelogenous leukemia in blastic crisis.	imatinib	40-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
11342454-0	2001	Tyrosine kinase inhibitor STI571 potentiates the pharmacologic activity of retinoic acid in acute promyelocytic leukemia cells: effects on the degradation of RARalpha and PML-RARalpha.	imatinib	26-32	retinoic acid receptor alpha	Homo sapiens	158-166
11342454-0	2001	Tyrosine kinase inhibitor STI571 potentiates the pharmacologic activity of retinoic acid in acute promyelocytic leukemia cells: effects on the degradation of RARalpha and PML-RARalpha.	imatinib	26-32	PML nuclear body scaffold	Homo sapiens	171-174
11342454-0	2001	Tyrosine kinase inhibitor STI571 potentiates the pharmacologic activity of retinoic acid in acute promyelocytic leukemia cells: effects on the degradation of RARalpha and PML-RARalpha.	imatinib	26-32	retinoic acid receptor alpha	Homo sapiens	175-183
11342454-1	2001	The 2-phenylaminopyrimidine derivative STI571 is a selective inhibitor of c-Abl, c-kit, and platelet-derived growth factor-receptor tyrosine kinases and is presently in phase II-III clinical studies.	imatinib	39-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-79
11342454-1	2001	The 2-phenylaminopyrimidine derivative STI571 is a selective inhibitor of c-Abl, c-kit, and platelet-derived growth factor-receptor tyrosine kinases and is presently in phase II-III clinical studies.	imatinib	39-45	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	81-86
11342454-5	2001	In NB4 promyelocytes, a RARalpha agonist, but not an RXR agonist, can substitute for ATRA and interact with STI571.	imatinib	108-114	retinoic acid receptor alpha	Homo sapiens	24-32
11342454-6	2001	By contrast, STI571 is unique among c-Abl-specific tyrosine kinase inhibitors in modulating the pharmacologic activity of ATRA.	imatinib	13-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-41
11313280-5	2001	STI-571 inhibited cell growth and induced apoptosis in bcr-abl-expressing cells (MBA, K562, BV-173, KBM5) but not in bcr-abl(-) tumor cells (Mo7e, KG-1, ME-180, Daudi).	imatinib	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
11313280-6	2001	STI-571-mediated apoptosis correlated with the inhibition of Stat-5 and MAP kinase activation and a reduction in overexpressed bcl-x(L) but not in PTP1B.	imatinib	0-7	signal transducer and activator of transcription 5A	Homo sapiens	61-67
11313280-6	2001	STI-571-mediated apoptosis correlated with the inhibition of Stat-5 and MAP kinase activation and a reduction in overexpressed bcl-x(L) but not in PTP1B.	imatinib	0-7	BCL2 like 1	Homo sapiens	127-135
11313280-8	2001	However, neither IL-3 nor GM-CSF could reactivate Stat-5 after the STI-571-mediated inhibition of bcr-abl.	imatinib	67-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
11378651-8	2001	The remarkable clinical response of tumors that express c-kit to treatment with the tyrosine kinase inhibitor STI571 is a triumph of molecular pharmacology.	imatinib	110-116	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	56-61
11237055-0	2001	Synergistic activity of the new ABL-specific tyrosine kinase inhibitor STI571 and chemotherapeutic drugs on BCR-ABL-positive chronic myelogenous leukemia cells.	imatinib	71-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-35
11383207-1	2001	STI571 selectively inhibits the ABL-tyrosine kinase, the activity of which is activated by the formation of chimeric BCR/ABL.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-35
11383207-1	2001	STI571 selectively inhibits the ABL-tyrosine kinase, the activity of which is activated by the formation of chimeric BCR/ABL.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
11291071-0	2001	Growth-inhibitory effect of STI571 on cells transformed by the COL1A1/PDGFB rearrangement.	imatinib	28-34	collagen, type I, alpha 1	Mus musculus	63-69
11291071-0	2001	Growth-inhibitory effect of STI571 on cells transformed by the COL1A1/PDGFB rearrangement.	imatinib	28-34	platelet derived growth factor, B polypeptide	Mus musculus	70-75
11291071-11	2001	Our data indicate that STI571 might be a candidate compound for the pharmacological treatment of DP and demonstrate that the same compound may act in different ways (cytotoxic vs. cytostatic), according to the specificity of the inhibited tyrosine kinase, namely, ABL or PDGFrbeta.	imatinib	23-29	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	264-267
11291071-11	2001	Our data indicate that STI571 might be a candidate compound for the pharmacological treatment of DP and demonstrate that the same compound may act in different ways (cytotoxic vs. cytostatic), according to the specificity of the inhibited tyrosine kinase, namely, ABL or PDGFrbeta.	imatinib	23-29	platelet derived growth factor receptor, beta polypeptide	Mus musculus	271-280
11290609-1	2001	The tyrosine kinase inhibitor STI571 inhibits BCR/ABL and induces hematologic remission in most patients with chronic myeloid leukemia.	imatinib	30-36	BCR activator of RhoGEF and GTPase	Mus musculus	46-53
11290609-2	2001	In addition to BCR/ABL, STI571 also inhibits v-Abl, TEL/ABL, the native platelet-derived growth factor (PDGF)beta receptor, and c-KIT, but it does not inhibit SRC family kinases, c-FMS, FLT3, the epidermal growth factor receptor, or multiple other tyrosine kinases.	imatinib	24-30	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	47-50
11290609-2	2001	In addition to BCR/ABL, STI571 also inhibits v-Abl, TEL/ABL, the native platelet-derived growth factor (PDGF)beta receptor, and c-KIT, but it does not inhibit SRC family kinases, c-FMS, FLT3, the epidermal growth factor receptor, or multiple other tyrosine kinases.	imatinib	24-30	ets variant 6	Mus musculus	52-59
11290609-2	2001	In addition to BCR/ABL, STI571 also inhibits v-Abl, TEL/ABL, the native platelet-derived growth factor (PDGF)beta receptor, and c-KIT, but it does not inhibit SRC family kinases, c-FMS, FLT3, the epidermal growth factor receptor, or multiple other tyrosine kinases.	imatinib	24-30	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	128-133
11290609-2	2001	In addition to BCR/ABL, STI571 also inhibits v-Abl, TEL/ABL, the native platelet-derived growth factor (PDGF)beta receptor, and c-KIT, but it does not inhibit SRC family kinases, c-FMS, FLT3, the epidermal growth factor receptor, or multiple other tyrosine kinases.	imatinib	24-30	colony stimulating factor 1 receptor	Mus musculus	179-184
11290609-2	2001	In addition to BCR/ABL, STI571 also inhibits v-Abl, TEL/ABL, the native platelet-derived growth factor (PDGF)beta receptor, and c-KIT, but it does not inhibit SRC family kinases, c-FMS, FLT3, the epidermal growth factor receptor, or multiple other tyrosine kinases.	imatinib	24-30	FMS-like tyrosine kinase 3	Mus musculus	186-190
11290609-2	2001	In addition to BCR/ABL, STI571 also inhibits v-Abl, TEL/ABL, the native platelet-derived growth factor (PDGF)beta receptor, and c-KIT, but it does not inhibit SRC family kinases, c-FMS, FLT3, the epidermal growth factor receptor, or multiple other tyrosine kinases.	imatinib	24-30	epidermal growth factor receptor	Mus musculus	196-228
11287972-3	2001	METHODS: We conducted a phase 1, dose-escalating trial of STI571 (formerly known as CGP 57148B), a specific inhibitor of the BCR-ABL tyrosine kinase.	imatinib	58-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
11287973-3	2001	On the basis of the substantial activity of the inhibitor in patients in the chronic phase, we evaluated STI571 (formerly known as CGP 57148B), a specific inhibitor of the BCR-ABL tyrosine kinase, in patients who had CML in blast crisis and in patients with ALL who had the Ph chromosome.	imatinib	105-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-179
11287973-11	2001	CONCLUSIONS: The BCR-ABL tyrosine kinase inhibitor STI571 is well tolerated and has substantial activity in the blast crises of CML and in Ph-positive ALL.	imatinib	51-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
11264164-2	2001	STI571 is a novel anticancer agent that selectively inhibits the BCR/ABL tyrosine kinase.	imatinib	0-6	BCR activator of RhoGEF and GTPase	Homo sapiens	65-88
11264165-4	2001	STI571 was a more potent inhibitor of (3)H-thymidine incorporation in p210(bcr-abl)-expressing cells than was AG957, and it showed superior discrimination between inhibitory effects on parental cell lines and effects on their p210(bcr-abl)-expressing derivatives.	imatinib	0-6	envoplakin	Mus musculus	70-74
11264165-4	2001	STI571 was a more potent inhibitor of (3)H-thymidine incorporation in p210(bcr-abl)-expressing cells than was AG957, and it showed superior discrimination between inhibitory effects on parental cell lines and effects on their p210(bcr-abl)-expressing derivatives.	imatinib	0-6	envoplakin	Mus musculus	226-230
11368361-0	2001	Effect of a selective Abl tyrosine kinase inhibitor, STI571, on in vitro growth of BCR-ABL-positive acute lymphoblastic leukemia cells.	imatinib	53-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
11368361-7	2001	STI571 inhibited CA formation of BCR-ABL-positive ALL cells virtually 100% at 0.1-1.0 micromol/l.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
11368361-9	2001	Our results indicate that STI571 selectively inhibits in vitro growth of BCR-ABL-positive ALL cells.	imatinib	26-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
11368438-3	2001	Here, we demonstrate that compared to treatment with STI-571 (0.25 to 1.0 microM) or As2O3 (0.5 to 2.0 microM) alone, combined treatment with As2O3 and STI-571 induced significantly more apoptosis of HL-60/Bcr-Abl and K562 but not HL-60/neo cells (P < 0.05).	imatinib	152-159	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	206-213
11368438-4	2001	Combined treatment with As2O3 and STI-571 also resulted in greater reductions in the levels of Bcl-x(L), XIAP and Akt, and inhibition of Akt kinase activity.	imatinib	34-41	BCL2 like 1	Homo sapiens	95-103
11368438-4	2001	Combined treatment with As2O3 and STI-571 also resulted in greater reductions in the levels of Bcl-x(L), XIAP and Akt, and inhibition of Akt kinase activity.	imatinib	34-41	X-linked inhibitor of apoptosis	Homo sapiens	105-109
11368438-4	2001	Combined treatment with As2O3 and STI-571 also resulted in greater reductions in the levels of Bcl-x(L), XIAP and Akt, and inhibition of Akt kinase activity.	imatinib	34-41	AKT serine/threonine kinase 1	Homo sapiens	114-117
11368438-4	2001	Combined treatment with As2O3 and STI-571 also resulted in greater reductions in the levels of Bcl-x(L), XIAP and Akt, and inhibition of Akt kinase activity.	imatinib	34-41	AKT serine/threonine kinase 1	Homo sapiens	137-140
11290609-8	2001	STI571 inhibited tyrosine phosphorylation and cell growth of Ba/F3 cells expressing BCR/ABL, TEL/ABL, TEL/PDGFbetaR, and TEL/ARG with an IC(50) of approximately 0.5 microM in each case, but it had no effect on untransformed Ba/F3 cells growing in IL-3 or on Ba/F3 cells transformed by TEL/JAK2.	imatinib	0-6	BCR activator of RhoGEF and GTPase	Mus musculus	84-91
11290609-8	2001	STI571 inhibited tyrosine phosphorylation and cell growth of Ba/F3 cells expressing BCR/ABL, TEL/ABL, TEL/PDGFbetaR, and TEL/ARG with an IC(50) of approximately 0.5 microM in each case, but it had no effect on untransformed Ba/F3 cells growing in IL-3 or on Ba/F3 cells transformed by TEL/JAK2.	imatinib	0-6	ets variant 6	Mus musculus	93-100
11290609-8	2001	STI571 inhibited tyrosine phosphorylation and cell growth of Ba/F3 cells expressing BCR/ABL, TEL/ABL, TEL/PDGFbetaR, and TEL/ARG with an IC(50) of approximately 0.5 microM in each case, but it had no effect on untransformed Ba/F3 cells growing in IL-3 or on Ba/F3 cells transformed by TEL/JAK2.	imatinib	0-6	ets variant 6	Mus musculus	93-96
11290609-8	2001	STI571 inhibited tyrosine phosphorylation and cell growth of Ba/F3 cells expressing BCR/ABL, TEL/ABL, TEL/PDGFbetaR, and TEL/ARG with an IC(50) of approximately 0.5 microM in each case, but it had no effect on untransformed Ba/F3 cells growing in IL-3 or on Ba/F3 cells transformed by TEL/JAK2.	imatinib	0-6	ets variant 6	Mus musculus	102-105
11290609-8	2001	STI571 inhibited tyrosine phosphorylation and cell growth of Ba/F3 cells expressing BCR/ABL, TEL/ABL, TEL/PDGFbetaR, and TEL/ARG with an IC(50) of approximately 0.5 microM in each case, but it had no effect on untransformed Ba/F3 cells growing in IL-3 or on Ba/F3 cells transformed by TEL/JAK2.	imatinib	0-6	interleukin 3	Mus musculus	247-251
11290609-8	2001	STI571 inhibited tyrosine phosphorylation and cell growth of Ba/F3 cells expressing BCR/ABL, TEL/ABL, TEL/PDGFbetaR, and TEL/ARG with an IC(50) of approximately 0.5 microM in each case, but it had no effect on untransformed Ba/F3 cells growing in IL-3 or on Ba/F3 cells transformed by TEL/JAK2.	imatinib	0-6	ets variant 6	Mus musculus	102-105
11290609-8	2001	STI571 inhibited tyrosine phosphorylation and cell growth of Ba/F3 cells expressing BCR/ABL, TEL/ABL, TEL/PDGFbetaR, and TEL/ARG with an IC(50) of approximately 0.5 microM in each case, but it had no effect on untransformed Ba/F3 cells growing in IL-3 or on Ba/F3 cells transformed by TEL/JAK2.	imatinib	0-6	Janus kinase 2	Mus musculus	289-293
11290609-9	2001	Culture of TEL/ARG-transfected Ba/F3 cells with IL-3 completely prevented STI571-induced apoptosis in these cells, similar to what has been observed with BCR/ABL- or TEL/ABL-transformed cells.	imatinib	74-80	ets variant 6	Mus musculus	11-14
11290609-9	2001	Culture of TEL/ARG-transfected Ba/F3 cells with IL-3 completely prevented STI571-induced apoptosis in these cells, similar to what has been observed with BCR/ABL- or TEL/ABL-transformed cells.	imatinib	74-80	interleukin 3	Mus musculus	48-52
11264165-7	2001	However, for p210(bcr-abl)-expressing clones from all 3 cell lines, synergistic inhibition was demonstrated between STI571 and concentrations of AG490 with no independent inhibitory effect.	imatinib	116-122	envoplakin	Mus musculus	13-17
11264165-10	2001	This study concludes that, for the cell lines studied, (1) STI571 is a more potent and more selective inhibitor of a p210(bcr-abl)-dependent phenotype than AG957; (2) AG490 synergizes with STI571 to enhance its inhibitory effect on p210(bcr-abl)-driven proliferation; and (3) the combination of p210(bcr-abl)-tyrosine kinase inhibition and growth factor signal withdrawal can be sufficient to induce apoptotic death of transformed cells.	imatinib	59-65	envoplakin	Mus musculus	117-121
11264165-10	2001	This study concludes that, for the cell lines studied, (1) STI571 is a more potent and more selective inhibitor of a p210(bcr-abl)-dependent phenotype than AG957; (2) AG490 synergizes with STI571 to enhance its inhibitory effect on p210(bcr-abl)-driven proliferation; and (3) the combination of p210(bcr-abl)-tyrosine kinase inhibition and growth factor signal withdrawal can be sufficient to induce apoptotic death of transformed cells.	imatinib	59-65	envoplakin	Mus musculus	232-236
11264165-10	2001	This study concludes that, for the cell lines studied, (1) STI571 is a more potent and more selective inhibitor of a p210(bcr-abl)-dependent phenotype than AG957; (2) AG490 synergizes with STI571 to enhance its inhibitory effect on p210(bcr-abl)-driven proliferation; and (3) the combination of p210(bcr-abl)-tyrosine kinase inhibition and growth factor signal withdrawal can be sufficient to induce apoptotic death of transformed cells.	imatinib	59-65	envoplakin	Mus musculus	232-236
11298594-0	2001	Sensitivity to the abl inhibitor STI571 in fresh leukaemic cells obtained from chronic myelogenous leukaemia patients in different stages of disease.	imatinib	33-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-22
11298594-1	2001	STI571 (CGP57148B) is an inhibitor of BCR/ABL, the cause of chronic myeloid leukaemia (CML).	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
11298594-1	2001	STI571 (CGP57148B) is an inhibitor of BCR/ABL, the cause of chronic myeloid leukaemia (CML).	imatinib	8-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
11179439-6	2001	Use of the Bcr-Abl tyrosine kinase inhibitor STI-571 resulted in a reduction in Bcl-xL levels and potentiation of dexrazoxane-induced apoptosis related to an earlier onset and more extensive cleavage of caspase-3.	imatinib	45-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-18
11179439-6	2001	Use of the Bcr-Abl tyrosine kinase inhibitor STI-571 resulted in a reduction in Bcl-xL levels and potentiation of dexrazoxane-induced apoptosis related to an earlier onset and more extensive cleavage of caspase-3.	imatinib	45-52	BCL2 like 1	Homo sapiens	80-86
11179439-6	2001	Use of the Bcr-Abl tyrosine kinase inhibitor STI-571 resulted in a reduction in Bcl-xL levels and potentiation of dexrazoxane-induced apoptosis related to an earlier onset and more extensive cleavage of caspase-3.	imatinib	45-52	caspase 3	Homo sapiens	203-212
11237055-0	2001	Synergistic activity of the new ABL-specific tyrosine kinase inhibitor STI571 and chemotherapeutic drugs on BCR-ABL-positive chronic myelogenous leukemia cells.	imatinib	71-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-115
11237055-1	2001	The ABL-specific tyrosine kinase inhibitor STI571 (formerly CGP57148B) induced cytogenetic remissions in 33% of chronic myelogenous leukemia (CML) patients in a phase I trial (Druker et al 1999).	imatinib	43-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
11237055-1	2001	The ABL-specific tyrosine kinase inhibitor STI571 (formerly CGP57148B) induced cytogenetic remissions in 33% of chronic myelogenous leukemia (CML) patients in a phase I trial (Druker et al 1999).	imatinib	60-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
11237055-3	2001	We tested whether combinations of STI571 and cytarabine or other chemotherapeutic agents such as hydroxyurea, mafosfamide or etoposide would display synergistic activity in BCR-ABL-positive chronic myelogenous leukemia (CML) cell lines derived from patients in blast crisis.	imatinib	34-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	177-180
11237055-8	2001	At growth inhibition levels of over 50%, STI571 + cytarabine as well as STI571 + etoposide were significantly synergistic (CI < 1, P < 0.05) in the BCR-ABL-positive cell lines evaluated.	imatinib	41-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-161
11237055-8	2001	At growth inhibition levels of over 50%, STI571 + cytarabine as well as STI571 + etoposide were significantly synergistic (CI < 1, P < 0.05) in the BCR-ABL-positive cell lines evaluated.	imatinib	72-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-161
11036109-0	2000	Role of alpha1 acid glycoprotein in the in vivo resistance of human BCR-ABL(+) leukemic cells to the abl inhibitor STI571.	imatinib	115-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
11512148-1	2001	Imatinib (STI571, Glivec) is a small molecule drug selected for its ability to inhibit the Bcr-Abl kinase, the pathogenic molecular abnormality in chronic myelogenous leukemia (CML).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
11512149-1	2001	The tyrosine kinase inhibitor imatinib (STI571, Glivec) blocks the activity of the BCR/ABL oncogene and induces hematologic remissions in the majority of patients with chronic myeloid leukemia (CML).	imatinib	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-90
11512149-1	2001	The tyrosine kinase inhibitor imatinib (STI571, Glivec) blocks the activity of the BCR/ABL oncogene and induces hematologic remissions in the majority of patients with chronic myeloid leukemia (CML).	imatinib	40-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-90
11512149-1	2001	The tyrosine kinase inhibitor imatinib (STI571, Glivec) blocks the activity of the BCR/ABL oncogene and induces hematologic remissions in the majority of patients with chronic myeloid leukemia (CML).	imatinib	48-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-90
11512149-2	2001	Glivec is an aminopyrimidine derivative that interacts with the ATP-binding site within the kinase domain of ABL and several other tyrosine kinases, including c-KIT, PDGF beta receptor, and ARG.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-112
11512149-2	2001	Glivec is an aminopyrimidine derivative that interacts with the ATP-binding site within the kinase domain of ABL and several other tyrosine kinases, including c-KIT, PDGF beta receptor, and ARG.	imatinib	0-6	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	159-164
11512149-2	2001	Glivec is an aminopyrimidine derivative that interacts with the ATP-binding site within the kinase domain of ABL and several other tyrosine kinases, including c-KIT, PDGF beta receptor, and ARG.	imatinib	0-6	platelet derived growth factor subunit B	Homo sapiens	166-175
10964922-1	2000	Using the specific Abl tyrosine kinase inhibitor STI 571, we purified unphosphorylated murine type IV c-Abl and measured the kinetic parameters of c-Abl tyrosine kinase activity in a solution with a peptide-based assay.	imatinib	49-56	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	19-22
11085460-3	2000	In preclinical studies, ST1571 (formerly CGP57148B), an abl-specific, tyrosine kinase inhibitor, selectively killed bcr-abl-expressing cells both in vitro and in vivo.	imatinib	41-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
11234890-0	2001	Cotreatment with STI-571 enhances tumor necrosis factor alpha-related apoptosis-inducing ligand (TRAIL or apo-2L)-induced apoptosis of Bcr-Abl-positive human acute leukemia cells.	imatinib	17-24	TNF superfamily member 10	Homo sapiens	97-102
11234890-0	2001	Cotreatment with STI-571 enhances tumor necrosis factor alpha-related apoptosis-inducing ligand (TRAIL or apo-2L)-induced apoptosis of Bcr-Abl-positive human acute leukemia cells.	imatinib	17-24	TNF superfamily member 10	Homo sapiens	106-112
11234890-0	2001	Cotreatment with STI-571 enhances tumor necrosis factor alpha-related apoptosis-inducing ligand (TRAIL or apo-2L)-induced apoptosis of Bcr-Abl-positive human acute leukemia cells.	imatinib	17-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
11234890-1	2001	Bcr-Abl tyrosine kinase inhibitor STI-571 induces differentiation and apoptosis of HL-60/Bcr-Abl (with ectopic expression of p190 Bcr-Abl) and K562 (with endogenous expression of p210 Bcr-Abl) cells (Blood, 96: 2246-2253, 2000).	imatinib	34-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
11234890-1	2001	Bcr-Abl tyrosine kinase inhibitor STI-571 induces differentiation and apoptosis of HL-60/Bcr-Abl (with ectopic expression of p190 Bcr-Abl) and K562 (with endogenous expression of p210 Bcr-Abl) cells (Blood, 96: 2246-2253, 2000).	imatinib	34-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
11234890-1	2001	Bcr-Abl tyrosine kinase inhibitor STI-571 induces differentiation and apoptosis of HL-60/Bcr-Abl (with ectopic expression of p190 Bcr-Abl) and K562 (with endogenous expression of p210 Bcr-Abl) cells (Blood, 96: 2246-2253, 2000).	imatinib	34-41	contactin associated protein 1	Homo sapiens	125-129
11234890-1	2001	Bcr-Abl tyrosine kinase inhibitor STI-571 induces differentiation and apoptosis of HL-60/Bcr-Abl (with ectopic expression of p190 Bcr-Abl) and K562 (with endogenous expression of p210 Bcr-Abl) cells (Blood, 96: 2246-2253, 2000).	imatinib	34-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
11234890-1	2001	Bcr-Abl tyrosine kinase inhibitor STI-571 induces differentiation and apoptosis of HL-60/Bcr-Abl (with ectopic expression of p190 Bcr-Abl) and K562 (with endogenous expression of p210 Bcr-Abl) cells (Blood, 96: 2246-2253, 2000).	imatinib	34-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
11234890-2	2001	Cotreatment with STI-571 partially overcomes the resistance to antileukemic drug-induced apoptosis of HL-60/Bcr-Abl and K562 cells.	imatinib	17-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
11234890-9	2001	Cotreatment with STI-571 significantly enhanced Apo-2L/TRAIL-induced apoptosis (P < 0.01) as well as increased the processing of caspase-9 and -3 and XIAP, without affecting the levels of DR4, DR5, decoy receptors, or c-FLIP(L).	imatinib	17-24	TNF superfamily member 10	Homo sapiens	48-54
11234890-9	2001	Cotreatment with STI-571 significantly enhanced Apo-2L/TRAIL-induced apoptosis (P < 0.01) as well as increased the processing of caspase-9 and -3 and XIAP, without affecting the levels of DR4, DR5, decoy receptors, or c-FLIP(L).	imatinib	17-24	TNF superfamily member 10	Homo sapiens	55-60
11234890-9	2001	Cotreatment with STI-571 significantly enhanced Apo-2L/TRAIL-induced apoptosis (P < 0.01) as well as increased the processing of caspase-9 and -3 and XIAP, without affecting the levels of DR4, DR5, decoy receptors, or c-FLIP(L).	imatinib	17-24	caspase 9	Homo sapiens	132-148
11234890-9	2001	Cotreatment with STI-571 significantly enhanced Apo-2L/TRAIL-induced apoptosis (P < 0.01) as well as increased the processing of caspase-9 and -3 and XIAP, without affecting the levels of DR4, DR5, decoy receptors, or c-FLIP(L).	imatinib	17-24	X-linked inhibitor of apoptosis	Homo sapiens	153-157
11234890-9	2001	Cotreatment with STI-571 significantly enhanced Apo-2L/TRAIL-induced apoptosis (P < 0.01) as well as increased the processing of caspase-9 and -3 and XIAP, without affecting the levels of DR4, DR5, decoy receptors, or c-FLIP(L).	imatinib	17-24	TNF receptor superfamily member 10a	Homo sapiens	191-194
11234890-9	2001	Cotreatment with STI-571 significantly enhanced Apo-2L/TRAIL-induced apoptosis (P < 0.01) as well as increased the processing of caspase-9 and -3 and XIAP, without affecting the levels of DR4, DR5, decoy receptors, or c-FLIP(L).	imatinib	17-24	TNF receptor superfamily member 10b	Homo sapiens	196-199
11234890-9	2001	Cotreatment with STI-571 significantly enhanced Apo-2L/TRAIL-induced apoptosis (P < 0.01) as well as increased the processing of caspase-9 and -3 and XIAP, without affecting the levels of DR4, DR5, decoy receptors, or c-FLIP(L).	imatinib	17-24	CASP8 and FADD like apoptosis regulator	Homo sapiens	221-227
11234890-11	2001	These studies suggest that a combined treatment with STI-571 may be an effective strategy to selectively sensitize Bcr-Abl-positive leukemic blasts to Apo-2L/TRAIL-induced apoptosis.	imatinib	53-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
11234890-11	2001	These studies suggest that a combined treatment with STI-571 may be an effective strategy to selectively sensitize Bcr-Abl-positive leukemic blasts to Apo-2L/TRAIL-induced apoptosis.	imatinib	53-60	TNF superfamily member 10	Homo sapiens	151-157
11234890-11	2001	These studies suggest that a combined treatment with STI-571 may be an effective strategy to selectively sensitize Bcr-Abl-positive leukemic blasts to Apo-2L/TRAIL-induced apoptosis.	imatinib	53-60	TNF superfamily member 10	Homo sapiens	158-163
11010972-6	2000	Second, inhibition of BCR/ABL kinase activity with the Abl tyrosine kinase inhibitor STI571 rapidly increases p27(Kip1) levels.	imatinib	85-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
11010972-6	2000	Second, inhibition of BCR/ABL kinase activity with the Abl tyrosine kinase inhibitor STI571 rapidly increases p27(Kip1) levels.	imatinib	85-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-58
11010972-6	2000	Second, inhibition of BCR/ABL kinase activity with the Abl tyrosine kinase inhibitor STI571 rapidly increases p27(Kip1) levels.	imatinib	85-91	interferon alpha inducible protein 27	Homo sapiens	110-113
11010972-6	2000	Second, inhibition of BCR/ABL kinase activity with the Abl tyrosine kinase inhibitor STI571 rapidly increases p27(Kip1) levels.	imatinib	85-91	cyclin dependent kinase inhibitor 1B	Homo sapiens	114-118
11905636-0	2000	STI571: an inhibitor of the BCR-ABL tyrosine kinase for the treatment of chronic myelogenous leukaemia.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
11905636-3	2000	STI571 (formerly CGP57148B), is an ABL-specific inhibitor of tyrosine kinase that, in preclinical studies, selectively killed BCR-ABL-containing cells in vitro and in vivo.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
11905636-3	2000	STI571 (formerly CGP57148B), is an ABL-specific inhibitor of tyrosine kinase that, in preclinical studies, selectively killed BCR-ABL-containing cells in vitro and in vivo.	imatinib	17-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
11036109-12	2000	The plasma protein alpha1 acid glycoprotein (AGP) bound STI571 at physiologic concentrations in vitro and blocked the ability of STI571 to inhibit Bcr-Abl kinase activity in a dose-dependent manner.	imatinib	129-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-154
11071360-6	2000	The most exciting prospect is the discovery of drugs that inhibit specific oncogenes, as illustrated by the BCR-ABL tyrosine kinase inhibitor STI-571.	imatinib	142-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
10991971-0	2000	Abl protein-tyrosine kinase inhibitor STI571 inhibits in vitro signal transduction mediated by c-kit and platelet-derived growth factor receptors.	imatinib	38-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
10991971-0	2000	Abl protein-tyrosine kinase inhibitor STI571 inhibits in vitro signal transduction mediated by c-kit and platelet-derived growth factor receptors.	imatinib	38-44	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	95-100
10991971-2	2000	STI571 selectively inhibits the Abl and platelet-derived growth factor (PDGF) receptor tyrosine kinases in vitro and blocks cellular proliferation and tumor growth of Bcr-abl- or v-abl-expressing cells.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-35
10991971-2	2000	STI571 selectively inhibits the Abl and platelet-derived growth factor (PDGF) receptor tyrosine kinases in vitro and blocks cellular proliferation and tumor growth of Bcr-abl- or v-abl-expressing cells.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-175
10991971-2	2000	STI571 selectively inhibits the Abl and platelet-derived growth factor (PDGF) receptor tyrosine kinases in vitro and blocks cellular proliferation and tumor growth of Bcr-abl- or v-abl-expressing cells.	imatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-174
10991971-4	2000	STI571 was found to potently inhibit the kinase activity of the alpha- and beta-PDGF receptors and the receptor for stem cell factor, but not the closely related c-Fms, Flt-3, Kdr, Flt-1, and Tek tyrosine kinases.	imatinib	0-6	KIT ligand	Homo sapiens	116-132
10991971-6	2000	In cell-based assays, STI571 selectively inhibited PDGF and stem cell factor-mediated cellular signaling, including ligand-stimulated receptor autophosphorylation, inositol phosphate formation, and mitogen-activated protein kinase activation and proliferation.	imatinib	22-28	KIT ligand	Homo sapiens	60-76
10962572-4	2000	Incubation of cells with BCR/ABL tyrosine kinase inhibitor STI571 abrogated the "re-activation" of Akt or STAT5 by BCR/ABL SH3+SH2 mutants in some clones, in the others Akt and STAT5 activation became independent on BCR/ABL kinase activity.	imatinib	59-65	BCR activator of RhoGEF and GTPase	Mus musculus	25-28
10988075-2	2000	A small-molecule inhibitor of Abl (STI-571) is effective in the treatment of CML.	imatinib	35-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-33
10979973-0	2000	CGP57148B (STI-571) induces differentiation and apoptosis and sensitizes Bcr-Abl-positive human leukemia cells to apoptosis due to antileukemic drugs.	imatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
10979973-0	2000	CGP57148B (STI-571) induces differentiation and apoptosis and sensitizes Bcr-Abl-positive human leukemia cells to apoptosis due to antileukemic drugs.	imatinib	11-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
10979973-1	2000	The differentiation and apoptosis-sensitizing effects of the Bcr-Abl-specific tyrosine kinase inhibitor CGP57148B, also known as STI-571, were determined in human Bcr-Abl-positive HL-60/Bcr-Abl and K562 cells.	imatinib	104-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
10979973-1	2000	The differentiation and apoptosis-sensitizing effects of the Bcr-Abl-specific tyrosine kinase inhibitor CGP57148B, also known as STI-571, were determined in human Bcr-Abl-positive HL-60/Bcr-Abl and K562 cells.	imatinib	104-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
10979973-1	2000	The differentiation and apoptosis-sensitizing effects of the Bcr-Abl-specific tyrosine kinase inhibitor CGP57148B, also known as STI-571, were determined in human Bcr-Abl-positive HL-60/Bcr-Abl and K562 cells.	imatinib	104-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
10979973-5	2000	Exposure to CGP57148B alone increased hemoglobin levels and CD11b expression and induced apoptosis of HL-60/Bcr-Abl and K562 cells.	imatinib	12-21	integrin subunit alpha M	Homo sapiens	60-65
10979973-5	2000	Exposure to CGP57148B alone increased hemoglobin levels and CD11b expression and induced apoptosis of HL-60/Bcr-Abl and K562 cells.	imatinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
10979973-7	2000	CGP57148B also inhibited constitutively active Akt kinase and NFkappaB in Bcr-Abl-positive cells.	imatinib	0-9	nuclear factor kappa B subunit 1	Homo sapiens	62-70
10979973-7	2000	CGP57148B also inhibited constitutively active Akt kinase and NFkappaB in Bcr-Abl-positive cells.	imatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
10979973-9	2000	Importantly, cotreatment with CGP57148B significantly increased Ara-C- or doxorubicin-induced apoptosis of HL-60/Bcr-Abl and K562 cells.	imatinib	30-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
10979973-11	2000	These in vitro data indicate that combinations of CGP57148B and antileukemic drugs such as Ara-C may have improved in vivo efficacy against Bcr-Abl-positive acute leukemia.	imatinib	50-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
10962572-4	2000	Incubation of cells with BCR/ABL tyrosine kinase inhibitor STI571 abrogated the "re-activation" of Akt or STAT5 by BCR/ABL SH3+SH2 mutants in some clones, in the others Akt and STAT5 activation became independent on BCR/ABL kinase activity.	imatinib	59-65	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	29-32
10962572-4	2000	Incubation of cells with BCR/ABL tyrosine kinase inhibitor STI571 abrogated the "re-activation" of Akt or STAT5 by BCR/ABL SH3+SH2 mutants in some clones, in the others Akt and STAT5 activation became independent on BCR/ABL kinase activity.	imatinib	59-65	thymoma viral proto-oncogene 1	Mus musculus	99-102
10962572-4	2000	Incubation of cells with BCR/ABL tyrosine kinase inhibitor STI571 abrogated the "re-activation" of Akt or STAT5 by BCR/ABL SH3+SH2 mutants in some clones, in the others Akt and STAT5 activation became independent on BCR/ABL kinase activity.	imatinib	59-65	signal transducer and activator of transcription 5A	Mus musculus	106-111
10962572-4	2000	Incubation of cells with BCR/ABL tyrosine kinase inhibitor STI571 abrogated the "re-activation" of Akt or STAT5 by BCR/ABL SH3+SH2 mutants in some clones, in the others Akt and STAT5 activation became independent on BCR/ABL kinase activity.	imatinib	59-65	BCR activator of RhoGEF and GTPase	Mus musculus	25-32
10962572-4	2000	Incubation of cells with BCR/ABL tyrosine kinase inhibitor STI571 abrogated the "re-activation" of Akt or STAT5 by BCR/ABL SH3+SH2 mutants in some clones, in the others Akt and STAT5 activation became independent on BCR/ABL kinase activity.	imatinib	59-65	sperm hammerhead 3	Mus musculus	123-126
10962572-4	2000	Incubation of cells with BCR/ABL tyrosine kinase inhibitor STI571 abrogated the "re-activation" of Akt or STAT5 by BCR/ABL SH3+SH2 mutants in some clones, in the others Akt and STAT5 activation became independent on BCR/ABL kinase activity.	imatinib	59-65	sperm hammerhead 2	Mus musculus	127-130
10962572-4	2000	Incubation of cells with BCR/ABL tyrosine kinase inhibitor STI571 abrogated the "re-activation" of Akt or STAT5 by BCR/ABL SH3+SH2 mutants in some clones, in the others Akt and STAT5 activation became independent on BCR/ABL kinase activity.	imatinib	59-65	thymoma viral proto-oncogene 1	Mus musculus	169-172
10962572-4	2000	Incubation of cells with BCR/ABL tyrosine kinase inhibitor STI571 abrogated the "re-activation" of Akt or STAT5 by BCR/ABL SH3+SH2 mutants in some clones, in the others Akt and STAT5 activation became independent on BCR/ABL kinase activity.	imatinib	59-65	signal transducer and activator of transcription 5A	Mus musculus	177-182
10962572-4	2000	Incubation of cells with BCR/ABL tyrosine kinase inhibitor STI571 abrogated the "re-activation" of Akt or STAT5 by BCR/ABL SH3+SH2 mutants in some clones, in the others Akt and STAT5 activation became independent on BCR/ABL kinase activity.	imatinib	59-65	BCR activator of RhoGEF and GTPase	Mus musculus	115-118
10962572-4	2000	Incubation of cells with BCR/ABL tyrosine kinase inhibitor STI571 abrogated the "re-activation" of Akt or STAT5 by BCR/ABL SH3+SH2 mutants in some clones, in the others Akt and STAT5 activation became independent on BCR/ABL kinase activity.	imatinib	59-65	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	119-122
10910924-12	2000	We conclude that BCR-ABL-positive cells can evade the inhibitory effect of STI571 by different mechanisms, such as Bcr-Abl overexpression, reduced intake mediated by Pgp, and, possibly, acquisition of compensatory mutations in genes other than BCR-ABL.	imatinib	75-81	phosphoglycolate phosphatase	Mus musculus	166-169
10833515-3	2000	The increase in ROS was directly due to BCR/ABL because it was blocked by the ABL-specific tyrosine kinase inhibitor STI571.	imatinib	117-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
10833515-3	2000	The increase in ROS was directly due to BCR/ABL because it was blocked by the ABL-specific tyrosine kinase inhibitor STI571.	imatinib	117-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-47
10955819-5	2000	Pretreatment of the H526 small cell lung cancer (SCLC) cell line with STI571 inhibited SCF-mediated Kit activation with an IC50 of 0.1 microM as measured by inhibition of receptor tyrosine phosphorylation and 0.2 microM as measured by immune complex kinase assay.	imatinib	70-76	KIT ligand	Homo sapiens	87-90
10910906-0	2000	Inhibition of c-kit receptor tyrosine kinase activity by STI 571, a selective tyrosine kinase inhibitor.	imatinib	57-64	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-19
10910906-5	2000	STI 571 inhibited c-kit autophosphorylation, activation of mitogen-activated protein (MAP) kinase, and activation of Akt without altering total protein levels of c-kit, MAP kinase, or Akt.	imatinib	0-7	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	18-23
10910906-5	2000	STI 571 inhibited c-kit autophosphorylation, activation of mitogen-activated protein (MAP) kinase, and activation of Akt without altering total protein levels of c-kit, MAP kinase, or Akt.	imatinib	0-7	AKT serine/threonine kinase 1	Homo sapiens	117-120
10910906-11	2000	These findings show that STI 571 selectively inhibits c-kit tyrosine kinase activity and downstream activation of target proteins involved in cellular proliferation and survival.	imatinib	25-32	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	54-59
10955819-5	2000	Pretreatment of the H526 small cell lung cancer (SCLC) cell line with STI571 inhibited SCF-mediated Kit activation with an IC50 of 0.1 microM as measured by inhibition of receptor tyrosine phosphorylation and 0.2 microM as measured by immune complex kinase assay.	imatinib	70-76	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	100-103
10955819-6	2000	This paralleled the inhibition of SCF-mediated growth by STI571, which had an IC50 of approximately 0.3 microM.	imatinib	57-63	KIT ligand	Homo sapiens	34-37
10955819-8	2000	STI571 efficiently blocked SCF-mediated activation of mitogen-activated protein kinase and Akt, but did not affect insulin-like growth factor-1 or serum-mediated mitogen-activated protein kinase or Akt activation.	imatinib	0-6	KIT ligand	Homo sapiens	27-30
10955819-8	2000	STI571 efficiently blocked SCF-mediated activation of mitogen-activated protein kinase and Akt, but did not affect insulin-like growth factor-1 or serum-mediated mitogen-activated protein kinase or Akt activation.	imatinib	0-6	AKT serine/threonine kinase 1	Homo sapiens	91-94
10918610-11	2000	These data imply that STI 571 inhibits growth of SCLC cells through a mechanism that involves inactivation of the tyrosine kinase c-Kit.	imatinib	22-29	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	130-135
12578692-5	2000	CGP57148B could increase the beta1 integrin activation potential of CMLBMMNCs but had no effects on that of NBMMNCs.	imatinib	0-9	integrin subunit beta 1	Homo sapiens	29-43
10828035-0	2000	Mechanism of resistance to the ABL tyrosine kinase inhibitor STI571 in BCR/ABL-transformed hematopoietic cell lines.	imatinib	61-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-34
10828035-0	2000	Mechanism of resistance to the ABL tyrosine kinase inhibitor STI571 in BCR/ABL-transformed hematopoietic cell lines.	imatinib	61-67	BCR activator of RhoGEF and GTPase	Homo sapiens	71-74
10828035-0	2000	Mechanism of resistance to the ABL tyrosine kinase inhibitor STI571 in BCR/ABL-transformed hematopoietic cell lines.	imatinib	61-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-78
10828035-2	2000	The tyrosine kinase inhibitor STI571 (formerly called CGP57148B, Novartis Pharmaceuticals) inhibits BCR/ABL, TEL/ABL, and v-ABL kinase activity and inhibits growth and viability of cells transformed by any of these ABL oncogenes.	imatinib	30-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
10828035-2	2000	The tyrosine kinase inhibitor STI571 (formerly called CGP57148B, Novartis Pharmaceuticals) inhibits BCR/ABL, TEL/ABL, and v-ABL kinase activity and inhibits growth and viability of cells transformed by any of these ABL oncogenes.	imatinib	30-36	ETS variant transcription factor 6	Homo sapiens	109-116
10828035-2	2000	The tyrosine kinase inhibitor STI571 (formerly called CGP57148B, Novartis Pharmaceuticals) inhibits BCR/ABL, TEL/ABL, and v-ABL kinase activity and inhibits growth and viability of cells transformed by any of these ABL oncogenes.	imatinib	30-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-127
10828035-2	2000	The tyrosine kinase inhibitor STI571 (formerly called CGP57148B, Novartis Pharmaceuticals) inhibits BCR/ABL, TEL/ABL, and v-ABL kinase activity and inhibits growth and viability of cells transformed by any of these ABL oncogenes.	imatinib	30-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-107
10828035-2	2000	The tyrosine kinase inhibitor STI571 (formerly called CGP57148B, Novartis Pharmaceuticals) inhibits BCR/ABL, TEL/ABL, and v-ABL kinase activity and inhibits growth and viability of cells transformed by any of these ABL oncogenes.	imatinib	54-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
10828035-2	2000	The tyrosine kinase inhibitor STI571 (formerly called CGP57148B, Novartis Pharmaceuticals) inhibits BCR/ABL, TEL/ABL, and v-ABL kinase activity and inhibits growth and viability of cells transformed by any of these ABL oncogenes.	imatinib	54-63	ETS variant transcription factor 6	Homo sapiens	109-116
10828035-2	2000	The tyrosine kinase inhibitor STI571 (formerly called CGP57148B, Novartis Pharmaceuticals) inhibits BCR/ABL, TEL/ABL, and v-ABL kinase activity and inhibits growth and viability of cells transformed by any of these ABL oncogenes.	imatinib	54-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-127
10828035-2	2000	The tyrosine kinase inhibitor STI571 (formerly called CGP57148B, Novartis Pharmaceuticals) inhibits BCR/ABL, TEL/ABL, and v-ABL kinase activity and inhibits growth and viability of cells transformed by any of these ABL oncogenes.	imatinib	54-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-107
12578692-6	2000	The results indicate that decreased activation potential of beta1 integrin in CMLBMMNCs is the major cause of adhesion defects of Ph(+) CML cells; beta1 integrin functional insufficiency in CMLBMMNCs could not be directly reversed by ABL tyrosine kinase inhibitor CGP57148B.	imatinib	264-273	integrin subunit beta 1	Homo sapiens	60-74
10658679-6	2000	[corrected] Treatment of Bcr-Abl expressing cells with CGP57148, but not LY294002, resulted in reversion of cells to a near-normal phenotype, as assessed by immunofluorescence and attachment of Bcr-Abl transformed fibroblasts.	imatinib	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
10815921-0	2000	The tyrosine kinase inhibitor CGP 57148 (ST1 571) induces apoptosis in BCR-ABL-positive cells by down-regulating BCL-X.	imatinib	30-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
10815921-0	2000	The tyrosine kinase inhibitor CGP 57148 (ST1 571) induces apoptosis in BCR-ABL-positive cells by down-regulating BCL-X.	imatinib	30-39	BCL2 like 1	Homo sapiens	113-118
10812245-1	2000	OBJECTIVE: To determine whether the compound STI571 (formerly known as CGP571418B), a selective inhibitor of the protein tyrosine kinase (PTK) activity of ABL and BCR-ABL proteins, preferentially reduces the capacity for amplification of granulocyte-macrophage progenitors (CFU-GM) from patients with chronic myeloid leukemia while sparing normal CFU-GM and to compare responses of CML and normal cells with STI571 and IFN-alpha.	imatinib	45-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-158
10812245-1	2000	OBJECTIVE: To determine whether the compound STI571 (formerly known as CGP571418B), a selective inhibitor of the protein tyrosine kinase (PTK) activity of ABL and BCR-ABL proteins, preferentially reduces the capacity for amplification of granulocyte-macrophage progenitors (CFU-GM) from patients with chronic myeloid leukemia while sparing normal CFU-GM and to compare responses of CML and normal cells with STI571 and IFN-alpha.	imatinib	45-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
10812245-1	2000	OBJECTIVE: To determine whether the compound STI571 (formerly known as CGP571418B), a selective inhibitor of the protein tyrosine kinase (PTK) activity of ABL and BCR-ABL proteins, preferentially reduces the capacity for amplification of granulocyte-macrophage progenitors (CFU-GM) from patients with chronic myeloid leukemia while sparing normal CFU-GM and to compare responses of CML and normal cells with STI571 and IFN-alpha.	imatinib	45-51	interferon alpha 1	Homo sapiens	419-428
10688835-1	2000	The 2-phenylaminopyrimidine derivative STI571 has been shown to selectively inhibit the tyrosine kinase domain of the oncogenic bcr/abl fusion protein.	imatinib	39-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
10658679-6	2000	[corrected] Treatment of Bcr-Abl expressing cells with CGP57148, but not LY294002, resulted in reversion of cells to a near-normal phenotype, as assessed by immunofluorescence and attachment of Bcr-Abl transformed fibroblasts.	imatinib	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	194-201
10446987-4	1999	The PDGF receptor kinase inhibitor CGP57148B reversed the transformed phenotype and reduced the growth rate of COLIA1/PDGFB-expressing cells but had no effects on control cells.	imatinib	35-44	collagen, type I, alpha 1	Mus musculus	111-117
10523635-7	1999	Also, an ABL-specific tyrosine kinase inhibitor, CGP57148B (STI571), rapidly caused reexpression of SHIP, indicating that BCR/ABL directly, but reversibly, regulates the expression of SHIP protein.	imatinib	49-58	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	9-12
10523635-7	1999	Also, an ABL-specific tyrosine kinase inhibitor, CGP57148B (STI571), rapidly caused reexpression of SHIP, indicating that BCR/ABL directly, but reversibly, regulates the expression of SHIP protein.	imatinib	49-58	inositol polyphosphate-5-phosphatase D	Mus musculus	100-104
10523635-7	1999	Also, an ABL-specific tyrosine kinase inhibitor, CGP57148B (STI571), rapidly caused reexpression of SHIP, indicating that BCR/ABL directly, but reversibly, regulates the expression of SHIP protein.	imatinib	49-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
10523635-7	1999	Also, an ABL-specific tyrosine kinase inhibitor, CGP57148B (STI571), rapidly caused reexpression of SHIP, indicating that BCR/ABL directly, but reversibly, regulates the expression of SHIP protein.	imatinib	49-58	inositol polyphosphate-5-phosphatase D	Mus musculus	184-188
10446987-4	1999	The PDGF receptor kinase inhibitor CGP57148B reversed the transformed phenotype and reduced the growth rate of COLIA1/PDGFB-expressing cells but had no effects on control cells.	imatinib	35-44	platelet derived growth factor, B polypeptide	Mus musculus	118-123
10446987-7	1999	Finally, COLIA1/PDGFB-expressing cells generated tumors after s.c. injection into nude mice, and tumor growth was reduced by treatment with CGP57148B.	imatinib	140-149	collagen, type I, alpha 1	Mus musculus	9-15
10446987-7	1999	Finally, COLIA1/PDGFB-expressing cells generated tumors after s.c. injection into nude mice, and tumor growth was reduced by treatment with CGP57148B.	imatinib	140-149	platelet derived growth factor, B polypeptide	Mus musculus	16-21
9389713-1	1997	CGP 57148 is a compound of the 2-phenylaminopyrimidine class that selectively inhibits the tyrosine kinase activity of the ABL and the platelet-derived growth factor receptor (PDGFR) protein tyrosine kinases.	imatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-126
10200527-2	1998	We report herein that CGP 57148, a selective inhibitor of the ABL tyrosine kinase, caused apoptosis specifically in bcr - abl-positive chronic myelogenous leukemia (CML) cells, K562 and KYO-1.	imatinib	22-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-125
10200527-5	1998	Caspase activation and cleavage of retinoblastoma protein (pRB) accompanied the development of CGP 57148-induced apoptosis.	imatinib	95-104	RB transcriptional corepressor 1	Homo sapiens	59-62
10029600-5	1999	Treatment of TEL/PDGFbetaR transgenic animals with a protein tyrosine kinase inhibitor with in vitro activity against PDGFbetaR (CGP57148) resulted in suppression of disease and a prolongation of survival.	imatinib	129-137	ets variant 6	Mus musculus	13-16
9923858-3	1999	In this study, we evaluated the antineoplastic activity of CGP57148B, which is a competitive inhibitor of the Bcr/Abl tyrosine kinase.	imatinib	59-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
9923858-8	1999	A single administration of CGP57148B caused substantial (>50%) but short-lived (2-5 hours) inhibition of Bcr/Abl kinase activity.	imatinib	27-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
9389713-1	1997	CGP 57148 is a compound of the 2-phenylaminopyrimidine class that selectively inhibits the tyrosine kinase activity of the ABL and the platelet-derived growth factor receptor (PDGFR) protein tyrosine kinases.	imatinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	135-174
9389713-1	1997	CGP 57148 is a compound of the 2-phenylaminopyrimidine class that selectively inhibits the tyrosine kinase activity of the ABL and the platelet-derived growth factor receptor (PDGFR) protein tyrosine kinases.	imatinib	0-9	platelet derived growth factor receptor beta	Homo sapiens	176-181
9345054-0	1997	The tyrosine kinase inhibitor CGP57148B selectively inhibits the growth of BCR-ABL-positive cells.	imatinib	30-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
9446752-4	1997	CGP57148B is an ATP-competitive inhibitor of the ABL protein kinase; it has been shown to inhibit the kinase activity of ABL both in vitro and in vivo and to inhibit the growth of v-abl and bcr/abl transfectants, as well as the in vitro formation of bone marrow (BM)-derived colonies in the presence of growth factors in some CML patients.	imatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-52
9446752-4	1997	CGP57148B is an ATP-competitive inhibitor of the ABL protein kinase; it has been shown to inhibit the kinase activity of ABL both in vitro and in vivo and to inhibit the growth of v-abl and bcr/abl transfectants, as well as the in vitro formation of bone marrow (BM)-derived colonies in the presence of growth factors in some CML patients.	imatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-124
9446752-4	1997	CGP57148B is an ATP-competitive inhibitor of the ABL protein kinase; it has been shown to inhibit the kinase activity of ABL both in vitro and in vivo and to inhibit the growth of v-abl and bcr/abl transfectants, as well as the in vitro formation of bone marrow (BM)-derived colonies in the presence of growth factors in some CML patients.	imatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	180-185
9446752-4	1997	CGP57148B is an ATP-competitive inhibitor of the ABL protein kinase; it has been shown to inhibit the kinase activity of ABL both in vitro and in vivo and to inhibit the growth of v-abl and bcr/abl transfectants, as well as the in vitro formation of bone marrow (BM)-derived colonies in the presence of growth factors in some CML patients.	imatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	190-197
9446752-5	1997	These studies were performed to investigate the activity of CGP57148B on the spontaneous proliferation of both fresh and cultured, leukemic and normal, BCR/ABL positive and negative cells, and to study its mechanism of action.	imatinib	60-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-159
9345054-3	1997	CGP57148B, a 2-phenylaminopyrimidine derivative, has been shown to selectively inhibit the tyrosine kinase of ABL and BCR-ABL.	imatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-113
9345054-3	1997	CGP57148B, a 2-phenylaminopyrimidine derivative, has been shown to selectively inhibit the tyrosine kinase of ABL and BCR-ABL.	imatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
33809714-2	2021	Small molecule inhibitors and monoclonal antibodies directed at relevant cancer-related proteins have been instrumental in delivering successful treatments of some blood malignancies (e.g., imatinib with chronic myelogenous leukemia (CML)) and solid tumors (e.g., tamoxifen with ER positive breast cancer and trastuzumab for HER2-positive breast cancer).	imatinib	190-198	erb-b2 receptor tyrosine kinase 2	Homo sapiens	325-329
33824300-0	2021	LncRNA-HOTAIR activates autophagy and promotes the imatinib resistance of gastrointestinal stromal tumor cells through a mechanism involving the miR-130a/ATG2B pathway.	imatinib	51-59	HOX transcript antisense RNA (non-protein coding)	Mus musculus	7-13
33824300-0	2021	LncRNA-HOTAIR activates autophagy and promotes the imatinib resistance of gastrointestinal stromal tumor cells through a mechanism involving the miR-130a/ATG2B pathway.	imatinib	51-59	microRNA 130a	Mus musculus	145-153
33824300-0	2021	LncRNA-HOTAIR activates autophagy and promotes the imatinib resistance of gastrointestinal stromal tumor cells through a mechanism involving the miR-130a/ATG2B pathway.	imatinib	51-59	autophagy related 2B	Mus musculus	154-159
33824300-1	2021	Gastrointestinal stromal tumors (GISTs) are common neoplasms of the gastrointestinal tract that can be treated successfully using C-kit target therapy and surgery; however, imatinib chemoresistance is a major barrier to success in therapy.	imatinib	173-181	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	130-135
33824300-5	2021	In this study, we analyzed differentially expressed lncRNAs after imatinib treatment and found that HOTAIR displayed the largest increase.	imatinib	66-74	HOX transcript antisense RNA (non-protein coding)	Mus musculus	100-106
33824300-6	2021	The distribution of HOTAIR in GISTs was shifted from nucleus to cytoplasm after imatinib treatments.	imatinib	80-88	HOX transcript antisense RNA (non-protein coding)	Mus musculus	20-26
33824300-10	2021	The downregulation of miRNA-130a reversed HOTAIR-small interfering RNA-induced suppression of autophagy and imatinib sensitivity.	imatinib	108-116	HOX transcript antisense RNA (non-protein coding)	Mus musculus	42-48
33824300-12	2021	ATG2B downregulation reversed the effect of pEX-3-HOTAIR/miR-130a inhibitor on imatinib sensitivity.	imatinib	79-87	autophagy related 2B	Mus musculus	0-5
33824300-12	2021	ATG2B downregulation reversed the effect of pEX-3-HOTAIR/miR-130a inhibitor on imatinib sensitivity.	imatinib	79-87	peroxisomal biogenesis factor 3	Mus musculus	44-49
33824300-12	2021	ATG2B downregulation reversed the effect of pEX-3-HOTAIR/miR-130a inhibitor on imatinib sensitivity.	imatinib	79-87	HOX transcript antisense RNA (non-protein coding)	Mus musculus	50-56
33824300-12	2021	ATG2B downregulation reversed the effect of pEX-3-HOTAIR/miR-130a inhibitor on imatinib sensitivity.	imatinib	79-87	microRNA 130a	Mus musculus	57-65
33824300-13	2021	Finally, HOTAIR was shown to influence the autophagy and imatinib sensitivity of GIST cells in mouse tumor models.	imatinib	57-65	HOX transcript antisense RNA (non-protein coding)	Mus musculus	9-15
33824300-14	2021	Our results suggested that HOTAIR targets the ATG2B inhibitor miR-130a to upregulate the level of cell autophagy so that promotes the imatinib resistance in GISTs.	imatinib	134-142	HOX transcript antisense RNA (non-protein coding)	Mus musculus	27-33
33824300-14	2021	Our results suggested that HOTAIR targets the ATG2B inhibitor miR-130a to upregulate the level of cell autophagy so that promotes the imatinib resistance in GISTs.	imatinib	134-142	autophagy related 2B	Mus musculus	46-51
33824300-14	2021	Our results suggested that HOTAIR targets the ATG2B inhibitor miR-130a to upregulate the level of cell autophagy so that promotes the imatinib resistance in GISTs.	imatinib	134-142	microRNA 130a	Mus musculus	62-70
33772839-2	2021	A simple analytical method using high-performance liquid chromatography/electrospray ionization tandem mass spectrometry has been developed and validated for simultaneous quantification of BCR-ABL and Bruton"s tyrosine kinase inhibitors (TKIs) used for chronic leukemia (imatinib, dasatinib, bosutinib, nilotinib, and ibrutinib) in human plasma.	imatinib	271-279	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	189-196
33772839-2	2021	A simple analytical method using high-performance liquid chromatography/electrospray ionization tandem mass spectrometry has been developed and validated for simultaneous quantification of BCR-ABL and Bruton"s tyrosine kinase inhibitors (TKIs) used for chronic leukemia (imatinib, dasatinib, bosutinib, nilotinib, and ibrutinib) in human plasma.	imatinib	271-279	Bruton tyrosine kinase	Homo sapiens	201-225
28261657-0	2016	Impact of CYP3A4*18 and CYP3A5*3 Polymorphisms on Imatinib Mesylate Response Among Chronic Myeloid Leukemia Patients in Malaysia.	imatinib	50-67	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	10-16
33235741-0	2020	Effects of imatinib mesylate on cutaneous neurofibromas associated with neurofibromatosis type 1.	imatinib	11-28	neurofibromin 1	Homo sapiens	72-96
33235741-1	2020	Imatinib mesylate seemed to inhibit development of cutaneous neurofibromas (c-NFs) and promote growth of pre-existing c-NFs in our neurofibromatosis type 1 case.	imatinib	0-17	neurofibromin 1	Homo sapiens	131-155
28261657-0	2016	Impact of CYP3A4*18 and CYP3A5*3 Polymorphisms on Imatinib Mesylate Response Among Chronic Myeloid Leukemia Patients in Malaysia.	imatinib	50-67	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	24-30
20007137-1	2010	BACKGROUND: Tyrosine kinase inhibitors, such as imatinib, are not considered curative for chronic myeloid leukemia--regardless of the significant reduction of disease burden during treatment--since they do not affect the leukemic stem cells.	imatinib	48-56	TXK tyrosine kinase	Homo sapiens	12-27
25871397-4	2015	We found that miR-203 expression was significantly lower in imatinib-resistant GBM cells (U251AR, U87AR) that underwent EMT than in their parental cells (U251, U87).	imatinib	60-68	microRNA 203a	Homo sapiens	14-21
25501350-0	2015	Impact of IKZF1 deletions on long-term outcomes of allo-SCT following imatinib-based chemotherapy in adult Philadelphia chromosome-positive ALL.	imatinib	70-78	IKAROS family zinc finger 1	Homo sapiens	10-15
24331439-1	2014	BACKGROUND: The first-line treatment in chronic myeloid leukemia (CML), imatinib, has been shown to decrease the production of amyloid-beta (Abeta) in vitro and in animal studies.	imatinib	72-80	amyloid beta precursor protein	Homo sapiens	127-139
24331439-1	2014	BACKGROUND: The first-line treatment in chronic myeloid leukemia (CML), imatinib, has been shown to decrease the production of amyloid-beta (Abeta) in vitro and in animal studies.	imatinib	72-80	amyloid beta precursor protein	Homo sapiens	141-146
24331439-4	2014	The effect of imatinib on Abeta production was also investigated in human embryonic kidney 293 (HEK293) cells overexpressing the amyloid precursor protein (APP) with the Swedish mutation, in mouse primary cortical neurons and in human Down syndrome embryonic stem-cell-derived cortical neurons.	imatinib	14-22	amyloid beta precursor protein	Homo sapiens	26-31
21893472-0	2011	Complex effects of imatinib on spontaneous and oxytocin-induced contractions in human non-pregnant myometrium.	imatinib	19-27	oxytocin/neurophysin I prepropeptide	Homo sapiens	47-55
21893472-3	2011	The aim of this study was to investigate the effects of imatinib as a c-kit receptor antagonist on the spontaneous or oxytocin (OT) induced contractions of human non-pregnant myometrium in vitro.	imatinib	56-64	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	70-75
21893472-3	2011	The aim of this study was to investigate the effects of imatinib as a c-kit receptor antagonist on the spontaneous or oxytocin (OT) induced contractions of human non-pregnant myometrium in vitro.	imatinib	56-64	oxytocin/neurophysin I prepropeptide	Homo sapiens	118-126
17317816-3	2007	RESULTS: Imatinib, which targets the ABL kinase activity of BCR-ABL, has prolonged survival in CML.	imatinib	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
17403535-1	2007	Acquired imatinib resistance in chronic myelogenous leukemia (CML) can be the consequence of mutations in the kinase domain of BCR-ABL or increased protein levels.	imatinib	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
19052557-0	2009	Early in vivo changes of the transcriptome in Philadelphia chromosome-positive CD34+ cells from patients with chronic myelogenous leukaemia following imatinib therapy.	imatinib	150-158	CD34 molecule	Homo sapiens	79-83
17317816-4	2007	Despite the efficacy of imatinib, some patients in chronic phase and more in advanced phases of CML develop resistance, frequently as a result of BCR-ABL tyrosine kinase domain mutants that impair imatinib binding but retain enzymatic activity.	imatinib	24-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	146-153
17317816-4	2007	Despite the efficacy of imatinib, some patients in chronic phase and more in advanced phases of CML develop resistance, frequently as a result of BCR-ABL tyrosine kinase domain mutants that impair imatinib binding but retain enzymatic activity.	imatinib	197-205	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	146-153
17317816-5	2007	New tyrosine kinase inhibitors inhibit BCR-ABL more potently than imatinib and maintain activity against an array of imatinib-resistant BCR-ABL mutants.	imatinib	117-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
17317816-5	2007	New tyrosine kinase inhibitors inhibit BCR-ABL more potently than imatinib and maintain activity against an array of imatinib-resistant BCR-ABL mutants.	imatinib	117-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-143
34496035-0	2022	BCR-ABL1 transcript doubling time as a predictor for treatment-free remission failure after imatinib discontinuation in chronic myeloid leukaemia in chronic phase.	imatinib	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-8
34774565-1	2022	Imatinib is an ATP-competitive inhibitor of Bcr-Abl kinase and the first drug approved for chronic myelogenous leukemia (CML) treatment.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
34774565-8	2022	Our results highlight the benefit of combining imatinib with allosteric inhibitors to maximize their inhibitory effect on Bcr-Abl.	imatinib	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
34973290-10	2022	The in vivo results revealed that IMA treatment significantly increased serum CK, LDH and AST.	imatinib	34-37	cytidine/uridine monophosphate kinase 1	Homo sapiens	78-80
34973290-10	2022	The in vivo results revealed that IMA treatment significantly increased serum CK, LDH and AST.	imatinib	34-37	solute carrier family 17 member 5	Homo sapiens	90-93
34895916-0	2022	The tyrosine kinase inhibitor Bosutinib does not inhibit angiotensin II-induced abdominal aortic aneurysm: Validation of the importance of PDGFR and c-Kit tyrosine kinases by Imatinib.	imatinib	175-183	platelet derived growth factor receptor beta	Homo sapiens	139-144
34902507-0	2022	Expression Dynamics Of The Immune Mediators ARG1, TBET, CIITA, IL10 AND TGFB1 IN Chronic Myeloid Leukaemia Patients During The First Year Of Imatinib Therapy.	imatinib	141-149	arginase 1	Homo sapiens	44-48
34902507-0	2022	Expression Dynamics Of The Immune Mediators ARG1, TBET, CIITA, IL10 AND TGFB1 IN Chronic Myeloid Leukaemia Patients During The First Year Of Imatinib Therapy.	imatinib	141-149	T-box transcription factor 21	Homo sapiens	50-54
34902507-0	2022	Expression Dynamics Of The Immune Mediators ARG1, TBET, CIITA, IL10 AND TGFB1 IN Chronic Myeloid Leukaemia Patients During The First Year Of Imatinib Therapy.	imatinib	141-149	class II major histocompatibility complex transactivator	Homo sapiens	56-61
34902507-0	2022	Expression Dynamics Of The Immune Mediators ARG1, TBET, CIITA, IL10 AND TGFB1 IN Chronic Myeloid Leukaemia Patients During The First Year Of Imatinib Therapy.	imatinib	141-149	interleukin 10	Homo sapiens	63-67
34902507-0	2022	Expression Dynamics Of The Immune Mediators ARG1, TBET, CIITA, IL10 AND TGFB1 IN Chronic Myeloid Leukaemia Patients During The First Year Of Imatinib Therapy.	imatinib	141-149	transforming growth factor beta 1	Homo sapiens	72-77
34963561-9	2022	In addition, DNR induced the expression of drug exporter ABCB1 in K562 cells through the p38 MAPK/NFkappaB-mediated pathway, while imatinib or ABT-199 inhibited the DNR-induced effect.	imatinib	131-139	ATP binding cassette subfamily B member 1	Homo sapiens	57-62
34973290-0	2022	Role of ferroptosis in promoting cardiotoxicity induced by Imatinib Mesylate via down-regulating Nrf2 pathways in vitro and in vivo.	imatinib	59-76	NFE2 like bZIP transcription factor 2	Homo sapiens	97-101
34709443-2	2022	The treatment of GISTs has been revolutionized since imatinib and other tyrosine kinase inhibitors were introduced for the treatment of GISTs, which inhibit the tyrosine kinases c-KIT and platelet-derived growth factor receptor (PDGFR) alpha.	imatinib	53-61	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	178-183
34709443-2	2022	The treatment of GISTs has been revolutionized since imatinib and other tyrosine kinase inhibitors were introduced for the treatment of GISTs, which inhibit the tyrosine kinases c-KIT and platelet-derived growth factor receptor (PDGFR) alpha.	imatinib	53-61	platelet derived growth factor receptor alpha	Homo sapiens	229-241
34379028-2	2022	We aimed to identify potential predictors of future achievement of stable MR4.5, defined as a sustained 4.5-log reduction in BCR-ABL1 transcripts for a minimum of 2 years, in 593 patients treated with imatinib as first-line TKI therapy.	imatinib	201-209	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-133
34822800-0	2022	Imatinib mesylate inhibits androgen-independent PC-3 cell viability, proliferation, migration, and tumor growth by targeting platelet-derived growth factor receptor-alpha.	imatinib	0-17	platelet derived growth factor receptor alpha	Homo sapiens	125-170
34738628-16	2022	Therefore, the present study suggests that GLUT-1 is involved in the acquisition of imatinib resistance by GIST cells, which can be overcome by combined treatment with WZB117 and imatinib.	imatinib	84-92	solute carrier family 2 member 1	Homo sapiens	43-49
34822800-9	2022	Imatinib reduced the phosphorylation of the PDGFRalpha/Akt axis.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	44-54
34822800-9	2022	Imatinib reduced the phosphorylation of the PDGFRalpha/Akt axis.	imatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	55-58
34738628-7	2022	The expression of glycolysis-related molecules (GLUT-1, hexokinase 2, pyruvate kinase M2 and lactate dehydrogenase) was assessed in parental and imatinib-resistant cells by western blotting, reverse transcription-quantitative PCR and glucose and lactate measurement kits.	imatinib	145-153	solute carrier family 2 member 1	Homo sapiens	48-54
34738628-16	2022	Therefore, the present study suggests that GLUT-1 is involved in the acquisition of imatinib resistance by GIST cells, which can be overcome by combined treatment with WZB117 and imatinib.	imatinib	179-187	solute carrier family 2 member 1	Homo sapiens	43-49
34738628-7	2022	The expression of glycolysis-related molecules (GLUT-1, hexokinase 2, pyruvate kinase M2 and lactate dehydrogenase) was assessed in parental and imatinib-resistant cells by western blotting, reverse transcription-quantitative PCR and glucose and lactate measurement kits.	imatinib	145-153	hexokinase 2	Homo sapiens	56-68
34820006-6	2022	The present study revealed that tanshinone IIA markedly potentiated the cytotoxic and apoptotic induction effects of imatinib by regulating the AKT-MDM2-P53 signaling pathway and inhibiting the anti-apoptotic proteins BCL2 and MCL1 apoptosis regulator, BCL2 family member in Ph+ ALL cell lines.	imatinib	117-125	MDM2 proto-oncogene	Homo sapiens	148-152
34738628-9	2022	The potential effects of GLUT-1 inhibition on the expression of proteins in the glycolysis (GLUT-1, hexokinase 2, pyruvate kinase M2 and lactate dehydrogenase) and apoptosis pathways (Bcl-2, cleaved PARP, caspase-3 and caspase-9) in imatinib-resistant cells were then investigated following gene silencing and treatment using the GLUT-1 inhibitor WZB117 by western blotting.	imatinib	233-241	solute carrier family 2 member 1	Homo sapiens	92-98
34738628-9	2022	The potential effects of GLUT-1 inhibition on the expression of proteins in the glycolysis (GLUT-1, hexokinase 2, pyruvate kinase M2 and lactate dehydrogenase) and apoptosis pathways (Bcl-2, cleaved PARP, caspase-3 and caspase-9) in imatinib-resistant cells were then investigated following gene silencing and treatment using the GLUT-1 inhibitor WZB117 by western blotting.	imatinib	233-241	BCL2 apoptosis regulator	Homo sapiens	184-189
34738628-12	2022	Although imatinib treatment downregulated GLUT-1 expression and other glycolysis pathway components hexokinase 2, pyruvate kinase M2, and lactate dehydrogenase in parental GIST-T1 cells even at low concentrations.	imatinib	9-17	solute carrier family 2 member 1	Homo sapiens	42-48
34738628-12	2022	Although imatinib treatment downregulated GLUT-1 expression and other glycolysis pathway components hexokinase 2, pyruvate kinase M2, and lactate dehydrogenase in parental GIST-T1 cells even at low concentrations.	imatinib	9-17	hexokinase 2	Homo sapiens	100-112
34738628-14	2022	WZB117 administration significantly downregulated AKT phosphorylation and Bcl-2 expression in imatinib-resistant cells, whereas the combined administration of imatinib and WZB117 conferred synergistic growth inhibition effects in apoptosis assay.	imatinib	94-102	AKT serine/threonine kinase 1	Homo sapiens	50-53
34820006-0	2022	Tanshinone IIA potentiates the efficacy of imatinib by regulating the AKT-MDM2-P53 signaling pathway in Philadelphia chromosome-positive acute lymphoblastic leukemia.	imatinib	43-51	ATPase, class II, type 9A	Mus musculus	11-14
34820006-0	2022	Tanshinone IIA potentiates the efficacy of imatinib by regulating the AKT-MDM2-P53 signaling pathway in Philadelphia chromosome-positive acute lymphoblastic leukemia.	imatinib	43-51	AKT serine/threonine kinase 1	Homo sapiens	70-73
34738628-14	2022	WZB117 administration significantly downregulated AKT phosphorylation and Bcl-2 expression in imatinib-resistant cells, whereas the combined administration of imatinib and WZB117 conferred synergistic growth inhibition effects in apoptosis assay.	imatinib	94-102	BCL2 apoptosis regulator	Homo sapiens	74-79
34820006-6	2022	The present study revealed that tanshinone IIA markedly potentiated the cytotoxic and apoptotic induction effects of imatinib by regulating the AKT-MDM2-P53 signaling pathway and inhibiting the anti-apoptotic proteins BCL2 and MCL1 apoptosis regulator, BCL2 family member in Ph+ ALL cell lines.	imatinib	117-125	tumor protein p53	Homo sapiens	153-156
34738628-14	2022	WZB117 administration significantly downregulated AKT phosphorylation and Bcl-2 expression in imatinib-resistant cells, whereas the combined administration of imatinib and WZB117 conferred synergistic growth inhibition effects in apoptosis assay.	imatinib	159-167	AKT serine/threonine kinase 1	Homo sapiens	50-53
34820006-0	2022	Tanshinone IIA potentiates the efficacy of imatinib by regulating the AKT-MDM2-P53 signaling pathway in Philadelphia chromosome-positive acute lymphoblastic leukemia.	imatinib	43-51	MDM2 proto-oncogene	Homo sapiens	74-78
34820006-0	2022	Tanshinone IIA potentiates the efficacy of imatinib by regulating the AKT-MDM2-P53 signaling pathway in Philadelphia chromosome-positive acute lymphoblastic leukemia.	imatinib	43-51	tumor protein p53	Homo sapiens	79-82
34820006-6	2022	The present study revealed that tanshinone IIA markedly potentiated the cytotoxic and apoptotic induction effects of imatinib by regulating the AKT-MDM2-P53 signaling pathway and inhibiting the anti-apoptotic proteins BCL2 and MCL1 apoptosis regulator, BCL2 family member in Ph+ ALL cell lines.	imatinib	117-125	BCL2 apoptosis regulator	Homo sapiens	218-222
34820006-6	2022	The present study revealed that tanshinone IIA markedly potentiated the cytotoxic and apoptotic induction effects of imatinib by regulating the AKT-MDM2-P53 signaling pathway and inhibiting the anti-apoptotic proteins BCL2 and MCL1 apoptosis regulator, BCL2 family member in Ph+ ALL cell lines.	imatinib	117-125	ATPase, class II, type 9A	Mus musculus	43-46
34820006-6	2022	The present study revealed that tanshinone IIA markedly potentiated the cytotoxic and apoptotic induction effects of imatinib by regulating the AKT-MDM2-P53 signaling pathway and inhibiting the anti-apoptotic proteins BCL2 and MCL1 apoptosis regulator, BCL2 family member in Ph+ ALL cell lines.	imatinib	117-125	AKT serine/threonine kinase 1	Homo sapiens	144-147
34820006-6	2022	The present study revealed that tanshinone IIA markedly potentiated the cytotoxic and apoptotic induction effects of imatinib by regulating the AKT-MDM2-P53 signaling pathway and inhibiting the anti-apoptotic proteins BCL2 and MCL1 apoptosis regulator, BCL2 family member in Ph+ ALL cell lines.	imatinib	117-125	BCL2 apoptosis regulator	Homo sapiens	253-257
34969396-0	2021	Correction to: Pristimerin induces apoptosis in imatinib-resistant chronic myelogenous leukemia cells harboring T315I mutation by blocking NF-kappaB signaling and depleting Bcr-Abl.	imatinib	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	173-180
34890638-7	2022	The estrogenic activity of imatinib was confirmed as mediated through ERalpha, and interference of the TKIs with the reporter gene assays was ruled out in a cell-lysate-based firefly luciferase enzyme inhibition assay.	imatinib	27-35	estrogen receptor 1	Homo sapiens	70-77
34890638-8	2022	Imatinib in combination with 4-hydroxytamoxifen showed concentration-dependent effects on the metabolic activity of ERalpha-expressing AN3CA, MCF-7, and SKOV3 cells, and on cell proliferation and adhesion of MCF-7 cells.	imatinib	0-8	estrogen receptor 1	Homo sapiens	116-123
34957688-7	2022	In xenografts, targeting DDR with imatinib enhances BRAF inhibitor efficacy, counteracts drug-induced collagen remodeling, and delays tumor relapse.	imatinib	34-42	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	52-56
34959482-5	2021	The first, second, and third generation inhibitors (imatinib, dasatinib, nilotinib, bosutinib, and ponatinib) of BCR-ABL1 and the allosteric inhibitor asciminib showed deep genetic and molecular remission rates in CML, leading to the evaluation of treatment discontinuation in prospective trials.	imatinib	52-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-121
34993140-13	2021	Moreover, we found that RPL13 and RPL14 exhibited exceptional upregulation in imatinib-resistant CML patients, which were further confirmed by PRM and WB.	imatinib	78-86	ribosomal protein L13	Homo sapiens	24-29
34993140-13	2021	Moreover, we found that RPL13 and RPL14 exhibited exceptional upregulation in imatinib-resistant CML patients, which were further confirmed by PRM and WB.	imatinib	78-86	ribosomal protein L14	Homo sapiens	34-39
34843676-0	2021	Simvastatin potentiates the cell-killing activity of imatinib in imatinib-resistant chronic myeloid leukemia cells mainly through PI3K/AKT pathway attenuation and Myc downregulation.	imatinib	53-61	AKT serine/threonine kinase 1	Homo sapiens	135-138
34922009-6	2022	In particular, IDH2 was identified as a potential drug target correlated with the drug resistance phenotype, and its inhibition by the antagonist AGI-6780 reversed the acquired resistance in K562 cells to either ADR or IMA.	imatinib	219-222	isocitrate dehydrogenase (NADP(+)) 2	Homo sapiens	15-19
34922009-7	2022	Together, our study has implicated IDH2 as a potential target that can be therapeutically leveraged to alleviate the drug resistance in K562 cells when treated with IMA and ADR.	imatinib	165-168	isocitrate dehydrogenase (NADP(+)) 2	Homo sapiens	35-39
34843676-0	2021	Simvastatin potentiates the cell-killing activity of imatinib in imatinib-resistant chronic myeloid leukemia cells mainly through PI3K/AKT pathway attenuation and Myc downregulation.	imatinib	53-61	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	163-166
34843676-8	2021	Mechanistically, the cooperative interaction of simvastatin and imatinib was associated with the inactivation of the PI3K/Akt signaling pathway, which was a classical downstream pro-survival cascade of the BCR-ABL kinase.	imatinib	64-72	AKT serine/threonine kinase 1	Homo sapiens	122-125
34894066-2	2022	Imatinib, a receptor tyrosine kinase (RTK) inhibitor, has been used in Penttinen syndrome (PS) patients with good results.	imatinib	0-8	ret proto-oncogene	Homo sapiens	12-36
34894066-2	2022	Imatinib, a receptor tyrosine kinase (RTK) inhibitor, has been used in Penttinen syndrome (PS) patients with good results.	imatinib	0-8	ret proto-oncogene	Homo sapiens	38-41
34944663-8	2021	Based on this finding, we tested the efficacy of hydrazostat in combination with RTK inhibitor imatinib.	imatinib	95-103	ret proto-oncogene	Homo sapiens	81-84
34889232-4	2021	Imatinib mesylate, a small-molecule inhibitor of the KIT tyrosine kinase, provides a rapid but not durable clinical response in KIT-mutant melanoma.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	53-56
34889232-4	2021	Imatinib mesylate, a small-molecule inhibitor of the KIT tyrosine kinase, provides a rapid but not durable clinical response in KIT-mutant melanoma.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	128-131
34889232-6	2021	Herein, we designed clinical trial of co-administrating imatinib mesylate and pembrolizumab (anti-PD-1 antibody) to evaluate its safety and efficacy.	imatinib	56-73	programmed cell death 1	Homo sapiens	98-102
34875133-12	2022	Interestingly, the PDGFRA protein fusions can be targeted by tyrosine kinase inhibitors such as imatinib, sunitinib and sorafenib.	imatinib	96-104	platelet derived growth factor receptor alpha	Homo sapiens	19-25
34875133-13	2022	Moreover, we identified BCR-ABL1 (in 8% of patients), COL1A1-PDGFB (8%), NIN-PDGFRB (8%) and FGFR1-BCR (4%) in cfDNA of patients, which can be targeted by analogues of imatinib.	imatinib	168-176	BCR activator of RhoGEF and GTPase	Homo sapiens	24-32
34875133-13	2022	Moreover, we identified BCR-ABL1 (in 8% of patients), COL1A1-PDGFB (8%), NIN-PDGFRB (8%) and FGFR1-BCR (4%) in cfDNA of patients, which can be targeted by analogues of imatinib.	imatinib	168-176	collagen type I alpha 1 chain	Homo sapiens	54-60
34875133-13	2022	Moreover, we identified BCR-ABL1 (in 8% of patients), COL1A1-PDGFB (8%), NIN-PDGFRB (8%) and FGFR1-BCR (4%) in cfDNA of patients, which can be targeted by analogues of imatinib.	imatinib	168-176	platelet derived growth factor subunit B	Homo sapiens	61-66
34875133-13	2022	Moreover, we identified BCR-ABL1 (in 8% of patients), COL1A1-PDGFB (8%), NIN-PDGFRB (8%) and FGFR1-BCR (4%) in cfDNA of patients, which can be targeted by analogues of imatinib.	imatinib	168-176	fibroblast growth factor receptor 1	Homo sapiens	93-98
34875133-13	2022	Moreover, we identified BCR-ABL1 (in 8% of patients), COL1A1-PDGFB (8%), NIN-PDGFRB (8%) and FGFR1-BCR (4%) in cfDNA of patients, which can be targeted by analogues of imatinib.	imatinib	168-176	BCR activator of RhoGEF and GTPase	Homo sapiens	99-102
34673425-0	2021	JKST6, a novel multikinase modulator of the BCR-ABL1/STAT5 signaling pathway that potentiates direct BCR-ABL1 inhibition and overcomes imatinib resistance in chronic myelogenous leukemia.	imatinib	135-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-52
34938656-12	2021	Results of Western blot confirmed the inhibitory effects of imatinib on DH82 by targeting activation of MAPK and PI3K/AKT pathways.	imatinib	60-68	AKT serine/threonine kinase 1	Homo sapiens	118-121
34781823-0	2021	Protein disulfide isomerase family 6 promotes the imatinib-resistance of renal cell carcinoma by regulation of Wnt3a-Frizzled1 axis.	imatinib	50-58	protein disulfide isomerase family A member 6	Homo sapiens	0-36
34781823-0	2021	Protein disulfide isomerase family 6 promotes the imatinib-resistance of renal cell carcinoma by regulation of Wnt3a-Frizzled1 axis.	imatinib	50-58	Wnt family member 3A	Homo sapiens	111-116
34781823-0	2021	Protein disulfide isomerase family 6 promotes the imatinib-resistance of renal cell carcinoma by regulation of Wnt3a-Frizzled1 axis.	imatinib	50-58	frizzled class receptor 1	Homo sapiens	117-126
34781823-4	2021	The effect of PDIA6 on imatinib-resistance of renal cell carcinoma was investigated in this study.	imatinib	23-31	protein disulfide isomerase family A member 6	Homo sapiens	14-19
34781823-5	2021	Firstly, PDIA6 was found to be up-regulated in the imatinib-resistant renal cell carcinoma tissues and cells.	imatinib	51-59	protein disulfide isomerase family A member 6	Homo sapiens	9-14
34781823-6	2021	Functional assays showed that knockdown of PDIA6 sensitized imatinib-resistant renal cell carcinoma cells to imatinib through decreasing the half-maximal inhibitory concentration (IC50) of imatinib-resistant renal cell carcinoma cells.	imatinib	60-68	protein disulfide isomerase family A member 6	Homo sapiens	43-48
34781823-6	2021	Functional assays showed that knockdown of PDIA6 sensitized imatinib-resistant renal cell carcinoma cells to imatinib through decreasing the half-maximal inhibitory concentration (IC50) of imatinib-resistant renal cell carcinoma cells.	imatinib	109-117	protein disulfide isomerase family A member 6	Homo sapiens	43-48
34781823-6	2021	Functional assays showed that knockdown of PDIA6 sensitized imatinib-resistant renal cell carcinoma cells to imatinib through decreasing the half-maximal inhibitory concentration (IC50) of imatinib-resistant renal cell carcinoma cells.	imatinib	189-197	protein disulfide isomerase family A member 6	Homo sapiens	43-48
34781823-7	2021	Secondly, cell proliferation of imatinib-resistant renal cell carcinoma cells was suppressed by PDIA6 silencing, and the apoptosis was promoted with reduced Bcl-2, enhanced Bax and cleaved caspase-3.	imatinib	32-40	protein disulfide isomerase family A member 6	Homo sapiens	96-101
34781823-7	2021	Secondly, cell proliferation of imatinib-resistant renal cell carcinoma cells was suppressed by PDIA6 silencing, and the apoptosis was promoted with reduced Bcl-2, enhanced Bax and cleaved caspase-3.	imatinib	32-40	BCL2 apoptosis regulator	Homo sapiens	157-162
34781823-7	2021	Secondly, cell proliferation of imatinib-resistant renal cell carcinoma cells was suppressed by PDIA6 silencing, and the apoptosis was promoted with reduced Bcl-2, enhanced Bax and cleaved caspase-3.	imatinib	32-40	BCL2 associated X, apoptosis regulator	Homo sapiens	173-176
34781823-7	2021	Secondly, cell proliferation of imatinib-resistant renal cell carcinoma cells was suppressed by PDIA6 silencing, and the apoptosis was promoted with reduced Bcl-2, enhanced Bax and cleaved caspase-3.	imatinib	32-40	caspase 3	Homo sapiens	189-198
34673425-0	2021	JKST6, a novel multikinase modulator of the BCR-ABL1/STAT5 signaling pathway that potentiates direct BCR-ABL1 inhibition and overcomes imatinib resistance in chronic myelogenous leukemia.	imatinib	135-143	signal transducer and activator of transcription 5A	Homo sapiens	53-58
34781823-8	2021	Moreover, interference of PDIA6 increased phosphorylation of H2A histone family member X (gammaH2AX), while decreased Rad51 and phosphorylated DNA-dependent protein kinase (DNA-PK) (p-DNA-PK) in imatinib-resistant renal cell carcinoma cells.	imatinib	195-203	protein disulfide isomerase family A member 6	Homo sapiens	26-31
34781823-9	2021	Lastly, protein expression levels of Wnt3a and Frizzled1 (FZD1) in imatinib-resistant renal cell carcinoma cells were down-regulated by silencing of PDIA6.	imatinib	67-75	Wnt family member 3A	Homo sapiens	37-42
34608769-5	2021	Further covariate modeling with this combined dataset showed that in addition to AAG; age, bodyweight, albumin, CRP and ICU admission were predictive of total imatinib oral clearance.	imatinib	159-167	C-reactive protein	Homo sapiens	112-115
34781823-9	2021	Lastly, protein expression levels of Wnt3a and Frizzled1 (FZD1) in imatinib-resistant renal cell carcinoma cells were down-regulated by silencing of PDIA6.	imatinib	67-75	frizzled class receptor 1	Homo sapiens	47-56
34781823-9	2021	Lastly, protein expression levels of Wnt3a and Frizzled1 (FZD1) in imatinib-resistant renal cell carcinoma cells were down-regulated by silencing of PDIA6.	imatinib	67-75	frizzled class receptor 1	Homo sapiens	58-62
34781823-9	2021	Lastly, protein expression levels of Wnt3a and Frizzled1 (FZD1) in imatinib-resistant renal cell carcinoma cells were down-regulated by silencing of PDIA6.	imatinib	67-75	protein disulfide isomerase family A member 6	Homo sapiens	149-154
34781823-10	2021	Over-expression of FZD1 attenuated PDIA6 silencing-induced increase in cell apoptosis and decrease in cell proliferation in imatinib-resistant renal cell carcinoma cells.	imatinib	124-132	protein disulfide isomerase family A member 6	Homo sapiens	35-40
34781823-11	2021	In conclusion, knockdown of PDIA6 sensitized imatinib-resistant renal cell carcinoma cells to imatinib through inactivation of Wnt3a-FZD1 axis.	imatinib	45-53	protein disulfide isomerase family A member 6	Homo sapiens	28-33
34781823-11	2021	In conclusion, knockdown of PDIA6 sensitized imatinib-resistant renal cell carcinoma cells to imatinib through inactivation of Wnt3a-FZD1 axis.	imatinib	94-102	protein disulfide isomerase family A member 6	Homo sapiens	28-33
34781823-11	2021	In conclusion, knockdown of PDIA6 sensitized imatinib-resistant renal cell carcinoma cells to imatinib through inactivation of Wnt3a-FZD1 axis.	imatinib	94-102	Wnt family member 3A	Homo sapiens	127-132
34781823-11	2021	In conclusion, knockdown of PDIA6 sensitized imatinib-resistant renal cell carcinoma cells to imatinib through inactivation of Wnt3a-FZD1 axis.	imatinib	94-102	frizzled class receptor 1	Homo sapiens	133-137
34214017-9	2021	Furthermore, CPT and imatinib increased the apoptotic rates and markedly decreased the phosphorylation levels of STAT3 and eIF4E.	imatinib	21-29	signal transducer and activator of transcription 3	Homo sapiens	113-118
34621020-7	2021	Buttressed on these findings, we established in vitro and in vivo the preclinical proof-of-concept for co-targeting KIT and the ubiquitin pathway to maximize the therapeutic response to first-line imatinib treatment.	imatinib	197-205	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	116-119
34398495-13	2021	The clinical benefit with KIT inhibitors, such as imatinib, remains to be determined.	imatinib	50-58	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	26-29
34214017-9	2021	Furthermore, CPT and imatinib increased the apoptotic rates and markedly decreased the phosphorylation levels of STAT3 and eIF4E.	imatinib	21-29	eukaryotic translation initiation factor 4E	Homo sapiens	123-128
34917498-0	2021	Case Report: Evolution of KIT D816V-Positive Systemic Mastocytosis to Myeloid Neoplasm With PDGFRA Rearrangement Responsive to Imatinib.	imatinib	127-135	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	26-29
34893099-7	2021	CONCLUSION: CML imatinib resistance is associated with oxidative phosphorylation, during which the pathway of TGF-beta and mTOR are significantly up-regulated.	imatinib	16-24	transforming growth factor alpha	Homo sapiens	110-118
34893099-7	2021	CONCLUSION: CML imatinib resistance is associated with oxidative phosphorylation, during which the pathway of TGF-beta and mTOR are significantly up-regulated.	imatinib	16-24	mechanistic target of rapamycin kinase	Homo sapiens	123-127
34917498-0	2021	Case Report: Evolution of KIT D816V-Positive Systemic Mastocytosis to Myeloid Neoplasm With PDGFRA Rearrangement Responsive to Imatinib.	imatinib	127-135	platelet derived growth factor receptor alpha	Homo sapiens	92-98
34917498-4	2021	Here, we present a patient with indolent SM who subsequently developed a myeloid neoplasm with PDGFRA rearrangement with complete response to low-dose imatinib.	imatinib	151-159	platelet derived growth factor receptor alpha	Homo sapiens	95-101
34837064-7	2021	Imatinib, as well as specific inhibitors of ABL and PDGFR, demonstrated a highly selective cytotoxic effect targeting the HEY1-NCoA2 fusion-driven cellular model.	imatinib	0-8	hes related family bHLH transcription factor with YRPW motif 1	Homo sapiens	122-126
34837064-7	2021	Imatinib, as well as specific inhibitors of ABL and PDGFR, demonstrated a highly selective cytotoxic effect targeting the HEY1-NCoA2 fusion-driven cellular model.	imatinib	0-8	nuclear receptor coactivator 2	Homo sapiens	127-132
34944576-5	2021	Imatinib block the binding site of ATP in the BCR/ABL protein and is also a platelet-derived growth factor receptor (PDGFR) and a KIT (CD117) kinase inhibitor.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-53
34976304-9	2021	Tyrosine kinase inhibitors (TKIs), including imatinib and nilotinib, have a non-specific target, namely plateletderived growth factor receptor (PDGFR), which indirectly affects blood potassium and calcium levels in CML patients.	imatinib	45-53	platelet derived growth factor receptor beta	Homo sapiens	104-142
34976304-9	2021	Tyrosine kinase inhibitors (TKIs), including imatinib and nilotinib, have a non-specific target, namely plateletderived growth factor receptor (PDGFR), which indirectly affects blood potassium and calcium levels in CML patients.	imatinib	45-53	platelet derived growth factor receptor beta	Homo sapiens	144-149
34944576-5	2021	Imatinib block the binding site of ATP in the BCR/ABL protein and is also a platelet-derived growth factor receptor (PDGFR) and a KIT (CD117) kinase inhibitor.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	76-115
34944576-5	2021	Imatinib block the binding site of ATP in the BCR/ABL protein and is also a platelet-derived growth factor receptor (PDGFR) and a KIT (CD117) kinase inhibitor.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	117-122
34944576-5	2021	Imatinib block the binding site of ATP in the BCR/ABL protein and is also a platelet-derived growth factor receptor (PDGFR) and a KIT (CD117) kinase inhibitor.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	130-133
34944576-5	2021	Imatinib block the binding site of ATP in the BCR/ABL protein and is also a platelet-derived growth factor receptor (PDGFR) and a KIT (CD117) kinase inhibitor.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	135-140
34830455-6	2021	In this study, we used specific gene knockdown to clearly demonstrate that the deficiency of p38alpha greatly enhanced the therapeutic efficacy in growth suppression and cytotoxicity of TKIs, first-generation imatinib, and second generation dasatinib by approximately 2.5-3.0-fold in BCR-ABL-positive CML-derived leukemia K562 and KMB5 cells.	imatinib	209-217	mitogen-activated protein kinase 14	Homo sapiens	93-101
34830455-9	2021	A highly specific p38alpha inhibitor, TAK715, also significantly enhanced the imatinib- and dasatinib-mediated therapeutic efficacy, supporting the feasibility of p38alpha deficiency in future clinic application.	imatinib	78-86	mitogen-activated protein kinase 14	Homo sapiens	18-26
34830455-9	2021	A highly specific p38alpha inhibitor, TAK715, also significantly enhanced the imatinib- and dasatinib-mediated therapeutic efficacy, supporting the feasibility of p38alpha deficiency in future clinic application.	imatinib	78-86	mitogen-activated protein kinase 14	Homo sapiens	163-171
34938856-0	2021	Targeting SOS1 overcomes imatinib resistance with BCR-ABL independence through uptake transporter SLC22A4 in CML.	imatinib	25-33	SOS Ras/Rac guanine nucleotide exchange factor 1	Homo sapiens	10-14
34938856-0	2021	Targeting SOS1 overcomes imatinib resistance with BCR-ABL independence through uptake transporter SLC22A4 in CML.	imatinib	25-33	solute carrier family 22 member 4	Homo sapiens	98-105
34867354-6	2021	Phosphorylation was ABL1-mediated, as demonstrated by the specific inhibition of imatinib (p < 0.001 for K562, NALM6, ALL-SIL and p < 0.01 for REH) in contrast to ruxolitinib (JAK2-inhibitor), and occurred on the ABL1 Y-site, as demonstrated by PABL-F whose phosphorylation was comparable to basal levels.	imatinib	81-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-24
34938856-1	2021	Resistance to the BCR-ABL inhibitor imatinib mesylate poses a major problem for the treatment of chronic myeloid leukemia.	imatinib	36-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
34938856-2	2021	Imatinib resistance often results from a secondary mutation in BCR-ABL that interferes with drug binding.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
34938856-3	2021	However, sometimes there is no mutation in BCR-ABL, and the basis of such BCR-ABL-independent imatinib mesylate resistance remains to be elucidated.	imatinib	94-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
34938856-4	2021	SOS1, a guanine nucleotide exchange factor for Ras protein, affects drug sensitivity and resistance to imatinib.	imatinib	103-111	SOS Ras/Rac guanine nucleotide exchange factor 1	Homo sapiens	0-4
34938856-5	2021	The depletion of SOS1 markedly inhibits cell growth either in vitro or in vivo and significantly increases the sensitivity of chronic myeloid leukemia cells to imatinib.	imatinib	160-168	SOS Ras/Rac guanine nucleotide exchange factor 1	Homo sapiens	17-21
34938856-6	2021	Furthermore, LC-MS/MS and RNA-seq assays reveal that SOS1 negatively regulates the expression of SLC22A4, a member of the carnitine/organic cation transporter family, which mediates the active uptake of imatinib into chronic myeloid leukemia cells.	imatinib	203-211	SOS Ras/Rac guanine nucleotide exchange factor 1	Homo sapiens	53-57
34938856-6	2021	Furthermore, LC-MS/MS and RNA-seq assays reveal that SOS1 negatively regulates the expression of SLC22A4, a member of the carnitine/organic cation transporter family, which mediates the active uptake of imatinib into chronic myeloid leukemia cells.	imatinib	203-211	solute carrier family 22 member 4	Homo sapiens	97-104
34938856-7	2021	HPLC assay confirms that intracellular accumulation of imatinib is accompanied by upregulation of SLC22A4 through SOS1 inhibition in both sensitive and resistant chronic myeloid leukemia cells.	imatinib	55-63	solute carrier family 22 member 4	Homo sapiens	98-105
34938856-7	2021	HPLC assay confirms that intracellular accumulation of imatinib is accompanied by upregulation of SLC22A4 through SOS1 inhibition in both sensitive and resistant chronic myeloid leukemia cells.	imatinib	55-63	SOS Ras/Rac guanine nucleotide exchange factor 1	Homo sapiens	114-118
34938856-9	2021	Altogether these findings indicate that targeting SOS1 inhibition promotes imatinib sensitivity and overcomes resistance with BCR-ABL independence by SLC22A4-mediated uptake transport.	imatinib	75-83	SOS Ras/Rac guanine nucleotide exchange factor 1	Homo sapiens	50-54
34938856-9	2021	Altogether these findings indicate that targeting SOS1 inhibition promotes imatinib sensitivity and overcomes resistance with BCR-ABL independence by SLC22A4-mediated uptake transport.	imatinib	75-83	solute carrier family 22 member 4	Homo sapiens	150-157
34867354-6	2021	Phosphorylation was ABL1-mediated, as demonstrated by the specific inhibition of imatinib (p < 0.001 for K562, NALM6, ALL-SIL and p < 0.01 for REH) in contrast to ruxolitinib (JAK2-inhibitor), and occurred on the ABL1 Y-site, as demonstrated by PABL-F whose phosphorylation was comparable to basal levels.	imatinib	81-89	STIL centriolar assembly protein	Homo sapiens	122-125
34867354-8	2021	Phosphorylation of PABL was specifically inhibited after the incubation of BCR-ABL1 positive cell lysates with imatinib, but not with ruxolitinib.	imatinib	111-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-83
34750265-2	2021	For example, the Bcr-Abl kinase inhibitor imatinib decreases mortality for chronic myeloid leukemia by 80%, but 22 to 41% of patients acquire resistance to imatinib.	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-24
34750265-2	2021	For example, the Bcr-Abl kinase inhibitor imatinib decreases mortality for chronic myeloid leukemia by 80%, but 22 to 41% of patients acquire resistance to imatinib.	imatinib	156-164	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-24
34750265-9	2021	Surprisingly, one-third of mutations in the Abl kinase domain still remain sensitive to imatinib and bind with similar or higher affinity than wild type.	imatinib	88-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-47
34750265-10	2021	Intriguingly, we identified three clinical Abl mutations that bind imatinib with wild type-like affinity but dissociate from imatinib considerably faster.	imatinib	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-46
34750265-10	2021	Intriguingly, we identified three clinical Abl mutations that bind imatinib with wild type-like affinity but dissociate from imatinib considerably faster.	imatinib	125-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-46
34781898-0	2021	Global identification of circular RNAs in imatinib (IM) resistance of chronic myeloid leukemia (CML) by modulating signaling pathways of circ_0080145/miR-203/ABL1 and circ 0051886/miR-637/ABL1.	imatinib	42-50	microRNA 203a	Homo sapiens	150-157
34858182-7	2021	Combined exposure of rapamycin with the PDGFR inhibitor, imatinib significantly reduced the proliferation and migration of hPASMCs compared to either agent alone.	imatinib	57-65	platelet derived growth factor receptor beta	Homo sapiens	40-45
34775854-14	2022	DISCUSSION: Imatinib is an oral signal inhibitor that targets tyrosine kinase for BCR/ABL, platelet-derived growth factor, stem cell factor, and c-kit (CD117).	imatinib	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-89
34775854-14	2022	DISCUSSION: Imatinib is an oral signal inhibitor that targets tyrosine kinase for BCR/ABL, platelet-derived growth factor, stem cell factor, and c-kit (CD117).	imatinib	12-20	KIT ligand	Homo sapiens	123-139
34775854-14	2022	DISCUSSION: Imatinib is an oral signal inhibitor that targets tyrosine kinase for BCR/ABL, platelet-derived growth factor, stem cell factor, and c-kit (CD117).	imatinib	12-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	145-150
34775854-14	2022	DISCUSSION: Imatinib is an oral signal inhibitor that targets tyrosine kinase for BCR/ABL, platelet-derived growth factor, stem cell factor, and c-kit (CD117).	imatinib	12-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	152-157
34775854-15	2022	The conjunctiva and sclera have a large amount of c-kit positive mast cells which are inhibited by imatinib.	imatinib	99-107	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	50-55
34775854-16	2022	The inhibition of c-kit positive mast cells by imatinib may be responsible for further exposure of the conjunctival mucosa to injuries.	imatinib	47-55	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	18-23
34781898-0	2021	Global identification of circular RNAs in imatinib (IM) resistance of chronic myeloid leukemia (CML) by modulating signaling pathways of circ_0080145/miR-203/ABL1 and circ 0051886/miR-637/ABL1.	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-162
34781898-0	2021	Global identification of circular RNAs in imatinib (IM) resistance of chronic myeloid leukemia (CML) by modulating signaling pathways of circ_0080145/miR-203/ABL1 and circ 0051886/miR-637/ABL1.	imatinib	42-50	microRNA 637	Homo sapiens	180-187
34781898-0	2021	Global identification of circular RNAs in imatinib (IM) resistance of chronic myeloid leukemia (CML) by modulating signaling pathways of circ_0080145/miR-203/ABL1 and circ 0051886/miR-637/ABL1.	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	188-192
34771705-8	2021	The growth-inhibitory effects of the statin/imatinib combination against CD34+/CML primary cells were higher than those against CD34+/Norm cells (p = 0.005), suggesting that the combination of rosuvastatin and imatinib exerted growth-inhibitory effects against CML CD34+ cells, but not against normal CD34+ cells.	imatinib	44-52	CD34 molecule	Homo sapiens	73-77
34771705-8	2021	The growth-inhibitory effects of the statin/imatinib combination against CD34+/CML primary cells were higher than those against CD34+/Norm cells (p = 0.005), suggesting that the combination of rosuvastatin and imatinib exerted growth-inhibitory effects against CML CD34+ cells, but not against normal CD34+ cells.	imatinib	44-52	CD34 molecule	Homo sapiens	265-269
34771705-8	2021	The growth-inhibitory effects of the statin/imatinib combination against CD34+/CML primary cells were higher than those against CD34+/Norm cells (p = 0.005), suggesting that the combination of rosuvastatin and imatinib exerted growth-inhibitory effects against CML CD34+ cells, but not against normal CD34+ cells.	imatinib	210-218	CD34 molecule	Homo sapiens	73-77
34771705-8	2021	The growth-inhibitory effects of the statin/imatinib combination against CD34+/CML primary cells were higher than those against CD34+/Norm cells (p = 0.005), suggesting that the combination of rosuvastatin and imatinib exerted growth-inhibitory effects against CML CD34+ cells, but not against normal CD34+ cells.	imatinib	210-218	CD34 molecule	Homo sapiens	265-269
34128532-0	2021	Association of SLC22A1,SLCO1B3 Drug Transporter Polymorphisms and Smoking with Disease Risk and Cytogenetic Response to Imatinib in Patients with Chronic Myeloid Leukemia.	imatinib	120-128	solute carrier organic anion transporter family member 1B3	Homo sapiens	23-30
34128532-1	2021	OBJECTIVE: To determine whether polymorphisms of SLC22A1 and SLCO1B3 genes could predict imatinib (IM) response and chronic myeloid leukemia (CML) risk.	imatinib	89-97	solute carrier family 22 member 1	Homo sapiens	49-56
34128532-1	2021	OBJECTIVE: To determine whether polymorphisms of SLC22A1 and SLCO1B3 genes could predict imatinib (IM) response and chronic myeloid leukemia (CML) risk.	imatinib	89-97	solute carrier organic anion transporter family member 1B3	Homo sapiens	61-68
34517025-6	2021	Two drugs, imatinib, and decitabine have been identified as putative modulators of G3BP1/2 genes and their regulators, suggesting their role as COVID-19 mitigation agents.	imatinib	11-19	G3BP stress granule assembly factor 1	Homo sapiens	83-90
34517025-8	2021	This study reports imatinib and decitabine as candidate drugs against N protein and G3BP1/2 protein.	imatinib	19-27	G3BP stress granule assembly factor 1	Homo sapiens	84-91
34569605-0	2021	Imatinib protects against human beta-cell death via inhibition of mitochondrial respiration and activation of AMPK.	imatinib	0-8	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	110-114
34556815-6	2021	In a therapeutic setting, we showed that among six selected growth factors, EPO, and NGF showed the most pronounced protective effects in vitro against several promising anti-NB multikinase inhibitors: imatinib, dasatinib, crizotinib, cabozantinib, and axitinib.	imatinib	202-210	erythropoietin	Homo sapiens	76-79
34899250-8	2021	However, the clinical symptoms reappeared more severely 2 months after restart of imatinib, and the peripheral absolute eosinophil count increased to 1,690/muL.	imatinib	82-90	tripartite motif containing 37	Homo sapiens	156-159
34899250-9	2021	A diagnosis of imatinib-induced DRESS syndrome was made, based on the Registry of Severe Cutaneous Adverse Reactions (RegiSCAR) criteria.	imatinib	15-23	ribosomal protein S4 X-linked	Homo sapiens	118-126
34700368-6	2021	Interestingly, the proliferation behavior of TGF-beta1-induced cells was changed with the combination therapy, and STI-571-induced apoptosis was also prompted by this combination.	imatinib	115-122	transforming growth factor beta 1	Homo sapiens	45-54
34667163-0	2021	BRD9 inhibition promotes PUMA-dependent apoptosis and augments the effect of imatinib in gastrointestinal stromal tumors.	imatinib	77-85	bromodomain containing 9	Homo sapiens	0-4
34667163-7	2021	BRD9 inhibition could promote PUMA-dependent apoptosis in GISTs and enhance imatinib activity in vitro and in vivo.	imatinib	76-84	bromodomain containing 9	Homo sapiens	0-4
34667163-8	2021	BRD9 inhibition synergizes with imatinib in GISTs by inducing PUMA upregulation.	imatinib	32-40	BCL2 binding component 3	Homo sapiens	62-66
34667163-10	2021	Furthermore, imatinib also upregulates PUMA by targeting AKT/GSK-3beta/p65 axis.	imatinib	13-21	BCL2 binding component 3	Homo sapiens	39-43
34667163-10	2021	Furthermore, imatinib also upregulates PUMA by targeting AKT/GSK-3beta/p65 axis.	imatinib	13-21	AKT serine/threonine kinase 1	Homo sapiens	57-60
34667163-10	2021	Furthermore, imatinib also upregulates PUMA by targeting AKT/GSK-3beta/p65 axis.	imatinib	13-21	glycogen synthase kinase 3 alpha	Homo sapiens	61-70
34667163-10	2021	Furthermore, imatinib also upregulates PUMA by targeting AKT/GSK-3beta/p65 axis.	imatinib	13-21	RELA proto-oncogene, NF-kB subunit	Homo sapiens	71-74
34667163-12	2021	Inhibition of BRD9 is a novel therapeutic strategy in GISTs treated alone or in combination with imatinib.	imatinib	97-105	bromodomain containing 9	Homo sapiens	14-18
34569605-3	2021	Treatment of NOD mice with imatinib resulted in increased beta-cell AMPK phosphorylation.	imatinib	27-35	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	68-72
34569605-4	2021	Imatinib activated AMPK also in vitro, resulting in decreased ribosomal protein S6 phosphorylation and protection against IAPP-aggregation, TXNIP upregulation and beta-cell death.	imatinib	0-8	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	19-23
34569605-4	2021	Imatinib activated AMPK also in vitro, resulting in decreased ribosomal protein S6 phosphorylation and protection against IAPP-aggregation, TXNIP upregulation and beta-cell death.	imatinib	0-8	ribosomal protein S6	Homo sapiens	62-82
34569605-4	2021	Imatinib activated AMPK also in vitro, resulting in decreased ribosomal protein S6 phosphorylation and protection against IAPP-aggregation, TXNIP upregulation and beta-cell death.	imatinib	0-8	islet amyloid polypeptide	Homo sapiens	122-126
34569605-4	2021	Imatinib activated AMPK also in vitro, resulting in decreased ribosomal protein S6 phosphorylation and protection against IAPP-aggregation, TXNIP upregulation and beta-cell death.	imatinib	0-8	thioredoxin interacting protein	Homo sapiens	140-145
34569605-6	2021	Imatinib-induced AMPK activation was preceded by reduced glucose/pyruvate-dependent respiration, increased glycolysis rates, and a lowered ATP/AMP ratio.	imatinib	0-8	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	17-21
34569605-7	2021	Imatinib augmented the fractional oxidation of fatty acids/malate, possibly via a direct interaction with the beta-oxidation enzyme ECHS1.	imatinib	0-8	enoyl-CoA hydratase, short chain 1	Homo sapiens	132-137
34561421-4	2021	Here, we reveal that the m6A methyltransferase complex METTL3/METTL14 is upregulated in CML patients and that is required for proliferation of primary CML cells and CML cell lines sensitive and resistant to the TKI imatinib.	imatinib	215-223	methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit	Homo sapiens	55-61
34547714-1	2021	Despite the success of imatinib in CML therapy through Bcr-Abl inhibition, acquired drug resistance occurs over time in patients.	imatinib	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
34599372-0	2021	Investigation on the interaction behavior of afatinib, dasatinib, and imatinib docked to the BCR-ABL protein.	imatinib	70-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
34599372-2	2021	Imatinib was the first drug that could effectively treat this condition, but its use is hindered by the development of mutations of the BCR-ABL protein, which are the cause of resistance.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-143
34564697-4	2021	Here, we show that combining TKI (imatinib, nilotinib, dasatinib, or asciminib) treatment with the small-molecule MCL1 inhibitor S63845 exerted strong synergistic antiviability and proapoptotic effects on CML lines and CD34+ stem/progenitor cells isolated from untreated CML patients in chronic phase.	imatinib	34-42	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	114-118
34564697-4	2021	Here, we show that combining TKI (imatinib, nilotinib, dasatinib, or asciminib) treatment with the small-molecule MCL1 inhibitor S63845 exerted strong synergistic antiviability and proapoptotic effects on CML lines and CD34+ stem/progenitor cells isolated from untreated CML patients in chronic phase.	imatinib	34-42	CD34 molecule	Homo sapiens	219-223
34636293-3	2022	Initially, imatinib was the first small molecule BCR-ABL Tyrosine kinases inhibitors (TKIs) for the effective treatment of chronic myelogenous leukemia.	imatinib	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
34636293-4	2022	Later, due to the emergence of various BCR-ABL mutations, especially T315I mutation, imatinib developed strong resistance.	imatinib	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-46
34611140-0	2021	Aberrantly reduced expression of miR-342-5p contributes to CCND1-associated chronic myeloid leukemia progression and imatinib resistance.	imatinib	117-125	microRNA 342	Homo sapiens	33-40
34611140-6	2021	Furthermore, overexpression of miR-342-5p enhanced imatinib-induced DNA double-strand breaks and apoptosis.	imatinib	51-59	microRNA 342	Homo sapiens	31-38
34596797-1	2022	Chronic myeloid leukemia (CML) epitomises successful targeted therapy, where inhibition of tyrosine kinase activity of oncoprotein Bcr-Abl1 by imatinib, induces remission in 86% patients in initial chronic phase (CP).	imatinib	143-151	BCR activator of RhoGEF and GTPase	Homo sapiens	131-134
34596797-1	2022	Chronic myeloid leukemia (CML) epitomises successful targeted therapy, where inhibition of tyrosine kinase activity of oncoprotein Bcr-Abl1 by imatinib, induces remission in 86% patients in initial chronic phase (CP).	imatinib	143-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-139
34596797-5	2022	Their levels and activity respectively, indicated active Bcr-Abl1 pathway in CML-BC resistant cells, though Bcr-Abl1 is inhibited by imatinib.	imatinib	133-141	BCR activator of RhoGEF and GTPase	Homo sapiens	108-111
34596797-5	2022	Their levels and activity respectively, indicated active Bcr-Abl1 pathway in CML-BC resistant cells, though Bcr-Abl1 is inhibited by imatinib.	imatinib	133-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-116
34144313-9	2021	There was also a significant decrease in the mRNA levels of the major drug efflux genes (ABCB1, ABCB10, ABCC1 and ABCG2) when treated with a combination of imatinib and MBF in comparison to imatinib treatment alone.	imatinib	156-164	ATP binding cassette subfamily B member 1	Homo sapiens	89-94
34144313-9	2021	There was also a significant decrease in the mRNA levels of the major drug efflux genes (ABCB1, ABCB10, ABCC1 and ABCG2) when treated with a combination of imatinib and MBF in comparison to imatinib treatment alone.	imatinib	156-164	ATP binding cassette subfamily B member 10	Homo sapiens	96-102
34144313-9	2021	There was also a significant decrease in the mRNA levels of the major drug efflux genes (ABCB1, ABCB10, ABCC1 and ABCG2) when treated with a combination of imatinib and MBF in comparison to imatinib treatment alone.	imatinib	156-164	ATP binding cassette subfamily C member 1	Homo sapiens	104-109
34144313-9	2021	There was also a significant decrease in the mRNA levels of the major drug efflux genes (ABCB1, ABCB10, ABCC1 and ABCG2) when treated with a combination of imatinib and MBF in comparison to imatinib treatment alone.	imatinib	156-164	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	114-119
34144313-9	2021	There was also a significant decrease in the mRNA levels of the major drug efflux genes (ABCB1, ABCB10, ABCC1 and ABCG2) when treated with a combination of imatinib and MBF in comparison to imatinib treatment alone.	imatinib	190-198	ATP binding cassette subfamily B member 1	Homo sapiens	89-94
34144313-9	2021	There was also a significant decrease in the mRNA levels of the major drug efflux genes (ABCB1, ABCB10, ABCC1 and ABCG2) when treated with a combination of imatinib and MBF in comparison to imatinib treatment alone.	imatinib	190-198	ATP binding cassette subfamily B member 10	Homo sapiens	96-102
34144313-9	2021	There was also a significant decrease in the mRNA levels of the major drug efflux genes (ABCB1, ABCB10, ABCC1 and ABCG2) when treated with a combination of imatinib and MBF in comparison to imatinib treatment alone.	imatinib	190-198	ATP binding cassette subfamily C member 1	Homo sapiens	104-109
34144313-9	2021	There was also a significant decrease in the mRNA levels of the major drug efflux genes (ABCB1, ABCB10, ABCC1 and ABCG2) when treated with a combination of imatinib and MBF in comparison to imatinib treatment alone.	imatinib	190-198	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	114-119
34376580-0	2021	KIT Low Cells Mediate Imatinib Resistance in Gastrointestinal Stromal Tumor.	imatinib	22-30	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
34376580-1	2021	Gastrointestinal stromal tumor (GIST) is commonly driven by oncogenic KIT mutations that are effectively targeted by imatinib, a tyrosine kinase inhibitor (TKI).	imatinib	117-125	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	70-73
34376580-4	2021	Here, we report a subpopulation of CD34+KITlow GIST cells that have intrinsic imatinib resistance.	imatinib	78-86	CD34 molecule	Homo sapiens	35-39
34376580-10	2021	We evaluated these targets in vitro and found that primary imatinib-resistant GIST cells were effectively targeted with either single agent bemcentinib (AXL inhibitor) or bardoxolone (NF-kappaB inhibitor), as well as with either agent in combination with imatinib.	imatinib	59-67	AXL receptor tyrosine kinase	Homo sapiens	153-156
34304603-2	2021	FIP1L1-PDGFRA fusion ((Fip1-like 1-platelet-derived growth factor receptor alpha); F/P) leads to the proliferation of the eosinophilic lineage and thus to a clonal hypereosinophilic syndrome that is highly responsive to imatinib.	imatinib	220-228	factor interacting with PAPOLA and CPSF1	Homo sapiens	0-6
34304603-2	2021	FIP1L1-PDGFRA fusion ((Fip1-like 1-platelet-derived growth factor receptor alpha); F/P) leads to the proliferation of the eosinophilic lineage and thus to a clonal hypereosinophilic syndrome that is highly responsive to imatinib.	imatinib	220-228	platelet derived growth factor receptor alpha	Homo sapiens	7-13
34729261-4	2021	We present a case of a 46-year-old man diagnosed with CML who responded well to imatinib as evidenced by a downtrend in quantitative BCR-ABL mutation to less than 1.	imatinib	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-140
34561421-4	2021	Here, we reveal that the m6A methyltransferase complex METTL3/METTL14 is upregulated in CML patients and that is required for proliferation of primary CML cells and CML cell lines sensitive and resistant to the TKI imatinib.	imatinib	215-223	methyltransferase 14, N6-adenosine-methyltransferase subunit	Homo sapiens	62-69
34616682-9	2021	We show that the percentage of HR and NHEJ efficient HeLa cells decreased more than 50% by combining c-Abl inhibitor imatinib with mitoxantrone.	imatinib	117-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-106
34535920-6	2022	RESULTS: The PBPK model of imatinib demonstrated excellent predictive performance in describing pharmacokinetics and the attained Css,min in patients from different ethnic groups, shown by prediction differences that were within 1.25-fold of the clinically-reported values in published studies.	imatinib	27-35	cytidine monophosphate N-acetylneuraminic acid synthetase	Homo sapiens	130-133
34535920-7	2022	PBPK simulation suggested a similar dose of imatinib (400 - 600 mg/d) to achieve the desirable range of Css,min (1,000 - 3,200 ng/mL) in populations of European, Japanese and Chinese ancestry.	imatinib	44-52	cytidine monophosphate N-acetylneuraminic acid synthetase	Homo sapiens	104-107
34301758-4	2021	This technique was validated by identifying clinically relevant EGFR resistance mutations, then applied to two additional clinical anti-cancer drugs: imatinib, a BCR-ABL inhibitor, and AMG 510, a KRAS G12C inhibitor.	imatinib	150-158	epidermal growth factor receptor	Homo sapiens	64-68
34477162-8	2021	OUTCOMES: After treatment with imatinib for 3 months, the BCR/ABLIS was less than 0.1% and achieved major molecular response.	imatinib	31-39	BCR activator of RhoGEF and GTPase	Homo sapiens	58-61
34301758-5	2021	Novel deletions in BCR-ABL1 conferred resistance to imatinib.	imatinib	52-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-27
34087223-5	2021	Imatinib treatment decreased the phosphorylation of AKT and increased the levels of both p62 (protein sequestosome 1) and LC3 (microtubule-associated protein 1A/1B-light chain 3) in HCC cells and HCC xenografts.	imatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	52-55
34087223-5	2021	Imatinib treatment decreased the phosphorylation of AKT and increased the levels of both p62 (protein sequestosome 1) and LC3 (microtubule-associated protein 1A/1B-light chain 3) in HCC cells and HCC xenografts.	imatinib	0-8	sequestosome 1	Homo sapiens	89-92
34087223-5	2021	Imatinib treatment decreased the phosphorylation of AKT and increased the levels of both p62 (protein sequestosome 1) and LC3 (microtubule-associated protein 1A/1B-light chain 3) in HCC cells and HCC xenografts.	imatinib	0-8	sequestosome 1	Homo sapiens	102-116
34087223-5	2021	Imatinib treatment decreased the phosphorylation of AKT and increased the levels of both p62 (protein sequestosome 1) and LC3 (microtubule-associated protein 1A/1B-light chain 3) in HCC cells and HCC xenografts.	imatinib	0-8	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	122-125
34087223-6	2021	Scanning confocal microscopy analysis with a mRFP-GFP-LC3 reporter and transmission electron microscopy analysis revealed that imatinib suppressed the autophagic flux by obstructing the formation of autolysosomes.	imatinib	127-135	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	54-57
34650853-11	2021	Imatinib has also been used to treat NF1.	imatinib	0-8	neurofibromin 1	Homo sapiens	37-40
34236401-2	2021	KIT inhibitors commonly used to treat GIST (eg, imatinib and sunitinib) are inactive-state (type II) inhibitors.	imatinib	48-56	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
34410954-0	2021	Combined Therapy of ATRA and Imatinib Mesylate Decreases BCR-ABL and ABCB1/MDR1 Expression Through Cellular Differentiation in a Chronic Myeloid Leukemia Model.	imatinib	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
34410954-0	2021	Combined Therapy of ATRA and Imatinib Mesylate Decreases BCR-ABL and ABCB1/MDR1 Expression Through Cellular Differentiation in a Chronic Myeloid Leukemia Model.	imatinib	29-37	ATP binding cassette subfamily B member 1	Homo sapiens	69-74
34410954-0	2021	Combined Therapy of ATRA and Imatinib Mesylate Decreases BCR-ABL and ABCB1/MDR1 Expression Through Cellular Differentiation in a Chronic Myeloid Leukemia Model.	imatinib	29-37	ATP binding cassette subfamily B member 1	Homo sapiens	75-79
34310076-6	2021	Molecular docking identifies several bioactive DDIT4-inteacting compounds including imatinib, nilotinib, and nateglinide, all of which are confirmed to attenuate hepatic ROS production, dampen p38-MAPK signaling, and ameliorate liver injury by influencing DDIT4 S-nitrosylation.	imatinib	84-92	DNA damage inducible transcript 4	Homo sapiens	47-52
34310076-6	2021	Molecular docking identifies several bioactive DDIT4-inteacting compounds including imatinib, nilotinib, and nateglinide, all of which are confirmed to attenuate hepatic ROS production, dampen p38-MAPK signaling, and ameliorate liver injury by influencing DDIT4 S-nitrosylation.	imatinib	84-92	mitogen-activated protein kinase 14	Homo sapiens	193-201
34310076-6	2021	Molecular docking identifies several bioactive DDIT4-inteacting compounds including imatinib, nilotinib, and nateglinide, all of which are confirmed to attenuate hepatic ROS production, dampen p38-MAPK signaling, and ameliorate liver injury by influencing DDIT4 S-nitrosylation.	imatinib	84-92	DNA damage inducible transcript 4	Homo sapiens	256-261
34410954-7	2021	CONCLUSION: Combined ATRA and IM therapy was shown to be effective in decreasing BCR-ABL and ABCB1 genes, possibly through the differentiation of blast cells, demonstrating that the therapy could be potentially effective in the blast crisis of the disease and for those patients who develop resistance to available CML treatments.	imatinib	30-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-88
34410954-7	2021	CONCLUSION: Combined ATRA and IM therapy was shown to be effective in decreasing BCR-ABL and ABCB1 genes, possibly through the differentiation of blast cells, demonstrating that the therapy could be potentially effective in the blast crisis of the disease and for those patients who develop resistance to available CML treatments.	imatinib	30-32	ATP binding cassette subfamily B member 1	Homo sapiens	93-98
34403880-1	2021	Tyrosine kinase inhibitors (TKIs) such as imatinib, nilotinib, dasatinib, and ponatinib have significantly improved the life expectancy of Philadelphia chromosome-positive (Ph+) acute lymphocytic leukemia (ALL) patients; however, resistance to TKIs remains a major clinical challenge.	imatinib	42-50	phenylalanine hydroxylase	Homo sapiens	173-175
34446510-0	2021	Sustained response to imatinib in patient with extraskeletal myxoid chondrosarcoma and novel KIT mutation.	imatinib	22-30	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	93-96
34589354-3	2021	Imatinib mesylate, a tyrosine kinase inhibitor with activity against ABL, BCR-ABL, platelet-derived growth factor receptor-alpha (PDGFRA), and c-KIT (CD117), constitutes the cornerstone of treatment for inoperable or metastatic GIST.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-72
34589354-3	2021	Imatinib mesylate, a tyrosine kinase inhibitor with activity against ABL, BCR-ABL, platelet-derived growth factor receptor-alpha (PDGFRA), and c-KIT (CD117), constitutes the cornerstone of treatment for inoperable or metastatic GIST.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
34589354-3	2021	Imatinib mesylate, a tyrosine kinase inhibitor with activity against ABL, BCR-ABL, platelet-derived growth factor receptor-alpha (PDGFRA), and c-KIT (CD117), constitutes the cornerstone of treatment for inoperable or metastatic GIST.	imatinib	0-17	platelet derived growth factor receptor alpha	Homo sapiens	83-128
34589354-3	2021	Imatinib mesylate, a tyrosine kinase inhibitor with activity against ABL, BCR-ABL, platelet-derived growth factor receptor-alpha (PDGFRA), and c-KIT (CD117), constitutes the cornerstone of treatment for inoperable or metastatic GIST.	imatinib	0-17	platelet derived growth factor receptor alpha	Homo sapiens	130-136
34589354-3	2021	Imatinib mesylate, a tyrosine kinase inhibitor with activity against ABL, BCR-ABL, platelet-derived growth factor receptor-alpha (PDGFRA), and c-KIT (CD117), constitutes the cornerstone of treatment for inoperable or metastatic GIST.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	143-148
34589354-3	2021	Imatinib mesylate, a tyrosine kinase inhibitor with activity against ABL, BCR-ABL, platelet-derived growth factor receptor-alpha (PDGFRA), and c-KIT (CD117), constitutes the cornerstone of treatment for inoperable or metastatic GIST.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	150-155
34157313-0	2021	Targeting HSPA8 inhibits proliferation via downregulating BCR-ABL and enhances chemosensitivity in imatinib-resistant chronic myeloid leukemia cells.	imatinib	99-107	heat shock protein family A (Hsp70) member 8	Homo sapiens	10-15
34540000-8	2021	The results showed that icaritin inhibited cell growth and induced cell senescence in imatinib-resistant CML cells, which is associated with the regulation of the JAK2/STAT3/P21 axis and accompanied by the accumulation of ROS.	imatinib	86-94	Janus kinase 2	Homo sapiens	163-167
34540000-8	2021	The results showed that icaritin inhibited cell growth and induced cell senescence in imatinib-resistant CML cells, which is associated with the regulation of the JAK2/STAT3/P21 axis and accompanied by the accumulation of ROS.	imatinib	86-94	signal transducer and activator of transcription 3	Homo sapiens	168-173
34540000-8	2021	The results showed that icaritin inhibited cell growth and induced cell senescence in imatinib-resistant CML cells, which is associated with the regulation of the JAK2/STAT3/P21 axis and accompanied by the accumulation of ROS.	imatinib	86-94	H3 histone pseudogene 16	Homo sapiens	174-177
34504783-5	2021	Then we used shRNA lentivirus to down-regulated RanBP3 in imatinib sensitive K562 cells and resistant K562/G01 cells and found RanBP3 silencing inhibited cell proliferation by up-regulating p21, induced caspase3-related cell apoptosis, and enhanced the drug sensitivity of IM in vitro.	imatinib	58-66	RAN binding protein 3	Homo sapiens	48-54
34504783-7	2021	Mechanistically, the nuclear aggregation of SMAD2/3 revealed that tumor suppressor axis (TGF-beta)-SMAD2/3-p21 was the anti-proliferation program related to RanBP3 knockdown, and the decrease of cytoplasmic ERK1/2 caused by RanBP3 interference leaded to the down-regulation of anti-apoptosis protein p(Ser112)-BAD, which was the mechanism of increased cell apoptosis and enhanced chemosensitivity to imatinib in CML.	imatinib	400-408	SMAD family member 2	Homo sapiens	44-51
34504783-7	2021	Mechanistically, the nuclear aggregation of SMAD2/3 revealed that tumor suppressor axis (TGF-beta)-SMAD2/3-p21 was the anti-proliferation program related to RanBP3 knockdown, and the decrease of cytoplasmic ERK1/2 caused by RanBP3 interference leaded to the down-regulation of anti-apoptosis protein p(Ser112)-BAD, which was the mechanism of increased cell apoptosis and enhanced chemosensitivity to imatinib in CML.	imatinib	400-408	transforming growth factor alpha	Homo sapiens	89-97
34504783-7	2021	Mechanistically, the nuclear aggregation of SMAD2/3 revealed that tumor suppressor axis (TGF-beta)-SMAD2/3-p21 was the anti-proliferation program related to RanBP3 knockdown, and the decrease of cytoplasmic ERK1/2 caused by RanBP3 interference leaded to the down-regulation of anti-apoptosis protein p(Ser112)-BAD, which was the mechanism of increased cell apoptosis and enhanced chemosensitivity to imatinib in CML.	imatinib	400-408	SMAD family member 2	Homo sapiens	99-106
34504783-7	2021	Mechanistically, the nuclear aggregation of SMAD2/3 revealed that tumor suppressor axis (TGF-beta)-SMAD2/3-p21 was the anti-proliferation program related to RanBP3 knockdown, and the decrease of cytoplasmic ERK1/2 caused by RanBP3 interference leaded to the down-regulation of anti-apoptosis protein p(Ser112)-BAD, which was the mechanism of increased cell apoptosis and enhanced chemosensitivity to imatinib in CML.	imatinib	400-408	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	107-110
34504783-7	2021	Mechanistically, the nuclear aggregation of SMAD2/3 revealed that tumor suppressor axis (TGF-beta)-SMAD2/3-p21 was the anti-proliferation program related to RanBP3 knockdown, and the decrease of cytoplasmic ERK1/2 caused by RanBP3 interference leaded to the down-regulation of anti-apoptosis protein p(Ser112)-BAD, which was the mechanism of increased cell apoptosis and enhanced chemosensitivity to imatinib in CML.	imatinib	400-408	RAN binding protein 3	Mus musculus	157-163
34504783-7	2021	Mechanistically, the nuclear aggregation of SMAD2/3 revealed that tumor suppressor axis (TGF-beta)-SMAD2/3-p21 was the anti-proliferation program related to RanBP3 knockdown, and the decrease of cytoplasmic ERK1/2 caused by RanBP3 interference leaded to the down-regulation of anti-apoptosis protein p(Ser112)-BAD, which was the mechanism of increased cell apoptosis and enhanced chemosensitivity to imatinib in CML.	imatinib	400-408	mitogen-activated protein kinase 3	Homo sapiens	207-213
34504783-7	2021	Mechanistically, the nuclear aggregation of SMAD2/3 revealed that tumor suppressor axis (TGF-beta)-SMAD2/3-p21 was the anti-proliferation program related to RanBP3 knockdown, and the decrease of cytoplasmic ERK1/2 caused by RanBP3 interference leaded to the down-regulation of anti-apoptosis protein p(Ser112)-BAD, which was the mechanism of increased cell apoptosis and enhanced chemosensitivity to imatinib in CML.	imatinib	400-408	RAN binding protein 3	Mus musculus	224-230
34157313-3	2021	Here, we determined HSPA8 was overexpressed in IR-CML cells and associated with imatinib resistance.	imatinib	80-88	heat shock protein family A (Hsp70) member 8	Homo sapiens	20-25
34439257-1	2021	Within the International Registry of Childhood Chronic Myeloid Leukemia (CML), we identified 18 patients less than 18 years old at diagnosis of CML who were in the chronic phase and exhibiting a sustained deep molecular response (DMR) to imatinib defined as BCR-ABL1/ABL1 < 0.01% (MR4) for at least two years followed by discontinuation of imatinib.	imatinib	238-246	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	262-266
34439257-1	2021	Within the International Registry of Childhood Chronic Myeloid Leukemia (CML), we identified 18 patients less than 18 years old at diagnosis of CML who were in the chronic phase and exhibiting a sustained deep molecular response (DMR) to imatinib defined as BCR-ABL1/ABL1 < 0.01% (MR4) for at least two years followed by discontinuation of imatinib.	imatinib	238-246	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	267-271
34157313-5	2021	Significantly, HSPA8 ablation enhanced the antitumor activity of imatinib via promoting apoptosis in vitro and vivo.These findings unraveled that HSPA8 ablation inhibits proliferation via downregulating BCR-ABL and enhances chemosensitivity of imatinib in IR-CML cells, which investigate the role and molecular mechanism of HSPA8 in IR-CML cells and suggest that HSPA8 may be a potential target for IR-CML treatment.	imatinib	65-73	heat shock protein family A (Hsp70) member 8	Homo sapiens	146-151
34157313-5	2021	Significantly, HSPA8 ablation enhanced the antitumor activity of imatinib via promoting apoptosis in vitro and vivo.These findings unraveled that HSPA8 ablation inhibits proliferation via downregulating BCR-ABL and enhances chemosensitivity of imatinib in IR-CML cells, which investigate the role and molecular mechanism of HSPA8 in IR-CML cells and suggest that HSPA8 may be a potential target for IR-CML treatment.	imatinib	65-73	heat shock protein family A (Hsp70) member 8	Homo sapiens	324-329
34157313-5	2021	Significantly, HSPA8 ablation enhanced the antitumor activity of imatinib via promoting apoptosis in vitro and vivo.These findings unraveled that HSPA8 ablation inhibits proliferation via downregulating BCR-ABL and enhances chemosensitivity of imatinib in IR-CML cells, which investigate the role and molecular mechanism of HSPA8 in IR-CML cells and suggest that HSPA8 may be a potential target for IR-CML treatment.	imatinib	65-73	heat shock protein family A (Hsp70) member 8	Homo sapiens	363-368
34157313-5	2021	Significantly, HSPA8 ablation enhanced the antitumor activity of imatinib via promoting apoptosis in vitro and vivo.These findings unraveled that HSPA8 ablation inhibits proliferation via downregulating BCR-ABL and enhances chemosensitivity of imatinib in IR-CML cells, which investigate the role and molecular mechanism of HSPA8 in IR-CML cells and suggest that HSPA8 may be a potential target for IR-CML treatment.	imatinib	244-252	heat shock protein family A (Hsp70) member 8	Homo sapiens	15-20
34157313-5	2021	Significantly, HSPA8 ablation enhanced the antitumor activity of imatinib via promoting apoptosis in vitro and vivo.These findings unraveled that HSPA8 ablation inhibits proliferation via downregulating BCR-ABL and enhances chemosensitivity of imatinib in IR-CML cells, which investigate the role and molecular mechanism of HSPA8 in IR-CML cells and suggest that HSPA8 may be a potential target for IR-CML treatment.	imatinib	244-252	heat shock protein family A (Hsp70) member 8	Homo sapiens	146-151
34157313-5	2021	Significantly, HSPA8 ablation enhanced the antitumor activity of imatinib via promoting apoptosis in vitro and vivo.These findings unraveled that HSPA8 ablation inhibits proliferation via downregulating BCR-ABL and enhances chemosensitivity of imatinib in IR-CML cells, which investigate the role and molecular mechanism of HSPA8 in IR-CML cells and suggest that HSPA8 may be a potential target for IR-CML treatment.	imatinib	244-252	heat shock protein family A (Hsp70) member 8	Homo sapiens	324-329
34157313-5	2021	Significantly, HSPA8 ablation enhanced the antitumor activity of imatinib via promoting apoptosis in vitro and vivo.These findings unraveled that HSPA8 ablation inhibits proliferation via downregulating BCR-ABL and enhances chemosensitivity of imatinib in IR-CML cells, which investigate the role and molecular mechanism of HSPA8 in IR-CML cells and suggest that HSPA8 may be a potential target for IR-CML treatment.	imatinib	244-252	heat shock protein family A (Hsp70) member 8	Homo sapiens	363-368
34414175-9	2021	The newly identified LNC000093 served as a competitive endogenous RNA for miR-675-5p and reversed the imatinib resistance in CML cells through regulating RUNX1 expression.	imatinib	102-110	RUNX family transcription factor 1	Homo sapiens	154-159
34489967-6	2021	In addition to inhibiting the KIT oncogene, imatinib appears to act by promoting cytotoxic T-cell activity, interacting with natural killer cells, and inhibiting the expression of PD-L1.	imatinib	44-52	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	30-33
34489967-6	2021	In addition to inhibiting the KIT oncogene, imatinib appears to act by promoting cytotoxic T-cell activity, interacting with natural killer cells, and inhibiting the expression of PD-L1.	imatinib	44-52	CD274 molecule	Homo sapiens	180-185
34214479-8	2021	The primary endpoint was the difference in the area under the curve (AUC) mean for C-peptide response in the first 2 h of an MMTT at 12 months in the imatinib group versus the placebo group, with use of an ANCOVA model adjusting for sex, baseline age, and baseline C-peptide, with further observation up to 24 months.	imatinib	150-158	insulin	Homo sapiens	83-92
34156283-6	2021	Knockdown of FEN1 by shRNA not only inhibited the proliferation and induced apoptosis but also enhanced the efficacy of imatinib (IM) in drug-resistant CML cell K562/G01.	imatinib	120-128	flap structure-specific endonuclease 1	Homo sapiens	13-17
34156283-6	2021	Knockdown of FEN1 by shRNA not only inhibited the proliferation and induced apoptosis but also enhanced the efficacy of imatinib (IM) in drug-resistant CML cell K562/G01.	imatinib	130-132	flap structure-specific endonuclease 1	Homo sapiens	13-17
34214479-15	2021	The study met its primary endpoint: the adjusted mean difference in 2-h C-peptide AUC at 12 months for imatinib versus placebo treatment was 0 095 (90% CI -0 003 to 0 191; p=0 048, one-tailed test).	imatinib	103-111	insulin	Homo sapiens	72-81
34361750-6	2021	Betulin was shown to modulate the mitogen-activated protein (MAP) kinase pathway, with activity similar to that of imatinib mesylate, a known ABL1 kinase inhibitor.	imatinib	115-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-146
34332577-0	2021	Aurora kinase A (AURKA) promotes the progression and imatinib resistance of advanced gastrointestinal stromal tumors.	imatinib	53-61	aurora kinase A	Homo sapiens	0-15
34332577-0	2021	Aurora kinase A (AURKA) promotes the progression and imatinib resistance of advanced gastrointestinal stromal tumors.	imatinib	53-61	aurora kinase A	Homo sapiens	17-22
34332577-14	2021	Additionally, overexpression of AURKA was experimentally demonstrated to promote cell proliferation, inhibit cell apoptosis, and enhance imatinib resistance in GIST/T1 cells.	imatinib	137-145	aurora kinase A	Homo sapiens	32-37
34332577-15	2021	CONCLUSIONS: These findings indicated that overexpression of AURKA promoted GIST progression and enhanced imatinib resistance, implying that AURKA is a potential therapeutic target for GISTs.	imatinib	106-114	aurora kinase A	Homo sapiens	61-66
34332577-15	2021	CONCLUSIONS: These findings indicated that overexpression of AURKA promoted GIST progression and enhanced imatinib resistance, implying that AURKA is a potential therapeutic target for GISTs.	imatinib	106-114	aurora kinase A	Homo sapiens	141-146
34324512-2	2021	KIT/PDGFRA inhibitors, such as imatinib do not evoke an effective cytocidal response, leaving room for quiescence and development of multiple secondary resistance mutations.	imatinib	31-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
34324512-2	2021	KIT/PDGFRA inhibitors, such as imatinib do not evoke an effective cytocidal response, leaving room for quiescence and development of multiple secondary resistance mutations.	imatinib	31-39	platelet derived growth factor receptor alpha	Homo sapiens	4-10
34272637-2	2021	Tyrosine kinase inhibitor such as imatinib is reported to interfere with the activation of vitamin D3 by inhibiting CYP27B1 enzyme.	imatinib	34-42	cytochrome P450 family 27 subfamily B member 1	Homo sapiens	116-123
34300312-0	2021	Impact of BCR-ABL1 Transcript Type on Response, Treatment-Free Remission Rate and Survival in Chronic Myeloid Leukemia Patients Treated with Imatinib.	imatinib	141-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-18
34359600-1	2021	The majority of gastrointestinal stromal tumor (GIST) patients develop resistance to the first-line KIT inhibitor, imatinib mesylate (IM), through acquisition of secondary mutations in KIT or bypass signaling pathway activation.	imatinib	115-132	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	100-103
34359600-1	2021	The majority of gastrointestinal stromal tumor (GIST) patients develop resistance to the first-line KIT inhibitor, imatinib mesylate (IM), through acquisition of secondary mutations in KIT or bypass signaling pathway activation.	imatinib	115-132	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	185-188
34359600-1	2021	The majority of gastrointestinal stromal tumor (GIST) patients develop resistance to the first-line KIT inhibitor, imatinib mesylate (IM), through acquisition of secondary mutations in KIT or bypass signaling pathway activation.	imatinib	134-136	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	100-103
34359600-1	2021	The majority of gastrointestinal stromal tumor (GIST) patients develop resistance to the first-line KIT inhibitor, imatinib mesylate (IM), through acquisition of secondary mutations in KIT or bypass signaling pathway activation.	imatinib	134-136	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	185-188
34298737-2	2021	The management of locally advanced or metastatic unresectable GIST involves detecting KIT, PDGFR, or other molecular alterations targeted by imatinib and other tyrosine kinase inhibitors.	imatinib	141-149	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	86-89
34298737-2	2021	The management of locally advanced or metastatic unresectable GIST involves detecting KIT, PDGFR, or other molecular alterations targeted by imatinib and other tyrosine kinase inhibitors.	imatinib	141-149	platelet derived growth factor receptor beta	Homo sapiens	91-96
34322383-2	2021	Approval of imatinib, a KIT/PDGFRA tyrosine kinase inhibitor (TKI), meaningfully improved the treatment of advanced GIST.	imatinib	12-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	24-27
34298678-8	2021	Accordingly, the ABL inhibitor imatinib and the FLT3 inhibitor quizartinib sensitize leukemic cells to pro-apoptotic effects of hydroxyurea.	imatinib	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-20
34327214-8	2021	In the pseudovirus assay, imatinib and lapatinib had IC50 values below 10 muM, while candesartan cilexetil had an IC50 value of approximately 67 microM against Mpro in a FRET-based activity assay.	imatinib	26-34	NEWENTRY	Severe acute respiratory syndrome-related coronavirus	160-164
34214082-3	2021	As the Abl kinase inhibitor imatinib was previously shown to reverse type 2 diabetes and to inhibit VEGF signaling via Abl kinases, we studied the effect of imatinib on vascular insulin sensitivity and fatty acid transport in vivo and in vitro.	imatinib	28-36	vascular endothelial growth factor A	Mus musculus	100-104
34295818-7	2021	Importantly, knockdown of HNRNPH1 in CML cells enhanced sensitivity to imatinib.	imatinib	71-79	heterogeneous nuclear ribonucleoprotein H1	Homo sapiens	26-33
34214082-12	2021	Although imatinib effectively prevented VEGF-B-mediated Abl kinase activation, it had no effect on VEGF-B mediated endothelial FA uptake.	imatinib	9-17	vascular endothelial growth factor B	Mus musculus	40-46
34214082-13	2021	CONCLUSION: Imatinib prevents weight gain and preserves insulin-mediated vasodilation in WD-fed mice, but does not affect endothelial FA transport despite inhibiting VEGF-B signaling.	imatinib	12-20	vascular endothelial growth factor B	Mus musculus	166-172
34090970-5	2021	By using in vitro models of tyrosine kinase inhibitor resistance, an increase in ZFP36L1 and ZFP36L2 expression was detected during the development of imatinib resistance.	imatinib	151-159	ZFP36 ring finger protein like 1	Homo sapiens	81-88
34090970-6	2021	CRISPR/Cas9-derived knockout of ZFP36L1, but not of ZFP36L2, in imatinib sensitive cells led to decreased proliferation rates in response to tyrosine kinase inhibitor treatment.	imatinib	64-72	ZFP36 ring finger protein like 1	Homo sapiens	32-39
34090970-5	2021	By using in vitro models of tyrosine kinase inhibitor resistance, an increase in ZFP36L1 and ZFP36L2 expression was detected during the development of imatinib resistance.	imatinib	151-159	ZFP36 ring finger protein like 2	Homo sapiens	93-100
34292760-0	2021	Spectrum of BCR-ABL Mutations and Treatment Outcomes in Ethiopian Imatinib-Resistant Patients With Chronic Myeloid Leukemia.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
34089444-1	2021	BACKGROUND: Retrospective analyses suggest that patients with advanced KIT exon 9-mutated gastrointestinal stromal tumors (GISTs) receiving imatinib 800 mg (rather than 400 mg) daily have better outcomes.	imatinib	140-148	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	71-74
34432780-4	2021	We showed that in the presence of imatinib autophagy was triggered via LC3I/II transformation, p62 protein expression and acidic vacuoles accumulation in tyrosine kinase inhibitor-sensitive K562 cells; whereas in the cell line K562-IR which is imatinib-resistant and Bcr-Abl independent, autophagy is not triggered.	imatinib	34-42	nucleoporin 62	Homo sapiens	95-98
34432780-4	2021	We showed that in the presence of imatinib autophagy was triggered via LC3I/II transformation, p62 protein expression and acidic vacuoles accumulation in tyrosine kinase inhibitor-sensitive K562 cells; whereas in the cell line K562-IR which is imatinib-resistant and Bcr-Abl independent, autophagy is not triggered.	imatinib	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	267-274
34292760-4	2021	We here report the types of BCR-ABL mutations in Ethiopian imatinib-resistant patients with CML and their outcome.	imatinib	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-35
34089444-12	2021	Patients with advanced disease receiving imatinib 400 mg with subsequent dose escalation had a TIF similar to that observed with an initial dose of 800 mg. Intra-patient dose escalation in this setting might be an option.	imatinib	41-49	TYRO3 protein tyrosine kinase	Homo sapiens	95-98
34458010-9	2021	By treating GIST cells with different doses of imatinib, we verified that RP11-616M22.7 knockdown promotes the sensitivity of tumor cells, whereas RP11-616M22.7 overexpression induces resistance to imatinib.	imatinib	198-206	pre-mRNA processing factor 31	Homo sapiens	147-151
34276365-7	2021	Moreover, employing immortalized cell lines and primary CD34-positive progenitors, we demonstrate that these modifications lead to reduced BCR-ABL1 sensitivity to imatinib, dasatinib and ponatinib but not nilotinib.	imatinib	163-171	CD34 molecule	Homo sapiens	56-60
34276365-7	2021	Moreover, employing immortalized cell lines and primary CD34-positive progenitors, we demonstrate that these modifications lead to reduced BCR-ABL1 sensitivity to imatinib, dasatinib and ponatinib but not nilotinib.	imatinib	163-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-147
34262462-5	2021	By binding to the BCR-ABL1 kinase and inhibition of downstream target phosphorylation, TKIs, such as imatinib or nilotinib, can be used as single agents to treat CML patients resulting in 80 % 10-year survival rates.	imatinib	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-26
34167562-7	2021	RESULTS: All NOTCH1-signaling-dependent T-ALL cell lines were sensitive to MRK-560 and its combination with ruxolitinib or imatinib in JAK1- or ABL1-dependent cell lines synergistically inhibited leukemia proliferation.	imatinib	123-131	notch receptor 1	Homo sapiens	13-19
34167562-7	2021	RESULTS: All NOTCH1-signaling-dependent T-ALL cell lines were sensitive to MRK-560 and its combination with ruxolitinib or imatinib in JAK1- or ABL1-dependent cell lines synergistically inhibited leukemia proliferation.	imatinib	123-131	mitogen-activated protein kinase kinase kinase 20	Homo sapiens	75-78
34167562-7	2021	RESULTS: All NOTCH1-signaling-dependent T-ALL cell lines were sensitive to MRK-560 and its combination with ruxolitinib or imatinib in JAK1- or ABL1-dependent cell lines synergistically inhibited leukemia proliferation.	imatinib	123-131	Janus kinase 1	Homo sapiens	135-139
34167562-7	2021	RESULTS: All NOTCH1-signaling-dependent T-ALL cell lines were sensitive to MRK-560 and its combination with ruxolitinib or imatinib in JAK1- or ABL1-dependent cell lines synergistically inhibited leukemia proliferation.	imatinib	123-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-148
34203261-0	2021	Imatinib (STI571) Inhibits the Expression of Angiotensin-Converting Enzyme 2 and Cell Entry of the SARS-CoV-2-Derived Pseudotyped Viral Particles.	imatinib	0-8	angiotensin converting enzyme 2	Homo sapiens	45-76
34203261-0	2021	Imatinib (STI571) Inhibits the Expression of Angiotensin-Converting Enzyme 2 and Cell Entry of the SARS-CoV-2-Derived Pseudotyped Viral Particles.	imatinib	10-16	angiotensin converting enzyme 2	Homo sapiens	45-76
34203261-2	2021	Here, we show that the receptor tyrosine kinase inhibitor imatinib (also known as STI571, Gleevec) can inhibit the expression of the endogenous ACE2 gene at both the transcript and protein levels.	imatinib	58-66	ret proto-oncogene	Homo sapiens	23-47
34203261-2	2021	Here, we show that the receptor tyrosine kinase inhibitor imatinib (also known as STI571, Gleevec) can inhibit the expression of the endogenous ACE2 gene at both the transcript and protein levels.	imatinib	58-66	angiotensin converting enzyme 2	Homo sapiens	144-148
34203261-4	2021	In FVB mice orally fed imatinib, tissue expression of ACE2 was reduced, specifically in the lungs and renal tubules, but not in the parenchyma of other organs such as the heart and intestine.	imatinib	23-31	angiotensin I converting enzyme (peptidyl-dipeptidase A) 2	Mus musculus	54-58
34458010-0	2021	RP11-616M22.7 recapitulates imatinib resistance in gastrointestinal stromal tumor.	imatinib	28-36	pre-mRNA processing factor 31	Homo sapiens	0-4
34458010-7	2021	RP11-616M22.7 was identified to increase in imatinib-resistant samples compared to those in non-resistant samples.	imatinib	44-52	pre-mRNA processing factor 31	Homo sapiens	0-4
34458010-9	2021	By treating GIST cells with different doses of imatinib, we verified that RP11-616M22.7 knockdown promotes the sensitivity of tumor cells, whereas RP11-616M22.7 overexpression induces resistance to imatinib.	imatinib	47-55	pre-mRNA processing factor 31	Homo sapiens	74-78
34458010-10	2021	We further confirmed reducing of resistance to imatinib by knocking down RP11-616M22.7 in vivo.	imatinib	47-55	pre-mRNA processing factor 31	Homo sapiens	73-77
34458010-12	2021	Our study revealed that deficiency of RP11-616M22.7 was able to reduce resistance of the GIST cell response to imatinib treatment both in vitro and in vivo.	imatinib	111-119	pre-mRNA processing factor 31	Homo sapiens	38-42
34065883-6	2021	The KIT inhibitors (Tyrosine kinase inhibitors: TKIs) imatinib and nilotinib could be the treatment options.	imatinib	54-62	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	4-7
34068907-3	2021	For this purpose, the cells harboring wild-type BCR/ABL, imatinib-resistant BCR/ABL (K562 and TCCYT315I), or Ba/F3 cells transfected with wild-type or mutant BCR/ABL genes were used.	imatinib	57-65	BCR activator of RhoGEF and GTPase	Mus musculus	76-79
34068907-3	2021	For this purpose, the cells harboring wild-type BCR/ABL, imatinib-resistant BCR/ABL (K562 and TCCYT315I), or Ba/F3 cells transfected with wild-type or mutant BCR/ABL genes were used.	imatinib	57-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
34068907-5	2021	The effect of MeST seems to be more sensitive in the cells that carry imatinib-resistant BCR/ABL (especially the T315I BCR/ABL mutation) than those with wild-type BCR/ABL.	imatinib	70-78	BCR activator of RhoGEF and GTPase	Mus musculus	89-96
34068907-5	2021	The effect of MeST seems to be more sensitive in the cells that carry imatinib-resistant BCR/ABL (especially the T315I BCR/ABL mutation) than those with wild-type BCR/ABL.	imatinib	70-78	BCR activator of RhoGEF and GTPase	Mus musculus	119-122
34068907-5	2021	The effect of MeST seems to be more sensitive in the cells that carry imatinib-resistant BCR/ABL (especially the T315I BCR/ABL mutation) than those with wild-type BCR/ABL.	imatinib	70-78	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	123-126
34068907-8	2021	The mechanism of the anti-leukemic effect of MeST on cells harboring imatinib-resistant BCR/ABL mutations could be due to the disruption of the BCR/ABL oncoprotein signaling cascade.	imatinib	69-77	BCR activator of RhoGEF and GTPase	Mus musculus	88-91
34068907-8	2021	The mechanism of the anti-leukemic effect of MeST on cells harboring imatinib-resistant BCR/ABL mutations could be due to the disruption of the BCR/ABL oncoprotein signaling cascade.	imatinib	69-77	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	92-95
34068907-8	2021	The mechanism of the anti-leukemic effect of MeST on cells harboring imatinib-resistant BCR/ABL mutations could be due to the disruption of the BCR/ABL oncoprotein signaling cascade.	imatinib	69-77	BCR activator of RhoGEF and GTPase	Mus musculus	144-147
34068907-8	2021	The mechanism of the anti-leukemic effect of MeST on cells harboring imatinib-resistant BCR/ABL mutations could be due to the disruption of the BCR/ABL oncoprotein signaling cascade.	imatinib	69-77	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	148-151
34268985-14	2021	In our study T315I mutation of the ABL gene and the increased values of LDH were associated with a higher rate of relapses and resistance to imatinib.	imatinib	141-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
34515193-2	2021	Therefore, this study was aimed to evaluate the clinical importance of miR-126 and miR-122 expression in concert to imatinib response in CML patients.	imatinib	116-124	microRNA 126	Homo sapiens	71-78
34466210-9	2021	Most of the Studies (n=4, 67% from 7 studies) considered BCR/ABL point mutation as main reason of imatinib resistance.	imatinib	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-64
34473615-6	2021	RESULTS: Imatinib exhibited the strongest inhibitory effect towards CYP3A, while the inhibitory potential of gefitinib and sunitinib were comparable to each other but weaker than imatinib.	imatinib	9-17	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	68-73
34473615-6	2021	RESULTS: Imatinib exhibited the strongest inhibitory effect towards CYP3A, while the inhibitory potential of gefitinib and sunitinib were comparable to each other but weaker than imatinib.	imatinib	179-187	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	68-73
34473615-12	2021	Therefore, caution should be taken when CYP3A-metabolizing drugs are co-administrated with imatinib, sunitinib, or gefitinib.	imatinib	91-99	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	40-45
34247157-10	2021	Mechanistically, Gleevec, but not rapamycin, induced a significant elevation in caspase-3 activity in EPCs, and it attenuated the expression of the endothelial protein marker platelet-derived growth factor receptor alpha.	imatinib	17-24	caspase 3	Mus musculus	80-89
34247157-10	2021	Mechanistically, Gleevec, but not rapamycin, induced a significant elevation in caspase-3 activity in EPCs, and it attenuated the expression of the endothelial protein marker platelet-derived growth factor receptor alpha.	imatinib	17-24	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	175-220
34515193-2	2021	Therefore, this study was aimed to evaluate the clinical importance of miR-126 and miR-122 expression in concert to imatinib response in CML patients.	imatinib	116-124	microRNA 122	Homo sapiens	83-90
34515193-9	2021	CONCLUSION: The study concludes that expression of miR-126 and miR-122 increases after imatinib treatment in CML patients and that miR-126 defines the good responders of imatinib therapy.	imatinib	87-95	microRNA 126	Homo sapiens	51-58
34515193-9	2021	CONCLUSION: The study concludes that expression of miR-126 and miR-122 increases after imatinib treatment in CML patients and that miR-126 defines the good responders of imatinib therapy.	imatinib	87-95	microRNA 122	Homo sapiens	63-70
34515193-9	2021	CONCLUSION: The study concludes that expression of miR-126 and miR-122 increases after imatinib treatment in CML patients and that miR-126 defines the good responders of imatinib therapy.	imatinib	87-95	microRNA 126	Homo sapiens	131-138
34723728-0	2021	LncRNA OIP5-AS1 Promotes the Autophagy-Related Imatinib Resistance in Chronic Myeloid Leukemia Cells by Regulating miR-30e-5p/ATG12 Axis.	imatinib	47-55	OIP5 antisense RNA 1	Homo sapiens	7-15
34515193-9	2021	CONCLUSION: The study concludes that expression of miR-126 and miR-122 increases after imatinib treatment in CML patients and that miR-126 defines the good responders of imatinib therapy.	imatinib	170-178	microRNA 126	Homo sapiens	51-58
34723728-0	2021	LncRNA OIP5-AS1 Promotes the Autophagy-Related Imatinib Resistance in Chronic Myeloid Leukemia Cells by Regulating miR-30e-5p/ATG12 Axis.	imatinib	47-55	autophagy related 12	Homo sapiens	126-131
34515193-9	2021	CONCLUSION: The study concludes that expression of miR-126 and miR-122 increases after imatinib treatment in CML patients and that miR-126 defines the good responders of imatinib therapy.	imatinib	170-178	microRNA 122	Homo sapiens	63-70
34515193-9	2021	CONCLUSION: The study concludes that expression of miR-126 and miR-122 increases after imatinib treatment in CML patients and that miR-126 defines the good responders of imatinib therapy.	imatinib	170-178	microRNA 126	Homo sapiens	131-138
34866089-0	2021	(Successful treatment with imatinib for a patient with myeloid neoplasms with eosinophilia and abnormalities of PDGFRB due to t (5;14)(q33;q22)).	imatinib	27-35	platelet derived growth factor receptor beta	Homo sapiens	112-118
35106640-0	2022	Successful treatment of imatinib-induced periorbital edema with a sodium-glucose cotransporter-2 inhibitor.	imatinib	24-32	solute carrier family 5 member 2	Homo sapiens	66-96
35597499-12	2022	Immunofluorescence experiments and western blot results showed that psoralen could affect ROS levels and downstream Nrf2 and mTOR protein changes, whereas the ABL1 inhibitor imatinib and ABL1 agonist DPH could enhance or inhibit this effect.	imatinib	174-182	NFE2 like bZIP transcription factor 2	Homo sapiens	116-120
35597499-12	2022	Immunofluorescence experiments and western blot results showed that psoralen could affect ROS levels and downstream Nrf2 and mTOR protein changes, whereas the ABL1 inhibitor imatinib and ABL1 agonist DPH could enhance or inhibit this effect.	imatinib	174-182	mechanistic target of rapamycin kinase	Homo sapiens	125-129
35597499-12	2022	Immunofluorescence experiments and western blot results showed that psoralen could affect ROS levels and downstream Nrf2 and mTOR protein changes, whereas the ABL1 inhibitor imatinib and ABL1 agonist DPH could enhance or inhibit this effect.	imatinib	174-182	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-163
35132891-4	2022	Metformin is a widely prescribed glucose-lowering agent for patients with diabetes and in preclinical studies, has been shown to suppress cell viability, induce apoptosis, and downregulate the mTORC1 signaling pathway in imatinib resistant CML cell lines (K562R).	imatinib	221-229	CREB regulated transcription coactivator 1	Mus musculus	193-199
35288241-0	2022	The nerve-tumour regulatory axis GDNF-GFRA1 promotes tumour dormancy, imatinib resistance and local recurrence of gastrointestinal stromal tumours by achieving autophagic flux.	imatinib	70-78	glial cell derived neurotrophic factor	Homo sapiens	33-37
35288241-0	2022	The nerve-tumour regulatory axis GDNF-GFRA1 promotes tumour dormancy, imatinib resistance and local recurrence of gastrointestinal stromal tumours by achieving autophagic flux.	imatinib	70-78	GDNF family receptor alpha 1	Homo sapiens	38-43
35487307-9	2022	Other KIT-targeting drugs, such as imatinib or masitinib, are less effective or even non-effective against KIT D816V and are thus only recommended for use in patients with other KIT mutant forms (non codon 816 mutations) or with wild type KIT.	imatinib	35-43	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	6-9
35613653-0	2022	Assessment of hyaluronic acid-modified imatinib mesylate cubosomes through CD44 targeted drug delivery in NDEA-induced hepatic carcinoma.	imatinib	39-47	CD44 molecule (Indian blood group)	Homo sapiens	75-79
35624462-0	2022	The HSP90 inhibitor KW-2478 depletes the malignancy of BCR/ABL and overcomes the imatinib-resistance caused by BCR/ABL amplification.	imatinib	81-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-118
35630697-2	2022	The newly designed and synthesized compounds are structurally related to nilotinib (NIL), a second-generation oral TKI, and to a series of imatinib (IM)-based TKIs, previously reported by our research group, these latter characterized by a hybrid structure between TKIs and heme oxygenase-1 (HO-1) inhibitors.	imatinib	139-147	heme oxygenase 1	Homo sapiens	274-290
35443205-0	2022	Pharmacological PDGFRbeta inhibitors imatinib and sunitinib cause human brain pericyte death in vitro.	imatinib	37-45	platelet derived growth factor receptor beta	Homo sapiens	16-25
35443205-3	2022	Some anti-cancer agents, like imatinib, target platelet-derived growth factor receptor-beta (PDGFRbeta).	imatinib	30-38	platelet derived growth factor receptor beta	Homo sapiens	47-91
35443205-3	2022	Some anti-cancer agents, like imatinib, target platelet-derived growth factor receptor-beta (PDGFRbeta).	imatinib	30-38	platelet derived growth factor receptor beta	Homo sapiens	93-102
35443205-7	2022	Imatinib and sunitinib, but not orantinib, inhibited PDGFRbeta phosphorylation in pericytes.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	53-62
35630697-2	2022	The newly designed and synthesized compounds are structurally related to nilotinib (NIL), a second-generation oral TKI, and to a series of imatinib (IM)-based TKIs, previously reported by our research group, these latter characterized by a hybrid structure between TKIs and heme oxygenase-1 (HO-1) inhibitors.	imatinib	139-147	heme oxygenase 1	Homo sapiens	292-296
35625893-2	2022	In chronic myeloid leukemia (CML), imatinib resistance has been associated with changes in BCR-ABL1 and intracellular drug concentration, controlled by SLC and ABC transporters.	imatinib	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-99
35585158-1	2022	Although KIT-mutant GISTs can be effectively treated with tyrosine kinase inhibitors (TKIs), many patients develop resistance to imatinib mesylate (IM) as well as the FDA-approved later-line agents sunitinib, regorafenib and ripretinib.	imatinib	129-146	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	9-12
35585158-1	2022	Although KIT-mutant GISTs can be effectively treated with tyrosine kinase inhibitors (TKIs), many patients develop resistance to imatinib mesylate (IM) as well as the FDA-approved later-line agents sunitinib, regorafenib and ripretinib.	imatinib	148-150	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	9-12
35551463-2	2022	The approval of BCR::ABL1 tyrosine kinase inhibitors (TKI) such as imatinib, dasatinib, nilotinib and ponatinib marked a milestone in targeted therapy only for a subset of patients carrying the translocation t(9;22)(q34;q11).	imatinib	67-75	BCR activator of RhoGEF and GTPase	Homo sapiens	16-19
35551463-2	2022	The approval of BCR::ABL1 tyrosine kinase inhibitors (TKI) such as imatinib, dasatinib, nilotinib and ponatinib marked a milestone in targeted therapy only for a subset of patients carrying the translocation t(9;22)(q34;q11).	imatinib	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-25
35302171-0	2022	TRIB2 regulates the expression of miR-33a-5p through the ERK/c-Fos pathway to affect the imatinib resistance of chronic myeloid leukemia cells.	imatinib	89-97	tribbles pseudokinase 2	Mus musculus	0-5
35349049-3	2022	Imatinib is first-line treatment for unresectable gastrointestinal stromal tumors (GISTs) unless they harbor a PDGFRA D842V mutation; it is recommended to escalate imatinib to twice daily dosing for KIT exon 9 mutant tumors.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	111-117
35349049-3	2022	Imatinib is first-line treatment for unresectable gastrointestinal stromal tumors (GISTs) unless they harbor a PDGFRA D842V mutation; it is recommended to escalate imatinib to twice daily dosing for KIT exon 9 mutant tumors.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	199-202
35551036-3	2022	Nevertheless, inevitable drug resistance of Imatinib has occurred frequently in clinical due to the several mutations in the BCR-ABL kinase.	imatinib	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
35551036-4	2022	Subsequently, the second-generation of tyrosine kinase inhibitors (TKIs) against BCR-ABL was developed to address the mutants of Imatinib resistance, except T315I.	imatinib	129-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
35149540-5	2022	To do so, three drugs were selected: nelfinavir (P-gp substrate), efavirenz (BCRP substrate), and imatinib (P-gp/BCRP substrate).	imatinib	98-106	phosphoglycolate phosphatase	Homo sapiens	108-112
35149540-5	2022	To do so, three drugs were selected: nelfinavir (P-gp substrate), efavirenz (BCRP substrate), and imatinib (P-gp/BCRP substrate).	imatinib	98-106	BCR pseudogene 1	Homo sapiens	113-117
35149540-10	2022	Significance Statement The in vivo Kp,uu,fetal of nelfinavir (P-gp substrate), efavirenz (BCRP substrate), and imatinib (P-gp and BCRP substrate) was successfully estimated using m-f- PBPK modeling.	imatinib	111-119	phosphoglycolate phosphatase	Homo sapiens	121-125
35302171-0	2022	TRIB2 regulates the expression of miR-33a-5p through the ERK/c-Fos pathway to affect the imatinib resistance of chronic myeloid leukemia cells.	imatinib	89-97	mitogen-activated protein kinase 1	Mus musculus	57-60
35302171-0	2022	TRIB2 regulates the expression of miR-33a-5p through the ERK/c-Fos pathway to affect the imatinib resistance of chronic myeloid leukemia cells.	imatinib	89-97	FBJ osteosarcoma oncogene	Mus musculus	61-66
35132195-2	2022	Among them, IKZF1 deletion was associated with poor prognosis in patients treated with imatinib-based or dasatinib-based regimens.	imatinib	87-95	IKAROS family zinc finger 1	Homo sapiens	12-17
35217782-2	2022	The discovery of KIT mutations as the first and most prevalent drivers of GIST and the subsequent development of the first KIT tyrosine kinase inhibitor (TKI), imatinib, revolutionized the treatment of patients with this disease.	imatinib	160-168	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	17-20
35367722-0	2022	LncRNA CCAT2 expression at diagnosis predicts imatinib response in chronic phase chronic myeloid leukemia patients.	imatinib	46-54	colon cancer associated transcript 2	Homo sapiens	7-12
35367722-3	2022	We aimed to examine the expression of lncRNA colon cancer-associated transcript 2 (CCAT2) in CML patients, as well as to correlate CCAT2 expression with response to imatinib therapy.	imatinib	165-173	colon cancer associated transcript 2	Homo sapiens	131-136
35367722-9	2022	LncRNA CCAT2 is highly expressed in the peripheral blood of CML patients, and the enhanced expression at diagnosis is linked to imatinib resistance.	imatinib	128-136	colon cancer associated transcript 2	Homo sapiens	7-12
35367722-10	2022	CCAT2 is expected to become a reliable molecular marker for predicting imatinib response in chronic phase CML patients.	imatinib	71-79	colon cancer associated transcript 2	Homo sapiens	0-5
35217782-2	2022	The discovery of KIT mutations as the first and most prevalent drivers of GIST and the subsequent development of the first KIT tyrosine kinase inhibitor (TKI), imatinib, revolutionized the treatment of patients with this disease.	imatinib	160-168	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	123-126
35528149-0	2022	Imatinib Mesylate Reduces Neurotrophic Factors and pERK and pAKT Expression in Urinary Bladder of Female Mice With Cyclophosphamide-Induced Cystitis.	imatinib	0-17	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	51-55
35573746-5	2022	The current gREST/REUS simulation protocols are tested for three kinase-inhibitor systems: c-Src kinase with PP1, c-Src kinase with Dasatinib, and c-Abl kinase with Imatinib.	imatinib	165-173	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-152
35451495-0	2022	AADAC promotes therapeutic activity of cisplatin and imatinib against ovarian cancer cells.	imatinib	53-61	arylacetamide deacetylase	Homo sapiens	0-5
35451495-9	2022	Both cisplatin and imatinib suppressed cancer cell malignant progression, while overexpressed AADAC synergistically enhanced such inhibition.	imatinib	19-27	arylacetamide deacetylase	Homo sapiens	94-99
35528149-1	2022	Imatinib mesylate is a tyrosine kinase inhibitor that inhibits platelet-derived growth factor receptor (PDGFR)-alpha, -beta, stem cell factor receptor (c-KIT), and BCR-ABL.	imatinib	0-17	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	63-123
35528149-1	2022	Imatinib mesylate is a tyrosine kinase inhibitor that inhibits platelet-derived growth factor receptor (PDGFR)-alpha, -beta, stem cell factor receptor (c-KIT), and BCR-ABL.	imatinib	0-17	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	152-157
35528149-8	2022	Imatinib prevention significantly (0.0001 <= p <= 0.05) reduced expression for all mediators examined except NGF, whereas imatinib treatment was without effect.	imatinib	0-8	nerve growth factor	Mus musculus	109-112
35528149-9	2022	Imatinib prevention and treatment significantly (0.0001 <= p <= 0.05) reduced pERK and pAKT expression in the upper LP (U. LP) and deeper LP (D. LP) in female mice with 4 h CYP-induced cystitis.	imatinib	0-8	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	78-82
35444236-6	2022	Administration of the well-known OXPHOS inhibitor metformin eradicated CML stem/progenitor cells and re-sensitized CD34+ CML cells to imatinib in vitro and in patient-derived tumor xenograft murine model.	imatinib	134-142	CD34 molecule	Homo sapiens	115-119
35443725-3	2022	The purpose of this study was to test metabolic modulation as a potential strategy to overcome imatinib resistance based on the possible crosstalk between BCR-ABL signaling and metabolic changes in CML.	imatinib	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-162
35144161-7	2022	Genetic variations in ABCG2, SLCO1B3, and SLCO1A2 may play important roles in the safety and pharmacokinetics of imatinib in Japanese patients with GIST, although a replication study is necessary for validation.	imatinib	113-121	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	22-27
35421941-8	2022	BCR/ABL1 specific TaqMan probe based qRT-PCR was used for assessing the molecular response of CML patients on imatinib therapy.	imatinib	110-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-8
35421941-10	2022	RESULTS: We observed that promoter hydroxymethylation of DAPK1, RIZ1, P16INK4A, RASSF1A and p14ARFARF genes characterize advanced CML disease and poor imatinib respondents.	imatinib	151-159	death associated protein kinase 1	Homo sapiens	57-62
35421941-10	2022	RESULTS: We observed that promoter hydroxymethylation of DAPK1, RIZ1, P16INK4A, RASSF1A and p14ARFARF genes characterize advanced CML disease and poor imatinib respondents.	imatinib	151-159	Ras association domain family member 1	Homo sapiens	80-87
35421941-11	2022	Although, cytokine signalling (SOCS1) gene was hypermethylated in advanced stages of CML and accumulated in patients with poor imatinib response, but the differences were not statistically significant.	imatinib	127-135	suppressor of cytokine signaling 1	Homo sapiens	31-36
35421941-12	2022	Moreover, we found hypermethylation of p14ARF, RASSF1 and p16INK4A genes and cytokine signalling gene (SOCS1) significantly associated with poor overall survival of CML patients on imatinib therapy.	imatinib	181-189	cyclin dependent kinase inhibitor 2A	Homo sapiens	39-45
35421941-12	2022	Moreover, we found hypermethylation of p14ARF, RASSF1 and p16INK4A genes and cytokine signalling gene (SOCS1) significantly associated with poor overall survival of CML patients on imatinib therapy.	imatinib	181-189	Ras association domain family member 1	Homo sapiens	47-53
35421941-12	2022	Moreover, we found hypermethylation of p14ARF, RASSF1 and p16INK4A genes and cytokine signalling gene (SOCS1) significantly associated with poor overall survival of CML patients on imatinib therapy.	imatinib	181-189	cyclin dependent kinase inhibitor 2A	Homo sapiens	58-66
35421941-12	2022	Moreover, we found hypermethylation of p14ARF, RASSF1 and p16INK4A genes and cytokine signalling gene (SOCS1) significantly associated with poor overall survival of CML patients on imatinib therapy.	imatinib	181-189	suppressor of cytokine signaling 1	Homo sapiens	103-108
35421941-14	2022	CONCLUSION: In this study, we report that promoter hydroxymethylation of DAPK1, RIZ1, P16INK4A, RASSF1A and p14ARFARF genes is a characteristic feature of CML disease progressions, defines poor imatinib respondents and poor overall survival of CML patients to imatinib therapy.	imatinib	194-202	Ras association domain family member 1	Homo sapiens	96-103
35421941-14	2022	CONCLUSION: In this study, we report that promoter hydroxymethylation of DAPK1, RIZ1, P16INK4A, RASSF1A and p14ARFARF genes is a characteristic feature of CML disease progressions, defines poor imatinib respondents and poor overall survival of CML patients to imatinib therapy.	imatinib	260-268	Ras association domain family member 1	Homo sapiens	96-103
35388061-8	2022	We utilized a system to quantify in real-time cell-cell membrane fusion mediated by the SARS-CoV-2 surface protein, Spike, and its receptor, hACE2, to demonstrate that imatinib inhibits this process in an Abl1 and Abl2 independent manner.	imatinib	168-176	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	116-121
35388061-8	2022	We utilized a system to quantify in real-time cell-cell membrane fusion mediated by the SARS-CoV-2 surface protein, Spike, and its receptor, hACE2, to demonstrate that imatinib inhibits this process in an Abl1 and Abl2 independent manner.	imatinib	168-176	angiotensin converting enzyme 2	Homo sapiens	141-146
35388061-8	2022	We utilized a system to quantify in real-time cell-cell membrane fusion mediated by the SARS-CoV-2 surface protein, Spike, and its receptor, hACE2, to demonstrate that imatinib inhibits this process in an Abl1 and Abl2 independent manner.	imatinib	168-176	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	205-209
35388061-8	2022	We utilized a system to quantify in real-time cell-cell membrane fusion mediated by the SARS-CoV-2 surface protein, Spike, and its receptor, hACE2, to demonstrate that imatinib inhibits this process in an Abl1 and Abl2 independent manner.	imatinib	168-176	ABL proto-oncogene 2, non-receptor tyrosine kinase	Homo sapiens	214-218
35388061-9	2022	Furthermore, cellular thermal shift assay revealed a direct imatinib-Spike interaction that affects Spike susceptibility to trypsin digest.	imatinib	60-68	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	69-74
35388061-9	2022	Furthermore, cellular thermal shift assay revealed a direct imatinib-Spike interaction that affects Spike susceptibility to trypsin digest.	imatinib	60-68	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	100-105
35388061-10	2022	Collectively, our data suggest that imatinib inhibits Spike mediated viral entry by an off-target mechanism.	imatinib	36-44	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	54-59
35190838-0	2022	Imatinib-induced hepatotoxicity via oxidative stress and activation of NLRP3 inflammasome: an in vitro and in vivo study.	imatinib	0-8	NLR family, pyrin domain containing 3	Rattus norvegicus	71-76
35410141-7	2022	The combination of preoperative Imatinib mesylate chemotherapy and tumor excision was accompanied by significant remission of proteinuria, and IgE level decreasing, without immunosuppressivetherapy.	imatinib	32-40	immunoglobulin heavy constant epsilon	Homo sapiens	143-146
35379145-7	2022	In 2001, the BCR-ABL kinase inhibitor imatinib came out, and that opened the new era of targeted therapy for CML.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
35333695-0	2022	Restoration of miR-23a expression by chidamide sensitizes CML cells to imatinib treatment with concomitant downregulation of CRYAB.	imatinib	71-79	crystallin alpha B	Homo sapiens	125-130
35333695-2	2022	In this report, we aimed to investigate the roles of miR-23a in the regulation of imatinib mesylate (IM) sensitivity in CML cells and the possible mechanisms involved in this process.	imatinib	82-99	microRNA 23a	Homo sapiens	53-60
35333695-3	2022	We demonstrated that the expression of miR-23a was markedly low in bone marrow mononuclear cells from patients in whom IM treatment had failed and imatinib-resistant K562/G01 cells when compared to patients with optimal responses and imatinib-sensitive K562 cells, respectively.	imatinib	147-155	microRNA 23a	Homo sapiens	39-46
35333695-3	2022	We demonstrated that the expression of miR-23a was markedly low in bone marrow mononuclear cells from patients in whom IM treatment had failed and imatinib-resistant K562/G01 cells when compared to patients with optimal responses and imatinib-sensitive K562 cells, respectively.	imatinib	234-242	microRNA 23a	Homo sapiens	39-46
35333695-4	2022	Overexpression of miR-23a was shown to induce apoptosis of K562/G01 cells and sensitize these cells to imatinib treatment.	imatinib	103-111	microRNA 23a	Homo sapiens	18-25
35144161-7	2022	Genetic variations in ABCG2, SLCO1B3, and SLCO1A2 may play important roles in the safety and pharmacokinetics of imatinib in Japanese patients with GIST, although a replication study is necessary for validation.	imatinib	113-121	solute carrier organic anion transporter family member 1B3	Homo sapiens	29-36
35144161-7	2022	Genetic variations in ABCG2, SLCO1B3, and SLCO1A2 may play important roles in the safety and pharmacokinetics of imatinib in Japanese patients with GIST, although a replication study is necessary for validation.	imatinib	113-121	solute carrier organic anion transporter family member 1A2	Homo sapiens	42-49
35419359-12	2022	As for therapeutic correlations, SLC1A5 was related to the efficacy of dasatinib, sunitinib, sorafenib, and imatinib but may not predict that of radiotherapy, chemotherapeutic drugs, and immune checkpoints inhibitors (ICIs).	imatinib	108-116	solute carrier family 1 (neutral amino acid transporter), member 5	Mus musculus	33-39
35038545-9	2022	CONCLUSIONS: These results suggest that the hnRNPK/Beclin1 signaling pathway may play a role in shaping imatinib resistance in Ph+ ALL cells.	imatinib	104-112	heterogeneous nuclear ribonucleoprotein K	Homo sapiens	44-50
35038545-9	2022	CONCLUSIONS: These results suggest that the hnRNPK/Beclin1 signaling pathway may play a role in shaping imatinib resistance in Ph+ ALL cells.	imatinib	104-112	beclin 1	Homo sapiens	51-58
35129779-4	2022	Imatinib is the only TKI whose absorption depends on both influx (OCT1 and OATP1A2) and efflux (ABCB1 and ABCG2) transporters, whereas the others rely only on efflux transporters.	imatinib	0-8	POU class 2 homeobox 1	Homo sapiens	66-70
35129779-4	2022	Imatinib is the only TKI whose absorption depends on both influx (OCT1 and OATP1A2) and efflux (ABCB1 and ABCG2) transporters, whereas the others rely only on efflux transporters.	imatinib	0-8	solute carrier organic anion transporter family member 1A2	Homo sapiens	75-82
35129779-4	2022	Imatinib is the only TKI whose absorption depends on both influx (OCT1 and OATP1A2) and efflux (ABCB1 and ABCG2) transporters, whereas the others rely only on efflux transporters.	imatinib	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	96-101
35129779-4	2022	Imatinib is the only TKI whose absorption depends on both influx (OCT1 and OATP1A2) and efflux (ABCB1 and ABCG2) transporters, whereas the others rely only on efflux transporters.	imatinib	0-8	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	106-111
35194937-0	2022	Nintedanib overcomes drug resistance from upregulation of FGFR signalling and imatinib-induced KIT mutations in gastrointestinal stromal tumours.	imatinib	78-86	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	95-98
35219798-11	2022	Imatinib, an inhibitor of tyrosine kinase c-Abl, significantly downregulated the elevated expression levels of p-YAPY357, p-p73Y99 and cleaved caspase-3 (p < 0.05) caused by BPA and then ameliorated the cell index of P19 cells in the BPA-treated group.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase S homeolog	Xenopus laevis	42-47
35219798-11	2022	Imatinib, an inhibitor of tyrosine kinase c-Abl, significantly downregulated the elevated expression levels of p-YAPY357, p-p73Y99 and cleaved caspase-3 (p < 0.05) caused by BPA and then ameliorated the cell index of P19 cells in the BPA-treated group.	imatinib	0-8	caspase 3, gene 2 L homeolog	Xenopus laevis	143-152
35219798-11	2022	Imatinib, an inhibitor of tyrosine kinase c-Abl, significantly downregulated the elevated expression levels of p-YAPY357, p-p73Y99 and cleaved caspase-3 (p < 0.05) caused by BPA and then ameliorated the cell index of P19 cells in the BPA-treated group.	imatinib	0-8	cyclin-dependent kinase inhibitor 2D S homeolog	Xenopus laevis	217-220
35038545-0	2022	hnRNPK/Beclin1 signaling regulates autophagy to promote imatinib resistance in Philadelphia chromosome-positive acute lymphoblastic leukemia cells.	imatinib	56-64	heterogeneous nuclear ribonucleoprotein K	Homo sapiens	0-6
35038545-0	2022	hnRNPK/Beclin1 signaling regulates autophagy to promote imatinib resistance in Philadelphia chromosome-positive acute lymphoblastic leukemia cells.	imatinib	56-64	beclin 1	Homo sapiens	7-14
35038545-1	2022	BACKGROUND: This study sought to clarify the role of hnRNPK as a regulator of imatinib resistance in Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL).	imatinib	78-86	heterogeneous nuclear ribonucleoprotein K	Homo sapiens	53-59
35038545-5	2022	RESULTS: Imatinib-resistant Ph+ ALL cell lines and patient bone marrow samples exhibited significant hnRNPK overexpression.	imatinib	9-17	heterogeneous nuclear ribonucleoprotein K	Homo sapiens	101-107
35038545-6	2022	The knockdown of hnRNPK increased the imatinib sensitivity of these tumor cells and decreased in vivo tumor burden in a xenograft model system as evidenced by a reduction in tumor volume.	imatinib	38-46	heterogeneous nuclear ribonucleoprotein K	Homo sapiens	17-23
35038545-7	2022	Levels of LC3I/IIand Beclin1, but not p-ERK and mTOR, were consistent with the regulatory activity of hnRNPK.Electronmicroscopy revealed that imatinib-resistant cells harbored significantly more autophagic vacuoles relative to wild-type cells, while hnRNPK knockdown reduced the number of these vacuoles.	imatinib	142-150	beclin 1	Homo sapiens	21-28
35038545-7	2022	Levels of LC3I/IIand Beclin1, but not p-ERK and mTOR, were consistent with the regulatory activity of hnRNPK.Electronmicroscopy revealed that imatinib-resistant cells harbored significantly more autophagic vacuoles relative to wild-type cells, while hnRNPK knockdown reduced the number of these vacuoles.	imatinib	142-150	heterogeneous nuclear ribonucleoprotein K	Homo sapiens	102-108
35038545-7	2022	Levels of LC3I/IIand Beclin1, but not p-ERK and mTOR, were consistent with the regulatory activity of hnRNPK.Electronmicroscopy revealed that imatinib-resistant cells harbored significantly more autophagic vacuoles relative to wild-type cells, while hnRNPK knockdown reduced the number of these vacuoles.	imatinib	142-150	heterogeneous nuclear ribonucleoprotein K	Homo sapiens	250-256
35050937-9	2022	Finally, in patients with BRAF/NRAS/NF1 wild-type melanoma, imatinib or nilotinib can be effective in cKIT mutant melanoma.	imatinib	60-68	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	26-30
35313299-0	2022	MiR-199a-3p Overexpression Suppressed Cell Proliferation and Sensitized Chronic Myeloid Leukaemia Cells to Imatinib by Inhibiting mTOR Signalling.	imatinib	107-115	microRNA 199a-1	Homo sapiens	0-11
35313299-0	2022	MiR-199a-3p Overexpression Suppressed Cell Proliferation and Sensitized Chronic Myeloid Leukaemia Cells to Imatinib by Inhibiting mTOR Signalling.	imatinib	107-115	mechanistic target of rapamycin kinase	Homo sapiens	130-134
35313299-4	2022	We aimed to analyse the role and mechanism of miR-199a-3p in regulating imatinib resistance in CML.	imatinib	72-80	microRNA 199a-1	Homo sapiens	46-57
35313299-11	2022	Both miR-199a-3p overexpression and mTOR silencing inhibited CML cell proliferation, promoted CML cell apoptosis and sensitized these cells to imatinib.	imatinib	143-151	microRNA 199a-1	Homo sapiens	5-16
35313299-11	2022	Both miR-199a-3p overexpression and mTOR silencing inhibited CML cell proliferation, promoted CML cell apoptosis and sensitized these cells to imatinib.	imatinib	143-151	mechanistic target of rapamycin kinase	Homo sapiens	36-40
35313299-12	2022	mTOR silencing reversed the promoting effect of miR-199a-3p inhibition on the proliferation of CML cells and the inhibitory effects on cell apoptosis and sensitivity to imatinib.	imatinib	169-177	mechanistic target of rapamycin kinase	Homo sapiens	0-4
35313299-12	2022	mTOR silencing reversed the promoting effect of miR-199a-3p inhibition on the proliferation of CML cells and the inhibitory effects on cell apoptosis and sensitivity to imatinib.	imatinib	169-177	microRNA 199a-1	Homo sapiens	48-59
35313299-14	2022	CONCLUSION: MiR-199a-3p suppressed cell propagation, facilitated apoptosis of CML cells and sensitized CML cells to imatinib by downregulating mTOR signalling.	imatinib	116-124	microRNA 199a-1	Homo sapiens	12-23
35313299-14	2022	CONCLUSION: MiR-199a-3p suppressed cell propagation, facilitated apoptosis of CML cells and sensitized CML cells to imatinib by downregulating mTOR signalling.	imatinib	116-124	mechanistic target of rapamycin kinase	Homo sapiens	143-147
35340014-0	2022	Myeloid Neoplasm with PCM1-PDGFRB Transcript Responded to Low-Dose Imatinib: One Case Report with Literature Review.	imatinib	67-75	pericentriolar material 1	Homo sapiens	22-26
35340014-0	2022	Myeloid Neoplasm with PCM1-PDGFRB Transcript Responded to Low-Dose Imatinib: One Case Report with Literature Review.	imatinib	67-75	platelet derived growth factor receptor beta	Homo sapiens	27-33
35399514-8	2022	Our data demonstrate that: 1) c-Abl is activated in-vitro as well as in-vivo NPA models; 2) imatinib, a clinical c-Abl inhibitor, reduces autophagy-lysosomal pathway alterations, restores autophagy flux, and lowers sphingomyelin accumulation in NPA patient fibroblasts and NPA neuronal models and 3) chronic treatment with nilotinib and neurotinib, two c-Abl inhibitors with differences in blood-brain barrier penetrance and target binding mode, show further benefits.	imatinib	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-35
35399514-8	2022	Our data demonstrate that: 1) c-Abl is activated in-vitro as well as in-vivo NPA models; 2) imatinib, a clinical c-Abl inhibitor, reduces autophagy-lysosomal pathway alterations, restores autophagy flux, and lowers sphingomyelin accumulation in NPA patient fibroblasts and NPA neuronal models and 3) chronic treatment with nilotinib and neurotinib, two c-Abl inhibitors with differences in blood-brain barrier penetrance and target binding mode, show further benefits.	imatinib	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-118
35399514-8	2022	Our data demonstrate that: 1) c-Abl is activated in-vitro as well as in-vivo NPA models; 2) imatinib, a clinical c-Abl inhibitor, reduces autophagy-lysosomal pathway alterations, restores autophagy flux, and lowers sphingomyelin accumulation in NPA patient fibroblasts and NPA neuronal models and 3) chronic treatment with nilotinib and neurotinib, two c-Abl inhibitors with differences in blood-brain barrier penetrance and target binding mode, show further benefits.	imatinib	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	353-358
35337107-1	2022	Imatinib (IMT) is the first-in-class BCR-ABL commercial tyrosine kinase inhibitor (TKI).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
35337107-1	2022	Imatinib (IMT) is the first-in-class BCR-ABL commercial tyrosine kinase inhibitor (TKI).	imatinib	10-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
35150639-0	2022	Imatinib and methazolamide ameliorate COVID-19-induced metabolic complications via elevating ACE2 enzymatic activity and inhibiting viral entry.	imatinib	0-8	angiotensin converting enzyme 2	Homo sapiens	93-97
35150639-4	2022	By using structure-based high-throughput virtual screening and connectivity map database, followed with experimental validations, we identify imatinib, methazolamide, and harpagoside as direct enzymatic activators of ACE2.	imatinib	142-150	angiotensin converting enzyme 2	Homo sapiens	217-221
35150639-5	2022	Imatinib and methazolamide remarkably improve metabolic perturbations in vivo in an ACE2-dependent manner under the insulin-resistant state and SARS-CoV-2-infected state.	imatinib	0-8	angiotensin converting enzyme 2	Homo sapiens	84-88
35150639-5	2022	Imatinib and methazolamide remarkably improve metabolic perturbations in vivo in an ACE2-dependent manner under the insulin-resistant state and SARS-CoV-2-infected state.	imatinib	0-8	insulin	Homo sapiens	116-123
35050937-9	2022	Finally, in patients with BRAF/NRAS/NF1 wild-type melanoma, imatinib or nilotinib can be effective in cKIT mutant melanoma.	imatinib	60-68	NRAS proto-oncogene, GTPase	Homo sapiens	31-35
35050937-9	2022	Finally, in patients with BRAF/NRAS/NF1 wild-type melanoma, imatinib or nilotinib can be effective in cKIT mutant melanoma.	imatinib	60-68	neurofibromin 1	Homo sapiens	36-39
35183792-0	2022	The synergistic therapeutic effect of Imatinib and Protein Kinase CK2 Inhibition correlates with PI3K-AKT activation in gastrointestinal stromal tumors.	imatinib	38-46	AKT serine/threonine kinase 1	Homo sapiens	102-105
35150639-7	2022	Taken together, our study shows that enzymatic activation of ACE2 via imatinib, methazolamide, or harpagoside may be a conceptually new strategy to treat metabolic sequelae of COVID-19.	imatinib	70-78	angiotensin converting enzyme 2	Homo sapiens	61-65
35220926-8	2022	Molecular dynamics simulations verified that imatinib interacts with RBD residues that are critical for ACE2 binding.	imatinib	45-53	angiotensin converting enzyme 2	Homo sapiens	104-108
35205374-0	2022	Impact of Variants in the ATIC and ARID5B Genes on Therapeutic Failure with Imatinib in Patients with Chronic Myeloid Leukemia.	imatinib	76-84	5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase	Homo sapiens	26-30
35182693-0	2022	Imatinib disturbs lysosomal function and morphology and impairs the activity of mTORC1 in human hepatocyte cell lines.	imatinib	0-8	CREB regulated transcription coactivator 1	Mus musculus	80-86
35182693-5	2022	In HepG2 cells, lapatinib and imatinib raised the lysosomal pH and destabilized the lysosomal membrane, thereby impairing lysosomal proteolytic activity such as cathepsin B processing.	imatinib	30-38	cathepsin B	Homo sapiens	161-172
35182693-6	2022	Imatinib activated the transcription factor EB (TFEB), a regulator of lysosomal biogenesis and function, as demonstrated by nuclear TFEB accumulation and increased expression of TFEB-target genes.	imatinib	0-8	transcription factor EB	Homo sapiens	23-46
35182693-6	2022	Imatinib activated the transcription factor EB (TFEB), a regulator of lysosomal biogenesis and function, as demonstrated by nuclear TFEB accumulation and increased expression of TFEB-target genes.	imatinib	0-8	transcription factor EB	Homo sapiens	48-52
35182693-6	2022	Imatinib activated the transcription factor EB (TFEB), a regulator of lysosomal biogenesis and function, as demonstrated by nuclear TFEB accumulation and increased expression of TFEB-target genes.	imatinib	0-8	transcription factor EB	Homo sapiens	132-136
35182693-6	2022	Imatinib activated the transcription factor EB (TFEB), a regulator of lysosomal biogenesis and function, as demonstrated by nuclear TFEB accumulation and increased expression of TFEB-target genes.	imatinib	0-8	transcription factor EB	Homo sapiens	178-182
35182693-7	2022	Because of lysosomal dysfunction, imatinib impaired mTORC1 activation, a protein complex activated on the lysosomal surface, which explained TFEB activation.	imatinib	34-42	CREB regulated transcription coactivator 1	Mus musculus	52-58
35182693-7	2022	Because of lysosomal dysfunction, imatinib impaired mTORC1 activation, a protein complex activated on the lysosomal surface, which explained TFEB activation.	imatinib	34-42	transcription factor EB	Homo sapiens	141-145
35182693-8	2022	HepG2 cells treated with imatinib showed increased levels of MAP1LC3A/B-II and of ATG13 (S318) phosphorylation, indicating induction of autophagy due to TFEB activation.	imatinib	25-33	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	61-69
35182693-8	2022	HepG2 cells treated with imatinib showed increased levels of MAP1LC3A/B-II and of ATG13 (S318) phosphorylation, indicating induction of autophagy due to TFEB activation.	imatinib	25-33	calcium voltage-gated channel subunit alpha1 E	Homo sapiens	70-74
35182693-8	2022	HepG2 cells treated with imatinib showed increased levels of MAP1LC3A/B-II and of ATG13 (S318) phosphorylation, indicating induction of autophagy due to TFEB activation.	imatinib	25-33	autophagy related 13	Homo sapiens	82-87
35182693-8	2022	HepG2 cells treated with imatinib showed increased levels of MAP1LC3A/B-II and of ATG13 (S318) phosphorylation, indicating induction of autophagy due to TFEB activation.	imatinib	25-33	transcription factor EB	Homo sapiens	153-157
35205374-0	2022	Impact of Variants in the ATIC and ARID5B Genes on Therapeutic Failure with Imatinib in Patients with Chronic Myeloid Leukemia.	imatinib	76-84	AT-rich interaction domain 5B	Homo sapiens	35-41
35205374-2	2022	The first-line treatment for CML is imatinib, a tyrosine kinase inhibitor that acts on the BCR-ABL protein.	imatinib	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
35205374-7	2022	In conclusion, we show that variants in the ATIC and ARIDB5 gene, never screened in previous studies, could potentially influence the therapeutic response to imatinib in patients treated for CML.	imatinib	158-166	5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase	Homo sapiens	44-48
35122213-10	2022	Finally, we show that treatment with a combination therapy that enhances endogenous fibrinolysis by inhibiting PAI-1 with MDI-2268 and reduces BBB permeability by inhibiting tPA-mediated PDGFRalpha signaling with imatinib significantly reduces infarct size compared to vehicle-treated mice and to mice with either treatment alone.	imatinib	213-221	plasminogen activator, tissue	Mus musculus	174-177
35154723-1	2022	Describe a novel use for a kinase inhibitor, imatinib, in young children with a known activated somatic mutation in PDGFR-beta.	imatinib	45-53	platelet derived growth factor receptor alpha	Homo sapiens	116-126
35120552-12	2022	Inhibiting the activation of c-kit by imatinib remarkably suppressed the proliferation and promoted the apoptosis of ESCs.	imatinib	38-46	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	29-34
35122213-10	2022	Finally, we show that treatment with a combination therapy that enhances endogenous fibrinolysis by inhibiting PAI-1 with MDI-2268 and reduces BBB permeability by inhibiting tPA-mediated PDGFRalpha signaling with imatinib significantly reduces infarct size compared to vehicle-treated mice and to mice with either treatment alone.	imatinib	213-221	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	187-197
35120552-13	2022	Additionally, the phosphorylation of AKT and expression of Cyclin D1, which were closely related with cellular growth, were distinctly lessened after treating with imatinib.	imatinib	164-172	AKT serine/threonine kinase 1	Homo sapiens	37-40
35120552-13	2022	Additionally, the phosphorylation of AKT and expression of Cyclin D1, which were closely related with cellular growth, were distinctly lessened after treating with imatinib.	imatinib	164-172	cyclin D1	Homo sapiens	59-68
35174150-1	2022	Gastrointestinal stromal tumor (GIST) is the most common mesenchymal tumor in the gastrointestinal tracts and a model for the targeted therapy of solid tumors because of the oncogenic driver mutations in KIT and PDGDRA genes, which could be effectively inhibited by the very first targeted agent, imatinib mesylate.	imatinib	297-305	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	204-207
35123611-0	2022	(The Relationship between MicroRNA Expression Profiling in Imatinib-Resistant Cell Line K562/G and Potential Mechanism through FOXO3/Bcl-6 Signaling Pathway).	imatinib	59-67	forkhead box O3	Homo sapiens	127-132
35123611-0	2022	(The Relationship between MicroRNA Expression Profiling in Imatinib-Resistant Cell Line K562/G and Potential Mechanism through FOXO3/Bcl-6 Signaling Pathway).	imatinib	59-67	BCL6 transcription repressor	Homo sapiens	133-138
35123611-11	2022	CONCLUSION: The FOXO3/Bcl-6 signaling pathway contributes to imatinib resistance in K562/G cell line, and the miRNA expression profiles showed significant differences between K562/G and K562 cells.	imatinib	61-69	forkhead box O3	Homo sapiens	16-21
35123611-11	2022	CONCLUSION: The FOXO3/Bcl-6 signaling pathway contributes to imatinib resistance in K562/G cell line, and the miRNA expression profiles showed significant differences between K562/G and K562 cells.	imatinib	61-69	BCL6 transcription repressor	Homo sapiens	22-27
34985875-6	2022	The sensor was successfully applied to quantify c-Abl activity in the brain tissue of AD transgenic mice, and the interaction between c-Abl and Abeta in AD mice was explored by administering the c-Abl inhibitor (imatinib) and the agonist (DPH).	imatinib	212-220	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	134-139
35091542-0	2022	HucMSC exosomes promoted imatinib-induced apoptosis in K562-R cells via a miR-145a-5p/USP6/GLS1 axis.	imatinib	25-33	ubiquitin specific peptidase 6	Homo sapiens	86-90
35091542-0	2022	HucMSC exosomes promoted imatinib-induced apoptosis in K562-R cells via a miR-145a-5p/USP6/GLS1 axis.	imatinib	25-33	glutaminase	Homo sapiens	91-95
35091542-7	2022	USP6 was significantly upregulated in imatinib (IM)-resistant clinical samples compared with IM-sensitive samples.	imatinib	38-46	ubiquitin specific peptidase 6	Homo sapiens	0-4
34985875-6	2022	The sensor was successfully applied to quantify c-Abl activity in the brain tissue of AD transgenic mice, and the interaction between c-Abl and Abeta in AD mice was explored by administering the c-Abl inhibitor (imatinib) and the agonist (DPH).	imatinib	212-220	amyloid beta (A4) precursor protein	Mus musculus	144-149
34985875-6	2022	The sensor was successfully applied to quantify c-Abl activity in the brain tissue of AD transgenic mice, and the interaction between c-Abl and Abeta in AD mice was explored by administering the c-Abl inhibitor (imatinib) and the agonist (DPH).	imatinib	212-220	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	195-200
35057108-2	2022	Targeted therapies based on tyrosine kinase inhibitors (TKIs), such as imatinib, dasatinib, nilotinib, bosutinib, and ponatinib, have revolutionized the treatment of BCR-ABL1-driven leukemia, particularly chronic myeloid leukemia (CML).	imatinib	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-174
35038826-0	2022	Whole-genome and Transcriptome Sequencing Identified NOTCH2 and HES1 as Potential Markers of Response to Imatinib in Desmoid Tumor (Aggressive Fibromatosis): A Phase II Trial Study.	imatinib	105-113	notch receptor 2	Homo sapiens	53-59
35038826-0	2022	Whole-genome and Transcriptome Sequencing Identified NOTCH2 and HES1 as Potential Markers of Response to Imatinib in Desmoid Tumor (Aggressive Fibromatosis): A Phase II Trial Study.	imatinib	105-113	hes family bHLH transcription factor 1	Homo sapiens	64-68
35038826-4	2022	Here, we describe potential roles of NOTCH2 and HES1 in clinical response to imatinib at genome and transcriptome levels.	imatinib	77-85	notch receptor 2	Homo sapiens	37-43
35038826-4	2022	Here, we describe potential roles of NOTCH2 and HES1 in clinical response to imatinib at genome and transcriptome levels.	imatinib	77-85	hes family bHLH transcription factor 1	Homo sapiens	48-52
35038826-9	2022	With gene-wise functional analyses, we detected significant correlation between recurrent NOTCH2 noncoding mutations and clinical response to imatinib.	imatinib	142-150	notch receptor 2	Homo sapiens	90-96
35038826-15	2022	Our results show that HES1, regulated by NOTCH2, as an indicator of sensitivity to imatinib, and an important therapeutic consideration for desmoid tumor.	imatinib	83-91	hes family bHLH transcription factor 1	Homo sapiens	22-26
35022428-6	2022	Intriguingly, IRAK1/4 inhibitors attenuate PD-L1 expression on CML LSCs, and blocking PD-L1 together with imatinib also effectively eliminates CML LSCs in the presence of T cell immunity.	imatinib	106-114	interleukin 1 receptor associated kinase 1	Homo sapiens	14-21
35053574-0	2022	Introduction of Mutant GNAQ into Endothelial Cells Induces a Vascular Malformation Phenotype with Therapeutic Response to Imatinib.	imatinib	122-130	G protein subunit alpha q	Homo sapiens	23-27
35053574-7	2022	Since c-Kit is targeted by the FDA-approved drug imatinib, we tested the ability of imatinib on the phenotype of the vascular malformations in vivo.	imatinib	49-57	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	6-11
35053574-9	2022	Imatinib may be useful in the treatment of human vascular malformations that express c-Kit, including Sturge-Weber syndrome.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	85-90
35022428-6	2022	Intriguingly, IRAK1/4 inhibitors attenuate PD-L1 expression on CML LSCs, and blocking PD-L1 together with imatinib also effectively eliminates CML LSCs in the presence of T cell immunity.	imatinib	106-114	CD274 molecule	Homo sapiens	43-48
34980123-0	2022	A novel imatinib-upregulated long noncoding RNA plays a critical role in inhibition of tumor growth induced by Abl oncogenes.	imatinib	8-16	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	111-114
34587239-3	2022	We first detected an ETV6-SCFD2 fusion by targeted RNA sequencing in a patient with t(4;12)(q12;p13) who had previously been diagnosed with an ETV6-PDGFRA fusion by FISH analysis but failed to respond to imatinib.	imatinib	204-212	ETS variant transcription factor 6	Homo sapiens	21-25
34587239-3	2022	We first detected an ETV6-SCFD2 fusion by targeted RNA sequencing in a patient with t(4;12)(q12;p13) who had previously been diagnosed with an ETV6-PDGFRA fusion by FISH analysis but failed to respond to imatinib.	imatinib	204-212	sec1 family domain containing 2	Homo sapiens	26-31
35070996-4	2021	In addition, miR-1301 is related to the anti-tumor effect of epirubicin on osteosarcoma and imatinib on chronic myeloid leukemia(CML) and can enhance the cisplatin sensitivity of ovarian cancer.	imatinib	92-100	microRNA 1301	Homo sapiens	13-21
35059434-15	2021	The IC50 scores of Sorafenib, Navitoclax, Veliparib, Luminespib, and Imatinib were found to be lower in BTBD10 high-expressing HCC group.	imatinib	69-77	BTB domain containing 10	Homo sapiens	104-110
34980123-5	2022	Abl-transformed cell survival and xenografted tumor growth in mice were evaluated to dissect the role of imatinib-upregulated lncRNA 1 (IUR1) in Abl-induced tumorigenesis.	imatinib	105-113	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	145-148
34980123-10	2022	Interestingly, it was significantly induced in Abl-positive leukemic cells treated by imatinib.	imatinib	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
34407970-2	2022	Tyrosine kinase inhibitor benefit is progressively less after imatinib failure.	imatinib	62-70	TXK tyrosine kinase	Homo sapiens	0-15
34980779-5	2022	Furthermore, frequency of interferon-gamma+ (IFN-gamma+) CD8+ T cells was increased in imatinib-treated CT26 tumors than control tumors, indicating induction of antitumor immunity by imatinib.	imatinib	87-95	interferon gamma	Mus musculus	26-42
34980779-5	2022	Furthermore, frequency of interferon-gamma+ (IFN-gamma+) CD8+ T cells was increased in imatinib-treated CT26 tumors than control tumors, indicating induction of antitumor immunity by imatinib.	imatinib	87-95	interferon gamma	Mus musculus	45-60
34980779-5	2022	Furthermore, frequency of interferon-gamma+ (IFN-gamma+) CD8+ T cells was increased in imatinib-treated CT26 tumors than control tumors, indicating induction of antitumor immunity by imatinib.	imatinib	183-191	interferon gamma	Mus musculus	26-42
34980779-5	2022	Furthermore, frequency of interferon-gamma+ (IFN-gamma+) CD8+ T cells was increased in imatinib-treated CT26 tumors than control tumors, indicating induction of antitumor immunity by imatinib.	imatinib	183-191	interferon gamma	Mus musculus	45-60
34533850-10	2022	Identification of rearranged PDGFRA or PDGFRB is critical because of the exquisite responsiveness of these diseases to imatinib.	imatinib	119-127	platelet derived growth factor receptor alpha	Homo sapiens	29-35
34533850-10	2022	Identification of rearranged PDGFRA or PDGFRB is critical because of the exquisite responsiveness of these diseases to imatinib.	imatinib	119-127	platelet derived growth factor receptor beta	Homo sapiens	39-45
34983047-7	2022	These characteristics may explain the limited activity of the tyrosine kinase inhibitor imatinib in the adjuvant setting in KIT exon 9-mutant GISTs, as well as their lower sensitivity to standard dose imatinib in the advanced setting.	imatinib	88-96	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	124-127
33848847-9	2021	c-Kit inhibition with both imatinib and monoclonal blocking antibody reduced expression of ARG-1, iNOS, PD-L1, and SAA3.	imatinib	27-35	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-5
35125711-4	2022	Moreover, BKM120 robustly enhanced the growth-suppressive effect of imatinib through p21-mediated induction of G2/M cell cycle arrest and induction of apoptotic cell death.	imatinib	68-76	H3 histone pseudogene 16	Homo sapiens	85-88
35125712-15	2022	Also, S. VEGF levels can be used to monitor patients on imatinib therapy and identify those who might benefit from antiangiogenesis therapy.	imatinib	56-64	vascular endothelial growth factor A	Homo sapiens	9-13
33984486-0	2021	AKR1C3 decreased CML sensitivity to Imatinib in bone marrow microenvironment via dysregulation of miR-379-5p.	imatinib	36-44	aldo-keto reductase family 1 member C3	Homo sapiens	0-6
33984486-0	2021	AKR1C3 decreased CML sensitivity to Imatinib in bone marrow microenvironment via dysregulation of miR-379-5p.	imatinib	36-44	microRNA 379	Mus musculus	98-105
33984486-7	2021	The CML murine model intravenous inoculated with K562-OE-vector and K562-OE-AKR1C3 cells were established to estimate the effect of AKR1C3 inhibitor Indomethacin on Imatinib resistance.	imatinib	165-173	aldo-keto reductase family 1 member C3	Homo sapiens	132-138
33984486-10	2021	And, the soft agar colony assay and Annexin V/PI were used to validate the effect of miR-379-5p in AKR1C3 induced Imatinib resistance.	imatinib	114-122	microRNA 379	Mus musculus	85-92
33984486-10	2021	And, the soft agar colony assay and Annexin V/PI were used to validate the effect of miR-379-5p in AKR1C3 induced Imatinib resistance.	imatinib	114-122	aldo-keto reductase family 1 member C3	Homo sapiens	99-105
33984486-12	2021	AKR1C3 decreased Imatinib activity in K562 and KU812 cells, while inhibition of AKR1C3 could enhance Imatinib sensitivity in vitro study.	imatinib	17-25	aldo-keto reductase family 1 member C3	Homo sapiens	0-6
33984486-12	2021	AKR1C3 decreased Imatinib activity in K562 and KU812 cells, while inhibition of AKR1C3 could enhance Imatinib sensitivity in vitro study.	imatinib	101-109	aldo-keto reductase family 1 member C3	Homo sapiens	80-86
33984486-13	2021	Furthermore, murine model results showed combination use of AKR1C3 inhibitor Indomethacin effectively prolong mice survival, indicating that AKR1C3 is a promising target to enhance Imatinib treatment.	imatinib	181-189	aldo-keto reductase family 1 member C3	Homo sapiens	60-66
33984486-13	2021	Furthermore, murine model results showed combination use of AKR1C3 inhibitor Indomethacin effectively prolong mice survival, indicating that AKR1C3 is a promising target to enhance Imatinib treatment.	imatinib	181-189	aldo-keto reductase family 1 member C3	Homo sapiens	141-147
33984486-16	2021	Further, gain of miR-379-5p rescued the imatinib resistance induced by AKR1C3 overexpression in CML cells.	imatinib	40-48	microRNA 379	Mus musculus	17-24
33984486-16	2021	Further, gain of miR-379-5p rescued the imatinib resistance induced by AKR1C3 overexpression in CML cells.	imatinib	40-48	aldo-keto reductase family 1 member C3	Homo sapiens	71-77
33844974-0	2021	Effect of l-carnitine on cardiotoxicity and apoptosis induced by imatinib through PDGF/ PPARgamma /MAPK pathways.	imatinib	65-73	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	88-97
33783002-1	2021	Imatinib (IM) is a pharmaceutical drug that inhibits tyrosine kinase enzymes that are responsible for the activation of many proteins by signal transduction cascades as c-Abl, c-Kit and the platelet-derived growth factor (PDGF) receptor.	imatinib	0-8	steroid sulfatase	Homo sapiens	166-170
33783002-1	2021	Imatinib (IM) is a pharmaceutical drug that inhibits tyrosine kinase enzymes that are responsible for the activation of many proteins by signal transduction cascades as c-Abl, c-Kit and the platelet-derived growth factor (PDGF) receptor.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-174
33783002-1	2021	Imatinib (IM) is a pharmaceutical drug that inhibits tyrosine kinase enzymes that are responsible for the activation of many proteins by signal transduction cascades as c-Abl, c-Kit and the platelet-derived growth factor (PDGF) receptor.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	176-181
33783002-1	2021	Imatinib (IM) is a pharmaceutical drug that inhibits tyrosine kinase enzymes that are responsible for the activation of many proteins by signal transduction cascades as c-Abl, c-Kit and the platelet-derived growth factor (PDGF) receptor.	imatinib	10-12	steroid sulfatase	Homo sapiens	166-170
33783002-1	2021	Imatinib (IM) is a pharmaceutical drug that inhibits tyrosine kinase enzymes that are responsible for the activation of many proteins by signal transduction cascades as c-Abl, c-Kit and the platelet-derived growth factor (PDGF) receptor.	imatinib	10-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-174
33783002-1	2021	Imatinib (IM) is a pharmaceutical drug that inhibits tyrosine kinase enzymes that are responsible for the activation of many proteins by signal transduction cascades as c-Abl, c-Kit and the platelet-derived growth factor (PDGF) receptor.	imatinib	10-12	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	176-181
33848847-9	2021	c-Kit inhibition with both imatinib and monoclonal blocking antibody reduced expression of ARG-1, iNOS, PD-L1, and SAA3.	imatinib	27-35	arginase 1	Homo sapiens	91-96
33848847-9	2021	c-Kit inhibition with both imatinib and monoclonal blocking antibody reduced expression of ARG-1, iNOS, PD-L1, and SAA3.	imatinib	27-35	inositol-3-phosphate synthase 1	Homo sapiens	98-102
33848847-9	2021	c-Kit inhibition with both imatinib and monoclonal blocking antibody reduced expression of ARG-1, iNOS, PD-L1, and SAA3.	imatinib	27-35	CD274 molecule	Homo sapiens	104-109
33848847-9	2021	c-Kit inhibition with both imatinib and monoclonal blocking antibody reduced expression of ARG-1, iNOS, PD-L1, and SAA3.	imatinib	27-35	serum amyloid A3, pseudogene	Homo sapiens	115-119
33403501-4	2021	In human K562 cells and in murine Ba/F3 cells, engineered to express either wild-type BCR-ABL1 or the imatinib-resistant BCR-ABL1T315I mutant, NT157 inhibited BCR-ABL1, IGF1R, IRS1/2, PI3K/AKT/mTOR, and STAT3/5 signaling, increased CDKN1A, FOS and JUN tumor suppressor gene expression, and reduced MYC and BCL2 oncogenes.	imatinib	102-110	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	125-129
34031270-11	2021	To translate this finding to the clinic, we used the most relevant multikinase inhibitor, imatinib, to inhibit PDGFRA signaling.	imatinib	90-98	platelet derived growth factor receptor alpha	Homo sapiens	111-117
34045202-4	2021	The patient was diagnosed as myeloproliferative neoplasm with a FIP1L1-PDGFRA fusion gene, and successfully treated with the tyrosine kinase inhibitor, imatinib.	imatinib	152-160	factor interacting with PAPOLA and CPSF1	Homo sapiens	64-70
34045202-4	2021	The patient was diagnosed as myeloproliferative neoplasm with a FIP1L1-PDGFRA fusion gene, and successfully treated with the tyrosine kinase inhibitor, imatinib.	imatinib	152-160	platelet derived growth factor receptor alpha	Homo sapiens	71-77
34031270-13	2021	Our developed noninvasive apoptosis detection sensor (NIADS) indicated that imatinib induced cell apoptosis through caspase-3 activation.	imatinib	76-84	caspase 3	Homo sapiens	116-125
33753340-5	2021	The PDGFRbeta inhibitor imatinib, which has been approved for the treatment of malignant metastatic cancer, protected mice against JEV-induced lethality by decreasing the viral load in the brain, while abrogating the histopathological changes associated with JEV infection.	imatinib	24-32	platelet derived growth factor receptor, beta polypeptide	Mus musculus	4-13
34027663-7	2021	Further, chrysin treatment reverses the effects of the specific PDGFRalpha inhibitor imatinib on browning differentiation of stromal vascular fraction cells from SAT.	imatinib	85-93	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	64-74
34011155-7	2021	Overall, the results indicate that 3a-P1 is a promising drug candidate for the treatment of CML to overcome the imatinib-resistant T315I BCR-ABL mutation.	imatinib	112-120	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	141-144
33753340-6	2021	These findings demonstrated that PDGFRbeta is important in viral infection and provided evidence for the potential to develop imatinib as a therapeutic intervention against JEV infection.	imatinib	126-134	platelet derived growth factor receptor beta	Homo sapiens	33-42
33976882-1	2021	Dasatinib is a potent and effective second-generation oral tyrosine kinase inhibitor that is clinically indicated for the treatment of imatinib-resistant or imatinib-intolerant breakpoint cluster region-Abelson (BCR-ABL)-positive chronic myeloid leukaemia (CML) or for Philadelphia chromosome-positive acute lymphocytic leukaemia.	imatinib	157-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	212-219
33979467-0	2021	Positive response to imatinib in PDGFRB-related Kosaki overgrowth syndrome.	imatinib	21-29	platelet derived growth factor receptor beta	Homo sapiens	33-39
33848469-8	2021	Treatment with the Abl inhibitor imatinib increased NSC activation without impairing NSC maintenance in the middle-aged brain.	imatinib	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-22
33784254-9	2021	Accordingly, the exacerbated aneurysmal phenotype in Tbeta4-null mice was rescued upon treatment with the PDGFRbeta antagonist, Imatinib.	imatinib	128-136	transforming growth factor alpha regulated gene 3	Mus musculus	53-59
33784254-9	2021	Accordingly, the exacerbated aneurysmal phenotype in Tbeta4-null mice was rescued upon treatment with the PDGFRbeta antagonist, Imatinib.	imatinib	128-136	platelet derived growth factor receptor, beta polypeptide	Mus musculus	106-115
34026165-0	2021	Efficacy and safety of low-dose imatinib in an elderly patient with mixed phenotype acute leukemia with t(9;22)(q34;q11.2);BCR-ABL1.	imatinib	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-131
33952281-15	2021	Furthermore, imatinib treatment ameliorated serum protein leakage, oligodendrocyte progenitor cell (OPC) activation, endothelial transcytosis, microglial activation, and aberrant TGF-beta/Smad2 signaling activation.	imatinib	13-21	transforming growth factor alpha	Rattus norvegicus	179-187
33952281-15	2021	Furthermore, imatinib treatment ameliorated serum protein leakage, oligodendrocyte progenitor cell (OPC) activation, endothelial transcytosis, microglial activation, and aberrant TGF-beta/Smad2 signaling activation.	imatinib	13-21	SMAD family member 2	Rattus norvegicus	188-193
33582440-0	2021	Spectroscopic studies of simultaneous binding of cyclophosphamide and imatinib mesylate to human holo-transferrin.	imatinib	70-87	transferrin	Homo sapiens	102-113
33582440-5	2021	In this study the effect of cyclophosphamide on the interaction of imatinib mesylate with human holo-transferrin has been investigated.	imatinib	67-84	transferrin	Homo sapiens	101-112
33947686-2	2021	Imatinib, sunitinib, and regorafenib are available as first, second, and third-line targeted therapies, respectively, for metastatic or unresectable KIT-driven GIST.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	149-152
33947686-8	2021	Here we show that ripretinib treatment in combination with MEK inhibitors is effective at inducing and enhancing the apoptotic response and preventing growth of resistant colonies in both imatinib-sensitive and -resistant GIST cell lines, even after long-term removal of drugs.	imatinib	188-196	mitogen-activated protein kinase kinase 7	Homo sapiens	59-62
33150465-0	2021	Effective treatment with imatinib for acute B-lymphoblastic leukaemia with EBF1-PDGFRB fusion.	imatinib	25-33	EBF transcription factor 1	Homo sapiens	75-79
33150465-0	2021	Effective treatment with imatinib for acute B-lymphoblastic leukaemia with EBF1-PDGFRB fusion.	imatinib	25-33	platelet derived growth factor receptor beta	Homo sapiens	80-86
33893334-8	2021	Treatment with TKIs nilotinib and Imatinib Mesylate restored the expression of PTPRG in the WBCs of CML patients to levels observed in healthy controls.	imatinib	34-51	protein tyrosine phosphatase receptor type G	Homo sapiens	79-84
33978360-9	2021	Results: Expression of SIRT1 is increased in patients with imatinib resistance.	imatinib	59-67	sirtuin 1	Homo sapiens	23-28
33978360-11	2021	The inhibition of SIRT1 in CML causes increased sensitivity to imatinib.	imatinib	63-71	sirtuin 1	Homo sapiens	18-23
33390067-3	2021	The patient-derived Ph-like ALL RANBP2-ABL1 fusion gene was transduced into Ba/F3 cells and allowed to become resistant to the tyrosine kinase inhibitors (TKIs) imatinib or dasatinib, followed by secondary resistance to ponatinib.	imatinib	161-169	RAN binding protein 2	Homo sapiens	32-38
33390067-3	2021	The patient-derived Ph-like ALL RANBP2-ABL1 fusion gene was transduced into Ba/F3 cells and allowed to become resistant to the tyrosine kinase inhibitors (TKIs) imatinib or dasatinib, followed by secondary resistance to ponatinib.	imatinib	161-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-43
33947031-3	2021	METHODS: We examined CIP2A protein levels in diagnostic samples from the SPIRIT2 trial in 172 unselected patients, of whom 90 received imatinib and 82 dasatinib as first-line treatment.	imatinib	135-143	cellular inhibitor of PP2A	Homo sapiens	21-26
33995081-0	2021	ABCG2 Single Nucleotide Polymorphism Affects Imatinib Pharmacokinetics in Lower Alpha-1-Acid Glycoprotein Levels in Humans.	imatinib	45-53	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
33995081-1	2021	Imatinib is transported extracellularly by ABCB1 and ABCG2 efflux transporters and bound to alpha-1-acid glycoprotein (AGP) in the bloodstream.	imatinib	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	43-48
33995081-1	2021	Imatinib is transported extracellularly by ABCB1 and ABCG2 efflux transporters and bound to alpha-1-acid glycoprotein (AGP) in the bloodstream.	imatinib	0-8	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	53-58
33995081-2	2021	However, the clinical and pharmacokinetic effects of ABCB1 and ABCG2 on imatinib were inconsistent in the previous literature and have not been confirmed.	imatinib	72-80	ATP binding cassette subfamily B member 1	Homo sapiens	53-58
33995081-2	2021	However, the clinical and pharmacokinetic effects of ABCB1 and ABCG2 on imatinib were inconsistent in the previous literature and have not been confirmed.	imatinib	72-80	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	63-68
33995081-3	2021	Therefore, in the present study, we explored the effects of the ABCG2 and ABCB1 genetic polymorphisms on imatinib pharmacokinetics in association with plasma AGP levels in healthy subjects.	imatinib	105-113	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	64-69
33995081-3	2021	Therefore, in the present study, we explored the effects of the ABCG2 and ABCB1 genetic polymorphisms on imatinib pharmacokinetics in association with plasma AGP levels in healthy subjects.	imatinib	105-113	ATP binding cassette subfamily B member 1	Homo sapiens	74-79
33995081-7	2021	ABCG2 c.421C>A single nucleotide polymorphism showed a statistically significant effect on imatinib pharmacokinetics in low plasma AGP levels groups (<80 mg/dl); subjects with high plasma AGP levels (n = 5, >=80 mg/dl) were excluded.	imatinib	91-99	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
33995081-8	2021	The results indicate that plasma AGP levels and ABCG2 polymorphisms modulated imatinib pharmacokinetics; however, the effects of the ABCG2 transporter was masked at high plasma AGP levels.	imatinib	78-86	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	48-53
33995081-8	2021	The results indicate that plasma AGP levels and ABCG2 polymorphisms modulated imatinib pharmacokinetics; however, the effects of the ABCG2 transporter was masked at high plasma AGP levels.	imatinib	78-86	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	133-138
33549745-9	2021	Furthermore, its pharmacological inhibition with the FDA-approved drug Imatinib decreased RIPK3 signaling.	imatinib	71-79	receptor-interacting serine-threonine kinase 3	Mus musculus	90-95
33727226-1	2021	Oncogenic KIT or PDGFRA receptor tyrosine kinase mutations are compelling therapeutic targets in gastrointestinal stromal tumor (GIST), and treatment with the KIT/PDGFRA inhibitor imatinib is the standard of care for patients with advanced GIST.	imatinib	180-188	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	10-13
33727226-1	2021	Oncogenic KIT or PDGFRA receptor tyrosine kinase mutations are compelling therapeutic targets in gastrointestinal stromal tumor (GIST), and treatment with the KIT/PDGFRA inhibitor imatinib is the standard of care for patients with advanced GIST.	imatinib	180-188	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	159-162
33727226-1	2021	Oncogenic KIT or PDGFRA receptor tyrosine kinase mutations are compelling therapeutic targets in gastrointestinal stromal tumor (GIST), and treatment with the KIT/PDGFRA inhibitor imatinib is the standard of care for patients with advanced GIST.	imatinib	180-188	platelet derived growth factor receptor alpha	Homo sapiens	17-23
33727226-2	2021	Polyclonal emergence of KIT/PDGFRA secondary mutations is the main mechanism of imatinib progression, making it challenging to overcome KIT/PDGFRA-inhibitor resistance.	imatinib	80-88	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	24-27
33727226-2	2021	Polyclonal emergence of KIT/PDGFRA secondary mutations is the main mechanism of imatinib progression, making it challenging to overcome KIT/PDGFRA-inhibitor resistance.	imatinib	80-88	platelet derived growth factor receptor alpha	Homo sapiens	28-34
33727226-2	2021	Polyclonal emergence of KIT/PDGFRA secondary mutations is the main mechanism of imatinib progression, making it challenging to overcome KIT/PDGFRA-inhibitor resistance.	imatinib	80-88	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	136-139
33727226-2	2021	Polyclonal emergence of KIT/PDGFRA secondary mutations is the main mechanism of imatinib progression, making it challenging to overcome KIT/PDGFRA-inhibitor resistance.	imatinib	80-88	platelet derived growth factor receptor alpha	Homo sapiens	140-146
33727226-6	2021	CDK1 was critically required for advanced GIST, including imatinib-resistant GIST.	imatinib	58-66	cyclin dependent kinase 1	Homo sapiens	0-4
33947031-6	2021	Imatinib recipients with low CIP2A levels had a greater risk of treatment failure (p = 0.0008).	imatinib	0-8	cellular inhibitor of PP2A	Homo sapiens	29-34
33581133-0	2021	Discovery of a highly potent kinase inhibitor capable of overcoming multiple imatinib-resistant ABL mutants for chronic myeloid leukemia (CML).	imatinib	77-85	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	96-99
33924068-1	2021	Chronic myeloid leukemia (CML) develops due to the presence of the BCR-ABL1 protein, a target of tyrosine kinase inhibitors (TKIs), such as imatinib (IM), used in a CML therapy.	imatinib	140-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-75
33924068-1	2021	Chronic myeloid leukemia (CML) develops due to the presence of the BCR-ABL1 protein, a target of tyrosine kinase inhibitors (TKIs), such as imatinib (IM), used in a CML therapy.	imatinib	150-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-75
33662676-11	2021	Yet, immunoassays revealed a suppression of the STAT5 phosphorylation status by co-application of the most active derivatives with imatinib.	imatinib	131-139	signal transducer and activator of transcription 5A	Homo sapiens	48-53
33581133-2	2021	Although imatinib has achieved tremendous success as the first-line treatment for CML, the long-term application ultimately leads to resistance, primarily via various acquired mutations occurring in the BCR-ABL kinase.	imatinib	9-17	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	207-210
33524167-14	2021	Imatinib has a limited therapeutic role in SM; effective cytoreduction is limited to those with imatinib-sensitive KIT mutations.	imatinib	96-104	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	115-118
33843813-2	2022	Imatinib, a tyrosine kinase inhibitor, can trigger BMN during the treatment of malignant disease.	imatinib	0-8	TXK tyrosine kinase	Homo sapiens	12-27
33829606-3	2021	The objective of the present study was to assess the relationship between the XPC Ala499Val (rs2228000 C>T) and Lys939Gln (rs2228001 A>C) non-synonymous polymorphisms and susceptibility to CML pathogenesis, disease progression, and response to targeted therapeutic regimen, Imatinib Mesylate.	imatinib	274-282	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	78-81
33587348-10	2021	HULC overexpression increased imatinib resistance in K562 cells, and HULC depletion enhanced imatinib sensitivity in imatinib-resistant cells (K562-R).	imatinib	30-38	hepatocellular carcinoma up-regulated long non-coding RNA	Homo sapiens	0-4
33587348-0	2021	LncRNA highly upregulated in liver cancer regulates imatinib resistance in chronic myeloid leukemia via the miR-150-5p/MCL1 axis.	imatinib	52-60	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	119-123
33587348-10	2021	HULC overexpression increased imatinib resistance in K562 cells, and HULC depletion enhanced imatinib sensitivity in imatinib-resistant cells (K562-R).	imatinib	93-101	hepatocellular carcinoma up-regulated long non-coding RNA	Homo sapiens	69-73
33587348-10	2021	HULC overexpression increased imatinib resistance in K562 cells, and HULC depletion enhanced imatinib sensitivity in imatinib-resistant cells (K562-R).	imatinib	93-101	hepatocellular carcinoma up-regulated long non-coding RNA	Homo sapiens	69-73
33587348-12	2021	HULC contributed to imatinib resistance through regulation of miR-150-5p.	imatinib	20-28	hepatocellular carcinoma up-regulated long non-coding RNA	Homo sapiens	0-4
33587348-13	2021	MCL1 bound to miR-150-5p and reversed the effect of HULC on imatinib resistance.	imatinib	60-68	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	0-4
33587348-13	2021	MCL1 bound to miR-150-5p and reversed the effect of HULC on imatinib resistance.	imatinib	60-68	hepatocellular carcinoma up-regulated long non-coding RNA	Homo sapiens	52-56
33587348-15	2021	These findings indicated that HULC enhanced imatinib resistance in CML by modulating the miR-150-5p/MCL1 axis, providing a promising biomarker for CML.	imatinib	44-52	hepatocellular carcinoma up-regulated long non-coding RNA	Homo sapiens	30-34
33587348-15	2021	These findings indicated that HULC enhanced imatinib resistance in CML by modulating the miR-150-5p/MCL1 axis, providing a promising biomarker for CML.	imatinib	44-52	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	100-104
33539723-5	2021	These metabolic benefits are mimicked by treatment of obese mice with the PDGFR antagonist Imatinib, which promotes adipocyte hyperplasia and glucose tolerance in a progenitor cell PPARgamma-dependent manner.	imatinib	91-99	platelet derived growth factor receptor, beta polypeptide	Mus musculus	74-79
33556367-2	2021	SOR inhibits several human CYPs, including CYP2C8, which is a major enzyme in the elimination of oncology drugs like paclitaxel and imatinib.	imatinib	132-140	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	43-49
33539723-5	2021	These metabolic benefits are mimicked by treatment of obese mice with the PDGFR antagonist Imatinib, which promotes adipocyte hyperplasia and glucose tolerance in a progenitor cell PPARgamma-dependent manner.	imatinib	91-99	peroxisome proliferator activated receptor gamma	Mus musculus	181-190
33449152-6	2021	Functional analysis of these variants has led to the preclinical validation of tyrosine kinase inhibitors targeting PDGF receptors, such as imatinib, as a treatment for some of these conditions.	imatinib	140-148	platelet derived growth factor receptor beta	Homo sapiens	116-120
33903307-1	2021	INTRODUCTION: The advent of BCR-ABL1-targeted therapy with the tyrosine kinase inhibitor (TKI), for example, imatinib and nilotinib, marked a turning point in the therapy of chronic myeloid leukaemia (CML).	imatinib	109-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-36
33389076-3	2021	The aim of our study was to explore the feasibility of blocking KIT dimerisation upstream of the phosphorylation in imatinib-resistant GIST.	imatinib	116-124	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	64-67
33737510-5	2021	Patients with GIST with KIT or PDGFRA mutations sensitive to the tyrosine kinase inhibitor (TKI) imatinib that are at high risk of relapse have improved survival with adjuvant imatinib treatment.	imatinib	97-105	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	24-27
33743084-2	2021	Unfortunately, acquired c-kit mutations cause secondary resistance to imatinib in a median of 18-24 months.	imatinib	70-78	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	24-29
33743084-5	2021	The TKI avapritinib has been approved for metastatic GIST harboring the imatinib-resistant PDGFRA exon 18 mutation.	imatinib	72-80	platelet derived growth factor receptor alpha	Homo sapiens	91-97
32956651-2	2021	The identification of the COL1A1-PDGFB t(17;22) translocation activating the PDGF pathway led to the use of imatinib in unresectable DFSP, with a response rate of 36-80%.	imatinib	108-116	collagen type I alpha 1 chain	Homo sapiens	26-32
32956651-2	2021	The identification of the COL1A1-PDGFB t(17;22) translocation activating the PDGF pathway led to the use of imatinib in unresectable DFSP, with a response rate of 36-80%.	imatinib	108-116	platelet derived growth factor subunit B	Homo sapiens	33-38
33842339-5	2021	TKIs have revolutionized the current clinical approach, which involves combinations of imatinib plus standard chemotherapy that can abrogate the negative prognostic impact conferred by the presence of BCR/ABL1 rearrangement, resulting in the probability of event-free survival (EFS) being significantly better than that recorded in the pre-TKI era.	imatinib	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	205-209
33737510-5	2021	Patients with GIST with KIT or PDGFRA mutations sensitive to the tyrosine kinase inhibitor (TKI) imatinib that are at high risk of relapse have improved survival with adjuvant imatinib treatment.	imatinib	97-105	platelet derived growth factor receptor alpha	Homo sapiens	31-37
33737510-5	2021	Patients with GIST with KIT or PDGFRA mutations sensitive to the tyrosine kinase inhibitor (TKI) imatinib that are at high risk of relapse have improved survival with adjuvant imatinib treatment.	imatinib	176-184	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	24-27
33737510-5	2021	Patients with GIST with KIT or PDGFRA mutations sensitive to the tyrosine kinase inhibitor (TKI) imatinib that are at high risk of relapse have improved survival with adjuvant imatinib treatment.	imatinib	176-184	platelet derived growth factor receptor alpha	Homo sapiens	31-37
33707419-6	2021	It is the upregulation of Bcl2 that is involved in conferring Imatinib resistance to the CD34(+) LSCs.	imatinib	62-70	CD34 molecule	Homo sapiens	89-93
33451979-9	2021	HAND1 and BARX1 expression were superior predictors of relapse-free survival, as compared to standard risk stratification, and they predict progression-free survival on imatinib.	imatinib	169-177	heart and neural crest derivatives expressed 1	Homo sapiens	0-5
33451979-9	2021	HAND1 and BARX1 expression were superior predictors of relapse-free survival, as compared to standard risk stratification, and they predict progression-free survival on imatinib.	imatinib	169-177	BARX homeobox 1	Homo sapiens	10-15
33910311-0	2021	[CRISPR/Cas9-mediated microRNA-21 knockout increased imatinib sensitivity in chronic myeloid leukemia cells].	imatinib	53-61	microRNA 21	Homo sapiens	22-33
33910311-1	2021	Objective: To observe the effects of miR-21 knockout on proliferation and drug resistance in K562/G01 cells, and to preliminarily explore the mechanism of imatinib sensitivity by knocking out miR-21 in K562/G01 cells.	imatinib	155-163	microRNA 21	Homo sapiens	192-198
33910311-4	2021	Using western blot, we examined the potential mechanisms affecting imatinib sensitivity by knocking out miR-21 in K562/G01 cells.	imatinib	67-75	microRNA 21	Homo sapiens	104-110
33910311-8	2021	MiR-21 knockout increased the sensitivity of K562/G01 cells to imatinib, IC(50) of imatinib in WT, and 1#, 2#, 6# K562/G01 single-cell clones were (21.92+-1.36) micromol/ml, (3.98+-0.39) micromol/ml, (5.38+-1.01) micromol/ml, (9.24+-1.36) micromol/ml.	imatinib	63-71	microRNA 21	Homo sapiens	0-6
33910311-8	2021	MiR-21 knockout increased the sensitivity of K562/G01 cells to imatinib, IC(50) of imatinib in WT, and 1#, 2#, 6# K562/G01 single-cell clones were (21.92+-1.36) micromol/ml, (3.98+-0.39) micromol/ml, (5.38+-1.01) micromol/ml, (9.24+-1.36) micromol/ml.	imatinib	83-91	microRNA 21	Homo sapiens	0-6
33910311-10	2021	Conclusion: The knockout of miR-21 can suppress cell proliferation and improve sensitivity to imatinib in K562/G01 cells, which may be achieved by inhibiting the PI3K/AKT signaling pathway and BCR-ABL expression.	imatinib	94-102	microRNA 21	Homo sapiens	28-34
33910311-10	2021	Conclusion: The knockout of miR-21 can suppress cell proliferation and improve sensitivity to imatinib in K562/G01 cells, which may be achieved by inhibiting the PI3K/AKT signaling pathway and BCR-ABL expression.	imatinib	94-102	AKT serine/threonine kinase 1	Homo sapiens	167-170
33910311-10	2021	Conclusion: The knockout of miR-21 can suppress cell proliferation and improve sensitivity to imatinib in K562/G01 cells, which may be achieved by inhibiting the PI3K/AKT signaling pathway and BCR-ABL expression.	imatinib	94-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	193-200
33707419-0	2021	Exovesicular-Shh confers Imatinib resistance by upregulating Bcl2 expression in chronic myeloid leukemia with variant chromosomes.	imatinib	25-33	sonic hedgehog signaling molecule	Homo sapiens	13-16
33707419-0	2021	Exovesicular-Shh confers Imatinib resistance by upregulating Bcl2 expression in chronic myeloid leukemia with variant chromosomes.	imatinib	25-33	BCL2 apoptosis regulator	Homo sapiens	61-65
33707419-3	2021	Sonic hedgehog (Shh) signaling has been implicated in proliferation of this Imatinib-resistant CD34(+) LSCs.	imatinib	76-84	sonic hedgehog signaling molecule	Homo sapiens	0-14
33707419-7	2021	Sub-toxic doses of Bcl2 inhibitor or Shh inhibitor (<<IC50), when used as adjuvants along with Imatinib, can re-sensitize Shh signaling cells to Imatinib.	imatinib	95-103	BCL2 apoptosis regulator	Homo sapiens	19-23
33707419-3	2021	Sonic hedgehog (Shh) signaling has been implicated in proliferation of this Imatinib-resistant CD34(+) LSCs.	imatinib	76-84	sonic hedgehog signaling molecule	Homo sapiens	16-19
33707419-3	2021	Sonic hedgehog (Shh) signaling has been implicated in proliferation of this Imatinib-resistant CD34(+) LSCs.	imatinib	76-84	CD34 molecule	Homo sapiens	95-99
33707419-4	2021	Our work here identifies the molecular mechanism of Shh-mediated mutation-independent Imatinib resistance that is most relevant for treating CML-variants and non-compliant patients.	imatinib	86-94	sonic hedgehog signaling molecule	Homo sapiens	52-55
33707419-7	2021	Sub-toxic doses of Bcl2 inhibitor or Shh inhibitor (<<IC50), when used as adjuvants along with Imatinib, can re-sensitize Shh signaling cells to Imatinib.	imatinib	95-103	sonic hedgehog signaling molecule	Homo sapiens	37-40
33707419-6	2021	It is the upregulation of Bcl2 that is involved in conferring Imatinib resistance to the CD34(+) LSCs.	imatinib	62-70	BCL2 apoptosis regulator	Homo sapiens	26-30
33707419-7	2021	Sub-toxic doses of Bcl2 inhibitor or Shh inhibitor (<<IC50), when used as adjuvants along with Imatinib, can re-sensitize Shh signaling cells to Imatinib.	imatinib	95-103	sonic hedgehog signaling molecule	Homo sapiens	122-125
33707419-7	2021	Sub-toxic doses of Bcl2 inhibitor or Shh inhibitor (<<IC50), when used as adjuvants along with Imatinib, can re-sensitize Shh signaling cells to Imatinib.	imatinib	145-153	BCL2 apoptosis regulator	Homo sapiens	19-23
33707419-7	2021	Sub-toxic doses of Bcl2 inhibitor or Shh inhibitor (<<IC50), when used as adjuvants along with Imatinib, can re-sensitize Shh signaling cells to Imatinib.	imatinib	145-153	sonic hedgehog signaling molecule	Homo sapiens	37-40
33707419-7	2021	Sub-toxic doses of Bcl2 inhibitor or Shh inhibitor (<<IC50), when used as adjuvants along with Imatinib, can re-sensitize Shh signaling cells to Imatinib.	imatinib	145-153	sonic hedgehog signaling molecule	Homo sapiens	122-125
33289342-7	2021	At the transcriptional level, imatinib and sulfasalazine were found to synergistically down-regulate c-MET gene expression.	imatinib	30-38	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	101-106
33663368-7	2022	3c &3l were promoted in the CDK2/CyclinA2 Kinase assay against standard reference Imatinib.	imatinib	82-90	cyclin dependent kinase 2	Homo sapiens	28-32
33439175-3	2021	The efficient binding of imatinib to the aptamer was demonstrated by means of surface plasmon resonance (SPR) analysis, which allowed the development of a quantitative assay in the concentration range between 400 and 6000 ng mL-1 (0.7-10 muM), where a lower limit of quantification (LLOQ) of 400 ng mL-1 was achieved.	imatinib	25-33	L1 cell adhesion molecule	Mus musculus	225-229
33439175-3	2021	The efficient binding of imatinib to the aptamer was demonstrated by means of surface plasmon resonance (SPR) analysis, which allowed the development of a quantitative assay in the concentration range between 400 and 6000 ng mL-1 (0.7-10 muM), where a lower limit of quantification (LLOQ) of 400 ng mL-1 was achieved.	imatinib	25-33	L1 cell adhesion molecule	Mus musculus	299-303
33748144-3	2021	Although the use of the BCR-ABL tyrosine kinase inhibitors (TKIs), such as imatinib, nilotinib, dasatinib, bosutinib, and ponatinib have increased the overall survival of CML patients, their use is limited by drug resistance and severe adverse effects.	imatinib	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
33307872-1	2021	INTRODUCTION: 90% of gastrointestinal stromal tumors (GISTs) harbor an activating mutation in the KIT or PDGFRalpha oncogene, and these are known to confer imatinib sensitivity.	imatinib	156-164	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	98-101
33307872-1	2021	INTRODUCTION: 90% of gastrointestinal stromal tumors (GISTs) harbor an activating mutation in the KIT or PDGFRalpha oncogene, and these are known to confer imatinib sensitivity.	imatinib	156-164	platelet derived growth factor receptor alpha	Homo sapiens	105-115
33307872-3	2021	EXPERT OPINION: Several studies have shown that the response to imatinib in GIST patients mainly depends on the mutational status of KIT or PDGFRalpha.	imatinib	64-72	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	133-136
33307872-3	2021	EXPERT OPINION: Several studies have shown that the response to imatinib in GIST patients mainly depends on the mutational status of KIT or PDGFRalpha.	imatinib	64-72	platelet derived growth factor receptor alpha	Homo sapiens	140-150
33289342-0	2021	Sulfasalazine synergistically enhances the inhibitory effects of imatinib against hepatocellular carcinoma (HCC) cells by targeting NFkappaB, BCR/ABL, and PI3K/AKT signaling pathway-related proteins.	imatinib	65-73	nuclear factor kappa B subunit 1	Homo sapiens	132-140
33289342-0	2021	Sulfasalazine synergistically enhances the inhibitory effects of imatinib against hepatocellular carcinoma (HCC) cells by targeting NFkappaB, BCR/ABL, and PI3K/AKT signaling pathway-related proteins.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
33289342-0	2021	Sulfasalazine synergistically enhances the inhibitory effects of imatinib against hepatocellular carcinoma (HCC) cells by targeting NFkappaB, BCR/ABL, and PI3K/AKT signaling pathway-related proteins.	imatinib	65-73	AKT serine/threonine kinase 1	Homo sapiens	160-163
33289342-5	2021	The aim of this work was to assess the potential anticarcinogenic effects of imatinib and sulfasalazine alone or in combination on the human HCC cell lines, HEPG2 and Huh-7.	imatinib	77-85	MIR7-3 host gene	Homo sapiens	167-172
33607534-2	2021	Imatinib (IMA), a tyrosine kinase inhibitor of BCR-ABL, is used as a frontline treatment.Although IMA aids in killing a majority of leukemia cells, it may not kill CML stem cells which are the primary roots of disease and therapy resistance.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
33030616-11	2021	Imatinib and apatinib augmented the sensitivity of pyrotinib-resistant cells and xenografts to pyrotinib, by blocking SCF/c-kit signaling.	imatinib	0-8	KIT ligand	Homo sapiens	118-121
33030616-11	2021	Imatinib and apatinib augmented the sensitivity of pyrotinib-resistant cells and xenografts to pyrotinib, by blocking SCF/c-kit signaling.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	122-127
33607534-2	2021	Imatinib (IMA), a tyrosine kinase inhibitor of BCR-ABL, is used as a frontline treatment.Although IMA aids in killing a majority of leukemia cells, it may not kill CML stem cells which are the primary roots of disease and therapy resistance.	imatinib	10-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
33607534-9	2021	Moreover, combination of AZT/IMA suppressed cell viability, induced apoptosis and caspase3/7 activity more effectively and significantly compared to K562R cells treated with only IMA or AZT.	imatinib	29-32	caspase 3	Homo sapiens	82-92
33607534-10	2021	Furthermore, AZT and AZT/IMA combination decreased Pgp function in K562R cells in comparison with their controls.	imatinib	25-28	ATP binding cassette subfamily B member 1	Homo sapiens	51-54
33607534-11	2021	Based on qRT-PCR data, single AZT and combined AZT/IMA treatment also induced BAX/BCL-2 ratio significantly in both K562S and K562R cells.	imatinib	51-54	BCL2 associated X, apoptosis regulator	Homo sapiens	78-81
33607534-11	2021	Based on qRT-PCR data, single AZT and combined AZT/IMA treatment also induced BAX/BCL-2 ratio significantly in both K562S and K562R cells.	imatinib	51-54	BCL2 apoptosis regulator	Homo sapiens	82-87
33607534-13	2021	One of the mechanisms underlying the potent anticancer effect of combined AZT/IMA could be its ability to inhibit Pgp function and increase intracellular accumulation of IMA which leads to the induction of apoptosis in K562R cells.	imatinib	78-81	ATP binding cassette subfamily B member 1	Homo sapiens	114-117
33673554-0	2021	Type and Gene Location of KIT Mutations Predict Progression-Free Survival to First-Line Imatinib in Gastrointestinal Stromal Tumors: A Look into the Exon.	imatinib	88-96	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	26-29
33709282-3	2021	This study reports, the influence of GSTP1*B and GSTT1/GSTM1null polymorphisms in response to imatinib in CML patients in a Brazilian population.	imatinib	94-102	glutathione S-transferase pi 1	Homo sapiens	37-42
33709282-3	2021	This study reports, the influence of GSTP1*B and GSTT1/GSTM1null polymorphisms in response to imatinib in CML patients in a Brazilian population.	imatinib	94-102	glutathione S-transferase theta 1	Homo sapiens	49-54
33709282-3	2021	This study reports, the influence of GSTP1*B and GSTT1/GSTM1null polymorphisms in response to imatinib in CML patients in a Brazilian population.	imatinib	94-102	glutathione S-transferase mu 1	Homo sapiens	55-60
33709282-11	2021	The "G allele" of GSTP1*B, is associated with later cytogenetic response in imatinib therapy.	imatinib	76-84	glutathione S-transferase pi 1	Homo sapiens	18-23
33603171-7	2021	Given that CAF paracrine signaling modulated GIST biology, we directly targeted CAFs with a dual PI3K/mTOR inhibitor, which synergized with imatinib to increase tumor cell killing and in vivo disease response.	imatinib	140-148	mechanistic target of rapamycin kinase	Homo sapiens	102-106
33641024-4	2021	Interestingly, KIT/PDGFRA genotype predicts the response to first-line imatinib and to all tyrosine kinase inhibitors (TKIs) approved or in investigation after imatinib failure.	imatinib	71-79	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	15-18
33641024-4	2021	Interestingly, KIT/PDGFRA genotype predicts the response to first-line imatinib and to all tyrosine kinase inhibitors (TKIs) approved or in investigation after imatinib failure.	imatinib	71-79	platelet derived growth factor receptor alpha	Homo sapiens	19-25
33673554-5	2021	Our data showed a predictive impact of KIT exon 11 pathogenic variant on PFS to imatinib treatment: patients with deletion or insertion/deletion (delins) in 557/558 codons had a shorter PFS (median PFS: 24 months) compared to the patients with a deletion in other codons, or duplication/insertion/SNV (median PFS: 43 and 49 months, respectively) (p < 0.001).	imatinib	80-88	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	39-42
33641024-4	2021	Interestingly, KIT/PDGFRA genotype predicts the response to first-line imatinib and to all tyrosine kinase inhibitors (TKIs) approved or in investigation after imatinib failure.	imatinib	160-168	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	15-18
33641024-4	2021	Interestingly, KIT/PDGFRA genotype predicts the response to first-line imatinib and to all tyrosine kinase inhibitors (TKIs) approved or in investigation after imatinib failure.	imatinib	160-168	platelet derived growth factor receptor alpha	Homo sapiens	19-25
33565361-1	2022	BACKGROUND: Our study aimed to investigate the association between multidrug resistance (MDR1) C1236T, C3435T and G2677T/A polymorphisms and the response to imatinib (IM) in chronic myeloid leukemia (CML).	imatinib	157-165	ATP binding cassette subfamily B member 1	Homo sapiens	89-93
33714638-3	2021	PDGFRA/B-rearranged patients usually manifest as imatinib-sensitive myeloproliferative neoplasms (MPNs).	imatinib	49-57	platelet derived growth factor receptor alpha	Homo sapiens	0-6
33663081-18	2021	Patients bearing PDGFRB abnormality have a good response to imatinib.	imatinib	60-68	platelet derived growth factor receptor beta	Homo sapiens	17-23
33626861-0	2021	The EBF1-PDGFRB T681I mutation is highly resistant to imatinib and dasatinib in vitro and detectable in clinical samples prior to treatment.	imatinib	54-62	EBF transcription factor 1	Homo sapiens	4-8
33626861-0	2021	The EBF1-PDGFRB T681I mutation is highly resistant to imatinib and dasatinib in vitro and detectable in clinical samples prior to treatment.	imatinib	54-62	platelet derived growth factor receptor beta	Homo sapiens	9-15
33670651-5	2021	KIT exon 11 mutant patients were more favorable in responding to imatinib than those with exon 9 mutant or wild-type GISTs, and compared to non-KIT exon 11 mutant GISTs (p = 0.041).	imatinib	65-73	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
33571522-1	2021	We have previously shown that the tyrosine kinase inhibitors (TKIs) dasatinib and imatinib can protect salivary glands from irradiation (IR) damage without impacting tumor therapy.	imatinib	82-90	TXK tyrosine kinase	Homo sapiens	34-49
33561320-4	2021	Blockage of its expression in CD34+ cells and CML cell lines increased sensitivity to imatinib.	imatinib	86-94	CD34 molecule	Homo sapiens	30-34
33728144-7	2021	It was postulated that peritoneal inflammation had resulted in increased capillary permeability, which was further augmented by imatinib via inhibition of platelet-derived growth factor receptor (PDGFR), a tyrosine kinase known to play a significant physiological role in the regulation of interstitial fluid pressure and capillary permeability.	imatinib	128-136	platelet derived growth factor receptor beta	Homo sapiens	155-194
33562088-10	2021	Notably, Cisplatin (2 muM) and Imatinib (10 muM) at low concentrations significantly promoted tumoroid formation (cell aggregation) and increased Mmp9 promoter activity in mCRC LuM1/m9, while not cytotoxic to them.	imatinib	31-39	matrix metallopeptidase 9	Mus musculus	146-150
33728144-7	2021	It was postulated that peritoneal inflammation had resulted in increased capillary permeability, which was further augmented by imatinib via inhibition of platelet-derived growth factor receptor (PDGFR), a tyrosine kinase known to play a significant physiological role in the regulation of interstitial fluid pressure and capillary permeability.	imatinib	128-136	platelet derived growth factor receptor beta	Homo sapiens	196-201
33247506-9	2021	Blocking c-KIT signaling using Imatinib or ISCK03 reduced p-ELK1 expression and consequently decreased CEA levels in CRC cells, as did blocking the ERK1/2 pathway by U0126.	imatinib	31-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	9-14
33527482-0	2021	Expression of inducible NOS is indispensable for the antiproliferative and proapoptotic effect of imatinib in BCR-ABL positive cells.	imatinib	98-106	nitric oxide synthase 2	Homo sapiens	14-27
33527482-0	2021	Expression of inducible NOS is indispensable for the antiproliferative and proapoptotic effect of imatinib in BCR-ABL positive cells.	imatinib	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
33527482-2	2021	Targeting tyrosine kinase activity of BCR-ABL with imatinib is an effective therapy for the newly diagnosed CML patients; however, 20%-30% of the patients initially treated with imatinib eventually experience treatment failure.	imatinib	51-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
33527482-2	2021	Targeting tyrosine kinase activity of BCR-ABL with imatinib is an effective therapy for the newly diagnosed CML patients; however, 20%-30% of the patients initially treated with imatinib eventually experience treatment failure.	imatinib	178-186	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
33527482-4	2021	In the present study, we by undertaking a direct comparison of inducible NOS (iNOS) status in neutrophils from healthy volunteers, newly diagnosed, imatinib responder, and resistant CML patients as well as by conducting in vitro studies in K562 cells demonstrated that inhibition of BCR-ABL by imatinib or siRNA significantly enhanced NO generation and iNOS expression.	imatinib	148-156	nitric oxide synthase 2	Homo sapiens	63-76
33527482-4	2021	In the present study, we by undertaking a direct comparison of inducible NOS (iNOS) status in neutrophils from healthy volunteers, newly diagnosed, imatinib responder, and resistant CML patients as well as by conducting in vitro studies in K562 cells demonstrated that inhibition of BCR-ABL by imatinib or siRNA significantly enhanced NO generation and iNOS expression.	imatinib	148-156	nitric oxide synthase 2	Homo sapiens	78-82
33527482-5	2021	Indeed, patients exhibiting treatment failure or imatinib resistance were less likely to induce NO generation/iNOS expression.	imatinib	49-57	nitric oxide synthase 2	Homo sapiens	110-114
33527482-6	2021	Our findings further demonstrated that imatinib mediated antiproliferative and proapoptotic effect in BCR-ABL+ cells associated with enhanced iNOS expression, and it was significantly prevented in the presence of L-NAME, 1400W, or iNOS siRNA.	imatinib	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
33527482-6	2021	Our findings further demonstrated that imatinib mediated antiproliferative and proapoptotic effect in BCR-ABL+ cells associated with enhanced iNOS expression, and it was significantly prevented in the presence of L-NAME, 1400W, or iNOS siRNA.	imatinib	39-47	nitric oxide synthase 2	Homo sapiens	142-146
33527482-6	2021	Our findings further demonstrated that imatinib mediated antiproliferative and proapoptotic effect in BCR-ABL+ cells associated with enhanced iNOS expression, and it was significantly prevented in the presence of L-NAME, 1400W, or iNOS siRNA.	imatinib	39-47	nitric oxide synthase 2	Homo sapiens	231-235
33527482-7	2021	Overexpression of iNOS in K562 cells expectedly enhanced imatinib sensitivity on cytostasis and apoptosis, even at lower concentration (0.1 muM) of imatinib.	imatinib	57-65	nitric oxide synthase 2	Homo sapiens	18-22
33527482-7	2021	Overexpression of iNOS in K562 cells expectedly enhanced imatinib sensitivity on cytostasis and apoptosis, even at lower concentration (0.1 muM) of imatinib.	imatinib	148-156	nitric oxide synthase 2	Homo sapiens	18-22
33527482-8	2021	Mechanistically, imatinib or BCR-ABL siRNA following deglutathionylation of NF-kappaB, enhanced its binding to iNOS promoter and induced iNOS transcription.	imatinib	17-25	nuclear factor kappa B subunit 1	Homo sapiens	76-85
33527482-8	2021	Mechanistically, imatinib or BCR-ABL siRNA following deglutathionylation of NF-kappaB, enhanced its binding to iNOS promoter and induced iNOS transcription.	imatinib	17-25	nitric oxide synthase 2	Homo sapiens	111-115
33527482-8	2021	Mechanistically, imatinib or BCR-ABL siRNA following deglutathionylation of NF-kappaB, enhanced its binding to iNOS promoter and induced iNOS transcription.	imatinib	17-25	nitric oxide synthase 2	Homo sapiens	137-141
33527482-10	2021	Taken together, results obtained suggest that monitoring NO/iNOS level could be useful to identify patients likely to be responsive or resistant to imatinib and can be used to personalized alternative therapy.	imatinib	148-156	nitric oxide synthase 2	Homo sapiens	60-64
32918673-12	2021	Vascular TGF-beta1 expression was downregulated in both imatinib-treated and C-KO mice, along with sustained levels of MMP9.	imatinib	56-64	transforming growth factor, beta 1	Mus musculus	9-18
33639675-0	2021	Impact of Fas/Fasl Gene Polymorphisms on Susceptibility Risk and Imatinib Mesylate Treatment Response in Chronic Myeloid Leukaemia Patients.	imatinib	65-82	Fas ligand	Homo sapiens	14-18
33639675-1	2021	BACKGROUND: The FAS mediated apoptosis pathway involving the FAS and FASL genes plays a crucial role in the regulation of apoptotic cell death and imatinib mesylate (IM) mechanism of action.	imatinib	147-164	Fas ligand	Homo sapiens	69-73
33129954-2	2021	This study evaluated the combined effect of an anti-PD-1 antibody and a platelet-derived growth factor receptor inhibitor (imatinib) on CRC progression using an orthotopic transplanted mouse model that reproduced the three histological phenotypes of CRC (inflamed-, excluded-, and desert-type).	imatinib	123-131	receptor-like tyrosine kinase	Mus musculus	89-111
33129954-5	2021	In the mouse model, imatinib suppressed stromal reaction and increased sensitivity to anti-PD-1 treatment in excluded-type CRC.	imatinib	20-28	programmed cell death 1	Mus musculus	91-95
33247506-9	2021	Blocking c-KIT signaling using Imatinib or ISCK03 reduced p-ELK1 expression and consequently decreased CEA levels in CRC cells, as did blocking the ERK1/2 pathway by U0126.	imatinib	31-39	ETS transcription factor ELK1	Homo sapiens	60-64
33247506-9	2021	Blocking c-KIT signaling using Imatinib or ISCK03 reduced p-ELK1 expression and consequently decreased CEA levels in CRC cells, as did blocking the ERK1/2 pathway by U0126.	imatinib	31-39	CEA cell adhesion molecule 3	Homo sapiens	103-106
33598481-12	2020	Both sunitinib and imatinib pre-treatment increased Angiotensin II-induced intracellular Ca2+ mobilization, with only sunitinib resulting in a significant effect and also causing increased CaMKII activation via oxidation.	imatinib	19-27	angiotensinogen	Rattus norvegicus	52-66
33422470-0	2021	A Phase II Trial of Imatinib Mesylate as Maintenance Therapy for Patients With Newly Diagnosed C-kit-positive Acute Myeloid Leukemia.	imatinib	20-37	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	95-100
33172871-11	2021	This study reported for the first time that measurement of the circulating miR-146a expression at 14 days can predict the early response to imatinib treatment in patients with CML.	imatinib	140-148	microRNA 146a	Homo sapiens	75-83
33491750-0	2021	Exosomes released by imatinib-resistant K562 cells contain specific membrane markers, IFITM3, CD146 and CD36 and increase the survival of imatinib-sensitive cells in the presence of imatinib.	imatinib	21-29	interferon induced transmembrane protein 3	Homo sapiens	86-92
33491750-0	2021	Exosomes released by imatinib-resistant K562 cells contain specific membrane markers, IFITM3, CD146 and CD36 and increase the survival of imatinib-sensitive cells in the presence of imatinib.	imatinib	21-29	melanoma cell adhesion molecule	Homo sapiens	94-99
33491750-12	2021	Using flow cytometric analysis, it was possible to further demonstrate the potential of CD146 as a cell surface marker associated with imatinib resistance in K562 cells.	imatinib	135-143	melanoma cell adhesion molecule	Homo sapiens	88-93
32951102-6	2021	Because her ALL had been identified as BCR-ABL1-like ALL with CCDC88C-PDGFRB fusion, she was treated with imatinib for 2 months accompanied by 2 intrathecal methotrexate therapies, and 1 course of L-asparaginase, vincristine, and prednisolone in an outpatient setting.	imatinib	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-47
32951102-6	2021	Because her ALL had been identified as BCR-ABL1-like ALL with CCDC88C-PDGFRB fusion, she was treated with imatinib for 2 months accompanied by 2 intrathecal methotrexate therapies, and 1 course of L-asparaginase, vincristine, and prednisolone in an outpatient setting.	imatinib	106-114	coiled-coil domain containing 88C	Homo sapiens	62-69
32951102-6	2021	Because her ALL had been identified as BCR-ABL1-like ALL with CCDC88C-PDGFRB fusion, she was treated with imatinib for 2 months accompanied by 2 intrathecal methotrexate therapies, and 1 course of L-asparaginase, vincristine, and prednisolone in an outpatient setting.	imatinib	106-114	platelet derived growth factor receptor beta	Homo sapiens	70-76
32951102-7	2021	MRD analysis revealed potent efficacy of 2 months imatinib therapy; IgH MRD decreased from 1 x 10-2 to 1 x 10-3, and CCDC88C-PDGFRB/104ABL from 37.3 to 0.	imatinib	50-58	immunoglobulin heavy locus	Homo sapiens	68-71
32951102-7	2021	MRD analysis revealed potent efficacy of 2 months imatinib therapy; IgH MRD decreased from 1 x 10-2 to 1 x 10-3, and CCDC88C-PDGFRB/104ABL from 37.3 to 0.	imatinib	50-58	coiled-coil domain containing 88C	Homo sapiens	117-124
32951102-7	2021	MRD analysis revealed potent efficacy of 2 months imatinib therapy; IgH MRD decreased from 1 x 10-2 to 1 x 10-3, and CCDC88C-PDGFRB/104ABL from 37.3 to 0.	imatinib	50-58	platelet derived growth factor receptor beta	Homo sapiens	125-131
33172871-0	2021	Circulating miR-146a expression predicts early treatment response to imatinib in adult chronic myeloid leukemia.	imatinib	69-77	microRNA 146a	Homo sapiens	12-20
33172871-1	2021	This study aimed to investigate the prognostic role of circulating miR-146a in the prediction of early response to imatinib treatment in patients with chronic myeloid leukemia (CML).	imatinib	115-123	microRNA 146a	Homo sapiens	67-75
33172871-3	2021	BCR-ABL was assessed by quantitative rt-PCR at days 0 and 90 of imatinib therapy.	imatinib	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
33172871-4	2021	Circulating miR-146a levels were assessed by quantitative rt-PCR at days 0, 14 and 90 of imatinib therapy for patients and once for controls.	imatinib	89-97	microRNA 146a	Homo sapiens	12-20
33707832-10	2021	Also, results suggest that ABCB1 3435TT genotype increases imatinib resistance in CML and influence therapeutic outcome in B-ALL.	imatinib	59-67	ATP binding cassette subfamily B member 1	Homo sapiens	27-32
33172871-8	2021	The circulating miR-146a level was significantly lower in patients with CML than in healthy subjects and showed a significant rise after 14 days of imatinib treatment and an inverse correlation with BCR-ABL expression levels at 90 days.	imatinib	148-156	microRNA 146a	Homo sapiens	16-24
33416164-0	2021	TCF7 knockdown inhibits the imatinib resistance of chronic myeloid leukemia K562/G01 cells by neutralizing the Wnt/beta-catenin/TCF7/ABC transporter signaling axis.	imatinib	28-36	transcription factor 7	Homo sapiens	0-4
33416164-0	2021	TCF7 knockdown inhibits the imatinib resistance of chronic myeloid leukemia K562/G01 cells by neutralizing the Wnt/beta-catenin/TCF7/ABC transporter signaling axis.	imatinib	28-36	catenin beta 1	Homo sapiens	115-127
33416164-0	2021	TCF7 knockdown inhibits the imatinib resistance of chronic myeloid leukemia K562/G01 cells by neutralizing the Wnt/beta-catenin/TCF7/ABC transporter signaling axis.	imatinib	28-36	transcription factor 7	Homo sapiens	128-132
33416164-0	2021	TCF7 knockdown inhibits the imatinib resistance of chronic myeloid leukemia K562/G01 cells by neutralizing the Wnt/beta-catenin/TCF7/ABC transporter signaling axis.	imatinib	28-36	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	133-148
33416164-1	2021	Clinical resistance to ABL tyrosine kinase inhibitor (TKI) imatinib remains a critical issue in the treatment of chronic myeloid leukemia (CML).	imatinib	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-26
33416164-7	2021	Silencing of TCF7 downregulated the expression levels of CTNNB1, CCND1, and ABCC2, and therefore inhibited proliferation, weakened colony formation, and increased the drug sensitivity of imatinib-resistant cells.	imatinib	187-195	transcription factor 7	Homo sapiens	13-17
33416164-7	2021	Silencing of TCF7 downregulated the expression levels of CTNNB1, CCND1, and ABCC2, and therefore inhibited proliferation, weakened colony formation, and increased the drug sensitivity of imatinib-resistant cells.	imatinib	187-195	cyclin D1	Homo sapiens	65-70
33416164-7	2021	Silencing of TCF7 downregulated the expression levels of CTNNB1, CCND1, and ABCC2, and therefore inhibited proliferation, weakened colony formation, and increased the drug sensitivity of imatinib-resistant cells.	imatinib	187-195	ATP binding cassette subfamily C member 2	Homo sapiens	76-81
33416164-10	2021	In summary, our results highlight that the upregulation of Wnt/beta-catenin and ABC transporter signaling pathways induced by imatinib treatment of resistant cells confers imatinib resistance, and reveal that targeting TCF7 to regulate the Wnt/beta-catenin/TCF7/ABC transporter signaling axis may represent an effective strategy for overcoming imatinib resistance.	imatinib	126-134	catenin beta 1	Homo sapiens	63-75
33416164-10	2021	In summary, our results highlight that the upregulation of Wnt/beta-catenin and ABC transporter signaling pathways induced by imatinib treatment of resistant cells confers imatinib resistance, and reveal that targeting TCF7 to regulate the Wnt/beta-catenin/TCF7/ABC transporter signaling axis may represent an effective strategy for overcoming imatinib resistance.	imatinib	126-134	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	80-95
33416164-10	2021	In summary, our results highlight that the upregulation of Wnt/beta-catenin and ABC transporter signaling pathways induced by imatinib treatment of resistant cells confers imatinib resistance, and reveal that targeting TCF7 to regulate the Wnt/beta-catenin/TCF7/ABC transporter signaling axis may represent an effective strategy for overcoming imatinib resistance.	imatinib	126-134	transcription factor 7	Homo sapiens	219-223
33416164-10	2021	In summary, our results highlight that the upregulation of Wnt/beta-catenin and ABC transporter signaling pathways induced by imatinib treatment of resistant cells confers imatinib resistance, and reveal that targeting TCF7 to regulate the Wnt/beta-catenin/TCF7/ABC transporter signaling axis may represent an effective strategy for overcoming imatinib resistance.	imatinib	126-134	catenin beta 1	Homo sapiens	244-256
33416164-10	2021	In summary, our results highlight that the upregulation of Wnt/beta-catenin and ABC transporter signaling pathways induced by imatinib treatment of resistant cells confers imatinib resistance, and reveal that targeting TCF7 to regulate the Wnt/beta-catenin/TCF7/ABC transporter signaling axis may represent an effective strategy for overcoming imatinib resistance.	imatinib	126-134	transcription factor 7	Homo sapiens	257-261
33416164-10	2021	In summary, our results highlight that the upregulation of Wnt/beta-catenin and ABC transporter signaling pathways induced by imatinib treatment of resistant cells confers imatinib resistance, and reveal that targeting TCF7 to regulate the Wnt/beta-catenin/TCF7/ABC transporter signaling axis may represent an effective strategy for overcoming imatinib resistance.	imatinib	126-134	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	262-277
33416164-10	2021	In summary, our results highlight that the upregulation of Wnt/beta-catenin and ABC transporter signaling pathways induced by imatinib treatment of resistant cells confers imatinib resistance, and reveal that targeting TCF7 to regulate the Wnt/beta-catenin/TCF7/ABC transporter signaling axis may represent an effective strategy for overcoming imatinib resistance.	imatinib	172-180	catenin beta 1	Homo sapiens	63-75
33416164-10	2021	In summary, our results highlight that the upregulation of Wnt/beta-catenin and ABC transporter signaling pathways induced by imatinib treatment of resistant cells confers imatinib resistance, and reveal that targeting TCF7 to regulate the Wnt/beta-catenin/TCF7/ABC transporter signaling axis may represent an effective strategy for overcoming imatinib resistance.	imatinib	172-180	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	80-95
33416164-10	2021	In summary, our results highlight that the upregulation of Wnt/beta-catenin and ABC transporter signaling pathways induced by imatinib treatment of resistant cells confers imatinib resistance, and reveal that targeting TCF7 to regulate the Wnt/beta-catenin/TCF7/ABC transporter signaling axis may represent an effective strategy for overcoming imatinib resistance.	imatinib	172-180	transcription factor 7	Homo sapiens	219-223
33416164-10	2021	In summary, our results highlight that the upregulation of Wnt/beta-catenin and ABC transporter signaling pathways induced by imatinib treatment of resistant cells confers imatinib resistance, and reveal that targeting TCF7 to regulate the Wnt/beta-catenin/TCF7/ABC transporter signaling axis may represent an effective strategy for overcoming imatinib resistance.	imatinib	172-180	catenin beta 1	Homo sapiens	244-256
33416164-10	2021	In summary, our results highlight that the upregulation of Wnt/beta-catenin and ABC transporter signaling pathways induced by imatinib treatment of resistant cells confers imatinib resistance, and reveal that targeting TCF7 to regulate the Wnt/beta-catenin/TCF7/ABC transporter signaling axis may represent an effective strategy for overcoming imatinib resistance.	imatinib	172-180	transcription factor 7	Homo sapiens	257-261
33416164-10	2021	In summary, our results highlight that the upregulation of Wnt/beta-catenin and ABC transporter signaling pathways induced by imatinib treatment of resistant cells confers imatinib resistance, and reveal that targeting TCF7 to regulate the Wnt/beta-catenin/TCF7/ABC transporter signaling axis may represent an effective strategy for overcoming imatinib resistance.	imatinib	172-180	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	262-277
33416164-10	2021	In summary, our results highlight that the upregulation of Wnt/beta-catenin and ABC transporter signaling pathways induced by imatinib treatment of resistant cells confers imatinib resistance, and reveal that targeting TCF7 to regulate the Wnt/beta-catenin/TCF7/ABC transporter signaling axis may represent an effective strategy for overcoming imatinib resistance.	imatinib	172-180	catenin beta 1	Homo sapiens	63-75
33416164-10	2021	In summary, our results highlight that the upregulation of Wnt/beta-catenin and ABC transporter signaling pathways induced by imatinib treatment of resistant cells confers imatinib resistance, and reveal that targeting TCF7 to regulate the Wnt/beta-catenin/TCF7/ABC transporter signaling axis may represent an effective strategy for overcoming imatinib resistance.	imatinib	172-180	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	80-95
33416164-10	2021	In summary, our results highlight that the upregulation of Wnt/beta-catenin and ABC transporter signaling pathways induced by imatinib treatment of resistant cells confers imatinib resistance, and reveal that targeting TCF7 to regulate the Wnt/beta-catenin/TCF7/ABC transporter signaling axis may represent an effective strategy for overcoming imatinib resistance.	imatinib	172-180	transcription factor 7	Homo sapiens	219-223
33416164-10	2021	In summary, our results highlight that the upregulation of Wnt/beta-catenin and ABC transporter signaling pathways induced by imatinib treatment of resistant cells confers imatinib resistance, and reveal that targeting TCF7 to regulate the Wnt/beta-catenin/TCF7/ABC transporter signaling axis may represent an effective strategy for overcoming imatinib resistance.	imatinib	172-180	catenin beta 1	Homo sapiens	244-256
33416164-10	2021	In summary, our results highlight that the upregulation of Wnt/beta-catenin and ABC transporter signaling pathways induced by imatinib treatment of resistant cells confers imatinib resistance, and reveal that targeting TCF7 to regulate the Wnt/beta-catenin/TCF7/ABC transporter signaling axis may represent an effective strategy for overcoming imatinib resistance.	imatinib	172-180	transcription factor 7	Homo sapiens	257-261
33416164-10	2021	In summary, our results highlight that the upregulation of Wnt/beta-catenin and ABC transporter signaling pathways induced by imatinib treatment of resistant cells confers imatinib resistance, and reveal that targeting TCF7 to regulate the Wnt/beta-catenin/TCF7/ABC transporter signaling axis may represent an effective strategy for overcoming imatinib resistance.	imatinib	172-180	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	262-277
33470551-0	2021	Glutathione S-transferase gene polymorphic sequence variations: Association with risk and response to Imatinib among Chronic Myeloid Leukemia patients of Kashmir.	imatinib	102-110	glutathione S-transferase kappa 1	Homo sapiens	0-25
33470551-2	2021	We aimed to analyze relation of different GST gene sequence variants with susceptibility and response to Imatinib in CML.	imatinib	105-113	glutathione S-transferase kappa 1	Homo sapiens	42-45
33458904-8	2021	RESULTS: Cisplatin-related PF apoptosis via the ABL/TAp63 pathway was targeted with a tyrosine kinase inhibitor, imatinib, in mice, but effects were recently challenged by findings on human ovarian xenografts in mice.	imatinib	113-121	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	48-51
33585207-1	2020	The treatment of chronic myeloid leukemia (CML) with BCR-ABL tyrosine kinase inhibitors (TKIs), such as imatinib, has yielded clinical success.	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
33131722-8	2021	Importantly, imatinib treatment in HFD-fed mice enhanced plasma levels of high-molecular-weight adiponectin by ~2-fold without affecting total adiponectin.	imatinib	13-21	adiponectin, C1Q and collagen domain containing	Mus musculus	96-107
33397955-3	2021	Functional analysis shows that USP47 knockdown represses proliferation of CML cells sensitive or resistant to imatinib in vitro and in vivo.	imatinib	110-118	ubiquitin specific peptidase 47	Mus musculus	31-36
33478278-0	2021	BCR-ABL1 kinase domain mutation analysis by next generation sequencing detected additional mutations in chronic myeloid leukemia patients with suboptimal response to imatinib.	imatinib	166-174	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-8
33511186-1	2021	BACKGROUND: Myeloid neoplasm (MN) with eosinophilia and rearrangement of platelet-derived growth factor receptor beta (PDGFRB) shows a good therapeutic response to imatinib in adults.	imatinib	164-172	platelet derived growth factor receptor beta	Homo sapiens	73-117
33511186-1	2021	BACKGROUND: Myeloid neoplasm (MN) with eosinophilia and rearrangement of platelet-derived growth factor receptor beta (PDGFRB) shows a good therapeutic response to imatinib in adults.	imatinib	164-172	platelet derived growth factor receptor beta	Homo sapiens	119-125
33511186-3	2021	CASE SUMMARY: We report 2 pediatric cases diagnosed with MN with eosinophilia and PDGFRB rearrangement who were treated with imatinib.	imatinib	125-133	platelet derived growth factor receptor beta	Homo sapiens	82-88
33402214-4	2021	The management of GIST was revolutionized by the introduction of imatinib, a KIT inhibitor, which has become the standard first line treatment for metastatic GIST.	imatinib	65-73	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	77-80
32972961-1	2021	Gastrointestinal stromal tumors (GIST) harboring activating mutations of PDGFRA respond to imatinib with the notable exception of the most common mutation, D842V.	imatinib	91-99	platelet derived growth factor receptor alpha	Homo sapiens	73-79
32972961-4	2021	Tumor and plasma biopsies in 6 of 7 patients with PDGFRA primary mutations who progressed on avapritinib or imatinib had secondary resistance mutations within PDGFRA exons 13, 14 and 15 that interfere with avapritinib binding.	imatinib	108-116	platelet derived growth factor receptor alpha	Homo sapiens	50-56
33075481-0	2021	Comprehensive in-silico analysis of damage associated SNPs in hOCT1 affecting Imatinib response in chronic myeloid leukemia.	imatinib	78-86	solute carrier family 22 member 1	Homo sapiens	62-67
33075481-1	2021	Non-synonymous single nucleotide polymorphisms (nsSNPs) in hOCT1 (encoded by SLC22A1 gene) are expected to affect Imatinib uptake in chronic myeloid leukemia (CML).	imatinib	114-122	solute carrier family 22 member 1	Homo sapiens	59-64
33075481-1	2021	Non-synonymous single nucleotide polymorphisms (nsSNPs) in hOCT1 (encoded by SLC22A1 gene) are expected to affect Imatinib uptake in chronic myeloid leukemia (CML).	imatinib	114-122	solute carrier family 22 member 1	Homo sapiens	77-84
33129240-3	2021	This study attempted to evaluate the influence of ABCB1 gene polymorphisms and smoking on CML risk and resistance to imatinib.	imatinib	117-125	ATP binding cassette subfamily B member 1	Homo sapiens	50-55
32968926-8	2021	Imatinib, a specific inhibitor of platelet-derived growth factor receptor, significantly inhibited the proliferation of dermal fibroblasts promoted by PES, suggesting that PDGFA expression, an early response of PES, was involved in promoting the cell proliferation.	imatinib	0-8	platelet derived growth factor subunit A	Homo sapiens	172-177
33357774-7	2021	Then, we treated CCI mice with an inhibitor of PDGFR signaling, imatinib, during the postoperative day 0-4 period.	imatinib	64-72	platelet derived growth factor receptor, beta polypeptide	Mus musculus	47-52
33361796-4	2020	These changes were antagonized by blocking PDGFRalpha signaling with the small tyrosine kinase inhibitor imatinib.	imatinib	105-113	platelet derived growth factor receptor alpha	Homo sapiens	43-53
33953878-7	2021	PDGFRA is the most important druggable up-and down-regulated gene and is considered an important gene in the IMATINIB pathway.	imatinib	109-117	platelet-derived growth factor receptor, alpha polypeptide	Danio rerio	0-6
33421986-6	2021	In addition, the CSNK2A1-PDGFRB fusion retained the entire kinase domain of PDGFRB and response to imatinib at low concentration.	imatinib	99-107	casein kinase 2 alpha 1	Homo sapiens	17-24
33421986-6	2021	In addition, the CSNK2A1-PDGFRB fusion retained the entire kinase domain of PDGFRB and response to imatinib at low concentration.	imatinib	99-107	platelet derived growth factor receptor beta	Homo sapiens	25-31
33421986-7	2021	the patient with CSNK2A1-PDGFRB was sensitive to imatinib treatment and acquired sustained complete remission.	imatinib	49-57	casein kinase 2 alpha 1	Homo sapiens	17-24
33421986-7	2021	the patient with CSNK2A1-PDGFRB was sensitive to imatinib treatment and acquired sustained complete remission.	imatinib	49-57	platelet derived growth factor receptor beta	Homo sapiens	25-31
33456567-0	2021	KDM6A promotes imatinib resistance through YY1-mediated transcriptional upregulation of TRKA independently of its demethylase activity in chronic myelogenous leukemia.	imatinib	15-23	lysine demethylase 6A	Homo sapiens	0-5
33456567-0	2021	KDM6A promotes imatinib resistance through YY1-mediated transcriptional upregulation of TRKA independently of its demethylase activity in chronic myelogenous leukemia.	imatinib	15-23	YY1 transcription factor	Homo sapiens	43-46
33456567-0	2021	KDM6A promotes imatinib resistance through YY1-mediated transcriptional upregulation of TRKA independently of its demethylase activity in chronic myelogenous leukemia.	imatinib	15-23	neurotrophic receptor tyrosine kinase 1	Homo sapiens	88-92
33456567-7	2021	Results: Amongst five KDMs upregulated in CML, only KDM6A depletion sensitized CML cells to imatinib-induced apoptosis.	imatinib	92-100	lysine demethylase 6A	Homo sapiens	52-57
33456567-8	2021	Re-introduction of demethylase-dead KDM6A as well as wild-type KDM6A restored imatinib resistance.	imatinib	78-86	methyl-CpG binding domain protein 2	Homo sapiens	19-30
33456567-8	2021	Re-introduction of demethylase-dead KDM6A as well as wild-type KDM6A restored imatinib resistance.	imatinib	78-86	lysine demethylase 6A	Homo sapiens	36-41
33456567-8	2021	Re-introduction of demethylase-dead KDM6A as well as wild-type KDM6A restored imatinib resistance.	imatinib	78-86	lysine demethylase 6A	Homo sapiens	63-68
33456567-11	2021	Mechanistically, KDM6A was recruited to the NTRK1 promoter by the transcription factor YY1 with subsequent TRKA upregulation activating down-stream survival pathways to invoke imatinib resistance.	imatinib	176-184	lysine demethylase 6A	Homo sapiens	17-22
33456567-12	2021	Conclusion: Contrary to its reported role as a tumor suppressor and independent of its demethylase function, KDM6A promotes imatinib-resistance in CML cells.	imatinib	124-132	lysine demethylase 6A	Homo sapiens	109-114
33456567-13	2021	The identification of the KDM6A/YY1/TRKA axis as a novel imatinib-resistance mechanism represents an unexplored avenue to overcome TKI resistance in CML.	imatinib	57-65	lysine demethylase 6A	Homo sapiens	26-31
33456567-13	2021	The identification of the KDM6A/YY1/TRKA axis as a novel imatinib-resistance mechanism represents an unexplored avenue to overcome TKI resistance in CML.	imatinib	57-65	YY1 transcription factor	Homo sapiens	32-35
33456567-13	2021	The identification of the KDM6A/YY1/TRKA axis as a novel imatinib-resistance mechanism represents an unexplored avenue to overcome TKI resistance in CML.	imatinib	57-65	neurotrophic receptor tyrosine kinase 1	Homo sapiens	36-40
33409258-0	2020	Imatinib and GNF-5 Exhibit an Inhibitory Effect on Growth of Hepatocellar Carcinoma Cells by Downregulating S-phase Kinase-associated Protein 2.	imatinib	0-8	S-phase kinase associated protein 2	Homo sapiens	108-143
33409258-9	2020	Imatinib and GNF-5 induced G0/G1 phase cell cycle arrest by downregulating Skp2 and upregulating p27 and p21.	imatinib	0-8	S-phase kinase associated protein 2	Homo sapiens	75-79
33409258-9	2020	Imatinib and GNF-5 induced G0/G1 phase cell cycle arrest by downregulating Skp2 and upregulating p27 and p21.	imatinib	0-8	dynactin subunit 6	Homo sapiens	97-100
33409258-9	2020	Imatinib and GNF-5 induced G0/G1 phase cell cycle arrest by downregulating Skp2 and upregulating p27 and p21.	imatinib	0-8	H3 histone pseudogene 16	Homo sapiens	105-108
33409258-10	2020	Overexpression of Skp2 reduced the effect of imatinib and GNF-5 on HepG2 cells.	imatinib	45-53	S-phase kinase associated protein 2	Homo sapiens	18-22
33409258-12	2020	Furthermore, knockdown of Skp2 enhanced the effect of imatinib and GNF-5 on growth of HepG2 cells.	imatinib	54-62	S-phase kinase associated protein 2	Homo sapiens	26-30
33409258-13	2020	In conclusion, imatinib and GNF-5 effectively suppress HepG2 cell growth by inhibiting Skp2 expression.	imatinib	15-23	S-phase kinase associated protein 2	Homo sapiens	87-91
33445855-0	2020	[Acute myeloid leukemia with FIP1L1-PDGFRA fusion gene treated with imatinib: a case report and literature review].	imatinib	68-76	factor interacting with PAPOLA and CPSF1	Homo sapiens	29-35
33086089-8	2020	Imatinib mesylate (IM), P-gp substrate, was used as a model drug.	imatinib	19-21	ATP binding cassette subfamily B member 1	Homo sapiens	24-28
33445855-0	2020	[Acute myeloid leukemia with FIP1L1-PDGFRA fusion gene treated with imatinib: a case report and literature review].	imatinib	68-76	platelet derived growth factor receptor alpha	Homo sapiens	36-42
33376671-2	2021	We reported a case of AML with BCR-ABL1 patient who was successfully treated with dasatinib alone; additionally, we previously reported another case of long-term remission maintained with imatinib monotherapy.	imatinib	188-196	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-39
32944951-3	2020	Activating gain-of-function mutations in KIT and PDGFRA are the most frequent driver events, and most of these tumors are responsive to the tyrosine kinase inhibitor imatinib.	imatinib	166-174	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	41-44
33415044-2	2020	Dasatinib is a multitargeted tyrosine kinase inhibitor with significant activity in Philadephia positive ALL which is resistant to imatinib, as well as in treatment-naive patients.	imatinib	131-139	TXK tyrosine kinase	Homo sapiens	29-44
33294307-10	2021	Our in silico study revealed that losartan and imatinib could probably: (1) decline SARS-CoV2 affinity to ACE2.	imatinib	47-55	angiotensin converting enzyme 2	Homo sapiens	106-110
33022360-6	2020	It was observed that Imatinib could function as an immunomodulator by breaking the feed-back loop between the proinflammatory cytokines (IL-1beta and TNF-alpha) and transcription factors (NF-kappaB, Jak3/Stat3) knowingly involved in increased cell proliferation during tumorigenesis via activating different intracellular signaling.	imatinib	21-29	interleukin 1 alpha	Homo sapiens	137-145
33022360-6	2020	It was observed that Imatinib could function as an immunomodulator by breaking the feed-back loop between the proinflammatory cytokines (IL-1beta and TNF-alpha) and transcription factors (NF-kappaB, Jak3/Stat3) knowingly involved in increased cell proliferation during tumorigenesis via activating different intracellular signaling.	imatinib	21-29	tumor necrosis factor	Homo sapiens	150-159
33022360-6	2020	It was observed that Imatinib could function as an immunomodulator by breaking the feed-back loop between the proinflammatory cytokines (IL-1beta and TNF-alpha) and transcription factors (NF-kappaB, Jak3/Stat3) knowingly involved in increased cell proliferation during tumorigenesis via activating different intracellular signaling.	imatinib	21-29	Janus kinase 3	Homo sapiens	199-203
33022360-6	2020	It was observed that Imatinib could function as an immunomodulator by breaking the feed-back loop between the proinflammatory cytokines (IL-1beta and TNF-alpha) and transcription factors (NF-kappaB, Jak3/Stat3) knowingly involved in increased cell proliferation during tumorigenesis via activating different intracellular signaling.	imatinib	21-29	signal transducer and activator of transcription 3	Homo sapiens	204-209
33022360-7	2020	Also, Imatinib could independently deregulate the other cell survival and proliferation signaling e.g. PI3-K/Akt/mTOR, Wnt/beta-catenin and MAPK.	imatinib	6-14	AKT serine/threonine kinase 1	Homo sapiens	109-112
33022360-7	2020	Also, Imatinib could independently deregulate the other cell survival and proliferation signaling e.g. PI3-K/Akt/mTOR, Wnt/beta-catenin and MAPK.	imatinib	6-14	mechanistic target of rapamycin kinase	Homo sapiens	113-117
33022360-7	2020	Also, Imatinib could independently deregulate the other cell survival and proliferation signaling e.g. PI3-K/Akt/mTOR, Wnt/beta-catenin and MAPK.	imatinib	6-14	catenin beta 1	Homo sapiens	123-135
33022360-9	2020	Restoration of physiological apoptosis by increasing the release of intracellular calcium to generate ROS thereby reducing the mitochondrial membrane potential for the release of cytochrome c and activation of caspase-3 was also reported with Imatinib administration.	imatinib	243-251	cytochrome c, somatic	Homo sapiens	179-191
33022360-9	2020	Restoration of physiological apoptosis by increasing the release of intracellular calcium to generate ROS thereby reducing the mitochondrial membrane potential for the release of cytochrome c and activation of caspase-3 was also reported with Imatinib administration.	imatinib	243-251	caspase 3	Homo sapiens	210-219
33468755-7	2020	Histopathological examination showed c-kit positivity and she was diagnosed with small intestinal GIST; as a result, a course of imatinib was started.	imatinib	129-137	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	37-42
33227183-10	2020	Conclusion: Coadministration of imatinib or dasatinib with Cp could preserve AMH production capacity in this in vitro mice preantral follicle culture model, and it did not affect MII oocyte acquisition.	imatinib	32-40	anti-Mullerian hormone	Mus musculus	77-80
32944951-3	2020	Activating gain-of-function mutations in KIT and PDGFRA are the most frequent driver events, and most of these tumors are responsive to the tyrosine kinase inhibitor imatinib.	imatinib	166-174	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	49-55
33361712-2	2020	Imatinib mesylate (IM), a BCR-ABL1 targeted tyrosine kinase inhibitor (TKI) drug, is the first line gold standard drug for CML treatment.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-34
33024275-3	2020	The small molecule imatinib inhibits KIT and has been a mainstay of therapy in GIST.	imatinib	19-27	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	37-40
33024275-4	2020	Unfortunately, imatinib-treated patients typically relapse, most often due to clonal emergence of the resistance-associated KIT V654A mutation.	imatinib	15-23	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	124-127
33024275-7	2020	GISTs driven by the V558Delta;V653A Kit double mutation were resistant to imatinib, while cabozantinib was more effective in overcoming resistance than sunitinib.	imatinib	74-82	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	36-39
33244077-4	2020	Patients carrying ABCB1-C1236T variants had high day29 plasma imatinib levels (P = 0.005), increased EMR at 3 months (P = 0.044) and a better 2 year FFS (P = 0.003) when compared to those with wild type genotype.	imatinib	62-70	ATP binding cassette subfamily B member 1	Homo sapiens	18-23
32932224-1	2020	Imatinib Mesylate (IM) blocks Colony Stimulating Factor1 Receptor (CSF1R), the driver mechanism in TGCT.	imatinib	0-17	colony stimulating factor 1 receptor	Homo sapiens	30-65
32932224-1	2020	Imatinib Mesylate (IM) blocks Colony Stimulating Factor1 Receptor (CSF1R), the driver mechanism in TGCT.	imatinib	0-17	colony stimulating factor 1 receptor	Homo sapiens	67-72
33244077-5	2020	This translates to patients with lower ABCB1 mRNA expression having a significantly higher intracellular imatinib levels (P = 0.029).	imatinib	105-113	ATP binding cassette subfamily B member 1	Homo sapiens	39-44
33244143-4	2020	Imatinib was loaded in gold nanoparticles (GNP) functionalized with antibody against CD44 (GNP-HCIm).	imatinib	0-8	CD44 molecule (Indian blood group)	Homo sapiens	85-89
33244143-9	2020	GNP-HCIm reduced cAbl-p (0.41 GNP-HCIm, 0.24 Imatinib vs. to control; p < 0.001).	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-21
33198812-14	2020	CONCLUSIONS: These results demonstrated that the pharmacokinetics of imatinib and N-desmethyl imatinib had been significantly affected by GS and/or GT extracts, which could be partially explained by the inhibition of CYP3A-mediated metabolism.	imatinib	69-77	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	217-222
33212994-8	2020	However, when compared to a classical imatinib-resistant KIT mutation (T670I), N655K was slightly more sensitive to imatinib, and encouraging responses were observed with last-generation TKIs.	imatinib	38-46	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	57-60
33212994-8	2020	However, when compared to a classical imatinib-resistant KIT mutation (T670I), N655K was slightly more sensitive to imatinib, and encouraging responses were observed with last-generation TKIs.	imatinib	116-124	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	57-60
33197900-5	2021	Investigating the molecular mechanisms involved in the growth-suppressive effect of ZnO/CNT@Fe3O4-plus-Imatinib clarified that the up-regulation of SIRT1 ceased the progression of the cell cycle, foremost by increasing the expression of p21 and p27 cyclin-dependent kinase inhibitors.	imatinib	103-111	sirtuin 1	Homo sapiens	148-153
33197900-6	2021	Notably, we reported for the first time that either direct or indirect suppression of c-Myc resulted in an enhanced anti-leukemic effect; suggesting that the overexpression of c-Myc could play a contributory role in attenuating the efficacy of ZnO/CNT@Fe3O4-plus-Imatinib in K562.	imatinib	263-271	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	86-91
33197900-6	2021	Notably, we reported for the first time that either direct or indirect suppression of c-Myc resulted in an enhanced anti-leukemic effect; suggesting that the overexpression of c-Myc could play a contributory role in attenuating the efficacy of ZnO/CNT@Fe3O4-plus-Imatinib in K562.	imatinib	263-271	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	176-181
32711219-0	2020	p19INK4d inhibits proliferation and enhances imatinib efficacy through BCR-ABL signaling pathway in chronic myeloid leukemia.	imatinib	45-53	cyclin dependent kinase inhibitor 2D	Homo sapiens	0-8
33168949-5	2021	p190Bcr-Abl CML patients demonstrated poor response to imatinib and frequent mutations in epigenetic modifiers genes.	imatinib	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-11
33196011-0	2020	Sustained Complete Molecular Remission With Imatinib Monotherapy in a Child Presenting With Blast Phase FIP1L1-PDGFRA-Associated Myeloid Neoplasm With Eosinophilia.	imatinib	44-52	factor interacting with PAPOLA and CPSF1	Homo sapiens	104-110
33196011-0	2020	Sustained Complete Molecular Remission With Imatinib Monotherapy in a Child Presenting With Blast Phase FIP1L1-PDGFRA-Associated Myeloid Neoplasm With Eosinophilia.	imatinib	44-52	platelet derived growth factor receptor alpha	Homo sapiens	111-117
33155931-2	2021	The therapeutic targets for CML patients which are mediated with BCR/ABL1 oncogenic are tyrosine kinase inhibitors such as imatinib, dasatinib, and nilotinib.	imatinib	123-131	BCR activator of RhoGEF and GTPase	Homo sapiens	65-68
33155931-2	2021	The therapeutic targets for CML patients which are mediated with BCR/ABL1 oncogenic are tyrosine kinase inhibitors such as imatinib, dasatinib, and nilotinib.	imatinib	123-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-73
33149116-0	2020	Correction: Imatinib mesylate inhibits STAT5 phosphorylation in response to IL-7 and promotes T cell lymphopenia in chronic myelogenous leukemia patients.	imatinib	12-29	signal transducer and activator of transcription 5A	Homo sapiens	39-44
33149116-0	2020	Correction: Imatinib mesylate inhibits STAT5 phosphorylation in response to IL-7 and promotes T cell lymphopenia in chronic myelogenous leukemia patients.	imatinib	12-29	interleukin 7	Homo sapiens	76-80
32711219-0	2020	p19INK4d inhibits proliferation and enhances imatinib efficacy through BCR-ABL signaling pathway in chronic myeloid leukemia.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
32711219-6	2020	p19INK4d overexpression inhibits cell proliferation through cell cycle arrest, and cooperates with imatinib to inhibit CML more effectively in vitro and in vivo.	imatinib	99-107	cyclin dependent kinase inhibitor 2D	Homo sapiens	0-8
32711219-8	2020	Collectively, p19INK4d inhibits proliferation and enhances imatinib efficacy in the treatment of CML.	imatinib	59-67	cyclin dependent kinase inhibitor 2D	Homo sapiens	14-22
32836055-2	2020	BRAF mutated GISTs usually do not respond to imatinib treatment, even more GISTs with imatinib sensitive KIT mutation.	imatinib	86-94	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	105-108
33284894-0	2020	Increased sensitivity of BCR-ABL-induced B-ALL to imatinib by releasing leukemia B cell differentiation blockage.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
33284894-2	2020	We aimed to investigate whether it was possible to promote pro/pre-B cell maturation beyond this phase and make them sensitive to imatinib treatment by overexpressing immunoregulatory tyrosine activation motif (ITAM) with BCR-ABL in a Ph+ B-ALL mouse model.	imatinib	130-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	222-229
33284894-6	2020	CONCLUSION: B-cell development blockage released by ITAM renders leukemia cells sensitive to imatinib treatment in BCR-ABL-induced B-ALL.	imatinib	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
32723769-10	2020	We also blocked tolerance by administering morphine or fentanyl with the PDGFR-beta inhibitor imatinib.	imatinib	94-102	platelet derived growth factor receptor alpha	Rattus norvegicus	73-83
33104726-4	2020	Therapeutic administration of imatinib, a c-Kit inhibitor known to inhibit mast cell survival, led to reduced mast cell accumulation and alleviated tactile genital pain.	imatinib	30-38	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	42-47
33195674-5	2020	Mutational analysis showed secondary mutation in KIT exon 13 (V564A), which is resistant to imatinib treatment.	imatinib	92-100	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	49-52
33066449-3	2020	The clinical use of the RTK inhibitor imatinib has significantly improved the management of GIST patients; however, imatinib resistance remains a challenge.	imatinib	38-46	ret proto-oncogene	Homo sapiens	24-27
33116851-1	2020	Purpose: KIT/PDGFRA wild-type (WT) gastrointestinal stromal tumors (GISTs) represent a heterogeneous subgroup of GISTs that lack KIT or PDGFRA mutations and possess distinct genetic alterations and primary resistance to imatinib.	imatinib	220-228	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	9-12
32877218-6	2020	We finally demonstrate that application of the c-KIT antagonist imatinib mesylate in organ culture specifically depletes the ICC network and inhibits the transition to a regular rhythmic wave pattern.	imatinib	64-81	KIT proto-oncogene, receptor tyrosine kinase	Gallus gallus	47-52
33134075-4	2020	We present the first known case of concomitant MDS and CML on imatinib that developed focal blastic transformation, where the leukemic clone was BCR-ABL1 positive.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-153
32910995-2	2020	Imatinib, a BCR-ABL1 tyrosine kinase inhibitor (TKI), is a revolutionary molecular target inhibitor for CML.	imatinib	0-8	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	16-20
32945456-0	2020	CD9 knockdown suppresses cell proliferation, adhesion, migration and invasion, while promoting apoptosis and the efficacy of chemotherapeutic drugs and imatinib in Ph+ ALL SUP-B15 cells.	imatinib	152-160	CD9 molecule	Homo sapiens	0-3
32945456-7	2020	In addition, CD9 knockdown could suppress cell proliferation, adhesion, migration and invasion, and promote apoptosis and the efficacy of chemotherapeutic drugs (such as vincristine, daunorubicin, cyclophosphamide and dexamethasone) and the tyrosine kinase inhibitor imatinib in SUP-B15 cells.	imatinib	267-275	CD9 molecule	Homo sapiens	13-16
32619722-0	2020	The HDAC6 inhibitor 7b induces BCR-ABL ubiquitination and downregulation and synergizes with imatinib to trigger apoptosis in chronic myeloid leukemia.	imatinib	93-101	histone deacetylase 6	Homo sapiens	4-9
32927512-2	2020	Most GIST with PDGFRA exon 18 mutations including D842V mutation are highly resistant to imatinib.	imatinib	89-97	platelet derived growth factor receptor alpha	Homo sapiens	15-21
32619820-2	2020	Tyrosine kinase inhibitors (TKIs) such as imatinib have proven effective since the discovery of KIT and PDGFRA.	imatinib	42-50	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	96-99
32619820-2	2020	Tyrosine kinase inhibitors (TKIs) such as imatinib have proven effective since the discovery of KIT and PDGFRA.	imatinib	42-50	platelet derived growth factor receptor alpha	Homo sapiens	104-110
32999756-0	2020	Expression differences of miR-142-5p between treatment-naive chronic myeloid leukemia patients responding and non-responding to imatinib therapy suggest a link to oncogenic ABL2, SRI, cKIT and MCL1 signaling pathways critical for development of therapy resistance.	imatinib	128-136	ABL proto-oncogene 2, non-receptor tyrosine kinase	Homo sapiens	173-177
32999756-0	2020	Expression differences of miR-142-5p between treatment-naive chronic myeloid leukemia patients responding and non-responding to imatinib therapy suggest a link to oncogenic ABL2, SRI, cKIT and MCL1 signaling pathways critical for development of therapy resistance.	imatinib	128-136	sorcin	Homo sapiens	179-182
32999756-0	2020	Expression differences of miR-142-5p between treatment-naive chronic myeloid leukemia patients responding and non-responding to imatinib therapy suggest a link to oncogenic ABL2, SRI, cKIT and MCL1 signaling pathways critical for development of therapy resistance.	imatinib	128-136	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	184-188
32999756-0	2020	Expression differences of miR-142-5p between treatment-naive chronic myeloid leukemia patients responding and non-responding to imatinib therapy suggest a link to oncogenic ABL2, SRI, cKIT and MCL1 signaling pathways critical for development of therapy resistance.	imatinib	128-136	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	193-197
33364286-0	2020	COL1A1-PDGFB fusion uterine sarcoma and its response to Imatinib therapy.	imatinib	56-64	collagen type I alpha 1 chain	Homo sapiens	0-6
33364286-0	2020	COL1A1-PDGFB fusion uterine sarcoma and its response to Imatinib therapy.	imatinib	56-64	platelet derived growth factor subunit B	Homo sapiens	7-12
32780298-11	2020	Furthermore, ponatinib was more effective than imatinib in reducing the percentage of CD26-expressing cells in primary CML cells, whereas imatinib and ponatinib showed similar efficacy on KCL22 cells.	imatinib	47-55	dipeptidyl peptidase 4	Homo sapiens	86-90
33040790-3	2020	After the CML cells were successfully resistant to imatinib, Twist1 expression increased again in the cells and the PI3K/AKT signaling pathway was further activated.	imatinib	51-59	twist family bHLH transcription factor 1	Homo sapiens	61-67
33040790-3	2020	After the CML cells were successfully resistant to imatinib, Twist1 expression increased again in the cells and the PI3K/AKT signaling pathway was further activated.	imatinib	51-59	AKT serine/threonine kinase 1	Homo sapiens	121-124
33040790-4	2020	After the silence of the Twist1 expression, the imatinib-resistant CML cells were more sensitive to imatinib, and the PI3K/AKT signaling pathway was inhibited, and the expression level of p-AKT protein significantly reduced.	imatinib	48-56	twist family bHLH transcription factor 1	Homo sapiens	25-31
33040790-4	2020	After the silence of the Twist1 expression, the imatinib-resistant CML cells were more sensitive to imatinib, and the PI3K/AKT signaling pathway was inhibited, and the expression level of p-AKT protein significantly reduced.	imatinib	48-56	AKT serine/threonine kinase 1	Homo sapiens	123-126
33040790-4	2020	After the silence of the Twist1 expression, the imatinib-resistant CML cells were more sensitive to imatinib, and the PI3K/AKT signaling pathway was inhibited, and the expression level of p-AKT protein significantly reduced.	imatinib	48-56	AKT serine/threonine kinase 1	Homo sapiens	190-193
33040790-4	2020	After the silence of the Twist1 expression, the imatinib-resistant CML cells were more sensitive to imatinib, and the PI3K/AKT signaling pathway was inhibited, and the expression level of p-AKT protein significantly reduced.	imatinib	100-108	twist family bHLH transcription factor 1	Homo sapiens	25-31
33040790-6	2020	In conclusion, Twist1 and the PI3K/AKT signaling pathway are over-activated during the formation of the CML cells resistant to imatinib.	imatinib	127-135	twist family bHLH transcription factor 1	Homo sapiens	15-21
33040790-6	2020	In conclusion, Twist1 and the PI3K/AKT signaling pathway are over-activated during the formation of the CML cells resistant to imatinib.	imatinib	127-135	AKT serine/threonine kinase 1	Homo sapiens	35-38
33145265-0	2020	Wogonin reverses the drug resistance of chronic myelogenous leukemia cells to imatinib through CXCL12-CXCR4/7 axis in bone marrow microenvironment.	imatinib	78-86	C-X-C motif chemokine ligand 12	Homo sapiens	95-101
32920590-3	2020	The addition of pegylated interferon-alpha2b to imatinib or dasatinib results in promising deep molecular responses.	imatinib	48-56	interferon alpha 2	Homo sapiens	26-44
32597702-14	2020	The excessive arterial damage in the miR-223 knockout could be res-cued by adoptive transfer of platelet, administration of miR-223 mimics, or the PDGFRbeta inhibitor imatinib mesylate.	imatinib	167-184	microRNA 223	Mus musculus	37-44
32597702-14	2020	The excessive arterial damage in the miR-223 knockout could be res-cued by adoptive transfer of platelet, administration of miR-223 mimics, or the PDGFRbeta inhibitor imatinib mesylate.	imatinib	167-184	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	147-156
32535098-7	2020	Single treatment with MSCs or imatinib and the combination therapy, all significantly reduced serum levels of ALT, AST, and ALP concomitant with down-regulation of alpha-SMA, pro-collagen I, pro-collagen III, collagen IV, and laminin.	imatinib	30-38	PDZ and LIM domain 3	Rattus norvegicus	124-127
33014780-7	2020	Then, after gene expression profiling experiments, we found that several "antiviral" genes, such as CD28 and IFN gamma, were upregulated, while genes with "proviral" action, such as ARG-1, CEACAM1, and FUT4, were less expressed during treatment with imatinib, thus demonstrating that TKIs are not detrimental from the immunological point of view.	imatinib	250-258	CD28 molecule	Homo sapiens	100-104
33014780-7	2020	Then, after gene expression profiling experiments, we found that several "antiviral" genes, such as CD28 and IFN gamma, were upregulated, while genes with "proviral" action, such as ARG-1, CEACAM1, and FUT4, were less expressed during treatment with imatinib, thus demonstrating that TKIs are not detrimental from the immunological point of view.	imatinib	250-258	interferon gamma	Homo sapiens	109-118
33145265-0	2020	Wogonin reverses the drug resistance of chronic myelogenous leukemia cells to imatinib through CXCL12-CXCR4/7 axis in bone marrow microenvironment.	imatinib	78-86	C-X-C motif chemokine receptor 4	Homo sapiens	102-109
32710900-1	2020	The present study was undertaken to assess the effect of imatinib mesylate; a tyrosine kinase inhibitor and a well-known anticancer with numerous medical benefits on blood sugar levels, insulin, and glucagon secretion in an experimental model of STZ-induced diabetes mellitus.	imatinib	57-74	glucagon	Rattus norvegicus	199-207
32563150-3	2020	Further, chidamide combined with imatinib (IM) induced synergistic lethality in CML cell line KBM5, as well as IM-resistant CML cells KBM5T315I, associated with a marked reduction of Bcr-Abl kinase activity and acetyl-histone H3 expression.	imatinib	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	183-190
32563150-6	2020	Collectively, our data show that combination of chidamide and imatinib synergistically targets tyrosine kinase inhibitor (TKI) -resistant BC-CML cells via inhibition of Bcr-Abl and beta-catenin signaling, suggesting that this combination has the potential for treating TKI-resistant CML and improving clinical outcomes of BC-CML patients.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	169-176
32563150-6	2020	Collectively, our data show that combination of chidamide and imatinib synergistically targets tyrosine kinase inhibitor (TKI) -resistant BC-CML cells via inhibition of Bcr-Abl and beta-catenin signaling, suggesting that this combination has the potential for treating TKI-resistant CML and improving clinical outcomes of BC-CML patients.	imatinib	62-70	catenin beta 1	Homo sapiens	181-193
32697050-2	2020	This study aimed to evaluate the prognostic value of mutations in KIT and PDGFRA in a large-scale cohort of GIST patients with current therapy including surgery and imatinib.	imatinib	165-173	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	66-69
32697050-7	2020	In high-risk GISTs treated with R0 resection and imatinib, patients with KIT exon 11 homozygous mutations and KIT intron 10/exon 11 junction deletions demonstrated the highest recurrence rate, indicating that these mutations can be independent prognostic factors of DFS.	imatinib	49-57	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
32697050-9	2020	CONCLUSION: Low-incidence mutations such as KIT exon 11 homozygous mutations or intron 10/exon 11 junction deletions in GISTs should be carefully evaluated to explore novel treatment strategies, as tumors with these mutations have a high recurrence rate and a very poor prognosis after surgery followed by imatinib adjuvant treatment.	imatinib	306-314	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	44-47
32710900-5	2020	Biomarkers of cell injury, tissue necrosis, and apoptosis; caspase-3 were significantly reduced with imatinib treatment.	imatinib	101-109	caspase 3	Rattus norvegicus	59-68
32590338-5	2020	In xenografts, imatinib therapy in BCPAP thyroid tumour-bearing mice significantly increased [18F]FDG uptake and retention (>30%) in BCPAP tumours with PDGFRbeta or both (alpha+beta) isoforms.	imatinib	15-23	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	152-161
32365249-0	2020	Erythropoietin Treatment in Chronic Phase Chronic Myeloid Leukemia Patients Treated with Frontline Imatinib who Developed Late Anemia.	imatinib	99-107	erythropoietin	Homo sapiens	0-14
32365249-9	2020	CONCLUSIONS: Results of EPO treatment for late chronic anemia during long-lasting imatinib therapy are encouraging, with a high rate of response.	imatinib	82-90	erythropoietin	Homo sapiens	24-27
32715517-0	2020	Overexpression of P-glycoprotein and resistance to Imatinib in chronic myeloid leukemia patients.	imatinib	51-59	ATP binding cassette subfamily B member 1	Homo sapiens	18-32
32291709-2	2020	Imatinib and sunitinib are approved KIT-inhibiting therapies.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	36-39
32291709-9	2020	Our data show that dasatinib is more potent than imatinib or sunitinib at inhibiting the activity of drug-resistant KIT mutants.	imatinib	49-57	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	116-119
32715517-1	2020	BACKGROUND: The P-glycoprotein (P-gp) is one of the mechanisms of Imatinib (IM) resistance in chronic myeloid leukemia (CML).	imatinib	66-74	ATP binding cassette subfamily B member 1	Homo sapiens	16-30
32715517-1	2020	BACKGROUND: The P-glycoprotein (P-gp) is one of the mechanisms of Imatinib (IM) resistance in chronic myeloid leukemia (CML).	imatinib	66-74	ATP binding cassette subfamily B member 1	Homo sapiens	32-36
32364815-1	2020	Imatinib-induced tyrosine kinase inhibition extends beyond the BCR-ABL mutation, resulting in adverse effects.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-70
32364409-0	2020	Progressive multifocal leukoencephalopathy responsive to withdrawal of imatinib in a patient with FIP1L1-PDGFRA positive myeloid neoplasm.	imatinib	71-79	factor interacting with PAPOLA and CPSF1	Homo sapiens	98-104
32364409-0	2020	Progressive multifocal leukoencephalopathy responsive to withdrawal of imatinib in a patient with FIP1L1-PDGFRA positive myeloid neoplasm.	imatinib	71-79	platelet derived growth factor receptor alpha	Homo sapiens	105-111
32986105-2	2020	Imatinib targeting of KIT marked a new era in GIST treatment and ushered in precision oncological treatment for all solid malignant neoplasms.	imatinib	0-8	kit	None	22-25
32986105-3	2020	However, studies on the molecular biological traits of GIST have found that tumors respond differentially to imatinib dosage based on the KIT exon with variation.	imatinib	109-117	kit	None	138-141
32843387-0	2020	Chronic mast cell leukaemia with exon 9 KIT mutation A502_Y503dup: a rare imatinib responsive variant.	imatinib	74-82	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	40-43
32736695-14	2020	In conclusion, five different imatinib-resistant GIST cell lines including the EXOC2-AK7 fusion gene derived from GIST-R5 represent important research tools for the investigation of cancer cell mechanisms underlying drug resistance and genetic variation.	imatinib	30-38	exocyst complex component 2	Homo sapiens	79-84
32736695-14	2020	In conclusion, five different imatinib-resistant GIST cell lines including the EXOC2-AK7 fusion gene derived from GIST-R5 represent important research tools for the investigation of cancer cell mechanisms underlying drug resistance and genetic variation.	imatinib	30-38	adenylate kinase 7	Homo sapiens	85-88
32799779-11	2021	The interaction most likely arose because imatinib is a CYP2D6 inhibitor and could therefore impair the metabolism of gefitinib (a CYP2D6 substrate) and increase its serum concentration.	imatinib	42-50	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	56-62
32799779-11	2021	The interaction most likely arose because imatinib is a CYP2D6 inhibitor and could therefore impair the metabolism of gefitinib (a CYP2D6 substrate) and increase its serum concentration.	imatinib	42-50	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	131-137
32719139-1	2020	Despite the outstanding success of the cancer drug imatinib, one obstacle in prolonged treatment is the emergence of resistance mutations within the kinase domain of its target, Abl.	imatinib	51-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-181
32719139-2	2020	We noticed that many patient-resistance mutations occur in the dynamic hot spots recently identified to be responsible for imatinib"s high selectivity toward Abl.	imatinib	123-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-161
32719139-5	2020	The mutations alter the energy landscape of Abl in complex ways: increased kinase activity, altered affinity, and cooperativity for the substrates, and, surprisingly, only a modestly decreased imatinib affinity.	imatinib	193-201	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-47
32592909-2	2020	Targeted drugs already changed the clinical practice in treatment of leukemias, such as imatinib (BCR/ABL inhibitor) in chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL), ibrutinib (Bruton"s tyrosine kinase inhibitor) in chronic lymphocytic leukemia (CLL), venetoclax (BCL2 inhibitor) in CLL and acute myeloid leukemia (AML) or midostaurin (FLT3 inhibitor) in AML.	imatinib	88-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
32098768-0	2020	Discovery of berberine that targetedly induce autophagic degradation of both BCR-ABL and BCR-ABL T315I through recruiting LRSAM1 for overcoming imatinib-resistance.	imatinib	144-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
32098768-0	2020	Discovery of berberine that targetedly induce autophagic degradation of both BCR-ABL and BCR-ABL T315I through recruiting LRSAM1 for overcoming imatinib-resistance.	imatinib	144-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
32098768-0	2020	Discovery of berberine that targetedly induce autophagic degradation of both BCR-ABL and BCR-ABL T315I through recruiting LRSAM1 for overcoming imatinib-resistance.	imatinib	144-152	leucine rich repeat and sterile alpha motif containing 1	Homo sapiens	122-128
32098768-1	2020	PURPOSE: Imatinib, the breakpoint cluster region protein (BCR)/Abelson murine leukemia viral oncogene homolog (ABL) inhibitor, is widely used to treat chronic myeloid leukemia (CML).	imatinib	9-17	BCR activator of RhoGEF and GTPase	Mus musculus	23-56
32098768-1	2020	PURPOSE: Imatinib, the breakpoint cluster region protein (BCR)/Abelson murine leukemia viral oncogene homolog (ABL) inhibitor, is widely used to treat chronic myeloid leukemia (CML).	imatinib	9-17	BCR activator of RhoGEF and GTPase	Mus musculus	58-61
32098768-4	2020	Berberine (BBR) is a potent BCR-ABL inhibitor for imatinib-sensitive and -resistant CML.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
32473019-12	2020	However, imatinib increased glucose-stimulated insulin secretion during the glucose challenge.	imatinib	9-17	insulin	Homo sapiens	47-54
32473019-14	2020	Our data shows that RIPK2 limits the insulin sensitizing effect of gefitinib, whereas imatinib increased insulin secretion.	imatinib	86-94	insulin	Homo sapiens	105-112
32903598-7	2020	S100A8 and S100A9 also induced apoptosis of imatinib-resistant EoL-1 cells (EoL-1-IR).	imatinib	44-52	S100 calcium binding protein A8	Homo sapiens	0-6
32903598-7	2020	S100A8 and S100A9 also induced apoptosis of imatinib-resistant EoL-1 cells (EoL-1-IR).	imatinib	44-52	S100 calcium binding protein A9	Homo sapiens	11-17
32764164-0	2020	Relationship between trough level of tyrosine kinase inhibitor (imatinib and nilotinib) and BCR-ABL ratios in an Indonesian chronic-phase chronic myeloid leukemia (CML) population.	imatinib	64-72	TXK tyrosine kinase	Homo sapiens	37-52
32764164-0	2020	Relationship between trough level of tyrosine kinase inhibitor (imatinib and nilotinib) and BCR-ABL ratios in an Indonesian chronic-phase chronic myeloid leukemia (CML) population.	imatinib	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
32764164-1	2020	Objectives Among Chronic Myeloid Leukemia (CML) patients treated with Tyrosine Kinase Inhibitor (TKI-imatinib-nilotinib), some showed a suboptimal response.	imatinib	101-109	TXK tyrosine kinase	Homo sapiens	70-85
32764164-14	2020	C m i n     ${C}_{min}\hat{\infty }$ imatinib was found to be significantly associated with BCR-ABL ratio.	imatinib	37-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
32764164-16	2020	Conclusions There were high interindividual variations of imatinib and nilotinib correlated with BCR-ABL ratio, but no correlation in nilotinib.	imatinib	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-104
32346864-7	2020	In view of reports that imatinib (a Syk inhibitor) successfully treats symptoms of sickle cell disease, we suggest that Syk tyrosine kinase inhibitors warrant repurposing as potential treatments for SCD.	imatinib	24-32	spleen associated tyrosine kinase	Homo sapiens	36-39
32080901-0	2020	Targeting MDR-1 gene expression, BAX/BCL2, caspase-3 and Ki-67 by nano-encapsulated imatinib and hesperidin to enhance anticancer activity and ameliorate cardiotoxicity.	imatinib	84-92	malic enzyme complex, mitochondrial	Mus musculus	10-15
32080901-0	2020	Targeting MDR-1 gene expression, BAX/BCL2, caspase-3 and Ki-67 by nano-encapsulated imatinib and hesperidin to enhance anticancer activity and ameliorate cardiotoxicity.	imatinib	84-92	BCL2-associated X protein	Mus musculus	33-36
32592909-2	2020	Targeted drugs already changed the clinical practice in treatment of leukemias, such as imatinib (BCR/ABL inhibitor) in chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL), ibrutinib (Bruton"s tyrosine kinase inhibitor) in chronic lymphocytic leukemia (CLL), venetoclax (BCL2 inhibitor) in CLL and acute myeloid leukemia (AML) or midostaurin (FLT3 inhibitor) in AML.	imatinib	88-96	Bruton tyrosine kinase	Homo sapiens	202-226
32080901-0	2020	Targeting MDR-1 gene expression, BAX/BCL2, caspase-3 and Ki-67 by nano-encapsulated imatinib and hesperidin to enhance anticancer activity and ameliorate cardiotoxicity.	imatinib	84-92	B cell leukemia/lymphoma 2	Mus musculus	37-41
32080901-0	2020	Targeting MDR-1 gene expression, BAX/BCL2, caspase-3 and Ki-67 by nano-encapsulated imatinib and hesperidin to enhance anticancer activity and ameliorate cardiotoxicity.	imatinib	84-92	caspase 3	Mus musculus	43-52
32592909-2	2020	Targeted drugs already changed the clinical practice in treatment of leukemias, such as imatinib (BCR/ABL inhibitor) in chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL), ibrutinib (Bruton"s tyrosine kinase inhibitor) in chronic lymphocytic leukemia (CLL), venetoclax (BCL2 inhibitor) in CLL and acute myeloid leukemia (AML) or midostaurin (FLT3 inhibitor) in AML.	imatinib	88-96	BCL2 apoptosis regulator	Homo sapiens	289-293
32080901-0	2020	Targeting MDR-1 gene expression, BAX/BCL2, caspase-3 and Ki-67 by nano-encapsulated imatinib and hesperidin to enhance anticancer activity and ameliorate cardiotoxicity.	imatinib	84-92	antigen identified by monoclonal antibody Ki 67	Mus musculus	57-62
32592909-2	2020	Targeted drugs already changed the clinical practice in treatment of leukemias, such as imatinib (BCR/ABL inhibitor) in chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL), ibrutinib (Bruton"s tyrosine kinase inhibitor) in chronic lymphocytic leukemia (CLL), venetoclax (BCL2 inhibitor) in CLL and acute myeloid leukemia (AML) or midostaurin (FLT3 inhibitor) in AML.	imatinib	88-96	fms related receptor tyrosine kinase 3	Homo sapiens	361-365
32356575-11	2020	Treatment of HCC-PDX xenograft tumor bearing mice with c-Kit inhibitor, imatinib, significantly reduced tumor growth, and phospho-Akt and cyclin D1 expression, as compared to untreated control tumors.	imatinib	72-80	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	55-60
32517495-3	2020	Importantly, the most common PDGFRA molecular subtype, the D842V mutation in exon 18 of the gene which alters the activation loop, is imatinib insensitive in in vitro studies.	imatinib	134-142	platelet derived growth factor receptor alpha	Homo sapiens	29-35
32356575-11	2020	Treatment of HCC-PDX xenograft tumor bearing mice with c-Kit inhibitor, imatinib, significantly reduced tumor growth, and phospho-Akt and cyclin D1 expression, as compared to untreated control tumors.	imatinib	72-80	thymoma viral proto-oncogene 1	Mus musculus	130-133
32356575-11	2020	Treatment of HCC-PDX xenograft tumor bearing mice with c-Kit inhibitor, imatinib, significantly reduced tumor growth, and phospho-Akt and cyclin D1 expression, as compared to untreated control tumors.	imatinib	72-80	cyclin D1	Mus musculus	138-147
32459399-0	2020	Early administration of imatinib mesylate reduces plexiform neurofibroma tumor burden with durable results after drug discontinuation in a mouse model of neurofibromatosis type 1.	imatinib	24-41	neurofibromin 1	Mus musculus	154-178
32439895-4	2020	We show in various models, that murine and human imatinib-resistant leukemia cells positive for the oncogene BCR-ABL1T315I differ from BCR-ABL1 native (BCR-ABL1) cells with regards to niche location and specific niche interactions.	imatinib	49-57	BCR activator of RhoGEF and GTPase	Homo sapiens	109-112
32439895-4	2020	We show in various models, that murine and human imatinib-resistant leukemia cells positive for the oncogene BCR-ABL1T315I differ from BCR-ABL1 native (BCR-ABL1) cells with regards to niche location and specific niche interactions.	imatinib	49-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-117
32439895-4	2020	We show in various models, that murine and human imatinib-resistant leukemia cells positive for the oncogene BCR-ABL1T315I differ from BCR-ABL1 native (BCR-ABL1) cells with regards to niche location and specific niche interactions.	imatinib	49-57	BCR activator of RhoGEF and GTPase	Homo sapiens	109-117
32459399-3	2020	A subsequent phase 2 clinical trial using imatinib mesylate to inhibit SCF/c-kit demonstrated tumor shrinkage in a subset of preexisting pNF; however, imatinib"s role on preventing pNF development has yet to be explored.	imatinib	42-59	kit ligand	Mus musculus	71-74
32459399-3	2020	A subsequent phase 2 clinical trial using imatinib mesylate to inhibit SCF/c-kit demonstrated tumor shrinkage in a subset of preexisting pNF; however, imatinib"s role on preventing pNF development has yet to be explored.	imatinib	42-59	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	75-80
32459399-3	2020	A subsequent phase 2 clinical trial using imatinib mesylate to inhibit SCF/c-kit demonstrated tumor shrinkage in a subset of preexisting pNF; however, imatinib"s role on preventing pNF development has yet to be explored.	imatinib	42-50	kit ligand	Mus musculus	71-74
32459399-3	2020	A subsequent phase 2 clinical trial using imatinib mesylate to inhibit SCF/c-kit demonstrated tumor shrinkage in a subset of preexisting pNF; however, imatinib"s role on preventing pNF development has yet to be explored.	imatinib	42-50	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	75-80
32459399-11	2020	These findings may guide clinical use of imatinib in young NF1 patients prior to the substantial development of pNF.	imatinib	41-49	neurofibromin 1	Homo sapiens	59-62
32667912-6	2020	ABL1 tyrosine kinase inhibitors (TKIs), including imatinib, nilotinib, and dasatinib, are used clinically for treating CML.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-4
32697563-0	2020	Evaluation of Imatinib Concentrations in Samples Submitted for BCR-ABL1 or Imatinib Testing-Evidence to Support Therapeutic Drug Monitoring for Dose Optimization?	imatinib	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-71
32697563-2	2020	Achieving a major molecular response early in treatment, as indicated by a BCR-ABL1 major international scale result of <=0.1% within 6 months, is associated with better patient outcomes and is statistically associated with a trough imatinib concentration of approximately 1000 ng/mL.	imatinib	233-241	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-83
32697563-8	2020	The frequency of imatinib concentrations achieving the therapeutic target was determined and correlated with BCR-ABL1 major international scale, age, and sex.	imatinib	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-117
32879093-5	2020	A 38-year-old male CML patient developed a BCR-ABL1 gene mutation of T315I after 2.5 years of TKI treatment, including imatinib and dasatinib.	imatinib	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-51
32792947-17	2020	The mRNA expression of atrogin-1 increased also in RD cells exposed to imatinib.	imatinib	71-79	F-box protein 32	Mus musculus	23-32
32719331-0	2020	HIF-1alpha regulates cellular metabolism, and Imatinib resistance by targeting phosphogluconate dehydrogenase in gastrointestinal stromal tumors.	imatinib	46-54	phosphogluconate dehydrogenase	Homo sapiens	79-109
32719331-5	2020	One of the rate-limiting enzymes of the PPP-phosphogluconate dehydrogenase (PGD), is dramatically upregulated in gastrointestinal stromal tumors (GISTs) and GIST cell lines resistant to Imatinib (IM) compared with sensitive controls.	imatinib	186-194	phosphoglycerate dehydrogenase	Homo sapiens	40-74
32719331-5	2020	One of the rate-limiting enzymes of the PPP-phosphogluconate dehydrogenase (PGD), is dramatically upregulated in gastrointestinal stromal tumors (GISTs) and GIST cell lines resistant to Imatinib (IM) compared with sensitive controls.	imatinib	186-194	phosphoglycerate dehydrogenase	Homo sapiens	76-79
32703220-6	2020	Adjuvant imatinib therapy is recommended for high-risk GIST; however, it is known that imatinib is less effective against GIST with a PDGFRA D842V mutation.	imatinib	87-95	platelet derived growth factor receptor alpha	Homo sapiens	134-140
32703220-11	2020	Because the tumor had a PDGFRA mutation (D842V substitution), imatinib was suspected to lack efficacy to the tumor.	imatinib	62-70	platelet derived growth factor receptor alpha	Homo sapiens	24-30
32647179-11	2020	Importantly, in vivo, the treatment of the inhibitors (imatinib and AG490) for PDGFRbeta and JAK-STAT signals were capable of attenuating the tooth movement.	imatinib	55-63	platelet derived growth factor receptor beta	Homo sapiens	79-88
32647179-11	2020	Importantly, in vivo, the treatment of the inhibitors (imatinib and AG490) for PDGFRbeta and JAK-STAT signals were capable of attenuating the tooth movement.	imatinib	55-63	signal transducer and activator of transcription 3	Homo sapiens	97-101
32647179-13	2020	Meanwhile, the expressions of PDGFRbeta, JAK2 and STAT3 were inhibited by imatinib and AG490.	imatinib	74-82	platelet derived growth factor receptor beta	Homo sapiens	30-39
32647179-13	2020	Meanwhile, the expressions of PDGFRbeta, JAK2 and STAT3 were inhibited by imatinib and AG490.	imatinib	74-82	Janus kinase 2	Homo sapiens	41-45
32647179-13	2020	Meanwhile, the expressions of PDGFRbeta, JAK2 and STAT3 were inhibited by imatinib and AG490.	imatinib	74-82	signal transducer and activator of transcription 3	Homo sapiens	50-55
32279331-5	2020	In ETV6-ABL1 positive patients, a durable CHR was achieved by 4/9 patients (imatinib 1/5, nilotinib 2/3, dasatinib 1/1).	imatinib	76-84	ETS variant transcription factor 6	Homo sapiens	3-7
32685125-1	2020	Imatinib mesylate is a small tyrosine kinase inhibitor that targets BCR-ABL, ckit and platelet-derived growth factor receptor.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
32753885-0	2020	Chloroquine Combined with Imatinib Overcomes Imatinib Resistance in Gastrointestinal Stromal Tumors by Inhibiting Autophagy via the MAPK/ERK Pathway.	imatinib	26-34	mitogen-activated protein kinase 1	Homo sapiens	137-140
32753885-10	2020	Detection of KIT and PDGFRA gene mutations in the transplanted imatinib-resistant GIST was done by denaturing high performance liquid chromatography (DHPLC) and direct sequencing.	imatinib	63-71	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	13-16
32753885-10	2020	Detection of KIT and PDGFRA gene mutations in the transplanted imatinib-resistant GIST was done by denaturing high performance liquid chromatography (DHPLC) and direct sequencing.	imatinib	63-71	platelet derived growth factor receptor alpha	Homo sapiens	21-27
32753885-14	2020	Conclusion: Our data suggest that autophagy through the MAPK/ERK pathway may play a pivotal role in imatinib-resistant GIST proliferation.	imatinib	100-108	mitogen-activated protein kinase 1	Homo sapiens	61-64
32500973-0	2020	Activating variants in PDGFRB result in a spectrum of disorders responsive to imatinib monotherapy.	imatinib	78-86	platelet derived growth factor receptor beta	Homo sapiens	23-29
32279331-5	2020	In ETV6-ABL1 positive patients, a durable CHR was achieved by 4/9 patients (imatinib 1/5, nilotinib 2/3, dasatinib 1/1).	imatinib	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-12
32051529-0	2020	SRSF1 mediates cytokine-induced impaired imatinib sensitivity in chronic myeloid leukemia.	imatinib	41-49	serine and arginine rich splicing factor 1	Homo sapiens	0-5
32415468-0	2020	Effect of Cytochrome P450 and ABCB1 Polymorphisms on Imatinib Pharmacokinetics After Single-Dose Administration to Healthy Subjects.	imatinib	53-61	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	10-25
32415468-0	2020	Effect of Cytochrome P450 and ABCB1 Polymorphisms on Imatinib Pharmacokinetics After Single-Dose Administration to Healthy Subjects.	imatinib	53-61	ATP binding cassette subfamily B member 1	Homo sapiens	30-35
32415468-3	2020	OBJECTIVE: To investigate whether polymorphisms in genes encoding cytochrome P450 (CYP) enzymes and ABCB1 transporter affect imatinib pharmacokinetic parameters.	imatinib	125-133	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	66-81
32415468-3	2020	OBJECTIVE: To investigate whether polymorphisms in genes encoding cytochrome P450 (CYP) enzymes and ABCB1 transporter affect imatinib pharmacokinetic parameters.	imatinib	125-133	ATP binding cassette subfamily B member 1	Homo sapiens	100-105
32415468-9	2020	CYP2B6 516GT carriers showed a significant reduction of imatinib concentration at 24 h (23%, 391 ng/dL vs 511 ng/dL in 516GG carriers, p = 0.005) and elimination half-life (11%, 12.6 h vs 14.1 h in 516GG carriers, p = 0.041).	imatinib	56-64	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	0-6
32415468-12	2020	CONCLUSION: CYP2B6 G516T and CYP3A4 *20,*22 polymorphisms could influence imatinib plasma concentrations and safety profile, after single-dose administration to healthy subjects.	imatinib	74-82	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	12-18
32415468-12	2020	CONCLUSION: CYP2B6 G516T and CYP3A4 *20,*22 polymorphisms could influence imatinib plasma concentrations and safety profile, after single-dose administration to healthy subjects.	imatinib	74-82	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	29-35
32647423-0	2020	MicroRNA 30a Mediated Autophagy and Imatinib Response in Egyptian Chronic Myeloid Leukemia Patients.	imatinib	36-44	microRNA 30a	Homo sapiens	0-12
32647423-9	2020	miR-30a was over expressed and Beclin 1 was under expressed in imatinib responders compared to resistant cases median 1.21(0.55-3.02) versus median 0.65 (0.03-1.0) (p = 0.001) and median 950.0 (400.0-2410.0) versus, median 1570.0 (920.0-5430.0) (p < 0.001) respectively.	imatinib	63-71	beclin 1	Homo sapiens	31-39
32647423-10	2020	Beclin 1 correlated significantly positively with miR-30a in new cases (p = 0.001) and negatively in imatinib responders (p = 0.021).	imatinib	101-109	beclin 1	Homo sapiens	0-8
32647423-11	2020	Receiver Operating Curves demonstrated the performances of miR-30a and Beclin 1 to detect imatinib resistance.	imatinib	90-98	microRNA 30a	Homo sapiens	59-66
32647423-11	2020	Receiver Operating Curves demonstrated the performances of miR-30a and Beclin 1 to detect imatinib resistance.	imatinib	90-98	beclin 1	Homo sapiens	71-79
32647423-13	2020	Both miR-30a and Beclin 1 levels showed a relation with imatinib response and can therefore be put forward as valuable markers for detection of resistance and may also have promising future therapeutic implications.	imatinib	56-64	microRNA 30a	Homo sapiens	5-12
32647423-13	2020	Both miR-30a and Beclin 1 levels showed a relation with imatinib response and can therefore be put forward as valuable markers for detection of resistance and may also have promising future therapeutic implications.	imatinib	56-64	beclin 1	Homo sapiens	17-25
32051529-6	2020	SRSF1 overexpression conferred cytokine independence to untransformed hematopoietic cells and impaired imatinib sensitivity in CML cells, while SRSF1 depletion in CD34+ CP CML cells prevented the ability of extrinsic cytokines to decrease imatinib sensitivity.	imatinib	103-111	serine and arginine rich splicing factor 1	Homo sapiens	0-5
32615108-1	2020	BACKGROUND: Targeting of KIT and PDGFRA with imatinib revolutionised treatment in gastrointestinal stromal tumour; however, PDGFRA Asp842Val (D842V)-mutated gastrointestinal stromal tumour is highly resistant to tyrosine kinase inhibitors.	imatinib	45-53	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	25-28
32051529-6	2020	SRSF1 overexpression conferred cytokine independence to untransformed hematopoietic cells and impaired imatinib sensitivity in CML cells, while SRSF1 depletion in CD34+ CP CML cells prevented the ability of extrinsic cytokines to decrease imatinib sensitivity.	imatinib	239-247	serine and arginine rich splicing factor 1	Homo sapiens	0-5
32615108-1	2020	BACKGROUND: Targeting of KIT and PDGFRA with imatinib revolutionised treatment in gastrointestinal stromal tumour; however, PDGFRA Asp842Val (D842V)-mutated gastrointestinal stromal tumour is highly resistant to tyrosine kinase inhibitors.	imatinib	45-53	platelet derived growth factor receptor alpha	Homo sapiens	33-39
32051529-7	2020	Mechanistically, PRKCH and PLCH1 were upregulated by elevated SRSF1 levels, and contributed to impaired imatinib sensitivity.	imatinib	104-112	protein kinase C eta	Homo sapiens	17-22
32051529-7	2020	Mechanistically, PRKCH and PLCH1 were upregulated by elevated SRSF1 levels, and contributed to impaired imatinib sensitivity.	imatinib	104-112	phospholipase C eta 1	Homo sapiens	27-32
32051529-7	2020	Mechanistically, PRKCH and PLCH1 were upregulated by elevated SRSF1 levels, and contributed to impaired imatinib sensitivity.	imatinib	104-112	serine and arginine rich splicing factor 1	Homo sapiens	62-67
32051529-10	2020	Together, our data support an SRSF1/PRKCH/PLCH1 axis in contributing to cytokine-induced impaired imatinib sensitivity in CML.	imatinib	98-106	serine and arginine rich splicing factor 1	Homo sapiens	30-35
32051529-10	2020	Together, our data support an SRSF1/PRKCH/PLCH1 axis in contributing to cytokine-induced impaired imatinib sensitivity in CML.	imatinib	98-106	protein kinase C eta	Homo sapiens	36-41
32051529-10	2020	Together, our data support an SRSF1/PRKCH/PLCH1 axis in contributing to cytokine-induced impaired imatinib sensitivity in CML.	imatinib	98-106	phospholipase C eta 1	Homo sapiens	42-47
32599808-0	2020	Inhibition of FGF2-Mediated Signaling in GIST-Promising Approach for Overcoming Resistance to Imatinib.	imatinib	94-102	fibroblast growth factor 2	Homo sapiens	14-18
32598170-0	2020	circ_0080145 Enhances Imatinib Resistance of Chronic Myeloid Leukemia by Regulating miR-326/PPFIA1 Axis.	imatinib	22-30	microRNA 326	Homo sapiens	84-91
32598170-0	2020	circ_0080145 Enhances Imatinib Resistance of Chronic Myeloid Leukemia by Regulating miR-326/PPFIA1 Axis.	imatinib	22-30	PTPRF interacting protein alpha 1	Homo sapiens	92-98
32298535-2	2020	Recently, we identified the partial PPARgamma agonist telmisartan as effective sensitizer of resistant K562 CML cells to imatinib treatment.	imatinib	121-129	peroxisome proliferator activated receptor gamma	Homo sapiens	36-45
32655803-17	2020	CONCLUSION: We proposed a novel molecular mechanism of imatinib resistance in CML in which the high expression of Lyn in imatinib-resistant cells inhibited Ac-Foxo1 and p53 expression through the BCR-ABL/SIRT1/Foxo1 signaling pathway, thus reducing apoptosis and mediating imatinib resistance.	imatinib	55-63	LYN proto-oncogene, Src family tyrosine kinase	Mus musculus	114-117
32606967-0	2020	Inhibition of Skp2 Sensitizes Chronic Myeloid Leukemia Cells to Imatinib.	imatinib	64-72	S-phase kinase associated protein 2	Homo sapiens	14-18
32606967-10	2020	Furthermore, inhibition of Skp2 expression by shRNAs or blocking the PI3K/Akt/CREB pathway greatly enhances the sensitivity of CML cells to Imatinib treatment.	imatinib	140-148	S-phase kinase associated protein 2	Homo sapiens	27-31
32606967-10	2020	Furthermore, inhibition of Skp2 expression by shRNAs or blocking the PI3K/Akt/CREB pathway greatly enhances the sensitivity of CML cells to Imatinib treatment.	imatinib	140-148	AKT serine/threonine kinase 1	Homo sapiens	74-77
32606967-10	2020	Furthermore, inhibition of Skp2 expression by shRNAs or blocking the PI3K/Akt/CREB pathway greatly enhances the sensitivity of CML cells to Imatinib treatment.	imatinib	140-148	cAMP responsive element binding protein 1	Homo sapiens	78-82
32606967-11	2020	Conclusion: We conclude that the PI3K/Akt/CREB axis regulates the sensitivity of K562 cells to Imatinib via mediating Skp2 expression.	imatinib	95-103	AKT serine/threonine kinase 1	Homo sapiens	38-41
32606967-11	2020	Conclusion: We conclude that the PI3K/Akt/CREB axis regulates the sensitivity of K562 cells to Imatinib via mediating Skp2 expression.	imatinib	95-103	cAMP responsive element binding protein 1	Homo sapiens	42-46
32606967-11	2020	Conclusion: We conclude that the PI3K/Akt/CREB axis regulates the sensitivity of K562 cells to Imatinib via mediating Skp2 expression.	imatinib	95-103	S-phase kinase associated protein 2	Homo sapiens	118-122
32655803-0	2020	The Lyn-SIRT1 signaling pathway is involved in imatinib resistance in chronic myeloid leukaemia.	imatinib	47-55	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	4-7
32655803-17	2020	CONCLUSION: We proposed a novel molecular mechanism of imatinib resistance in CML in which the high expression of Lyn in imatinib-resistant cells inhibited Ac-Foxo1 and p53 expression through the BCR-ABL/SIRT1/Foxo1 signaling pathway, thus reducing apoptosis and mediating imatinib resistance.	imatinib	55-63	forkhead box O1	Homo sapiens	159-164
32655803-0	2020	The Lyn-SIRT1 signaling pathway is involved in imatinib resistance in chronic myeloid leukaemia.	imatinib	47-55	sirtuin 1	Homo sapiens	8-13
32655803-1	2020	BACKGROUND: Imatinib resistance is commonly associated with the activation of BCR-ABL signaling in chronic myeloid leukaemia (CML).	imatinib	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
32655803-17	2020	CONCLUSION: We proposed a novel molecular mechanism of imatinib resistance in CML in which the high expression of Lyn in imatinib-resistant cells inhibited Ac-Foxo1 and p53 expression through the BCR-ABL/SIRT1/Foxo1 signaling pathway, thus reducing apoptosis and mediating imatinib resistance.	imatinib	55-63	tumor protein p53	Homo sapiens	169-172
32655803-2	2020	The activation of Lyn can result in imatinib resistance by regulating the formation of BCR-ABL protein complexes.	imatinib	36-44	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	18-21
32655803-17	2020	CONCLUSION: We proposed a novel molecular mechanism of imatinib resistance in CML in which the high expression of Lyn in imatinib-resistant cells inhibited Ac-Foxo1 and p53 expression through the BCR-ABL/SIRT1/Foxo1 signaling pathway, thus reducing apoptosis and mediating imatinib resistance.	imatinib	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	200-203
32655803-2	2020	The activation of Lyn can result in imatinib resistance by regulating the formation of BCR-ABL protein complexes.	imatinib	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
32655803-4	2020	This study aimed to investigate whether the signaling pathway of Lyn/BCR-ABL/SIRT1 could mediate imatinib resistance in CML.	imatinib	97-105	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	65-68
32655803-4	2020	This study aimed to investigate whether the signaling pathway of Lyn/BCR-ABL/SIRT1 could mediate imatinib resistance in CML.	imatinib	97-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
32655803-17	2020	CONCLUSION: We proposed a novel molecular mechanism of imatinib resistance in CML in which the high expression of Lyn in imatinib-resistant cells inhibited Ac-Foxo1 and p53 expression through the BCR-ABL/SIRT1/Foxo1 signaling pathway, thus reducing apoptosis and mediating imatinib resistance.	imatinib	55-63	sirtuin 1	Mus musculus	204-209
32655803-4	2020	This study aimed to investigate whether the signaling pathway of Lyn/BCR-ABL/SIRT1 could mediate imatinib resistance in CML.	imatinib	97-105	sirtuin 1	Homo sapiens	77-82
32655803-17	2020	CONCLUSION: We proposed a novel molecular mechanism of imatinib resistance in CML in which the high expression of Lyn in imatinib-resistant cells inhibited Ac-Foxo1 and p53 expression through the BCR-ABL/SIRT1/Foxo1 signaling pathway, thus reducing apoptosis and mediating imatinib resistance.	imatinib	55-63	forkhead box O1	Homo sapiens	210-215
32655803-12	2020	Imatinib suppressed BCR-ABL phosphorylation in both K562 and K562R cells.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
32655803-17	2020	CONCLUSION: We proposed a novel molecular mechanism of imatinib resistance in CML in which the high expression of Lyn in imatinib-resistant cells inhibited Ac-Foxo1 and p53 expression through the BCR-ABL/SIRT1/Foxo1 signaling pathway, thus reducing apoptosis and mediating imatinib resistance.	imatinib	121-129	LYN proto-oncogene, Src family tyrosine kinase	Mus musculus	114-117
32655803-16	2020	In vivo experiments showed that imatinib and/or SIRT1 inhibition both prolonged the survival of the CML mouse model and that the effects of imatinib were enhanced in combination with SIRT1 inhibition.	imatinib	140-148	sirtuin 1	Mus musculus	48-53
32655803-17	2020	CONCLUSION: We proposed a novel molecular mechanism of imatinib resistance in CML in which the high expression of Lyn in imatinib-resistant cells inhibited Ac-Foxo1 and p53 expression through the BCR-ABL/SIRT1/Foxo1 signaling pathway, thus reducing apoptosis and mediating imatinib resistance.	imatinib	121-129	forkhead box O1	Homo sapiens	159-164
32655803-17	2020	CONCLUSION: We proposed a novel molecular mechanism of imatinib resistance in CML in which the high expression of Lyn in imatinib-resistant cells inhibited Ac-Foxo1 and p53 expression through the BCR-ABL/SIRT1/Foxo1 signaling pathway, thus reducing apoptosis and mediating imatinib resistance.	imatinib	121-129	tumor protein p53	Homo sapiens	169-172
32655803-17	2020	CONCLUSION: We proposed a novel molecular mechanism of imatinib resistance in CML in which the high expression of Lyn in imatinib-resistant cells inhibited Ac-Foxo1 and p53 expression through the BCR-ABL/SIRT1/Foxo1 signaling pathway, thus reducing apoptosis and mediating imatinib resistance.	imatinib	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	200-203
32655803-17	2020	CONCLUSION: We proposed a novel molecular mechanism of imatinib resistance in CML in which the high expression of Lyn in imatinib-resistant cells inhibited Ac-Foxo1 and p53 expression through the BCR-ABL/SIRT1/Foxo1 signaling pathway, thus reducing apoptosis and mediating imatinib resistance.	imatinib	121-129	sirtuin 1	Mus musculus	204-209
32655803-17	2020	CONCLUSION: We proposed a novel molecular mechanism of imatinib resistance in CML in which the high expression of Lyn in imatinib-resistant cells inhibited Ac-Foxo1 and p53 expression through the BCR-ABL/SIRT1/Foxo1 signaling pathway, thus reducing apoptosis and mediating imatinib resistance.	imatinib	121-129	forkhead box O1	Homo sapiens	210-215
32655803-17	2020	CONCLUSION: We proposed a novel molecular mechanism of imatinib resistance in CML in which the high expression of Lyn in imatinib-resistant cells inhibited Ac-Foxo1 and p53 expression through the BCR-ABL/SIRT1/Foxo1 signaling pathway, thus reducing apoptosis and mediating imatinib resistance.	imatinib	121-129	LYN proto-oncogene, Src family tyrosine kinase	Mus musculus	114-117
32655803-17	2020	CONCLUSION: We proposed a novel molecular mechanism of imatinib resistance in CML in which the high expression of Lyn in imatinib-resistant cells inhibited Ac-Foxo1 and p53 expression through the BCR-ABL/SIRT1/Foxo1 signaling pathway, thus reducing apoptosis and mediating imatinib resistance.	imatinib	121-129	forkhead box O1	Homo sapiens	159-164
32655803-17	2020	CONCLUSION: We proposed a novel molecular mechanism of imatinib resistance in CML in which the high expression of Lyn in imatinib-resistant cells inhibited Ac-Foxo1 and p53 expression through the BCR-ABL/SIRT1/Foxo1 signaling pathway, thus reducing apoptosis and mediating imatinib resistance.	imatinib	121-129	tumor protein p53	Homo sapiens	169-172
32655803-17	2020	CONCLUSION: We proposed a novel molecular mechanism of imatinib resistance in CML in which the high expression of Lyn in imatinib-resistant cells inhibited Ac-Foxo1 and p53 expression through the BCR-ABL/SIRT1/Foxo1 signaling pathway, thus reducing apoptosis and mediating imatinib resistance.	imatinib	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	200-203
32655803-17	2020	CONCLUSION: We proposed a novel molecular mechanism of imatinib resistance in CML in which the high expression of Lyn in imatinib-resistant cells inhibited Ac-Foxo1 and p53 expression through the BCR-ABL/SIRT1/Foxo1 signaling pathway, thus reducing apoptosis and mediating imatinib resistance.	imatinib	121-129	sirtuin 1	Mus musculus	204-209
32655803-17	2020	CONCLUSION: We proposed a novel molecular mechanism of imatinib resistance in CML in which the high expression of Lyn in imatinib-resistant cells inhibited Ac-Foxo1 and p53 expression through the BCR-ABL/SIRT1/Foxo1 signaling pathway, thus reducing apoptosis and mediating imatinib resistance.	imatinib	121-129	forkhead box O1	Homo sapiens	210-215
32670260-2	2020	The most frequent PDGFRA mutation is the exon 18 D842V, which is correlated to specific clinico-pathological features, such as primary imatinib resistance and higher indolence.	imatinib	135-143	platelet derived growth factor receptor alpha	Homo sapiens	18-24
32654459-6	2020	In total, 291 (50.5%) imatinib-, 152 (63.9%) nilotinib-, and 160 (57.3%) dasatinib-resistant cases developed BCR-ABL mutation (s) .	imatinib	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-116
32654459-10	2020	Other variables associated with developing BCR-ABL mutation (s) in imatinib-, nilotinib-, or dasatinib-resistant cases included male gender, younger age, no comorbidity, advanced phase before starting current TKI therapy, longer interval from diagnosis to starting current TKI therapy, acquired resistance, and TKI resistance due to progression to advanced phase or hematologic failure.	imatinib	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
32529309-5	2020	RESULTS: Curcumin demonstrated potent reversible inhibition of cytochrome P450 (CYP)3A4-mediated N-demethylation of imatinib and bosutinib and CYP2C8-mediated metabolism of imatinib with inhibitory constants (ki,u) of <=1.5 mumol.	imatinib	116-124	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	63-87
32529309-5	2020	RESULTS: Curcumin demonstrated potent reversible inhibition of cytochrome P450 (CYP)3A4-mediated N-demethylation of imatinib and bosutinib and CYP2C8-mediated metabolism of imatinib with inhibitory constants (ki,u) of <=1.5 mumol.	imatinib	173-181	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	143-149
32671189-0	2020	A Small Molecule Inhibitor, OGP46, Is Effective against Imatinib-Resistant BCR-ABL Mutations via the BCR-ABL/JAK-STAT Pathway.	imatinib	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
32671189-0	2020	A Small Molecule Inhibitor, OGP46, Is Effective against Imatinib-Resistant BCR-ABL Mutations via the BCR-ABL/JAK-STAT Pathway.	imatinib	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-82
32671189-3	2020	However, mutations in the BCR-ABL kinase domain are a major cause of resistance to imatinib, demonstrating that BCR-ABL remains a critical drug target.	imatinib	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
32671189-3	2020	However, mutations in the BCR-ABL kinase domain are a major cause of resistance to imatinib, demonstrating that BCR-ABL remains a critical drug target.	imatinib	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
32671189-5	2020	OGP46 exhibits potent activity against imatinib-resistant BCR-ABL mutations, including T315I.	imatinib	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-65
32671189-10	2020	Thus, OGP46 may be a novel strategy for overcoming imatinib-resistance BCR-ABL mutations, including T315I.	imatinib	51-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
32476052-3	2020	METHODS: Here, we demonstrated that this Cycle could be enhanced by the synergistic knock down of PD-L1 through co-delivery of siRNA-PD-L1 (siPD-L1) and imatinib (IMT) in a liposomal nanoparticle.	imatinib	153-161	CD274 molecule	Sus scrofa	98-103
32179085-1	2020	The selective BCR-ABL tyrosine kinase inhibitor imatinib is one of the first-line therapies in the management of chronic myeloid leukaemia (CML).	imatinib	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
32179085-2	2020	However, acquired resistance to this inhibitor, which is especially conferred by the T315I point mutation in BCR-ABL, impedes the efficacy of imatinib therapy.	imatinib	142-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
32112424-1	2020	Imatinib was the first BCR-ABL inhibitor used in clinical practice to treat chronic myeloid leukemia (CML) and significantly improve the life expectancy of CML patients in the chronic phase.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
32371592-5	2020	Simultaneous PI3K and KIT inhibition with copanlisib and imatinib resulted in enhanced impairment of cell viability in both imatinib-sensitive and -resistant GIST cell models, although apoptosis was mostly triggered in GIST-T1.	imatinib	57-65	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	22-25
32371592-5	2020	Simultaneous PI3K and KIT inhibition with copanlisib and imatinib resulted in enhanced impairment of cell viability in both imatinib-sensitive and -resistant GIST cell models, although apoptosis was mostly triggered in GIST-T1.	imatinib	124-132	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	22-25
32371592-9	2020	Effective KIT inhibition is necessary in order to achieve synergistic or additive effects with the combination of imatinib and any given PI3K/mTOR pathway inhibition.	imatinib	114-122	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	10-13
32189339-0	2020	Correction of Bcl-x splicing improves responses to imatinib in chronic myeloid leukaemia cells and mouse models.	imatinib	51-59	BCL2-like 1	Mus musculus	14-19
32112424-0	2020	The potentiation of menadione on imatinib by down-regulation of ABCB1 expression.	imatinib	33-41	ATP binding cassette subfamily B member 1	Homo sapiens	64-69
32272420-9	2020	However, the repression of the STAT5 phosphorylation relates with the possibility to sensitize K562-resistant CML cells to imatinib treatment.	imatinib	123-131	signal transducer and activator of transcription 5A	Homo sapiens	31-36
32552937-0	2020	[MiR-124-3p Enhances the Sansitivity of Chronic Myelogenous Leukemia Cell K562-R to Imatinib by Targeting ABCA2].	imatinib	84-92	microRNA 124-3	Homo sapiens	1-11
32552937-0	2020	[MiR-124-3p Enhances the Sansitivity of Chronic Myelogenous Leukemia Cell K562-R to Imatinib by Targeting ABCA2].	imatinib	84-92	ATP binding cassette subfamily A member 2	Homo sapiens	106-111
32466502-6	2020	Imatinib also reduced the expression of mitochondrial biogenesis activators (peroxisome proliferator-activated receptor coactivator-1 alpha (PGC1alpha), nuclear respiratory factor 2 (NRF2), and mitochondrial transcription factor A (TFAM)) and mitochondrial mass in imatinib-sensitive GIST cells.	imatinib	0-8	PPARG coactivator 1 alpha	Homo sapiens	141-150
32485885-11	2020	ABL gene editing-based therapy might provide a potential strategy for imatinib-insensitive or resistant CML patients.	imatinib	70-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
32466502-6	2020	Imatinib also reduced the expression of mitochondrial biogenesis activators (peroxisome proliferator-activated receptor coactivator-1 alpha (PGC1alpha), nuclear respiratory factor 2 (NRF2), and mitochondrial transcription factor A (TFAM)) and mitochondrial mass in imatinib-sensitive GIST cells.	imatinib	0-8	GA binding protein transcription factor subunit beta 1	Homo sapiens	153-181
32466502-6	2020	Imatinib also reduced the expression of mitochondrial biogenesis activators (peroxisome proliferator-activated receptor coactivator-1 alpha (PGC1alpha), nuclear respiratory factor 2 (NRF2), and mitochondrial transcription factor A (TFAM)) and mitochondrial mass in imatinib-sensitive GIST cells.	imatinib	0-8	GA binding protein transcription factor subunit beta 1	Homo sapiens	183-187
32466502-6	2020	Imatinib also reduced the expression of mitochondrial biogenesis activators (peroxisome proliferator-activated receptor coactivator-1 alpha (PGC1alpha), nuclear respiratory factor 2 (NRF2), and mitochondrial transcription factor A (TFAM)) and mitochondrial mass in imatinib-sensitive GIST cells.	imatinib	0-8	transcription factor A, mitochondrial	Homo sapiens	194-230
32466502-6	2020	Imatinib also reduced the expression of mitochondrial biogenesis activators (peroxisome proliferator-activated receptor coactivator-1 alpha (PGC1alpha), nuclear respiratory factor 2 (NRF2), and mitochondrial transcription factor A (TFAM)) and mitochondrial mass in imatinib-sensitive GIST cells.	imatinib	0-8	transcription factor A, mitochondrial	Homo sapiens	232-236
32466502-7	2020	Lower TFAM levels were also observed in imatinib-sensitive GISTs than in tumors from untreated patients.	imatinib	40-48	transcription factor A, mitochondrial	Homo sapiens	6-10
32430012-0	2020	Novel HDAC inhibitor MAKV-8 and imatinib synergistically kill chronic myeloid leukemia cells via inhibition of BCR-ABL/MYC-signaling: effect on imatinib resistance and stem cells.	imatinib	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
32439979-0	2020	Serotonin re-uptake transporter gene polymorphisms are associated with imatinib-induced diarrhoea in chronic myeloid leukaemia patients.	imatinib	71-79	solute carrier family 6 member 4	Homo sapiens	0-31
32439979-8	2020	These data suggest SERT polymorphisms influence imatinib-induced diarrhoea but not that of dasatinib.	imatinib	48-56	solute carrier family 6 member 4	Homo sapiens	19-23
32430012-9	2020	We also showed that beclin-1 knockdown prevented MAKV-8-imatinib combination-induced apoptosis.	imatinib	56-64	beclin 1	Homo sapiens	20-28
32430012-0	2020	Novel HDAC inhibitor MAKV-8 and imatinib synergistically kill chronic myeloid leukemia cells via inhibition of BCR-ABL/MYC-signaling: effect on imatinib resistance and stem cells.	imatinib	32-40	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	119-122
32430012-10	2020	Moreover, MAKV-8 and imatinib co-treatment synergistically reduced BCR-ABL-related signaling pathways involved in CML cell growth and survival.	imatinib	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
32430012-2	2020	Since BCR-ABL displays abnormal constitutive tyrosine kinase activity, therapies using tyrosine kinase inhibitors (TKis) such as imatinib represent a major breakthrough for the outcome of CML patients.	imatinib	129-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-13
32430012-11	2020	Since our results showed that LSCs from CML patients overexpressed c-MYC, importantly MAKV-8-imatinib co-treatment reduced c-MYC levels and the LSC population.	imatinib	93-101	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	67-72
32457834-17	2020	Finally, targeted therapy with imatinib was induced in presence of a druggable c-KIT mutation, leading to a considerable response of all tumor sites that is still ongoing.	imatinib	31-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	79-84
32430012-11	2020	Since our results showed that LSCs from CML patients overexpressed c-MYC, importantly MAKV-8-imatinib co-treatment reduced c-MYC levels and the LSC population.	imatinib	93-101	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	123-128
32385283-6	2020	Our cryo-EM, biochemical, and functional analyses reveal the binding mode of three chemotherapeutic compounds, demonstrate how these molecules open the closed conformation of the transporter, and establish that imatinib is particularly effective in stabilizing the inward facing conformation of ABCG2.	imatinib	211-219	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	295-300
32084420-6	2020	Interestingly, p53 expression was elevated by the SN-38 mono-treatment, and was not further increased after the co-treatment; besides, knockdown of p53 could only reduce the expression of cleaved-PARP partially, and weaken the enhanced proliferation inhibition induced by SN-38 plus imatinib, indicating that there might be other factors involved in the synergistic effects besides p53.	imatinib	283-291	tumor protein p53	Homo sapiens	15-18
32084420-6	2020	Interestingly, p53 expression was elevated by the SN-38 mono-treatment, and was not further increased after the co-treatment; besides, knockdown of p53 could only reduce the expression of cleaved-PARP partially, and weaken the enhanced proliferation inhibition induced by SN-38 plus imatinib, indicating that there might be other factors involved in the synergistic effects besides p53.	imatinib	283-291	tumor protein p53	Homo sapiens	148-151
32084420-6	2020	Interestingly, p53 expression was elevated by the SN-38 mono-treatment, and was not further increased after the co-treatment; besides, knockdown of p53 could only reduce the expression of cleaved-PARP partially, and weaken the enhanced proliferation inhibition induced by SN-38 plus imatinib, indicating that there might be other factors involved in the synergistic effects besides p53.	imatinib	283-291	poly(ADP-ribose) polymerase 1	Homo sapiens	196-200
32084420-6	2020	Interestingly, p53 expression was elevated by the SN-38 mono-treatment, and was not further increased after the co-treatment; besides, knockdown of p53 could only reduce the expression of cleaved-PARP partially, and weaken the enhanced proliferation inhibition induced by SN-38 plus imatinib, indicating that there might be other factors involved in the synergistic effects besides p53.	imatinib	283-291	tumor protein p53	Homo sapiens	148-151
32293378-8	2020	Sixteen case reports of HES presented with cough as predominant or sole symptom, with nine male patients with positive PDGFRA fusion gene, who responded well to imatinib.	imatinib	161-169	platelet derived growth factor receptor alpha	Homo sapiens	119-125
32269633-0	2020	Imatinib therapy in acute myeloid leukemia with DEK-NUP214 and FIP1L1-PDGFRA rearrangement: A case report.	imatinib	0-8	DEK proto-oncogene	Homo sapiens	48-51
32269633-0	2020	Imatinib therapy in acute myeloid leukemia with DEK-NUP214 and FIP1L1-PDGFRA rearrangement: A case report.	imatinib	0-8	nucleoporin 214	Homo sapiens	52-58
32269633-0	2020	Imatinib therapy in acute myeloid leukemia with DEK-NUP214 and FIP1L1-PDGFRA rearrangement: A case report.	imatinib	0-8	factor interacting with PAPOLA and CPSF1	Homo sapiens	63-69
32269633-0	2020	Imatinib therapy in acute myeloid leukemia with DEK-NUP214 and FIP1L1-PDGFRA rearrangement: A case report.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	70-76
32269633-1	2020	The fusion product of FIP1-like-1 (FIP1L1) and platelet-derived growth factor receptor alpha (PDGFRA) gene rearrangement is a tyrosine kinase oncoprotein sensitive to imatinib.	imatinib	167-175	factor interacting with PAPOLA and CPSF1	Homo sapiens	22-33
32269633-1	2020	The fusion product of FIP1-like-1 (FIP1L1) and platelet-derived growth factor receptor alpha (PDGFRA) gene rearrangement is a tyrosine kinase oncoprotein sensitive to imatinib.	imatinib	167-175	factor interacting with PAPOLA and CPSF1	Homo sapiens	35-41
32269633-1	2020	The fusion product of FIP1-like-1 (FIP1L1) and platelet-derived growth factor receptor alpha (PDGFRA) gene rearrangement is a tyrosine kinase oncoprotein sensitive to imatinib.	imatinib	167-175	platelet derived growth factor receptor alpha	Homo sapiens	47-92
32269633-1	2020	The fusion product of FIP1-like-1 (FIP1L1) and platelet-derived growth factor receptor alpha (PDGFRA) gene rearrangement is a tyrosine kinase oncoprotein sensitive to imatinib.	imatinib	167-175	platelet derived growth factor receptor alpha	Homo sapiens	94-100
32350132-2	2020	Although first-line treatment, imatinib, has revolutionized GIST treatment, drug resistance due to acquisition of secondary KIT/PDGFRalpha mutations develops in a majority of patients.	imatinib	31-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	124-127
32350132-2	2020	Although first-line treatment, imatinib, has revolutionized GIST treatment, drug resistance due to acquisition of secondary KIT/PDGFRalpha mutations develops in a majority of patients.	imatinib	31-39	platelet derived growth factor receptor alpha	Homo sapiens	128-138
32350132-5	2020	Here, we report the discovery and pharmacological characterization of AZD3229, a potent and selective small-molecule inhibitor of KIT and PDGFRalpha designed to inhibit a broad range of primary and imatinib-resistant secondary mutations seen in GIST.	imatinib	198-206	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	130-133
32350132-5	2020	Here, we report the discovery and pharmacological characterization of AZD3229, a potent and selective small-molecule inhibitor of KIT and PDGFRalpha designed to inhibit a broad range of primary and imatinib-resistant secondary mutations seen in GIST.	imatinib	198-206	platelet derived growth factor receptor alpha	Homo sapiens	138-148
31371419-9	2020	Combined inhibition of BCR-ABL1 with imatinib and MDM2 with DS-5272 increased NOXA level, markedly reduced leukemic linage-SCA-1+C-KIT+ cells and hematopoiesis, decreased leukemia burden, significantly prolonged the survival of mice engrafted with bone marrow cells from Scl-tTa-BCR-ABL1 mice, and significantly decreased chronic myeloid leukemia stem cell frequency in secondary transplantations.	imatinib	37-45	BCR activator of RhoGEF and GTPase	Mus musculus	23-31
31371419-9	2020	Combined inhibition of BCR-ABL1 with imatinib and MDM2 with DS-5272 increased NOXA level, markedly reduced leukemic linage-SCA-1+C-KIT+ cells and hematopoiesis, decreased leukemia burden, significantly prolonged the survival of mice engrafted with bone marrow cells from Scl-tTa-BCR-ABL1 mice, and significantly decreased chronic myeloid leukemia stem cell frequency in secondary transplantations.	imatinib	37-45	phorbol-12-myristate-13-acetate-induced protein 1	Mus musculus	78-82
31371419-9	2020	Combined inhibition of BCR-ABL1 with imatinib and MDM2 with DS-5272 increased NOXA level, markedly reduced leukemic linage-SCA-1+C-KIT+ cells and hematopoiesis, decreased leukemia burden, significantly prolonged the survival of mice engrafted with bone marrow cells from Scl-tTa-BCR-ABL1 mice, and significantly decreased chronic myeloid leukemia stem cell frequency in secondary transplantations.	imatinib	37-45	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	129-134
32293378-11	2020	PDGFRA+ HES patients present with chronic cough respond well to imatinib.	imatinib	64-72	platelet derived growth factor receptor alpha	Homo sapiens	0-6
32293378-12	2020	Our case reports indicate that PDGFRA negative HES patients may respond to imatinib as well.	imatinib	75-83	platelet derived growth factor receptor alpha	Homo sapiens	31-37
31371410-2	2020	Peroxisome proliferator-activated receptor-gamma (PPARgamma) agonist pioglitazone downregulates signal transducer and activator of transcription 5 (STAT5) and in combination with imatinib induces complete molecular response in imatinib-refractory patients by eroding leukemia stem cells.	imatinib	179-187	peroxisome proliferator activated receptor gamma	Homo sapiens	50-59
32260484-5	2020	Here, we tested the hypothesis that imatinib, a chemotherapeutic agent and a potent PDGFR inhibitor, alters PC distribution and thus induces vascular atrophy.	imatinib	36-44	platelet derived growth factor receptor, beta polypeptide	Mus musculus	84-89
32260484-6	2020	We performed a morphometric analysis of the vascular elements in sham control and imatinib-treated NG2-DsRed mice.	imatinib	82-90	chondroitin sulfate proteoglycan 4	Mus musculus	99-102
31371410-2	2020	Peroxisome proliferator-activated receptor-gamma (PPARgamma) agonist pioglitazone downregulates signal transducer and activator of transcription 5 (STAT5) and in combination with imatinib induces complete molecular response in imatinib-refractory patients by eroding leukemia stem cells.	imatinib	179-187	signal transducer and activator of transcription 5A	Homo sapiens	148-153
31371410-2	2020	Peroxisome proliferator-activated receptor-gamma (PPARgamma) agonist pioglitazone downregulates signal transducer and activator of transcription 5 (STAT5) and in combination with imatinib induces complete molecular response in imatinib-refractory patients by eroding leukemia stem cells.	imatinib	227-235	peroxisome proliferator activated receptor gamma	Homo sapiens	0-48
31371410-2	2020	Peroxisome proliferator-activated receptor-gamma (PPARgamma) agonist pioglitazone downregulates signal transducer and activator of transcription 5 (STAT5) and in combination with imatinib induces complete molecular response in imatinib-refractory patients by eroding leukemia stem cells.	imatinib	227-235	peroxisome proliferator activated receptor gamma	Homo sapiens	50-59
31371410-2	2020	Peroxisome proliferator-activated receptor-gamma (PPARgamma) agonist pioglitazone downregulates signal transducer and activator of transcription 5 (STAT5) and in combination with imatinib induces complete molecular response in imatinib-refractory patients by eroding leukemia stem cells.	imatinib	227-235	signal transducer and activator of transcription 5A	Homo sapiens	148-153
31371410-9	2020	Combining imatinib with clofazimine caused a far superior synergy than pioglitazone where clofazimine reduced imatinib"s IC50 by &gt;4 logs and remarkably eroded quiescent CD34+ cells.	imatinib	10-18	CD34 molecule	Homo sapiens	172-176
32291914-0	2020	Successful treatment with imatinib of lymphomatoid papulosis associated with myeloproliferative hypereosinophilic syndrome with PDGFRA rearrangement.	imatinib	26-34	platelet derived growth factor receptor alpha	Homo sapiens	128-134
31702819-3	2020	Previous reports have found success with sunitinib in imatinib-resistant GIST, but we report a certain wild-type KIT mutation GIST with cutaneous and subcutaneous metastasis that was unresponsive to multiple tyrosine kinase inhibitor (TKI) treatments.	imatinib	54-62	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	113-116
32291924-0	2020	Erfolgreiche Imatinib-Therapie einer mit dem myeloproliferativen hypereosinophilen Syndrom mit PDGFRA-Rearrangement assoziierten lymphomatoiden Papulose.	imatinib	13-21	platelet derived growth factor receptor alpha	Homo sapiens	95-101
32125294-0	2020	Exquisite response to imatinib mesylate in FIP1L1-PDGFRA-mutated hypereosinophilic syndrome: a very long-term experience of Polish Hypereosinophilic Syndrome Study Group.	imatinib	22-39	factor interacting with PAPOLA and CPSF1	Homo sapiens	43-49
32386029-8	2020	The patient was treated with the tyrosine kinase inhibitor-imatinib mesylate which is the first choice for this disease currently.Myeloid neoplasm with the abnormality of PDGFRB gene is a rare hematologic tumor characterized by myeloid dysplasia, eosinophilia, and PDGFR gene rearrangement.	imatinib	59-76	platelet derived growth factor receptor beta	Homo sapiens	171-177
32386029-8	2020	The patient was treated with the tyrosine kinase inhibitor-imatinib mesylate which is the first choice for this disease currently.Myeloid neoplasm with the abnormality of PDGFRB gene is a rare hematologic tumor characterized by myeloid dysplasia, eosinophilia, and PDGFR gene rearrangement.	imatinib	59-76	platelet derived growth factor receptor beta	Homo sapiens	171-176
32319374-0	2020	[Relationship between PANTR1 and Imatinib Resistance of Chronic Myeloid Leukemia Cell Line K562 and Its Related Mechanisms].	imatinib	33-41	POU3F3 adjacent non-coding transcript 1	Homo sapiens	22-28
32319374-1	2020	OBJECTIVE: To investigate the relationship between long non-coding RNA (LncRNA) PANTR1 and imatinib resistance in chronic myeloid leukemia cell line K562 and its mechanism.	imatinib	91-99	POU3F3 adjacent non-coding transcript 1	Homo sapiens	80-86
32319374-10	2020	CONCLUSION: LncRNA PANTR1 can promote the expression of MDR and stem cell marker in chronic myeloid leukemia cell line K562, and mediate imatinib resistance.	imatinib	137-145	POU3F3 adjacent non-coding transcript 1	Homo sapiens	19-25
32125294-0	2020	Exquisite response to imatinib mesylate in FIP1L1-PDGFRA-mutated hypereosinophilic syndrome: a very long-term experience of Polish Hypereosinophilic Syndrome Study Group.	imatinib	22-39	platelet derived growth factor receptor alpha	Homo sapiens	50-56
32198455-1	2020	The majority of gastrointestinal stromal tumors (GISTs) are driven by oncogenic KIT signaling and can therefore be effectively treated with the tyrosine kinase inhibitor (TKI) imatinib mesylate.	imatinib	176-184	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	80-83
32097559-3	2020	A recent study showed that imatinib and its analogues were able to allosterically enhance agonist-induced FXR activation and its target gene expression.	imatinib	27-35	nuclear receptor subfamily 1 group H member 4	Homo sapiens	106-109
32097559-5	2020	In this work, the most effective imatinib analogue P16 was used as a probe to explore the above issue by computational approaches.	imatinib	33-41	cyclin dependent kinase inhibitor 2A	Homo sapiens	51-54
32251287-0	2020	MicroRNA-30a targets BECLIN-1 to inactivate autophagy and sensitizes gastrointestinal stromal tumor cells to imatinib.	imatinib	109-117	microRNA 30a	Homo sapiens	0-12
32198455-2	2020	However, most GISTs develop imatinib resistance through secondary KIT mutations.	imatinib	28-36	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	66-69
32127950-0	2020	BCR-ABL1 transcript decline ratio combined BCR-ABL1IS as a precise predictor for imatinib response and outcome in the patients with chronic myeloid leukemia.	imatinib	81-89	BCR activator of RhoGEF and GTPase	Homo sapiens	0-8
32195376-2	2020	We previously reported that gefitinib (GEF) and imatinib (IMA) induce autophagy in epidermal growth factor receptor (EGFR) knock-out A549 and non-BCR-ABL-expressing leukemia cell lines, respectively.	imatinib	48-56	epidermal growth factor receptor	Homo sapiens	83-115
32195376-2	2020	We previously reported that gefitinib (GEF) and imatinib (IMA) induce autophagy in epidermal growth factor receptor (EGFR) knock-out A549 and non-BCR-ABL-expressing leukemia cell lines, respectively.	imatinib	48-56	epidermal growth factor receptor	Homo sapiens	117-121
32195376-2	2020	We previously reported that gefitinib (GEF) and imatinib (IMA) induce autophagy in epidermal growth factor receptor (EGFR) knock-out A549 and non-BCR-ABL-expressing leukemia cell lines, respectively.	imatinib	58-61	epidermal growth factor receptor	Homo sapiens	83-115
32195376-2	2020	We previously reported that gefitinib (GEF) and imatinib (IMA) induce autophagy in epidermal growth factor receptor (EGFR) knock-out A549 and non-BCR-ABL-expressing leukemia cell lines, respectively.	imatinib	58-61	epidermal growth factor receptor	Homo sapiens	117-121
32138149-6	2020	Two TrxR inhibitors, auranofin and [Au(d2pype)2]Cl, increased intracellular ROS levels and elicited apoptosis in both sensitive and imatinib resistant CML cells.	imatinib	132-140	peroxiredoxin 5	Homo sapiens	4-8
32138149-8	2020	In addition, imatinib resistant CML cell lines showed upregulated expression of the Trx system.	imatinib	13-21	thioredoxin	Homo sapiens	84-87
31923418-0	2020	Circ_0009910 promotes imatinib resistance through ULK1-induced autophagy by sponging miR-34a-5p in chronic myeloid leukemia.	imatinib	22-30	unc-51 like autophagy activating kinase 1	Homo sapiens	50-54
31923418-13	2020	CONCLUSION: Circ_0009910 accelerated imatinib-resistance in CML cells by modulating ULK1-induced autophagy via targeting miR-34a-5p, providing a potential target in imatinib resistance of CML.	imatinib	37-45	unc-51 like autophagy activating kinase 1	Homo sapiens	84-88
31923418-13	2020	CONCLUSION: Circ_0009910 accelerated imatinib-resistance in CML cells by modulating ULK1-induced autophagy via targeting miR-34a-5p, providing a potential target in imatinib resistance of CML.	imatinib	165-173	unc-51 like autophagy activating kinase 1	Homo sapiens	84-88
32116689-14	2020	It enhanced the current of Na+ and K+ in ICCs and improved c-kit expression and signaling mediator phosphorylation in SCF/c-kit, which was inhibited by imatinib in vitro and downregulated in model rats in vivo.	imatinib	152-160	KIT ligand	Rattus norvegicus	118-121
32099073-11	2020	In conclusion, our study indicates that DTF may harbor a broader mutational spectrum beyond CTNNB1 mutations, comprising targetable alterations including the herewith first reported imatinib-sensitive KIT V559D mutation in DTF.	imatinib	182-190	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	201-204
32082541-0	2020	Loss of PI3 kinase association improves the sensitivity of secondary mutation of KIT to Imatinib.	imatinib	88-96	peptidase inhibitor 3	Homo sapiens	8-11
32082541-0	2020	Loss of PI3 kinase association improves the sensitivity of secondary mutation of KIT to Imatinib.	imatinib	88-96	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	81-84
32082541-3	2020	Results: In this study, we found that secondary mutation of KIT dramatically increases the ligand-independent activation of the receptor and their resistance to the often used KIT inhibitor Imatinib in the treatment of GISTs.	imatinib	190-198	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	60-63
32082541-3	2020	Results: In this study, we found that secondary mutation of KIT dramatically increases the ligand-independent activation of the receptor and their resistance to the often used KIT inhibitor Imatinib in the treatment of GISTs.	imatinib	190-198	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	176-179
32082541-5	2020	We found that loss of PI3 kinase association, but not the inhibition of the lipid kinase activity of PI3 kinase, inhibits the ligand-independent activation of secondary mutations of KIT, and increases their sensitivity to Imatinib, and loss of PI3 kinase association inhibits secondary mutations of KIT mediated cell survival and proliferation in vitro.	imatinib	222-230	peptidase inhibitor 3	Homo sapiens	22-25
32082541-6	2020	The in vivo assay further showed that the growth of tumors carrying secondary mutations of KIT is more sensitive to Imatinib when PI3 kinase association is blocked while inhibition of the lipid kinase activity of PI3 kinase cannot inhibit tumor growth, indicating that PI3 kinase is important for the drug resistance of secondary mutation of KIT independent of the lipid kinase activity of PI3 kinase.	imatinib	116-124	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	91-94
32082541-6	2020	The in vivo assay further showed that the growth of tumors carrying secondary mutations of KIT is more sensitive to Imatinib when PI3 kinase association is blocked while inhibition of the lipid kinase activity of PI3 kinase cannot inhibit tumor growth, indicating that PI3 kinase is important for the drug resistance of secondary mutation of KIT independent of the lipid kinase activity of PI3 kinase.	imatinib	116-124	peptidase inhibitor 3	Homo sapiens	130-133
32116712-0	2020	Clonal Selection of a Novel Deleterious TP53 Somatic Mutation Discovered in ctDNA of a KIT/PDGFRA Wild-Type Gastrointestinal Stromal Tumor Resistant to Imatinib.	imatinib	152-160	tumor protein p53	Homo sapiens	40-44
32116712-0	2020	Clonal Selection of a Novel Deleterious TP53 Somatic Mutation Discovered in ctDNA of a KIT/PDGFRA Wild-Type Gastrointestinal Stromal Tumor Resistant to Imatinib.	imatinib	152-160	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	87-90
32116712-0	2020	Clonal Selection of a Novel Deleterious TP53 Somatic Mutation Discovered in ctDNA of a KIT/PDGFRA Wild-Type Gastrointestinal Stromal Tumor Resistant to Imatinib.	imatinib	152-160	platelet derived growth factor receptor alpha	Homo sapiens	91-97
32116712-10	2020	The de novo TP53 (c.560-7_560-2delCTCTTAinsT) mutation was in silico predicted to be associated with an aberrant RNA splicing and with an aggressive phenotype which might have contributed to a rapid disease spread despite the administration of an increased imatinib dosage.	imatinib	257-265	tumor protein p53	Homo sapiens	12-16
31704808-0	2020	Tyrosine kinase inhibitor imatinib augments tumor immunity by depleting effector regulatory T cells.	imatinib	26-34	TXK tyrosine kinase	Homo sapiens	0-15
31704808-2	2020	Imatinib, a tyrosine kinase inhibitor of oncogenic BCR-ABL protein expressed by chronic myelogenous leukemia (CML) cells, possesses off-targets including LCK expressed in T cells.	imatinib	0-8	TXK tyrosine kinase	Homo sapiens	12-27
31704808-2	2020	Imatinib, a tyrosine kinase inhibitor of oncogenic BCR-ABL protein expressed by chronic myelogenous leukemia (CML) cells, possesses off-targets including LCK expressed in T cells.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
31704808-2	2020	Imatinib, a tyrosine kinase inhibitor of oncogenic BCR-ABL protein expressed by chronic myelogenous leukemia (CML) cells, possesses off-targets including LCK expressed in T cells.	imatinib	0-8	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	154-157
31704808-3	2020	We showed that imatinib-treated CML patients in complete molecular remission (CMR) exhibited selective depletion of effector T reg (eT reg) cells and significant increase in effector/memory CD8+ T cells while non-CMR patients did not.	imatinib	15-23	regenerating family member 1 alpha	Homo sapiens	127-130
31704808-3	2020	We showed that imatinib-treated CML patients in complete molecular remission (CMR) exhibited selective depletion of effector T reg (eT reg) cells and significant increase in effector/memory CD8+ T cells while non-CMR patients did not.	imatinib	15-23	CD8a molecule	Homo sapiens	190-193
31704808-4	2020	Imatinib at CML-therapeutic concentrations indeed induced apoptosis specifically in eT reg cells and expanded tumor antigen-specific CD8+ T cells in vitro in healthy individuals and melanoma patients, and suppressed colon tumor growth in vivo in mice.	imatinib	0-8	regenerating family member 1 alpha	Homo sapiens	87-90
31704808-4	2020	Imatinib at CML-therapeutic concentrations indeed induced apoptosis specifically in eT reg cells and expanded tumor antigen-specific CD8+ T cells in vitro in healthy individuals and melanoma patients, and suppressed colon tumor growth in vivo in mice.	imatinib	0-8	CD8a molecule	Homo sapiens	133-136
31704808-5	2020	Mechanistically, because of FoxP3-dependent much lower expression of LCK and ZAP-70 in T reg cells compared with other T cells, imatinib inhibition of LCK further reduced their TCR signal intensity, rendering them selectively susceptible to signal-deprived apoptotis.	imatinib	128-136	forkhead box P3	Homo sapiens	28-33
31704808-5	2020	Mechanistically, because of FoxP3-dependent much lower expression of LCK and ZAP-70 in T reg cells compared with other T cells, imatinib inhibition of LCK further reduced their TCR signal intensity, rendering them selectively susceptible to signal-deprived apoptotis.	imatinib	128-136	regenerating family member 1 alpha	Homo sapiens	89-92
31704808-5	2020	Mechanistically, because of FoxP3-dependent much lower expression of LCK and ZAP-70 in T reg cells compared with other T cells, imatinib inhibition of LCK further reduced their TCR signal intensity, rendering them selectively susceptible to signal-deprived apoptotis.	imatinib	128-136	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	151-154
31704808-6	2020	Taken together, eT reg cell depletion by imatinib is instrumental in evoking effective immune responses to various cancers.	imatinib	41-49	regenerating family member 1 alpha	Homo sapiens	19-22
31894340-0	2020	Tanshinone IIA enhances the inhibitory effect of imatinib on proliferation and motility of acute leukemia cell line TIB-152 in vivo and in vitro by inhibiting the PI3K/AKT/mTOR signaling pathway.	imatinib	49-57	ATPase, class II, type 9A	Mus musculus	11-14
32141572-0	2020	Effect of imatinib on DOCA-induced myocardial fibrosis in rats through P38 MAPK signaling pathway.	imatinib	10-18	mitogen activated protein kinase 14	Rattus norvegicus	71-74
32141572-1	2020	OBJECTIVE: To explore the role of imatinib in desoxycorticosterone acetate (DOCA)-induced myocardial fibrosis in rats by the p38 mitogen-activated protein kinase (MAPK) signaling pathway.	imatinib	34-42	mitogen activated protein kinase 14	Rattus norvegicus	125-161
32141572-11	2020	The results of the gene detection revealed that the expression levels of Chek1, alpha-SMA, p38 MAPK, and JNK were evidently higher in DOCA induction group than those in the imatinib treatment group (p<0.05), and the expression of p38 MAPK protein in the rat myocardial tissues was remarkably lower in the treatment group than that in the DOCA induction group (p<0.05).	imatinib	173-181	checkpoint kinase 1	Rattus norvegicus	73-78
32141572-11	2020	The results of the gene detection revealed that the expression levels of Chek1, alpha-SMA, p38 MAPK, and JNK were evidently higher in DOCA induction group than those in the imatinib treatment group (p<0.05), and the expression of p38 MAPK protein in the rat myocardial tissues was remarkably lower in the treatment group than that in the DOCA induction group (p<0.05).	imatinib	173-181	mitogen activated protein kinase 14	Rattus norvegicus	91-94
32141572-11	2020	The results of the gene detection revealed that the expression levels of Chek1, alpha-SMA, p38 MAPK, and JNK were evidently higher in DOCA induction group than those in the imatinib treatment group (p<0.05), and the expression of p38 MAPK protein in the rat myocardial tissues was remarkably lower in the treatment group than that in the DOCA induction group (p<0.05).	imatinib	173-181	mitogen-activated protein kinase 8	Rattus norvegicus	105-108
32141572-12	2020	CONCLUSIONS: Imatinib can regulate the repair of myocardial injury caused by DOCA-induced myocardial fibrosis in rats by repressing the p38 MAPK signaling pathway.	imatinib	13-21	mitogen activated protein kinase 14	Rattus norvegicus	136-139
31776458-8	2020	Coordinated inhibition of CK2 and KIT by CX4945 (or CK2 shRNA) and imatinib, respectively, leads to increased apoptosis, anti-proliferative effects and cell cycle arrest and decreased p-AKT and p-S6 expression, migration and invasiveness in all GIST cell lines compared with either intervention alone, indicating additive effects of inhibiting these two important regulators of GIST biology.	imatinib	67-75	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	34-37
31776458-8	2020	Coordinated inhibition of CK2 and KIT by CX4945 (or CK2 shRNA) and imatinib, respectively, leads to increased apoptosis, anti-proliferative effects and cell cycle arrest and decreased p-AKT and p-S6 expression, migration and invasiveness in all GIST cell lines compared with either intervention alone, indicating additive effects of inhibiting these two important regulators of GIST biology.	imatinib	67-75	AKT serine/threonine kinase 1	Homo sapiens	186-189
31776458-9	2020	CONCLUSION: Our findings suggest that combinatorial inhibition of CK2 and KIT warrants evaluation as a novel therapeutic strategy in GIST, especially in imatinib-resistant GIST.	imatinib	153-161	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	74-77
31894340-0	2020	Tanshinone IIA enhances the inhibitory effect of imatinib on proliferation and motility of acute leukemia cell line TIB-152 in vivo and in vitro by inhibiting the PI3K/AKT/mTOR signaling pathway.	imatinib	49-57	thymoma viral proto-oncogene 1	Mus musculus	168-171
31894340-0	2020	Tanshinone IIA enhances the inhibitory effect of imatinib on proliferation and motility of acute leukemia cell line TIB-152 in vivo and in vitro by inhibiting the PI3K/AKT/mTOR signaling pathway.	imatinib	49-57	mechanistic target of rapamycin kinase	Mus musculus	172-176
31894340-4	2020	Tan IIA and IM, alone and in combination, significantly inhibited proliferation, migration and invasion of TIB-152 cells, and promoted apoptosis; the effect of co-treatment with Tan IIA plus IM was enhanced.	imatinib	12-14	ATPase, class II, type 9A	Mus musculus	182-185
32560620-0	2020	Encapsulation of Imatinib in Targeted KIT-5 Nanoparticles for Reducing its Cardiotoxicity and Hepatotoxicity.	imatinib	17-25	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	38-41
32005261-2	2020	The events that drive GIST oncogenesis are primarily KIT or PDGFRA mutations, which lead to the susceptibility of these tumors to small-molecule tyrosine kinase inhibitors such as imatinib and sunitinib.	imatinib	180-188	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	53-56
32005261-2	2020	The events that drive GIST oncogenesis are primarily KIT or PDGFRA mutations, which lead to the susceptibility of these tumors to small-molecule tyrosine kinase inhibitors such as imatinib and sunitinib.	imatinib	180-188	platelet derived growth factor receptor alpha	Homo sapiens	60-66
32005261-3	2020	However, previous studies have shown that patients with a PDGFRA D842V mutation in GISTs have a very low rate of response to imatinib treatment.	imatinib	125-133	platelet derived growth factor receptor alpha	Homo sapiens	58-64
32005261-10	2020	In addition, ALK may be a potential therapeutic target for patients with imatinib-resistant stromal tumors.	imatinib	73-81	ALK receptor tyrosine kinase	Homo sapiens	13-16
32082165-8	2019	The simulations also highlighted that children and adults being treated with imatinib have similar vulnerability to CYP modulations.	imatinib	77-85	peptidylprolyl isomerase G	Homo sapiens	116-119
31734352-0	2020	Human telomerase reverse transcriptase depletion potentiates the growth-inhibitory activity of imatinib in chronic myeloid leukemia stem cells.	imatinib	95-103	telomerase reverse transcriptase	Homo sapiens	6-38
31734352-6	2020	Furthermore, we show that hTERT depletion exerts a growth-inhibitory effect in K-562 cells and potentiates imatinib through alteration of cell cycle progression leading to a senescence-like phenotype.	imatinib	107-115	telomerase reverse transcriptase	Homo sapiens	26-31
31734352-7	2020	Finally, we demonstrate that hTERT depletion potentiates the imatinib-induced reduction of the ALDH+-LSC population.	imatinib	61-69	telomerase reverse transcriptase	Homo sapiens	29-34
31952546-0	2020	De-regulated STAT5A/miR-202-5p/USP15/Caspase-6 regulatory axis suppresses CML cell apoptosis and contributes to Imatinib resistance.	imatinib	112-120	signal transducer and activator of transcription 5A	Homo sapiens	13-19
31952546-0	2020	De-regulated STAT5A/miR-202-5p/USP15/Caspase-6 regulatory axis suppresses CML cell apoptosis and contributes to Imatinib resistance.	imatinib	112-120	ubiquitin specific peptidase 15	Homo sapiens	31-36
31952546-0	2020	De-regulated STAT5A/miR-202-5p/USP15/Caspase-6 regulatory axis suppresses CML cell apoptosis and contributes to Imatinib resistance.	imatinib	112-120	caspase 6	Homo sapiens	37-46
31952546-10	2020	Depletion of USP15 increased, whereas overexpression of USP15 reduced the resistance of CML cells to Imatinib.	imatinib	101-109	ubiquitin specific peptidase 15	Homo sapiens	56-61
31892598-1	2020	AIM: The purpose of the Imadje study was to confirm the efficacy and safety of imatinib, following resection of kit-positive gastrointestinal stromal tumour (GIST), in the adjuvant setting in the Greek population.	imatinib	79-87	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	112-115
32999163-0	2020	Emodin Inhibits Resistance to Imatinib by Downregulation of Bcr-Abl and STAT5 and Allosteric Inhibition in Chronic Myeloid Leukemia Cells.	imatinib	30-38	signal transducer and activator of transcription 5A	Homo sapiens	72-77
32999163-1	2020	Imatinib-resistance is a significant concern for Bcr-Abl-positive chronic myelogenous leukemia (CML) treatment.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
32999163-5	2020	After treatment of emodin and imatinib together, the levels of p-Bcr-Abl and Bcr-Abl were significantly downregulated.	imatinib	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
32999163-5	2020	After treatment of emodin and imatinib together, the levels of p-Bcr-Abl and Bcr-Abl were significantly downregulated.	imatinib	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
31813475-8	2020	Docking study was carried out into PDGFR-alpha active site which showed comparable binding mode to that of FDA approved PDGFR-alpha inhibitor, imatinib.	imatinib	143-151	platelet derived growth factor receptor alpha	Homo sapiens	35-46
31813475-8	2020	Docking study was carried out into PDGFR-alpha active site which showed comparable binding mode to that of FDA approved PDGFR-alpha inhibitor, imatinib.	imatinib	143-151	platelet derived growth factor receptor alpha	Homo sapiens	120-131
33821851-6	2020	One patient died without treatment while the remaining 7 patients received treatment, including imatinib in 1 patient with BCR-ABL1+ acute lymphoblastic leukemia.	imatinib	96-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-131
33691306-3	2020	In this study, we treated adult mice with imatinib (a Kit signaling blocker) for 8 or 16 days and investigated whether CD44 is a specific marker for the Kit negative ICCs in the adult mouse colon.	imatinib	42-50	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	54-57
33691306-5	2020	Our results indicated that Kit expression was downregulated for both protein and mRNA levels after imatinib treatment for 8 or 16 days as compared to the vehicle-treated mice.	imatinib	99-107	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	27-30
33691306-8	2020	After imatinib treatment, a number of CD44+/Kit- cells with elaborated processes were observed with an evident decrease of Kit+ cell number within the muscular layers (ICC-IM) and around the myenteric nerve plexus (ICC-MY) as compared to vehicle-treated mice.	imatinib	6-14	CD44 antigen	Mus musculus	38-42
33691306-8	2020	After imatinib treatment, a number of CD44+/Kit- cells with elaborated processes were observed with an evident decrease of Kit+ cell number within the muscular layers (ICC-IM) and around the myenteric nerve plexus (ICC-MY) as compared to vehicle-treated mice.	imatinib	6-14	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	44-47
33691306-8	2020	After imatinib treatment, a number of CD44+/Kit- cells with elaborated processes were observed with an evident decrease of Kit+ cell number within the muscular layers (ICC-IM) and around the myenteric nerve plexus (ICC-MY) as compared to vehicle-treated mice.	imatinib	6-14	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	123-126
33691306-9	2020	After discontinuing imatinib for 16 days, Kit+ ICC-MY and ICC-IM were completely co-localized with normalization of CD44 and Kit+ cell numbers.	imatinib	20-28	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	42-45
33691306-9	2020	After discontinuing imatinib for 16 days, Kit+ ICC-MY and ICC-IM were completely co-localized with normalization of CD44 and Kit+ cell numbers.	imatinib	20-28	CD44 antigen	Mus musculus	116-120
33691306-9	2020	After discontinuing imatinib for 16 days, Kit+ ICC-MY and ICC-IM were completely co-localized with normalization of CD44 and Kit+ cell numbers.	imatinib	20-28	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	125-128
31197522-0	2020	Targeting the WEE1 kinase strengthens the antitumor activity of imatinib via promoting KIT autophagic degradation in gastrointestinal stromal tumors.	imatinib	64-72	WEE1 G2 checkpoint kinase	Homo sapiens	14-18
31197522-0	2020	Targeting the WEE1 kinase strengthens the antitumor activity of imatinib via promoting KIT autophagic degradation in gastrointestinal stromal tumors.	imatinib	64-72	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	87-90
31789418-7	2020	In conclusion, HHT induced p62-mediated autophagy in imatinib-resistant CML K562G cells, thus promoting autophagic degradation of the BCR-ABL protein and providing a novel strategy for the treatment of TKI-resistant CML.	imatinib	53-61	sequestosome 1	Homo sapiens	27-30
31018977-3	2020	We hypothesized that non-adhesion of chronic myeloid leukemia-initiating cells to E-selectin on the bone marrow endothelium may lead to superior eradication of leukemic stem cells in chronic myeloid leukemia after treatment with imatinib than imatinib alone.	imatinib	229-237	selectin, endothelial cell	Mus musculus	82-92
31018977-3	2020	We hypothesized that non-adhesion of chronic myeloid leukemia-initiating cells to E-selectin on the bone marrow endothelium may lead to superior eradication of leukemic stem cells in chronic myeloid leukemia after treatment with imatinib than imatinib alone.	imatinib	243-251	selectin, endothelial cell	Mus musculus	82-92
32027818-9	2020	Both trough concentrations and SLCO1A2 -361G>A genotypes are independent factors affecting imatinib efficacy.	imatinib	91-99	solute carrier organic anion transporter family member 1A2	Homo sapiens	31-38
32027818-12	2020	CONCLUSION: Imatinib trough concentrations and SLCO1A2 -361G>A genotypes are associated with imatinib efficacy in Chinese patients with CML.	imatinib	93-101	solute carrier organic anion transporter family member 1A2	Homo sapiens	47-54
31488872-0	2020	Oncogenic heterogeneous nuclear ribonucleoprotein D-like modulates the growth and imatinib response of human chronic myeloid leukemia CD34+ cells via pre-B-cell leukemia homeobox 1.	imatinib	82-90	PBX homeobox 1	Homo sapiens	150-180
32498644-6	2020	When treated with imatinib mesylate (STI571), a specific c-Abl family kinase inhibitor, the p38 expression was decreased and the loss of dopaminergic neurons was reduced.	imatinib	18-35	mitogen activated protein kinase 14	Rattus norvegicus	92-95
32498644-6	2020	When treated with imatinib mesylate (STI571), a specific c-Abl family kinase inhibitor, the p38 expression was decreased and the loss of dopaminergic neurons was reduced.	imatinib	37-43	mitogen activated protein kinase 14	Rattus norvegicus	92-95
31488872-6	2020	In addition, HNRPDL modulated imatinib response of K562 cells and HNRPDL silencing sensitized CML CD34+ cells to imatinib treatment.	imatinib	30-38	heterogeneous nuclear ribonucleoprotein D like	Homo sapiens	13-19
31488872-6	2020	In addition, HNRPDL modulated imatinib response of K562 cells and HNRPDL silencing sensitized CML CD34+ cells to imatinib treatment.	imatinib	113-121	heterogeneous nuclear ribonucleoprotein D like	Homo sapiens	66-72
31488872-8	2020	The expression of PBX1 was significantly higher in CML CD34+ cells than that in control cells and PBX silencing inhibited the growth of CML cells and sensitized them to imatinib treatment.	imatinib	169-177	PBX homeobox 1	Homo sapiens	18-22
31488872-9	2020	In contrast, overexpression of PBX1 elevated the CFC production of normal hematopoietic CD34+ cells and "rescued" HNRPDL silencing induced growth inhibition and imatinib sensitization.	imatinib	161-169	PBX homeobox 1	Homo sapiens	31-35
32369821-18	2020	Interestingly, 2 variants observed in the PDGFRA gene are classic imatinib-sensitive therapy.	imatinib	66-74	platelet derived growth factor receptor alpha	Homo sapiens	42-48
31758409-13	2020	Secondary mutations of KIT/PDGFRA were the most important contributors in GISTs developing resistance to imatinib treatment.	imatinib	105-113	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	23-26
31758409-13	2020	Secondary mutations of KIT/PDGFRA were the most important contributors in GISTs developing resistance to imatinib treatment.	imatinib	105-113	platelet derived growth factor receptor alpha	Homo sapiens	27-33
32640452-6	2020	A spectacular response to empirical imatinib treatment triggered further genetic analysis and led to the identification of a 45-bp duplication in KIT exon 11 undetectable by routine NGS.	imatinib	36-44	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	146-149
31701195-4	2019	Moreover, miR328 was found selectively degraded in the lysosomes of K562R cells, as inhibition of lysosome with chloroquine restored miR328 expression and increased sensitivity to imatinib.	imatinib	180-188	microRNA 328	Homo sapiens	10-16
32240815-3	2020	Recent preclinical studies suggest that the multi-tyrosine kinase inhibitor, imatinib, which targets the Abl kinases c-Abl and Arg, has the potential to restore endothelial dysfunction caused by inflammatory agonists.	imatinib	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-108
32240815-3	2020	Recent preclinical studies suggest that the multi-tyrosine kinase inhibitor, imatinib, which targets the Abl kinases c-Abl and Arg, has the potential to restore endothelial dysfunction caused by inflammatory agonists.	imatinib	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-122
32240815-5	2020	In the current study, we demonstrate that imatinib inhibits LPS induced increase in the phosphorylation of CrkL, a specific substrate of Abl kinases, in human pulmonary endothelial cells.	imatinib	42-50	CRK like proto-oncogene, adaptor protein	Homo sapiens	107-111
32240815-5	2020	In the current study, we demonstrate that imatinib inhibits LPS induced increase in the phosphorylation of CrkL, a specific substrate of Abl kinases, in human pulmonary endothelial cells.	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-140
32507808-0	2020	[BCR-ABL1-positive myelodysplastic syndrome with neutropenia and anemia treated successfully with imatinib mesylate].	imatinib	98-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	5-9
32507808-14	2020	Our results suggest that complete hematologic recovery in response to imatinib mesylate suggests a critical role for the BCR-ABL1 fusion in the pathogenesis of this disease.	imatinib	70-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-129
31471313-1	2019	PURPOSE: Polyclonal emergence of KIT secondary mutations is a main mechanism of imatinib progression in gastrointestinal stromal tumor (GIST).	imatinib	80-88	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	33-36
31701195-0	2019	Targeted blocking of miR328 lysosomal degradation with alkalized exosomes sensitizes the chronic leukemia cells to imatinib.	imatinib	115-123	microRNA 328	Homo sapiens	21-27
31701195-2	2019	In this study, we found that miR328 significantly and strikingly decreased among other miRNA candidates during the induction of imatinib resistance.	imatinib	128-136	microRNA 328	Homo sapiens	29-35
31701195-3	2019	Overexpression of miR328 sensitized resistant cells to imatinib via post-transcriptionally decreasing ABCG2 expression, while miR328 knockdown conferred imatinib resistance in parental K562 cells.	imatinib	55-63	microRNA 328	Homo sapiens	18-24
31701195-3	2019	Overexpression of miR328 sensitized resistant cells to imatinib via post-transcriptionally decreasing ABCG2 expression, while miR328 knockdown conferred imatinib resistance in parental K562 cells.	imatinib	55-63	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	102-107
31701195-3	2019	Overexpression of miR328 sensitized resistant cells to imatinib via post-transcriptionally decreasing ABCG2 expression, while miR328 knockdown conferred imatinib resistance in parental K562 cells.	imatinib	153-161	microRNA 328	Homo sapiens	126-132
31701195-6	2019	Compared with the corresponding controls, the alkalized exosomes with or without miR328 sensitized the chronic leukemia cells to imatinib.	imatinib	129-137	microRNA 328	Homo sapiens	81-87
31701195-7	2019	Taken together, our study has revealed that lysosomal clearance of miR328 in imatinib-resistant cells at least partially contributes to the drug resistance, while delivery of alkalized exosomes would sensitize the chromic leukemia cells to imatinib.	imatinib	77-85	microRNA 328	Homo sapiens	67-73
30929559-1	2019	Imatinib is the first molecularly targeted compound for chronic myeloid leukemia (CML) capable to inhibit BCR-ABL kinase activity.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-113
30929559-2	2019	However, recent clinical evidence indicates that a substantial proportion of CML patients exhibit BCR-ABL-dependent or independent resistance to imatinib.	imatinib	145-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-105
30929559-6	2019	We also highlighted the role of GCA-TRAF6-ULK1 autophagy regulatory axis in imatinib resistance.	imatinib	76-84	unc-51 like autophagy activating kinase 1	Homo sapiens	42-46
30929559-4	2019	Here, we identified GCA (grancalcin) as a critical regulator of imatinib resistance in chronic phase CML via activation of autophagy.	imatinib	64-72	grancalcin	Homo sapiens	20-23
30929559-4	2019	Here, we identified GCA (grancalcin) as a critical regulator of imatinib resistance in chronic phase CML via activation of autophagy.	imatinib	64-72	grancalcin	Homo sapiens	25-35
30929559-6	2019	We also highlighted the role of GCA-TRAF6-ULK1 autophagy regulatory axis in imatinib resistance.	imatinib	76-84	grancalcin	Homo sapiens	32-35
30929559-6	2019	We also highlighted the role of GCA-TRAF6-ULK1 autophagy regulatory axis in imatinib resistance.	imatinib	76-84	TNF receptor associated factor 6	Homo sapiens	36-41
31669139-7	2019	The small molecule receptor antagonists, ST1571 (imatinib) and LY2109761, were used to block the PDGFbeta/pErk and TGFbeta/pSmad2/3 signaling pathways, respectively.	imatinib	49-57	platelet derived growth factor subunit A	Homo sapiens	97-105
31376170-1	2019	Tyrosine kinase inhibitor treatments for chronic myeloid leukaemia based on nilotinib (NIL), dasatinib (DAS) and imatinib (IMA) have improved patient quality of life and have turned chronic myeloid leukemia from a fatal disease into a chronic disease.	imatinib	113-121	TXK tyrosine kinase	Homo sapiens	0-15
31376170-1	2019	Tyrosine kinase inhibitor treatments for chronic myeloid leukaemia based on nilotinib (NIL), dasatinib (DAS) and imatinib (IMA) have improved patient quality of life and have turned chronic myeloid leukemia from a fatal disease into a chronic disease.	imatinib	123-126	TXK tyrosine kinase	Homo sapiens	0-15
31669139-7	2019	The small molecule receptor antagonists, ST1571 (imatinib) and LY2109761, were used to block the PDGFbeta/pErk and TGFbeta/pSmad2/3 signaling pathways, respectively.	imatinib	49-57	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	106-110
31669139-7	2019	The small molecule receptor antagonists, ST1571 (imatinib) and LY2109761, were used to block the PDGFbeta/pErk and TGFbeta/pSmad2/3 signaling pathways, respectively.	imatinib	49-57	transforming growth factor alpha	Homo sapiens	115-122
31839033-0	2019	[BAX Gene Deletion Reduces the Sensitivity of BCR-ABL-Induced B-ALL Cells of Mice to Imatinib].	imatinib	85-93	BCL2-associated X protein	Mus musculus	1-4
32699984-2	2019	Imatinib, the first BCR-ABL1 TKI, was introduced into clinical practice in the early 2000s.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-28
31839033-4	2019	RESULTS: In BCR-ABL transfected bone marrow cells treated with imatinib, the numbers of viable cells of BAX deletion group was significantly higher than that of wild type groups with statristcal difference(P<0.05), and effect- and dose-dependency(r=-0.9533 for BAX deletion group, and r=-0.9812 for wild type group).	imatinib	63-71	BCL2-associated X protein	Mus musculus	104-107
31327842-3	2019	We herein report a patient with myeloid/lymphoid neoplasms with PDGFRB rearrangement with t (5;10) (q33;q22) who showed atypical chronic myeloid leukemia-like clinical features without eosinophilia and achieved an optimal response to imatinib.	imatinib	234-242	platelet derived growth factor receptor beta	Homo sapiens	64-70
31836165-6	2019	Imatinib, a tyrosine kinase inhibitor significantly potentiated the sensitivity of doxorubicin in P-gp-overexpressing doxorubicin-resistant cells.	imatinib	0-8	PGP	Canis lupus familiaris	98-102
31836165-8	2019	In conclusion, imatinib reversed doxorubicin resistance by decreasing drug efflux in P-gp-overexpressing doxorubicin-resistant canine lymphoma cells.	imatinib	15-23	PGP	Canis lupus familiaris	85-89
31839033-4	2019	RESULTS: In BCR-ABL transfected bone marrow cells treated with imatinib, the numbers of viable cells of BAX deletion group was significantly higher than that of wild type groups with statristcal difference(P<0.05), and effect- and dose-dependency(r=-0.9533 for BAX deletion group, and r=-0.9812 for wild type group).	imatinib	63-71	BCL2-associated X protein	Mus musculus	261-264
31839033-7	2019	CONCLUSION: BAX deletion can reduce the sensitivity of BCR-ABL-induced B-ALL cells to imatinib.	imatinib	86-94	BCL2-associated X protein	Mus musculus	12-15
31839033-1	2019	OBJECTIVE: To investigate the effect of BAX gene deletion on the sensitivity of BCR-ABL-induced B-ALL cells of mice to imatinib and the related mechanism.	imatinib	119-127	BCL2-associated X protein	Mus musculus	40-43
31518872-3	2019	Tyrosine kinase inhibitors (TKIs) targeting BCR-ABL1 tyrosine kinase activity, represented by imatinib, are currently the first-line treatment for CML.	imatinib	94-102	BCR activator of RhoGEF and GTPase	Homo sapiens	44-52
31744552-10	2019	Identification of PDGFRA rearrangement, as in the present case, is particularly critical given the sensitivity and excellent response to imatinib, which has completely changed the natural history of this neoplasm.	imatinib	137-145	platelet derived growth factor receptor alpha	Homo sapiens	18-24
31292142-6	2019	Droplet digital PCR (ddPCR) was used to evaluate more accurately low levels of BCR-ABL1 in 175 of 218 patients at imatinib cessation.	imatinib	114-122	BCR activator of RhoGEF and GTPase	Homo sapiens	79-87
31493871-0	2019	TAL1 mediates imatinib-induced CML cell apoptosis via the PTEN/PI3K/AKT pathway.	imatinib	14-22	TAL bHLH transcription factor 1, erythroid differentiation factor	Homo sapiens	0-4
31493871-0	2019	TAL1 mediates imatinib-induced CML cell apoptosis via the PTEN/PI3K/AKT pathway.	imatinib	14-22	phosphatase and tensin homolog	Homo sapiens	58-62
31493871-0	2019	TAL1 mediates imatinib-induced CML cell apoptosis via the PTEN/PI3K/AKT pathway.	imatinib	14-22	AKT serine/threonine kinase 1	Homo sapiens	68-71
31828114-0	2019	Inhibition of the Nrf2-TrxR Axis Sensitizes the Drug-Resistant Chronic Myelogenous Leukemia Cell Line K562/G01 to Imatinib Treatments.	imatinib	114-122	NFE2 like bZIP transcription factor 2	Homo sapiens	18-22
31828114-0	2019	Inhibition of the Nrf2-TrxR Axis Sensitizes the Drug-Resistant Chronic Myelogenous Leukemia Cell Line K562/G01 to Imatinib Treatments.	imatinib	114-122	peroxiredoxin 5	Homo sapiens	23-27
31828114-6	2019	Imatinib-resistant K562/G01 cells had higher levels of Nrf2 expression than the parental K562 cells at both mRNA and protein levels.	imatinib	0-8	NFE2 like bZIP transcription factor 2	Homo sapiens	55-59
31828114-8	2019	Knockdown of Nrf2 in K562/G01 cells enhanced the intracellular ROS level, suppressed cell proliferation, and increased apoptosis in response to imatinib treatments.	imatinib	144-152	NFE2 like bZIP transcription factor 2	Homo sapiens	13-17
31828114-9	2019	Nrf2 expression contributes to the imatinib resistance of K562/G01 cells and is positively correlated with TrxR expression.	imatinib	35-43	NFE2 like bZIP transcription factor 2	Homo sapiens	0-4
31828114-10	2019	Targeted inhibition of the Nrf2-TrxR axis represents a potential therapeutic approach for imatinib-resistant CML.	imatinib	90-98	NFE2 like bZIP transcription factor 2	Homo sapiens	27-31
31828114-10	2019	Targeted inhibition of the Nrf2-TrxR axis represents a potential therapeutic approach for imatinib-resistant CML.	imatinib	90-98	peroxiredoxin 5	Homo sapiens	32-36
31827510-10	2019	These data suggest a potential role for both H19 and MALAT1 lncRNAs as prognostic biomarker for the clinical selection of the best candidate to first-line treatment with imatinib.	imatinib	170-178	H19 imprinted maternally expressed transcript	Homo sapiens	45-48
31827510-10	2019	These data suggest a potential role for both H19 and MALAT1 lncRNAs as prognostic biomarker for the clinical selection of the best candidate to first-line treatment with imatinib.	imatinib	170-178	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	53-59
31759356-0	2019	Association between C1236T Genetic Variant of ABCB1 Gene and Molecular Response to Imatinib in Indonesian Chronic Myeloid Patients.	imatinib	83-91	ATP binding cassette subfamily B member 1	Homo sapiens	46-51
31759356-3	2019	Mutation in ABCB1 efflux transporters is one of the known mechanisms of resistance to imatinib in chronic myeloid leukemia patients.	imatinib	86-94	ATP binding cassette subfamily B member 1	Homo sapiens	12-17
31759356-4	2019	This study was aimed to investigate the association of ABCB1 C1236T polymorphism in Indonesian chronic myeloid patients with molecular response to imatinib treatment.	imatinib	147-155	ATP binding cassette subfamily B member 1	Homo sapiens	55-60
31518872-9	2019	In addition, re-expression of miR-96 could increase the sensitivity of CML-BC cells to imatinib.	imatinib	87-95	microRNA 96	Homo sapiens	30-36
31429941-4	2019	Furthermore, the advantages of adding ACN to the sample containing NaCl to combine efficient protein precipitation and on-line CZE stacking of imatinib were demonstrated.	imatinib	143-151	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	38-41
30580670-2	2019	Ponatinib, an oral drug, was discovered as an efficient BCR-ABL inhibitor by addressing imatinib drug resistance arising due to the point mutations at its active sites.	imatinib	88-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
31428968-3	2019	Treatment with imatinib or RK-20449 inhibited cell growth and decreased tyrosine phosphorylation of YAP in both CML lines.	imatinib	15-23	Yes1 associated transcriptional regulator	Homo sapiens	100-103
31428968-6	2019	YAP was phosphorylated at Y357 constitutively in BCR-ABL stable transfectant but not in control transfectant, and treatment with imatinib or RK-20449, a Src family kinase-specific inhibitor, inhibited cell growth, YAP tyrosine phosphorylation, and expression of Cyclin D1 in BCR-ABL stable transfectant.	imatinib	129-137	Yes1 associated transcriptional regulator	Homo sapiens	0-3
31428968-6	2019	YAP was phosphorylated at Y357 constitutively in BCR-ABL stable transfectant but not in control transfectant, and treatment with imatinib or RK-20449, a Src family kinase-specific inhibitor, inhibited cell growth, YAP tyrosine phosphorylation, and expression of Cyclin D1 in BCR-ABL stable transfectant.	imatinib	129-137	Yes1 associated transcriptional regulator	Homo sapiens	214-217
31428968-6	2019	YAP was phosphorylated at Y357 constitutively in BCR-ABL stable transfectant but not in control transfectant, and treatment with imatinib or RK-20449, a Src family kinase-specific inhibitor, inhibited cell growth, YAP tyrosine phosphorylation, and expression of Cyclin D1 in BCR-ABL stable transfectant.	imatinib	129-137	cyclin D1	Homo sapiens	262-271
31428968-6	2019	YAP was phosphorylated at Y357 constitutively in BCR-ABL stable transfectant but not in control transfectant, and treatment with imatinib or RK-20449, a Src family kinase-specific inhibitor, inhibited cell growth, YAP tyrosine phosphorylation, and expression of Cyclin D1 in BCR-ABL stable transfectant.	imatinib	129-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	275-282
32053767-2	2019	The use of targeted therapy against these mutations in GISTs is one of the most successful examples of precision medicine in solid tumors, beginning in 2002 with the development of imatinib, a small molecule tyrosine kinase inhibitor (TKI) of KIT.	imatinib	181-189	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	243-246
31645346-0	2019	Novel PDGFRB rearrangement in multifocal infantile myofibromatosis is tumorigenic and sensitive to imatinib.	imatinib	99-107	platelet derived growth factor receptor beta	Homo sapiens	6-12
31520987-0	2019	The dynamic of TNF and IL6 gene expression in chronic myeloid leukemia patients reveals early responders to imatinib.	imatinib	108-116	tumor necrosis factor	Homo sapiens	15-18
31520987-0	2019	The dynamic of TNF and IL6 gene expression in chronic myeloid leukemia patients reveals early responders to imatinib.	imatinib	108-116	interleukin 6	Homo sapiens	23-26
31645346-7	2019	The mutated protein enhanced MAPK activation and retained sensitivity to the PDGFRbeta inhibitor imatinib.	imatinib	97-105	platelet derived growth factor receptor beta	Homo sapiens	77-86
31645346-8	2019	Our findings reveal a new mechanism by which PDGFRB can be activated in IM, suggest that therapy with tyrosine kinase inhibitors including imatinib may be beneficial, and raise the possibility that this receptor tyrosine kinase might be altered in a similar fashion in additional cases that would similarly present annotation challenges in clinical DNA sequencing analysis pipelines.	imatinib	139-147	platelet derived growth factor receptor, beta polypeptide	Mus musculus	45-51
31567386-0	2019	Complete response of myeloid/lymphoid neoplasms with PDGFRA rearrangement presenting as leukemia/myeloid sarcoma to imatinib monotherapy.	imatinib	116-124	platelet derived growth factor receptor alpha	Homo sapiens	53-59
31325435-0	2019	Imatinib prevents elastase-induced abdominal aortic aneurysm progression by regulating macrophage-derived MMP9.	imatinib	0-8	matrix metallopeptidase 9	Rattus norvegicus	106-110
31325435-4	2019	Here, we demonstrated that the transcription level of MMP9 was suppressed with a concentration-dependent manner in macrophages after Imatinib treatment, which was accompanied by the down-regulation of MMP9 protein expression and reduced MMP9 secretion in vitro.	imatinib	133-141	matrix metallopeptidase 9	Rattus norvegicus	54-58
31325435-4	2019	Here, we demonstrated that the transcription level of MMP9 was suppressed with a concentration-dependent manner in macrophages after Imatinib treatment, which was accompanied by the down-regulation of MMP9 protein expression and reduced MMP9 secretion in vitro.	imatinib	133-141	matrix metallopeptidase 9	Rattus norvegicus	201-205
31325435-4	2019	Here, we demonstrated that the transcription level of MMP9 was suppressed with a concentration-dependent manner in macrophages after Imatinib treatment, which was accompanied by the down-regulation of MMP9 protein expression and reduced MMP9 secretion in vitro.	imatinib	133-141	matrix metallopeptidase 9	Rattus norvegicus	201-205
31325435-7	2019	Expression and activity of MMP9 in the artery tissues were significantly suppressed after Imatinib treatment via in situ assessment like immunohistochemistry and zymography, although macrophage infiltration was not affected.	imatinib	90-98	matrix metallopeptidase 9	Rattus norvegicus	27-31
31325435-8	2019	Furthermore, we found that Imatinib inhibited MMP9 transcription through reduction of STAT3 phosphorylation and translocation from nucleus to cytoplasm.	imatinib	27-35	matrix metallopeptidase 9	Rattus norvegicus	46-50
31325435-8	2019	Furthermore, we found that Imatinib inhibited MMP9 transcription through reduction of STAT3 phosphorylation and translocation from nucleus to cytoplasm.	imatinib	27-35	signal transducer and activator of transcription 3	Rattus norvegicus	86-91
31325435-9	2019	These observations indicated that Imatinib prevents aneurysm progression by inhibiting STAT3-mediated MMP9 expression and activation, suggesting a new application of Imatinib on AAA clinical therapy.	imatinib	34-42	signal transducer and activator of transcription 3	Rattus norvegicus	87-92
31325435-9	2019	These observations indicated that Imatinib prevents aneurysm progression by inhibiting STAT3-mediated MMP9 expression and activation, suggesting a new application of Imatinib on AAA clinical therapy.	imatinib	34-42	matrix metallopeptidase 9	Rattus norvegicus	102-106
31325435-9	2019	These observations indicated that Imatinib prevents aneurysm progression by inhibiting STAT3-mediated MMP9 expression and activation, suggesting a new application of Imatinib on AAA clinical therapy.	imatinib	166-174	signal transducer and activator of transcription 3	Rattus norvegicus	87-92
31325435-9	2019	These observations indicated that Imatinib prevents aneurysm progression by inhibiting STAT3-mediated MMP9 expression and activation, suggesting a new application of Imatinib on AAA clinical therapy.	imatinib	166-174	matrix metallopeptidase 9	Rattus norvegicus	102-106
30045148-0	2019	Acute Lymphoblastic Leukemia With INPP5D-ABL1 Fusion Responds to Imatinib Treatment.	imatinib	65-73	inositol polyphosphate-5-phosphatase D	Homo sapiens	34-40
31423623-11	2019	Identification of rearranged PDGFRA or PDGFRB is critical because of the exquisite responsiveness of these diseases to imatinib.	imatinib	119-127	platelet derived growth factor receptor alpha	Homo sapiens	29-35
31423623-11	2019	Identification of rearranged PDGFRA or PDGFRB is critical because of the exquisite responsiveness of these diseases to imatinib.	imatinib	119-127	platelet derived growth factor receptor beta	Homo sapiens	39-45
30045148-0	2019	Acute Lymphoblastic Leukemia With INPP5D-ABL1 Fusion Responds to Imatinib Treatment.	imatinib	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-45
31432109-0	2019	Homoharringtonine enhances the effect of imatinib on chronic myelogenous leukemia cells by downregulating ZFX.	imatinib	41-49	zinc finger protein X-linked	Homo sapiens	106-109
31286393-3	2019	The study was carried out to understand the role of DNA repair genes (XRCC1, XPD) polymorphisms in Imatinib mesylate (IM) resistant CML patients.	imatinib	99-116	X-ray repair cross complementing 1	Homo sapiens	70-75
31286393-3	2019	The study was carried out to understand the role of DNA repair genes (XRCC1, XPD) polymorphisms in Imatinib mesylate (IM) resistant CML patients.	imatinib	99-116	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	77-80
31432109-8	2019	ZFX overexpression reversed cell sensitivity to imatinib and HHT and also reduced the HHT-induced imatinib sensitization by increasing p-Akt expression.	imatinib	48-56	zinc finger protein X-linked	Homo sapiens	0-3
31432109-8	2019	ZFX overexpression reversed cell sensitivity to imatinib and HHT and also reduced the HHT-induced imatinib sensitization by increasing p-Akt expression.	imatinib	98-106	zinc finger protein X-linked	Homo sapiens	0-3
31432109-9	2019	In conclusion, HHT may enhance the effect of imatinib on CML cells by downregulating ZFX.	imatinib	45-53	zinc finger protein X-linked	Homo sapiens	85-88
30713339-0	2019	Genetic polymorphisms in ABCG2 and CYP1A2 are associated with imatinib dose reduction in patients treated for gastrointestinal stromal tumors.	imatinib	62-70	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	25-30
30713339-0	2019	Genetic polymorphisms in ABCG2 and CYP1A2 are associated with imatinib dose reduction in patients treated for gastrointestinal stromal tumors.	imatinib	62-70	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	35-41
31045869-0	2019	Association of Hepatic Nuclear Factor 4 Alpha Gene Polymorphisms With Free Imatinib Plasma Levels and Adverse Reactions in Chinese Gastrointestinal Stromal Tumor Patients.	imatinib	75-83	hepatocyte nuclear factor 4 alpha	Homo sapiens	15-45
31236647-2	2019	Desmoid is a tumour with a local aggressiveness; GIST with KIT mutation responds massively to target treatment as IMATINIB, whereas soft tissue sarcoma and leiomyosarcoma are very aggressive with poor response to systemic therapies.	imatinib	114-122	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	59-62
31570755-5	2019	An Abl family tyrosine kinase inhibitor imatinib, which reduces caveolae-mediated endocytosis, impairs IgG extravasation in the skin and attenuates the murine pemphigus manifestations.	imatinib	40-48	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	3-6
31574910-1	2019	Imatinib, an Abelson (ABL) tyrosine kinase inhibitor, is a lead molecular-targeted drug against chronic myelogenous leukemia (CML).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
31574910-1	2019	Imatinib, an Abelson (ABL) tyrosine kinase inhibitor, is a lead molecular-targeted drug against chronic myelogenous leukemia (CML).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-25
31291054-4	2019	This is the first report of an adult patient with PDGFRB c.1681C&gt;T mutation treated with imatinib.	imatinib	92-100	platelet derived growth factor receptor beta	Homo sapiens	50-56
30342021-5	2019	NVP-BEZ235 and imatinib reduced RAD51 levels and focus formation (an indication of HRR function), but VS-5584 did not.	imatinib	15-23	RAD51 recombinase	Homo sapiens	32-37
31349760-2	2019	The introduction of tyrosine kinase inhibitors (TKIs) targeting the ABL kinase (such as imatinib) has dramatically improved survival of CML and Ph+ ALL patients.	imatinib	88-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-71
31349760-8	2019	The combination of MLN4924 and imatinib furthermore triggered a dramatic shift in the expression of MCL1 and NOXA.	imatinib	31-39	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	100-104
31349760-8	2019	The combination of MLN4924 and imatinib furthermore triggered a dramatic shift in the expression of MCL1 and NOXA.	imatinib	31-39	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	109-113
31079264-1	2019	Imatinib, the first BCR/ABL kinase inhibitor approved for the treatment of chronic myeloid leukemia (CML), has changed the long-term outcome of patients affected by this disease.	imatinib	0-8	BCR activator of RhoGEF and GTPase	Homo sapiens	20-23
31363162-9	2019	Taken together, these results demonstrate the existence of a nuclear KIT-driven NFKBIB-RELA-KIT autoregulatory loop in GIST tumorigenesis, which are potential targets for developing combination therapy to overcome imatinib-resistant of KIT-expressing GISTs.	imatinib	214-222	NFKB inhibitor beta	Homo sapiens	80-86
31363162-9	2019	Taken together, these results demonstrate the existence of a nuclear KIT-driven NFKBIB-RELA-KIT autoregulatory loop in GIST tumorigenesis, which are potential targets for developing combination therapy to overcome imatinib-resistant of KIT-expressing GISTs.	imatinib	214-222	RELA proto-oncogene, NF-kB subunit	Homo sapiens	87-91
31363162-9	2019	Taken together, these results demonstrate the existence of a nuclear KIT-driven NFKBIB-RELA-KIT autoregulatory loop in GIST tumorigenesis, which are potential targets for developing combination therapy to overcome imatinib-resistant of KIT-expressing GISTs.	imatinib	214-222	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	92-95
31363162-9	2019	Taken together, these results demonstrate the existence of a nuclear KIT-driven NFKBIB-RELA-KIT autoregulatory loop in GIST tumorigenesis, which are potential targets for developing combination therapy to overcome imatinib-resistant of KIT-expressing GISTs.	imatinib	214-222	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	92-95
31371779-1	2019	Oncogenic KIT or PDGFRA tyrosine kinase mutations are compelling therapeutic targets in most gastrointestinal stromal tumors (GISTs), and the KIT inhibitor, imatinib, is therefore standard of care for patients with metastatic GIST.	imatinib	157-165	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	10-13
31371779-1	2019	Oncogenic KIT or PDGFRA tyrosine kinase mutations are compelling therapeutic targets in most gastrointestinal stromal tumors (GISTs), and the KIT inhibitor, imatinib, is therefore standard of care for patients with metastatic GIST.	imatinib	157-165	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	142-145
31497247-8	2019	In addition, fluorocoxib A uptake correlated with the AB1010- and imatinib-induced COX-2 expression in the K9TCC#5Lilly xenografts in vivo.	imatinib	66-74	prostaglandin-endoperoxide synthase 2	Homo sapiens	83-88
30079802-2	2019	Imatinib, a small molecule tyrosine kinase inhibitor, induces rapid and sustained clinical benefit by inhibiting a number of signaling pathways, including BCR-ABL and c-KIT.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-162
30079802-2	2019	Imatinib, a small molecule tyrosine kinase inhibitor, induces rapid and sustained clinical benefit by inhibiting a number of signaling pathways, including BCR-ABL and c-KIT.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	167-172
31363162-0	2019	Nuclear KIT induces a NFKBIB-RELA-KIT autoregulatory loop in imatinib-resistant gastrointestinal stromal tumors.	imatinib	61-69	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	8-11
31363162-0	2019	Nuclear KIT induces a NFKBIB-RELA-KIT autoregulatory loop in imatinib-resistant gastrointestinal stromal tumors.	imatinib	61-69	NFKB inhibitor beta	Homo sapiens	22-28
31363162-0	2019	Nuclear KIT induces a NFKBIB-RELA-KIT autoregulatory loop in imatinib-resistant gastrointestinal stromal tumors.	imatinib	61-69	RELA proto-oncogene, NF-kB subunit	Homo sapiens	29-33
31363162-0	2019	Nuclear KIT induces a NFKBIB-RELA-KIT autoregulatory loop in imatinib-resistant gastrointestinal stromal tumors.	imatinib	61-69	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	34-37
31363162-7	2019	These findings were further confirmed by either RELA overexpression or NFKB/RELA inducer, valproic acid, treatment to result in reduced KIT expression and relative cell viability of imatinib-resistant GIST cells.	imatinib	182-190	RELA proto-oncogene, NF-kB subunit	Homo sapiens	48-52
31363162-7	2019	These findings were further confirmed by either RELA overexpression or NFKB/RELA inducer, valproic acid, treatment to result in reduced KIT expression and relative cell viability of imatinib-resistant GIST cells.	imatinib	182-190	RELA proto-oncogene, NF-kB subunit	Homo sapiens	76-80
31363162-7	2019	These findings were further confirmed by either RELA overexpression or NFKB/RELA inducer, valproic acid, treatment to result in reduced KIT expression and relative cell viability of imatinib-resistant GIST cells.	imatinib	182-190	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	136-139
31363162-9	2019	Taken together, these results demonstrate the existence of a nuclear KIT-driven NFKBIB-RELA-KIT autoregulatory loop in GIST tumorigenesis, which are potential targets for developing combination therapy to overcome imatinib-resistant of KIT-expressing GISTs.	imatinib	214-222	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	69-72
31456947-3	2019	Thus, we retrospectively examined BCR-ABL1 evolution in 305 chronic-phase CML patients receiving imatinib mesylate (IM) as a first line treatment.	imatinib	97-114	BCR activator of RhoGEF and GTPase	Homo sapiens	34-42
31079264-1	2019	Imatinib, the first BCR/ABL kinase inhibitor approved for the treatment of chronic myeloid leukemia (CML), has changed the long-term outcome of patients affected by this disease.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-27
31145521-0	2019	Cysteine-rich protein 61 regulates the chemosensitivity of chronic myeloid leukemia to imatinib mesylate through the nuclear factor kappa B/Bcl-2 pathway.	imatinib	87-95	cellular communication network factor 1	Homo sapiens	0-24
31486501-0	2019	MicroRNA-577 promotes the sensitivity of chronic myeloid leukemia cells to imatinib by targeting NUP160.	imatinib	75-83	microRNA 577	Homo sapiens	0-12
31486501-0	2019	MicroRNA-577 promotes the sensitivity of chronic myeloid leukemia cells to imatinib by targeting NUP160.	imatinib	75-83	nucleoporin 160	Homo sapiens	97-103
31486501-3	2019	Meanwhile, the expression of microRNA-577 was detected in CML cell line after imatinib treatment.	imatinib	78-86	microRNA 577	Homo sapiens	29-41
31486501-6	2019	Cell reverse test was performed to figure out whether microRNA-577 can enhance the sensitivity of CML to imatinib.	imatinib	105-113	microRNA 577	Homo sapiens	54-66
31486501-9	2019	Lastly, cell reverse experiments confirmed that microRNA-577 can alleviate the resistance of CML to imatinib.	imatinib	100-108	microRNA 577	Homo sapiens	48-60
31486501-10	2019	CONCLUSIONS: We found that microRNA-577 promotes the sensitivity of chronic myeloid leukemia cells to imatinib by down-regulating the expression of NUP160.	imatinib	102-110	microRNA 577	Homo sapiens	27-39
31486501-10	2019	CONCLUSIONS: We found that microRNA-577 promotes the sensitivity of chronic myeloid leukemia cells to imatinib by down-regulating the expression of NUP160.	imatinib	102-110	nucleoporin 160	Homo sapiens	148-154
31145521-0	2019	Cysteine-rich protein 61 regulates the chemosensitivity of chronic myeloid leukemia to imatinib mesylate through the nuclear factor kappa B/Bcl-2 pathway.	imatinib	87-95	BCL2 apoptosis regulator	Homo sapiens	140-145
31017643-12	2019	All of the PDGFRB mutations were associated with ligand-independent receptor activation, and all but one were sensitive to imatinib at clinically relevant concentrations.	imatinib	123-131	platelet derived growth factor receptor beta	Homo sapiens	11-17
31233186-7	2019	We also demonstrated that RRM2 is involved in the Bcl-2/caspase cell apoptotic pathway and in the Akt cell signaling pathway, and therefore affects the cell survival following imatinib therapy.	imatinib	176-184	ribonucleotide reductase regulatory subunit M2	Homo sapiens	26-30
31276931-8	2019	In addition, the combination treatment of KPT-330 and imatinib, which induced the marked nuclear accumulation of PP2A and SET, reactivated PP2A through its dephosphorylation and inhibited SET expression, resulting in the effective induction of the apoptosis in the cells expressing SEPT9-ABL1.	imatinib	54-62	protein phosphatase 2, regulatory subunit A, alpha	Mus musculus	113-117
31276931-8	2019	In addition, the combination treatment of KPT-330 and imatinib, which induced the marked nuclear accumulation of PP2A and SET, reactivated PP2A through its dephosphorylation and inhibited SET expression, resulting in the effective induction of the apoptosis in the cells expressing SEPT9-ABL1.	imatinib	54-62	protein phosphatase 2, regulatory subunit A, alpha	Mus musculus	139-143
31276931-8	2019	In addition, the combination treatment of KPT-330 and imatinib, which induced the marked nuclear accumulation of PP2A and SET, reactivated PP2A through its dephosphorylation and inhibited SET expression, resulting in the effective induction of the apoptosis in the cells expressing SEPT9-ABL1.	imatinib	54-62	septin 9	Mus musculus	282-287
31233186-0	2019	Knockdown of ribonucleotide reductase regulatory subunit M2 increases the drug sensitivity of chronic myeloid leukemia to imatinib-based therapy.	imatinib	122-130	ribonucleotide reductase regulatory subunit M2	Homo sapiens	13-59
31233186-7	2019	We also demonstrated that RRM2 is involved in the Bcl-2/caspase cell apoptotic pathway and in the Akt cell signaling pathway, and therefore affects the cell survival following imatinib therapy.	imatinib	176-184	BCL2 apoptosis regulator	Homo sapiens	50-55
31233186-2	2019	Imatinib resistance can be ascribed to Bcr-Abl-dependent and independent resistance.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
31276931-8	2019	In addition, the combination treatment of KPT-330 and imatinib, which induced the marked nuclear accumulation of PP2A and SET, reactivated PP2A through its dephosphorylation and inhibited SET expression, resulting in the effective induction of the apoptosis in the cells expressing SEPT9-ABL1.	imatinib	54-62	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	288-292
31276931-9	2019	The combination treatment with KPT-330 and imatinib successfully reduced the subcutaneous masses expressing SEPT9-ABL1 and extended the survival of the mice intraperitoneally transplanted with SEPT9-ABL1-expressing cells.	imatinib	43-51	septin 9	Mus musculus	108-113
31233186-7	2019	We also demonstrated that RRM2 is involved in the Bcl-2/caspase cell apoptotic pathway and in the Akt cell signaling pathway, and therefore affects the cell survival following imatinib therapy.	imatinib	176-184	AKT serine/threonine kinase 1	Homo sapiens	98-101
31276931-9	2019	The combination treatment with KPT-330 and imatinib successfully reduced the subcutaneous masses expressing SEPT9-ABL1 and extended the survival of the mice intraperitoneally transplanted with SEPT9-ABL1-expressing cells.	imatinib	43-51	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	114-118
31276931-9	2019	The combination treatment with KPT-330 and imatinib successfully reduced the subcutaneous masses expressing SEPT9-ABL1 and extended the survival of the mice intraperitoneally transplanted with SEPT9-ABL1-expressing cells.	imatinib	43-51	septin 9	Mus musculus	193-198
31233186-6	2019	Using reverse-transcription PCR (RT-PCR) and western blot analysis, we indicated that imatinib can increase RRM2 level in a dose-dependent manner in IR cells.	imatinib	86-94	ribonucleotide reductase regulatory subunit M2	Homo sapiens	108-112
31233186-8	2019	The present study, for the first time, indicates that RRM2 is responsible for drug resistance in imatinib-based therapy.	imatinib	97-105	ribonucleotide reductase regulatory subunit M2	Homo sapiens	54-58
31276931-9	2019	The combination treatment with KPT-330 and imatinib successfully reduced the subcutaneous masses expressing SEPT9-ABL1 and extended the survival of the mice intraperitoneally transplanted with SEPT9-ABL1-expressing cells.	imatinib	43-51	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	199-203
31396300-8	2019	The effect of ABL1 on inflammation was detected with Imatinib/Nilotinib-treated GC cell lines.	imatinib	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-18
30237583-5	2019	We further confirmed the genotype of selected variants in an extended cohort of 49 patients (the original cohort and 15 new cases, all with exon 11 primary mutation), identifying 6 SNPs- ABCB4 rs1202283, ABCC2 rs2273697, ABCG1 rs1541290, CYP11B1 rs7003319, CYP7B1 rs6987861, and NQO1 rs10517-significantly associated with response to imatinib.	imatinib	334-342	ATP binding cassette subfamily B member 4	Homo sapiens	187-192
30910525-6	2019	Further, 10 muM imatinib increased mRNA expression of TGFB1 7-fold, (p < 0.01), IL6 6-fold (p < 0.01), and IL1B 7-fold (p < 0.05) and reduced PDGFD 15-fold (p < 0.01); whereas sunitinib specifically reduced IL1B mRNA expression 17-fold (p < 0.01).	imatinib	16-24	transforming growth factor, beta 1	Rattus norvegicus	54-59
30910525-6	2019	Further, 10 muM imatinib increased mRNA expression of TGFB1 7-fold, (p < 0.01), IL6 6-fold (p < 0.01), and IL1B 7-fold (p < 0.05) and reduced PDGFD 15-fold (p < 0.01); whereas sunitinib specifically reduced IL1B mRNA expression 17-fold (p < 0.01).	imatinib	16-24	interleukin 1 beta	Rattus norvegicus	107-111
30910525-6	2019	Further, 10 muM imatinib increased mRNA expression of TGFB1 7-fold, (p < 0.01), IL6 6-fold (p < 0.01), and IL1B 7-fold (p < 0.05) and reduced PDGFD 15-fold (p < 0.01); whereas sunitinib specifically reduced IL1B mRNA expression 17-fold (p < 0.01).	imatinib	16-24	interleukin 1 beta	Rattus norvegicus	207-211
31358779-4	2019	It is mainly treated with BCR-ABL inhibitors, such as imatinib.	imatinib	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
31358779-7	2019	We demonstrated that imatinib decreased HA levels and the surface expression of CD44 in both cell lines.	imatinib	21-29	CD44 molecule (Indian blood group)	Homo sapiens	80-84
31423283-1	2019	Tyrosine kinase inhibitors (TKIs), such as imatinib (IMA) and nilotinib (NIL), are the cornerstone of chronic myeloid leukemia (CML) treatment via the blockade of the oncogenic BCR-ABL1 fusion protein.	imatinib	43-51	BCR activator of RhoGEF and GTPase	Homo sapiens	177-185
31423283-1	2019	Tyrosine kinase inhibitors (TKIs), such as imatinib (IMA) and nilotinib (NIL), are the cornerstone of chronic myeloid leukemia (CML) treatment via the blockade of the oncogenic BCR-ABL1 fusion protein.	imatinib	53-56	BCR activator of RhoGEF and GTPase	Homo sapiens	177-185
31418359-0	2019	[Expression Levels of JARID1B, Hes1 and MMP-9 Genes in CML Patients Treated with Imatinib Mesylate].	imatinib	81-98	lysine demethylase 5B	Homo sapiens	22-29
31418359-0	2019	[Expression Levels of JARID1B, Hes1 and MMP-9 Genes in CML Patients Treated with Imatinib Mesylate].	imatinib	81-98	hes family bHLH transcription factor 1	Homo sapiens	31-35
31418359-0	2019	[Expression Levels of JARID1B, Hes1 and MMP-9 Genes in CML Patients Treated with Imatinib Mesylate].	imatinib	81-98	matrix metallopeptidase 9	Homo sapiens	40-45
31418359-1	2019	OBJECTIVE: To explore the relationship between the expression levels of JARID1B,Hes1 and MMP-9 genes and the stages of chronic myelogenous leukemia(CML) and the curative effect of imatinib mesylate (IM).	imatinib	180-197	lysine demethylase 5B	Homo sapiens	72-79
31418359-1	2019	OBJECTIVE: To explore the relationship between the expression levels of JARID1B,Hes1 and MMP-9 genes and the stages of chronic myelogenous leukemia(CML) and the curative effect of imatinib mesylate (IM).	imatinib	180-197	hes family bHLH transcription factor 1	Homo sapiens	80-84
31418359-1	2019	OBJECTIVE: To explore the relationship between the expression levels of JARID1B,Hes1 and MMP-9 genes and the stages of chronic myelogenous leukemia(CML) and the curative effect of imatinib mesylate (IM).	imatinib	180-197	matrix metallopeptidase 9	Homo sapiens	89-94
31417408-14	2019	The genetic polymorphisms of CYP3A4 rs755828176 and NR1I2 rs3814055 were significantly associated with unbound imatinib and N-desmethyl-imatinib dose-adjusted trough plasma levels.	imatinib	111-119	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	29-35
31417408-14	2019	The genetic polymorphisms of CYP3A4 rs755828176 and NR1I2 rs3814055 were significantly associated with unbound imatinib and N-desmethyl-imatinib dose-adjusted trough plasma levels.	imatinib	111-119	nuclear receptor subfamily 1 group I member 2	Homo sapiens	52-57
31372066-5	2019	Several approved tyrosine kinase inhibitors (TKIs), such as imatinib and nilotinib, have activity against wild-type KIT but lack activity against KITD816V.	imatinib	60-68	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	116-119
31262905-10	2019	CONCLUSION: These findings provide valuable information regarding the sensitizing of drug-resistant cells and indicate that imatinib and erlotinib may be used in patients with potentially resistant cancer without any toxic effects from P-gp inhibition.	imatinib	124-132	ATP binding cassette subfamily B member 1	Homo sapiens	236-240
31262854-5	2019	Imatinib was the first TKI for the fusion protein BCR-ABL and represented a breakthrough in the treatment of chronic myeloid leukemia.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
31089794-5	2019	In newly diagnosed patients who received imatinib treatment (n = 40), 24-h urine protein levels significantly increased after 6 months, and urinary beta2-microglobulin values significantly increased compared to those in the nilotinib cohort (n =15) at 36 months (P = 0.042) and 42 months (P = 0.039).	imatinib	41-49	beta-2-microglobulin	Homo sapiens	148-167
31004989-11	2019	Concerning selected microRNAs in the hearts of individual mice, only miR-34a was significantly increased after DOX treatment, and only miR-205 was significantly decreased after IMB and DOX treatment.	imatinib	177-180	microRNA 205	Mus musculus	135-142
30948162-6	2019	Early identification of PDGFR translocations is essential, as they confer profound imatinib sensitivity which may, in many instances, spare the need for chemotherapy.	imatinib	83-91	platelet derived growth factor receptor beta	Homo sapiens	24-29
30948162-8	2019	Unfortunately, many cases of PDGFR associated AML, particularly those with other concurrent cytogenetic abnormalities, demonstrate treatment emergent imatinib resistance.	imatinib	150-158	platelet derived growth factor receptor beta	Homo sapiens	29-34
30948162-10	2019	Patients with rare translocations such as ETV6-ABL1 are not well described however seem to follow an aggressive clinical course, with limited response to imatinib, and poor outcomes.	imatinib	154-162	ETS variant transcription factor 6	Homo sapiens	42-46
31263034-0	2019	Editor"s Note: Cotreatment with STI-571 Enhances Tumor Necrosis Factor alpha-related Apoptosis-inducing Ligand (TRAIL or Apo-2L)-induced Apoptosis of Bcr-Abl-positive Human Acute Leukemia Cells.	imatinib	32-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
30948162-10	2019	Patients with rare translocations such as ETV6-ABL1 are not well described however seem to follow an aggressive clinical course, with limited response to imatinib, and poor outcomes.	imatinib	154-162	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-51
31054182-0	2019	Downregulation of the histone methyltransferase SETD2 promotes imatinib resistance in chronic myeloid leukaemia cells.	imatinib	63-71	SET domain containing 2, histone lysine methyltransferase	Homo sapiens	48-53
31054182-4	2019	MATERIALS AND METHODS: The level of SETD2 in imatinib-sensitive and imatinib-resistant chronic myeloid leukaemia (CML) cells was examined by immunoblotting and quantitative real-time PCR.	imatinib	45-53	SET domain containing 2, histone lysine methyltransferase	Homo sapiens	36-41
31054182-4	2019	MATERIALS AND METHODS: The level of SETD2 in imatinib-sensitive and imatinib-resistant chronic myeloid leukaemia (CML) cells was examined by immunoblotting and quantitative real-time PCR.	imatinib	68-76	SET domain containing 2, histone lysine methyltransferase	Homo sapiens	36-41
31054182-9	2019	The novel oncogenic targets MYCN and ERG were shown to be the direct downstream targets of SETD2, where their overexpression induced by SETD2 knockdown caused imatinib insensitivity and leukaemic stem cell enrichment in CML cell lines.	imatinib	159-167	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	28-32
31054182-9	2019	The novel oncogenic targets MYCN and ERG were shown to be the direct downstream targets of SETD2, where their overexpression induced by SETD2 knockdown caused imatinib insensitivity and leukaemic stem cell enrichment in CML cell lines.	imatinib	159-167	SET domain containing 2, histone lysine methyltransferase	Homo sapiens	91-96
31054182-9	2019	The novel oncogenic targets MYCN and ERG were shown to be the direct downstream targets of SETD2, where their overexpression induced by SETD2 knockdown caused imatinib insensitivity and leukaemic stem cell enrichment in CML cell lines.	imatinib	159-167	SET domain containing 2, histone lysine methyltransferase	Homo sapiens	136-141
31054182-11	2019	CONCLUSIONS: Our study not only emphasizes the regulatory mechanism of SETD2 in CML, but also provides promising therapeutic strategies for overcoming the imatinib resistance in patients with CML.	imatinib	155-163	SET domain containing 2, histone lysine methyltransferase	Homo sapiens	71-76
31263034-0	2019	Editor"s Note: Cotreatment with STI-571 Enhances Tumor Necrosis Factor alpha-related Apoptosis-inducing Ligand (TRAIL or Apo-2L)-induced Apoptosis of Bcr-Abl-positive Human Acute Leukemia Cells.	imatinib	32-39	tumor necrosis factor	Homo sapiens	49-76
31263034-0	2019	Editor"s Note: Cotreatment with STI-571 Enhances Tumor Necrosis Factor alpha-related Apoptosis-inducing Ligand (TRAIL or Apo-2L)-induced Apoptosis of Bcr-Abl-positive Human Acute Leukemia Cells.	imatinib	32-39	TNF superfamily member 10	Homo sapiens	112-117
31135065-13	2019	The latter effect was pharmacologically mimicked by treating OHCs with the PDGFRbeta agonist PDGF-BB and it was diminished by the PDGFRbeta inhibitor imatinib.	imatinib	150-158	platelet derived growth factor receptor, beta polypeptide	Mus musculus	75-84
31263034-0	2019	Editor"s Note: Cotreatment with STI-571 Enhances Tumor Necrosis Factor alpha-related Apoptosis-inducing Ligand (TRAIL or Apo-2L)-induced Apoptosis of Bcr-Abl-positive Human Acute Leukemia Cells.	imatinib	32-39	TNF superfamily member 10	Homo sapiens	121-127
31135065-13	2019	The latter effect was pharmacologically mimicked by treating OHCs with the PDGFRbeta agonist PDGF-BB and it was diminished by the PDGFRbeta inhibitor imatinib.	imatinib	150-158	platelet derived growth factor receptor, beta polypeptide	Mus musculus	130-139
31079870-0	2019	Corrigendum to "Adaphostin and bortezomib induce oxidative injury and apoptosis in imatinib mesylate-resistant hematopoietic cells expressing mutant forms of Bcr/Abl" [Leuk.	imatinib	83-100	BCR activator of RhoGEF and GTPase	Homo sapiens	158-161
31115499-2	2019	Pharmacological inhibition of BCR-ABL with imatinib (Gleevec) has been reported as an effective targeted therapy; however, mutations (including the kinase domain of ABL) suppress the efficacy of inhibitors.	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
31115499-2	2019	Pharmacological inhibition of BCR-ABL with imatinib (Gleevec) has been reported as an effective targeted therapy; however, mutations (including the kinase domain of ABL) suppress the efficacy of inhibitors.	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-37
30516071-0	2019	MicroRNA-221 sensitizes chronic myeloid leukemia cells to imatinib by targeting STAT5.	imatinib	58-66	signal transducer and activator of transcription 5A	Homo sapiens	80-85
30516071-2	2019	In this study, we examined the STAT5-related miRNA-expression profile in CML cell lines (K562 and imatinib-resistant K562/G) by quantitative real-time reverse-transcriptase polymerase chain reactions.	imatinib	98-106	signal transducer and activator of transcription 5A	Homo sapiens	31-36
30516071-3	2019	MiR-221 expression was markedly decreased in K562/G cells and peripheral blood mononuclear cells from patients with treatment failure, when compared to imatinib-sensitive CML cells and patients with optimal responses respectively.	imatinib	152-160	microRNA 221	Homo sapiens	0-7
31152921-0	2019	Age, gender and efflux transporter activity influence imatinib efficacy in chronic myeloid leukemia patients.	imatinib	54-62	renin binding protein	Homo sapiens	0-3
30516071-6	2019	MiR-221 restoration and STAT5 knockdown in K562/G cells increased the sensitivity of CML cells to imatinib by reducing the Bcl2: Bax ratio.	imatinib	98-106	microRNA 221	Homo sapiens	0-7
30516071-6	2019	MiR-221 restoration and STAT5 knockdown in K562/G cells increased the sensitivity of CML cells to imatinib by reducing the Bcl2: Bax ratio.	imatinib	98-106	signal transducer and activator of transcription 5A	Homo sapiens	24-29
30516071-6	2019	MiR-221 restoration and STAT5 knockdown in K562/G cells increased the sensitivity of CML cells to imatinib by reducing the Bcl2: Bax ratio.	imatinib	98-106	BCL2 apoptosis regulator	Homo sapiens	123-127
31111691-1	2019	BACKGROUND: Glutathione S-transferases (GSTs) polymorphisms may impact on chronic myeloid leukemia (CML) risk or heterogeneous responses to Imatinib mesylate (IM).	imatinib	140-157	glutathione S-transferase kappa 1	Homo sapiens	40-44
30516071-6	2019	MiR-221 restoration and STAT5 knockdown in K562/G cells increased the sensitivity of CML cells to imatinib by reducing the Bcl2: Bax ratio.	imatinib	98-106	BCL2 associated X, apoptosis regulator	Homo sapiens	129-132
30516071-7	2019	Collectively, our data suggested that miR-221-STAT5 axis played crucial roles in controlling the sensitivity of CML cells to imatinib.	imatinib	125-133	microRNA 221	Homo sapiens	38-45
30516071-7	2019	Collectively, our data suggested that miR-221-STAT5 axis played crucial roles in controlling the sensitivity of CML cells to imatinib.	imatinib	125-133	signal transducer and activator of transcription 5A	Homo sapiens	46-51
31258755-2	2019	Imatinib (Gleevec), a specific targeted drug for the treatment of chronic myeloid leukemia (CML), was developed for inhibiting the kinase activity of the BCR-ABL fusion protein.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-161
31308690-8	2019	Currently, the main strategy to combat imatinib resistance is to switch to another tyrosine kinase inhibitor, because imatinib-resistant GIST is usually still oncogenically addicted to KIT/PDGFRA signaling.	imatinib	39-47	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	185-188
31308690-8	2019	Currently, the main strategy to combat imatinib resistance is to switch to another tyrosine kinase inhibitor, because imatinib-resistant GIST is usually still oncogenically addicted to KIT/PDGFRA signaling.	imatinib	39-47	platelet derived growth factor receptor alpha	Homo sapiens	189-195
31308690-8	2019	Currently, the main strategy to combat imatinib resistance is to switch to another tyrosine kinase inhibitor, because imatinib-resistant GIST is usually still oncogenically addicted to KIT/PDGFRA signaling.	imatinib	118-126	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	185-188
31308690-8	2019	Currently, the main strategy to combat imatinib resistance is to switch to another tyrosine kinase inhibitor, because imatinib-resistant GIST is usually still oncogenically addicted to KIT/PDGFRA signaling.	imatinib	118-126	platelet derived growth factor receptor alpha	Homo sapiens	189-195
29770723-15	2019	The role of CYP2C8 in imatinib metabolism and imatinib autoinhibits CYP3A activity may explain this difference.	imatinib	22-30	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	12-18
31316860-5	2019	AIM: The aim of this study was to determine the frequency and types of PTCH1 gene mutations in Chronic Myeloid Leukemia (CML) patients and to correlate the effect of these mutations on the prognosis and outcome of CML and for predicting the imatinib response in CML patients.	imatinib	241-249	patched 1	Homo sapiens	71-76
31316860-11	2019	However there was significant association between PTCH1 gene mutation and imatinib failure (P=0.03).	imatinib	74-82	patched 1	Homo sapiens	50-55
31316860-12	2019	CONCLUSION: PTCH1 gene mutation should be considered a promising molecular marker for predicting the probability of imatinib response in CML patients.	imatinib	116-124	patched 1	Homo sapiens	12-17
31428517-10	2019	Analysis of the Gene Expression Omnibus database GIST samples pre- and post-treatment confirmed that imatinib downregulates PD-L1 and IRF1 expression through the inhibition of KIT and PDGFRA, thus contributing to counteract the suppressed adaptive immune response against GIST.	imatinib	101-109	CD274 antigen	Mus musculus	124-129
31428517-10	2019	Analysis of the Gene Expression Omnibus database GIST samples pre- and post-treatment confirmed that imatinib downregulates PD-L1 and IRF1 expression through the inhibition of KIT and PDGFRA, thus contributing to counteract the suppressed adaptive immune response against GIST.	imatinib	101-109	interferon regulatory factor 1	Mus musculus	134-138
31428517-10	2019	Analysis of the Gene Expression Omnibus database GIST samples pre- and post-treatment confirmed that imatinib downregulates PD-L1 and IRF1 expression through the inhibition of KIT and PDGFRA, thus contributing to counteract the suppressed adaptive immune response against GIST.	imatinib	101-109	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	176-179
31428517-10	2019	Analysis of the Gene Expression Omnibus database GIST samples pre- and post-treatment confirmed that imatinib downregulates PD-L1 and IRF1 expression through the inhibition of KIT and PDGFRA, thus contributing to counteract the suppressed adaptive immune response against GIST.	imatinib	101-109	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	184-190
31111691-1	2019	BACKGROUND: Glutathione S-transferases (GSTs) polymorphisms may impact on chronic myeloid leukemia (CML) risk or heterogeneous responses to Imatinib mesylate (IM).	imatinib	140-157	glutathione S-transferase kappa 1	Homo sapiens	12-38
31252559-0	2019	Coordinate Modulation of Glycolytic Enzymes and OXPHOS by Imatinib in BCR-ABL Driven Chronic Myelogenous Leukemia Cells.	imatinib	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
31252559-1	2019	Since many oncogenes, including BCR-ABL, may promote the acquisition and maintenance of the glycolytic phenotype, we tested whether treatment of BCR-ABL-driven human leukemia cells with imatinib, a selective BCR-ABL inhibitor, can modulate the expression of key glycolytic enzymes and mitochondrial complex subunits thus causing alterations of glucose metabolism.	imatinib	186-194	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-152
31252559-1	2019	Since many oncogenes, including BCR-ABL, may promote the acquisition and maintenance of the glycolytic phenotype, we tested whether treatment of BCR-ABL-driven human leukemia cells with imatinib, a selective BCR-ABL inhibitor, can modulate the expression of key glycolytic enzymes and mitochondrial complex subunits thus causing alterations of glucose metabolism.	imatinib	186-194	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-152
31252559-2	2019	BCR-ABL-driven K562 and KCL-22 cells were incubated with increasing concentrations of imatinib to preliminarily test drug sensitivity.	imatinib	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
31252559-5	2019	Furthermore, a strong reduction of the hexokinase II (HKII), phosphorylated form of PKM2 (at Tyr105 and Ser37) and lactate dehydrogenase A (LDH-A) was observed in response to imatinib along with a strong upregulation of mitochondrial complexes (OXPHOS).	imatinib	175-183	hexokinase 2	Homo sapiens	39-52
31252559-5	2019	Furthermore, a strong reduction of the hexokinase II (HKII), phosphorylated form of PKM2 (at Tyr105 and Ser37) and lactate dehydrogenase A (LDH-A) was observed in response to imatinib along with a strong upregulation of mitochondrial complexes (OXPHOS).	imatinib	175-183	hexokinase 2	Homo sapiens	54-58
31252559-5	2019	Furthermore, a strong reduction of the hexokinase II (HKII), phosphorylated form of PKM2 (at Tyr105 and Ser37) and lactate dehydrogenase A (LDH-A) was observed in response to imatinib along with a strong upregulation of mitochondrial complexes (OXPHOS).	imatinib	175-183	pyruvate kinase M1/2	Homo sapiens	84-88
31252559-5	2019	Furthermore, a strong reduction of the hexokinase II (HKII), phosphorylated form of PKM2 (at Tyr105 and Ser37) and lactate dehydrogenase A (LDH-A) was observed in response to imatinib along with a strong upregulation of mitochondrial complexes (OXPHOS).	imatinib	175-183	lactate dehydrogenase A	Homo sapiens	115-138
31252559-5	2019	Furthermore, a strong reduction of the hexokinase II (HKII), phosphorylated form of PKM2 (at Tyr105 and Ser37) and lactate dehydrogenase A (LDH-A) was observed in response to imatinib along with a strong upregulation of mitochondrial complexes (OXPHOS).	imatinib	175-183	lactate dehydrogenase A	Homo sapiens	140-145
31252559-7	2019	Our findings indicate that imatinib treatment of BCR-ABL-driven human leukemia cells reactivates mitochondrial oxidative phosphorylation thus allowing potential co-targeting of BCR-ABL and OXPHOS.	imatinib	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
31252559-7	2019	Our findings indicate that imatinib treatment of BCR-ABL-driven human leukemia cells reactivates mitochondrial oxidative phosphorylation thus allowing potential co-targeting of BCR-ABL and OXPHOS.	imatinib	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	177-184
31000683-3	2019	In mice, the antitumor effect of the Kit inhibitor imatinib is partially mediated by CD103+CD11b- DCs, and effector CD8+ T cells initially proliferate.	imatinib	51-59	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	37-40
31000683-3	2019	In mice, the antitumor effect of the Kit inhibitor imatinib is partially mediated by CD103+CD11b- DCs, and effector CD8+ T cells initially proliferate.	imatinib	51-59	integrin alpha E, epithelial-associated	Mus musculus	85-90
31000683-3	2019	In mice, the antitumor effect of the Kit inhibitor imatinib is partially mediated by CD103+CD11b- DCs, and effector CD8+ T cells initially proliferate.	imatinib	51-59	integrin subunit alpha M	Homo sapiens	91-96
31258755-4	2019	The main reason for the resistance is a decrease in sensitivity to imatinib caused by mutation or amplification of the BCR-ABL gene.	imatinib	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-126
30865840-7	2019	The PDGF-induced CaSR up-regulation was attenuated by small interfering RNA knockdown of PDGF receptors and STAT1/3, and by the treatment with imatinib.	imatinib	143-151	calcium sensing receptor	Homo sapiens	17-21
30707374-6	2019	KIT inhibitors that have been investigated in relevant clinical trials in advanced melanoma include imatinib, sunitinib, dasatinib, and nilotinib.	imatinib	100-108	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
30865840-8	2019	In monocrotaline-induced pulmonary hypertensive rats, the up-regulation of CaSR was reduced by imatinib.	imatinib	95-103	calcium-sensing receptor	Rattus norvegicus	75-79
30614559-0	2019	Response to imatinib in vaginal melanoma with KIT p.Val559Gly mutation previously treated with nivolumab, pembrolizumab and ipilimumab.	imatinib	12-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	46-49
31231484-4	2019	Results: Although tyrosine kinase inhibitors such as Imatinib significantly kill and remove the cell with BCR-ABL1 translocation, they are unable to target BCR-ABL1 leukemia stem cells.	imatinib	53-61	BCR activator of RhoGEF and GTPase	Homo sapiens	106-114
30548309-0	2019	Overexpression of Hes1 is involved in sensitization of K562 cells to Imatinib.	imatinib	69-77	hes family bHLH transcription factor 1	Homo sapiens	18-22
30548309-2	2019	Imatinib as a relatively specific inhibitor of Bcr-Abl is at present one of the undisputed therapeutic agent for newlydiagnosed patients with CML.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
30548309-9	2019	Conversely, treatment with imatinib attenuated Hes1 protein expression.	imatinib	27-35	hes family bHLH transcription factor 1	Homo sapiens	47-51
30565717-6	2019	Docking studies with 4153 phytochemicals revealed that GSAP having a better binding affinity with macaflavanone C, (E)-1-[2,4-dihydroxy-3-(3-methylbut-2-enyl)phenyl]-3-(2,2-dimethyl-8-hydroxy-2H-benzopyran-6-yl)prop-2-en-1-one, and monachosorin B as compared with the standard drug, imatinib.	imatinib	283-291	gamma-secretase activating protein	Homo sapiens	55-59
30585758-3	2019	The first generation TKI imatinib upregulated the expression of BCR-Abl in K562 cells as expected.	imatinib	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
31021002-5	2019	The FIP1L1-PDGFRA fusion gene (4q12) was detected by fluorescence in situ hybridization and the patient was treated with imatinib mesylate with complete response of the disease.	imatinib	121-138	factor interacting with PAPOLA and CPSF1	Homo sapiens	4-10
31021002-5	2019	The FIP1L1-PDGFRA fusion gene (4q12) was detected by fluorescence in situ hybridization and the patient was treated with imatinib mesylate with complete response of the disease.	imatinib	121-138	platelet derived growth factor receptor alpha	Homo sapiens	11-17
30555164-0	2019	HMGCLL1 is a predictive biomarker for deep molecular response to imatinib therapy in chronic myeloid leukemia.	imatinib	65-73	3-hydroxymethyl-3-methylglutaryl-CoA lyase like 1	Homo sapiens	0-7
30555164-2	2019	Herein, we report that an HMGCLL1 genetic variant located in 6p12.1 can be used as a predictive genetic biomarker for intrinsic sensitivity to imatinib (IM) therapy.	imatinib	143-151	3-hydroxymethyl-3-methylglutaryl-CoA lyase like 1	Homo sapiens	26-33
31080158-10	2019	Exposure to imatinib led also to a down-regulation of vimentin protein expression and up-regulation mRNA expression of FOXO3.	imatinib	12-20	vimentin	Rattus norvegicus	54-62
31080158-10	2019	Exposure to imatinib led also to a down-regulation of vimentin protein expression and up-regulation mRNA expression of FOXO3.	imatinib	12-20	forkhead box O3	Rattus norvegicus	119-124
31138788-9	2019	In vitro, both SCF isoforms were able to activate the Akt pathway in c-Kit+ cells, and this effect was counteracted by the tyrosine kinase inhibitor imatinib.	imatinib	149-157	KIT ligand	Homo sapiens	15-18
31138788-9	2019	In vitro, both SCF isoforms were able to activate the Akt pathway in c-Kit+ cells, and this effect was counteracted by the tyrosine kinase inhibitor imatinib.	imatinib	149-157	AKT serine/threonine kinase 1	Homo sapiens	54-57
31204920-0	2019	[Effect of Stably Down-regulating FMI Expression of K562 Cells on Sensitivity of K562 cells to Imatinib Mesylate].	imatinib	95-112	protein tyrosine phosphatase receptor type U	Homo sapiens	34-37
31204920-1	2019	OBJECTIVE: To investigate the effect of stably down-regulating the FMI expression of K562 cells on the sensitivity of K562 cells to Imatinib (IM) and its possible mechanism.	imatinib	132-140	protein tyrosine phosphatase receptor type U	Homo sapiens	67-70
31126916-1	2019	In chronic-phase chronic myeloid leukemia (CP-CML) patients treated with frontline imatinib, failure to achieve early molecular response (EMR; EMR failure: BCR-ABL1 >10% on the international scale at 3 months) is predictive of inferior outcomes.	imatinib	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-164
31138788-9	2019	In vitro, both SCF isoforms were able to activate the Akt pathway in c-Kit+ cells, and this effect was counteracted by the tyrosine kinase inhibitor imatinib.	imatinib	149-157	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	69-74
31046271-2	2019	Despite the success of imatinib as the first-line treatment of GISTs, dozens of drug-acquired resistant mutations emerge, and c-KIT T670I is one of the most common mutants among them.	imatinib	23-31	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	126-131
31205499-1	2019	The tyrosine kinase inhibitor (TKI) imatinib has radically changed the natural history of KIT-driven gastrointestinal stromal tumours (GISTs).	imatinib	36-44	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	90-93
31122263-9	2019	RESULTS: Here we proved that BCR-ABL1 TK-dependent hyper-activation of Aurora kinase A (AURKA)-Polo-like kinase 1 (PLK1)-FOXM1 axis is associated with the outcome of Imatinib (IM) resistance in an experimental model (K562 cell line) and bone marrow hematopoietic cells.	imatinib	166-174	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-37
31122263-9	2019	RESULTS: Here we proved that BCR-ABL1 TK-dependent hyper-activation of Aurora kinase A (AURKA)-Polo-like kinase 1 (PLK1)-FOXM1 axis is associated with the outcome of Imatinib (IM) resistance in an experimental model (K562 cell line) and bone marrow hematopoietic cells.	imatinib	166-174	aurora kinase A	Homo sapiens	71-86
31122263-9	2019	RESULTS: Here we proved that BCR-ABL1 TK-dependent hyper-activation of Aurora kinase A (AURKA)-Polo-like kinase 1 (PLK1)-FOXM1 axis is associated with the outcome of Imatinib (IM) resistance in an experimental model (K562 cell line) and bone marrow hematopoietic cells.	imatinib	166-174	aurora kinase A	Homo sapiens	88-93
31122263-9	2019	RESULTS: Here we proved that BCR-ABL1 TK-dependent hyper-activation of Aurora kinase A (AURKA)-Polo-like kinase 1 (PLK1)-FOXM1 axis is associated with the outcome of Imatinib (IM) resistance in an experimental model (K562 cell line) and bone marrow hematopoietic cells.	imatinib	166-174	polo like kinase 1	Homo sapiens	95-113
31122263-9	2019	RESULTS: Here we proved that BCR-ABL1 TK-dependent hyper-activation of Aurora kinase A (AURKA)-Polo-like kinase 1 (PLK1)-FOXM1 axis is associated with the outcome of Imatinib (IM) resistance in an experimental model (K562 cell line) and bone marrow hematopoietic cells.	imatinib	166-174	polo like kinase 1	Homo sapiens	115-119
31122263-9	2019	RESULTS: Here we proved that BCR-ABL1 TK-dependent hyper-activation of Aurora kinase A (AURKA)-Polo-like kinase 1 (PLK1)-FOXM1 axis is associated with the outcome of Imatinib (IM) resistance in an experimental model (K562 cell line) and bone marrow hematopoietic cells.	imatinib	166-174	forkhead box M1	Homo sapiens	121-126
31205508-0	2019	Axitinib overcomes multiple imatinib resistant cKIT mutations including the gatekeeper mutation T670I in gastrointestinal stromal tumors.	imatinib	28-36	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	47-51
31205508-9	2019	In addition, it could inhibit imatinib resistant cKIT T670I and V654A mutants in vitro and in vivo GIST preclinical models.	imatinib	30-38	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	49-53
30822403-0	2019	Andrographolide and its potent derivative exhibit anticancer effects against imatinib-resistant chronic myeloid leukemia cells by downregulating the Bcr-Abl oncoprotein.	imatinib	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
30929921-11	2019	Importantly, the CRC-CM derived from Flag-hUTP14a-expressing cells promotes angiogenesis in HUVECs, which is counteracted by PDGFR inhibitor imatinib.	imatinib	141-149	UTP14A small subunit processome component	Homo sapiens	42-49
30929921-11	2019	Importantly, the CRC-CM derived from Flag-hUTP14a-expressing cells promotes angiogenesis in HUVECs, which is counteracted by PDGFR inhibitor imatinib.	imatinib	141-149	platelet derived growth factor receptor beta	Homo sapiens	125-130
31123683-6	2019	Following treatment with imatinib for 3 mo, the patient had an optimal response and BCR-ABL1 (IS) was 0.143%, while the mutation rate of JAK2 V617F rose to 15%.	imatinib	25-33	BCR activator of RhoGEF and GTPase	Homo sapiens	84-92
31123683-6	2019	Following treatment with imatinib for 3 mo, the patient had an optimal response and BCR-ABL1 (IS) was 0.143%, while the mutation rate of JAK2 V617F rose to 15%.	imatinib	25-33	Janus kinase 2	Homo sapiens	137-141
30798348-0	2019	Impact of second decline rate of BCR-ABL1 transcript on clinical outcome of chronic phase chronic myeloid leukemia patients on imatinib first-line.	imatinib	127-135	BCR activator of RhoGEF and GTPase	Homo sapiens	33-41
31071955-0	2019	HDAC1,2 Knock-Out and HDACi Induced Cell Apoptosis in Imatinib-Resistant K562 Cells.	imatinib	54-62	histone deacetylase 1	Homo sapiens	0-5
31071955-1	2019	Since imatinib (Glivec or Gleevec) has been used to target the BCR-ABL fusion protein, chronic myeloid leukemia (CML) has become a manageable chronic disease with long-term survival.	imatinib	6-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
31073408-0	2019	Response to Imatinib therapy is inferior for e13a2 BCR-ABL1 transcript type in comparison to e14a2 transcript type in chronic myeloid leukaemia.	imatinib	12-20	BCR activator of RhoGEF and GTPase	Homo sapiens	51-59
30822403-1	2019	Chronic myelogenous leukemia (CML) is clinically treated with imatinib, which inhibits the kinase activity of the Bcr-Abl oncoprotein.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
30822403-5	2019	Both andrographolide and NCTU-322 downregulated the Bcr-Abl oncoprotein in imatinib-resistant CML cells through an Hsp90-dependent mechanism similar to that observed in imatinib-sensitive CML cells.	imatinib	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
30523507-2	2019	Imatinib, a potent inhibitor of mutated KIT, has revolutionized the clinical management of advanced, metastatic GIST.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	40-43
30864679-0	2019	[Corrigendum] Antiproliferative effects of imatinib mesylate on ZR-75-1 and MDA-MB-231 cell lines via PDGFR-beta, PDGF-BB, c-Kit and SCF expression.	imatinib	43-60	platelet derived growth factor receptor beta	Homo sapiens	102-112
30514803-2	2019	In the randomized German Chronic Myeloid Leukemia-Study IV, more potent BCR-ABL inhibition with 800 mg ("high-dose") imatinib accelerated achievement of a deep molecular remission.	imatinib	117-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-79
30864679-0	2019	[Corrigendum] Antiproliferative effects of imatinib mesylate on ZR-75-1 and MDA-MB-231 cell lines via PDGFR-beta, PDGF-BB, c-Kit and SCF expression.	imatinib	43-60	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	123-128
30864679-0	2019	[Corrigendum] Antiproliferative effects of imatinib mesylate on ZR-75-1 and MDA-MB-231 cell lines via PDGFR-beta, PDGF-BB, c-Kit and SCF expression.	imatinib	43-60	KIT ligand	Homo sapiens	133-136
30864683-7	2019	Overexpression of BCR/ABL or the presence of its inhibitor imatinib upregulated and downregulated TOPK expression, respectively, indicating that TOPK may be a target of BCR/ABL.	imatinib	59-67	PDZ binding kinase	Homo sapiens	98-102
30864683-7	2019	Overexpression of BCR/ABL or the presence of its inhibitor imatinib upregulated and downregulated TOPK expression, respectively, indicating that TOPK may be a target of BCR/ABL.	imatinib	59-67	PDZ binding kinase	Homo sapiens	145-149
30864683-7	2019	Overexpression of BCR/ABL or the presence of its inhibitor imatinib upregulated and downregulated TOPK expression, respectively, indicating that TOPK may be a target of BCR/ABL.	imatinib	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	169-176
30807397-0	2019	Myeloid Neoplasm With Eosinophilia and FIP1L1-PDGFRA Rearrangement Treated With Imatinib Mesylate: A Pediatric Case With Long-term Follow-up.	imatinib	80-97	factor interacting with PAPOLA and CPSF1	Homo sapiens	39-45
30807397-0	2019	Myeloid Neoplasm With Eosinophilia and FIP1L1-PDGFRA Rearrangement Treated With Imatinib Mesylate: A Pediatric Case With Long-term Follow-up.	imatinib	80-97	platelet derived growth factor receptor alpha	Homo sapiens	46-52
31083182-0	2019	Relationship between efficacy of sunitinib and KIT mutation of patients with advanced gastrointestinal stromal tumors after failure of imatinib: A systematic review.	imatinib	135-143	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	47-50
30684595-0	2019	Repurposing cabozantinib to GISTs: Overcoming multiple imatinib-resistant cKIT mutations including gatekeeper and activation loop mutants in GISTs preclinical models.	imatinib	55-63	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	74-78
30902661-2	2019	Being tyrosine kinase inhibitor, imatinib modulates the activities of Abelson gene (c-Abl), Abelson related gene (ARG), platelet-derived growth factor receptor (PDGFR), FMS-like tyrosine kinase 3 (FLT3), lymphocyte-specific protein (Lck), mitogen activated protein kinase (MAPK), amyloid precursor protein intracellular domain (AICD), alpha-synuclein and the stem-cell factor receptor (c-kit).	imatinib	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-89
30902661-2	2019	Being tyrosine kinase inhibitor, imatinib modulates the activities of Abelson gene (c-Abl), Abelson related gene (ARG), platelet-derived growth factor receptor (PDGFR), FMS-like tyrosine kinase 3 (FLT3), lymphocyte-specific protein (Lck), mitogen activated protein kinase (MAPK), amyloid precursor protein intracellular domain (AICD), alpha-synuclein and the stem-cell factor receptor (c-kit).	imatinib	33-41	ABL proto-oncogene 2, non-receptor tyrosine kinase	Homo sapiens	114-117
30902661-2	2019	Being tyrosine kinase inhibitor, imatinib modulates the activities of Abelson gene (c-Abl), Abelson related gene (ARG), platelet-derived growth factor receptor (PDGFR), FMS-like tyrosine kinase 3 (FLT3), lymphocyte-specific protein (Lck), mitogen activated protein kinase (MAPK), amyloid precursor protein intracellular domain (AICD), alpha-synuclein and the stem-cell factor receptor (c-kit).	imatinib	33-41	platelet derived growth factor receptor beta	Homo sapiens	120-159
30902661-2	2019	Being tyrosine kinase inhibitor, imatinib modulates the activities of Abelson gene (c-Abl), Abelson related gene (ARG), platelet-derived growth factor receptor (PDGFR), FMS-like tyrosine kinase 3 (FLT3), lymphocyte-specific protein (Lck), mitogen activated protein kinase (MAPK), amyloid precursor protein intracellular domain (AICD), alpha-synuclein and the stem-cell factor receptor (c-kit).	imatinib	33-41	platelet derived growth factor receptor beta	Homo sapiens	161-166
30902661-2	2019	Being tyrosine kinase inhibitor, imatinib modulates the activities of Abelson gene (c-Abl), Abelson related gene (ARG), platelet-derived growth factor receptor (PDGFR), FMS-like tyrosine kinase 3 (FLT3), lymphocyte-specific protein (Lck), mitogen activated protein kinase (MAPK), amyloid precursor protein intracellular domain (AICD), alpha-synuclein and the stem-cell factor receptor (c-kit).	imatinib	33-41	fms related receptor tyrosine kinase 3	Homo sapiens	169-195
30902661-2	2019	Being tyrosine kinase inhibitor, imatinib modulates the activities of Abelson gene (c-Abl), Abelson related gene (ARG), platelet-derived growth factor receptor (PDGFR), FMS-like tyrosine kinase 3 (FLT3), lymphocyte-specific protein (Lck), mitogen activated protein kinase (MAPK), amyloid precursor protein intracellular domain (AICD), alpha-synuclein and the stem-cell factor receptor (c-kit).	imatinib	33-41	fms related receptor tyrosine kinase 3	Homo sapiens	197-201
30902661-2	2019	Being tyrosine kinase inhibitor, imatinib modulates the activities of Abelson gene (c-Abl), Abelson related gene (ARG), platelet-derived growth factor receptor (PDGFR), FMS-like tyrosine kinase 3 (FLT3), lymphocyte-specific protein (Lck), mitogen activated protein kinase (MAPK), amyloid precursor protein intracellular domain (AICD), alpha-synuclein and the stem-cell factor receptor (c-kit).	imatinib	33-41	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	233-236
30902661-2	2019	Being tyrosine kinase inhibitor, imatinib modulates the activities of Abelson gene (c-Abl), Abelson related gene (ARG), platelet-derived growth factor receptor (PDGFR), FMS-like tyrosine kinase 3 (FLT3), lymphocyte-specific protein (Lck), mitogen activated protein kinase (MAPK), amyloid precursor protein intracellular domain (AICD), alpha-synuclein and the stem-cell factor receptor (c-kit).	imatinib	33-41	amyloid beta precursor protein	Homo sapiens	280-305
30902661-2	2019	Being tyrosine kinase inhibitor, imatinib modulates the activities of Abelson gene (c-Abl), Abelson related gene (ARG), platelet-derived growth factor receptor (PDGFR), FMS-like tyrosine kinase 3 (FLT3), lymphocyte-specific protein (Lck), mitogen activated protein kinase (MAPK), amyloid precursor protein intracellular domain (AICD), alpha-synuclein and the stem-cell factor receptor (c-kit).	imatinib	33-41	synuclein alpha	Homo sapiens	335-350
30902661-2	2019	Being tyrosine kinase inhibitor, imatinib modulates the activities of Abelson gene (c-Abl), Abelson related gene (ARG), platelet-derived growth factor receptor (PDGFR), FMS-like tyrosine kinase 3 (FLT3), lymphocyte-specific protein (Lck), mitogen activated protein kinase (MAPK), amyloid precursor protein intracellular domain (AICD), alpha-synuclein and the stem-cell factor receptor (c-kit).	imatinib	33-41	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	386-391
31044085-7	2019	Moreover, inhibition of USP10 significantly suppresses the proliferation of both imatinib-sensitive and imatinib-resistant CML cells, which likely depends on SKP2 status.	imatinib	81-89	ubiquitin specific peptidase 10	Homo sapiens	24-29
31044085-7	2019	Moreover, inhibition of USP10 significantly suppresses the proliferation of both imatinib-sensitive and imatinib-resistant CML cells, which likely depends on SKP2 status.	imatinib	81-89	S-phase kinase associated protein 2	Homo sapiens	158-162
31044085-7	2019	Moreover, inhibition of USP10 significantly suppresses the proliferation of both imatinib-sensitive and imatinib-resistant CML cells, which likely depends on SKP2 status.	imatinib	104-112	ubiquitin specific peptidase 10	Homo sapiens	24-29
31044085-7	2019	Moreover, inhibition of USP10 significantly suppresses the proliferation of both imatinib-sensitive and imatinib-resistant CML cells, which likely depends on SKP2 status.	imatinib	104-112	S-phase kinase associated protein 2	Homo sapiens	158-162
31044085-9	2019	Taken together, the present study not only provides a novel insight into the amplified activation of Bcr-Abl in CML, but also demonstrates that targeting the USP10/SKP2/Bcr-Abl axis is a potential strategy to overcome imatinib resistance in CML patients.	imatinib	218-226	ubiquitin specific peptidase 10	Homo sapiens	158-163
31044085-9	2019	Taken together, the present study not only provides a novel insight into the amplified activation of Bcr-Abl in CML, but also demonstrates that targeting the USP10/SKP2/Bcr-Abl axis is a potential strategy to overcome imatinib resistance in CML patients.	imatinib	218-226	S-phase kinase associated protein 2	Homo sapiens	164-168
31044085-9	2019	Taken together, the present study not only provides a novel insight into the amplified activation of Bcr-Abl in CML, but also demonstrates that targeting the USP10/SKP2/Bcr-Abl axis is a potential strategy to overcome imatinib resistance in CML patients.	imatinib	218-226	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	169-176
30126859-1	2019	BACKGROUND: Oncogenic KIT/PDGFRA signaling inhibition with imatinib achieves disease control in most patients with advanced/metastatic gastrointestinal stromal tumor (GIST), but resistance eventually develops after 20-24 months.	imatinib	59-67	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	22-25
30126859-1	2019	BACKGROUND: Oncogenic KIT/PDGFRA signaling inhibition with imatinib achieves disease control in most patients with advanced/metastatic gastrointestinal stromal tumor (GIST), but resistance eventually develops after 20-24 months.	imatinib	59-67	platelet derived growth factor receptor alpha	Homo sapiens	26-32
31014357-0	2019	Imatinib independent aberrant methylation of NOV/CCN3 in chronic myelogenous leukemia patients: a mechanism upstream of BCR-ABL1 function?	imatinib	0-8	cellular communication network factor 3	Homo sapiens	49-53
31014357-0	2019	Imatinib independent aberrant methylation of NOV/CCN3 in chronic myelogenous leukemia patients: a mechanism upstream of BCR-ABL1 function?	imatinib	0-8	BCR activator of RhoGEF and GTPase	Homo sapiens	120-128
31014357-11	2019	In the case of acting upstream of BCR-ABL1 signaling, the methylation marker can provide early detection and a novel platform for targeted epigenetic modifiers for efficient treatment in imatinib resistant patients.	imatinib	187-195	BCR activator of RhoGEF and GTPase	Homo sapiens	34-42
30684595-1	2019	Despite of the great success of imatinib as the first-line treatment for GISTs, the majority of patients will develop drug-acquired resistance due to secondary mutations in the cKIT kinase.	imatinib	32-40	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	177-181
30684595-3	2019	Through a drug repositioning approach, we found that cabozantinib exhibited higher potency than imatinib against primary gain-of-function mutations of cKIT.	imatinib	96-104	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	151-155
30984366-10	2019	Our data also support the hypothesis that the use of KIT/PDGFRA inhibitors, including non-approved agents, has improved OS for patients with imatinib- and sunitinib-resistant GIST.	imatinib	141-149	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	53-56
30984366-10	2019	Our data also support the hypothesis that the use of KIT/PDGFRA inhibitors, including non-approved agents, has improved OS for patients with imatinib- and sunitinib-resistant GIST.	imatinib	141-149	platelet derived growth factor receptor alpha	Homo sapiens	57-63
30726713-7	2019	Inhibition of BCR-ABL1 with imatinib not only blocks the inclusion of exon 10 but also deregulates PTBP2 expression in CML cells.	imatinib	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-22
30726713-7	2019	Inhibition of BCR-ABL1 with imatinib not only blocks the inclusion of exon 10 but also deregulates PTBP2 expression in CML cells.	imatinib	28-36	polypyrimidine tract binding protein 2	Homo sapiens	99-104
30866043-1	2019	Imatinib, the prototype BCR-ABL tyrosine kinase inhibitor (TKI), is the first-line treatment for Philadelphia chromosome-positive chronic myeloid leukemia (CML) in the chronic phase.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
30971550-0	2019	Distribution of common BCR-ABL fusion transcripts and their impact on treatment response in Imatinib treated CML patients: A study from India.	imatinib	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
30553841-13	2019	These effects were all suppressed by the PDGFRbeta inhibitor, imatinib.	imatinib	62-70	platelet derived growth factor receptor beta	Homo sapiens	41-50
30256411-0	2019	Heme oxygenase-1 reduces the sensitivity to imatinib through nonselective activation of histone deacetylases in chronic myeloid leukemia.	imatinib	44-52	heme oxygenase 1	Homo sapiens	0-16
30866043-7	2019	Cotreatment of neferine and imatinib significantly decreased the expression of BCR-ABL protein and its molecular chaperone heat shock protein 90 (Hsp90) mRNA and protein levels, and further decreased phospho-extracellular regulated protein kinase 1/2 (p-Erk1/2) and myeloid cell leukemia (Mcl-1) expression.	imatinib	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
30866043-7	2019	Cotreatment of neferine and imatinib significantly decreased the expression of BCR-ABL protein and its molecular chaperone heat shock protein 90 (Hsp90) mRNA and protein levels, and further decreased phospho-extracellular regulated protein kinase 1/2 (p-Erk1/2) and myeloid cell leukemia (Mcl-1) expression.	imatinib	28-36	heat shock protein 90 alpha family class A member 1	Homo sapiens	123-144
31015764-6	2019	The apoptosis was increased when TNF-alpha knockout cells were cultured with imatinib.	imatinib	77-85	tumor necrosis factor	Homo sapiens	33-42
30866043-7	2019	Cotreatment of neferine and imatinib significantly decreased the expression of BCR-ABL protein and its molecular chaperone heat shock protein 90 (Hsp90) mRNA and protein levels, and further decreased phospho-extracellular regulated protein kinase 1/2 (p-Erk1/2) and myeloid cell leukemia (Mcl-1) expression.	imatinib	28-36	heat shock protein 90 alpha family class A member 1	Homo sapiens	146-151
30866043-7	2019	Cotreatment of neferine and imatinib significantly decreased the expression of BCR-ABL protein and its molecular chaperone heat shock protein 90 (Hsp90) mRNA and protein levels, and further decreased phospho-extracellular regulated protein kinase 1/2 (p-Erk1/2) and myeloid cell leukemia (Mcl-1) expression.	imatinib	28-36	mitogen-activated protein kinase 3	Homo sapiens	254-260
30866043-7	2019	Cotreatment of neferine and imatinib significantly decreased the expression of BCR-ABL protein and its molecular chaperone heat shock protein 90 (Hsp90) mRNA and protein levels, and further decreased phospho-extracellular regulated protein kinase 1/2 (p-Erk1/2) and myeloid cell leukemia (Mcl-1) expression.	imatinib	28-36	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	289-294
29199506-7	2019	Potent inducers of cytochrome P450 isoenzyme CYP3A4, as phenytoin, could induce inadequate responses due to increased imatinib clearance and low imatinib trough plasma levels.	imatinib	118-126	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	45-51
29199506-7	2019	Potent inducers of cytochrome P450 isoenzyme CYP3A4, as phenytoin, could induce inadequate responses due to increased imatinib clearance and low imatinib trough plasma levels.	imatinib	145-153	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	45-51
30075827-2	2019	Current studies show that imatinib treatment is a promising approach in treating advanced melanoma patients harboring c-Kit mutations or amplifications.	imatinib	26-34	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	118-123
30075827-10	2019	Our study, combined with those studies targeting patients with a c-Kit alteration, validates the role of imatinib as an important and promising therapeutic agent in the treatment of patients with advanced melanoma.	imatinib	105-113	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	65-70
30873837-1	2019	Imatinib mesylate, 1a, inhibits production of beta-amyloid (Abeta) peptides both in cells and in animal models.	imatinib	0-17	amyloid beta (A4) precursor protein	Mus musculus	60-65
30536695-14	2019	Imatinib has a limited therapeutic role in SM; effective cytoreduction is limited to those with imatinib-sensitive KIT mutations.	imatinib	96-104	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	115-118
30773012-7	2019	Apart from ABL kinases, we identified a number of other kinases whose ATP-binding affinities are markedly diminished upon imatinib treatment, including CHK1, a checkpoint kinase involved in DNA damage response signaling.	imatinib	122-130	checkpoint kinase 1	Homo sapiens	152-156
30835732-0	2019	A new highly sensitive real-time quantitative-PCR method for detection of BCR-ABL1 to monitor minimal residual disease in chronic myeloid leukemia after discontinuation of imatinib.	imatinib	172-180	BCR activator of RhoGEF and GTPase	Homo sapiens	74-82
30998137-11	2019	Within the 17 patients treated with imatinib at induction stage,2 of which became BCR/ABLnegative.At consolidation chemotherapy stage, 9 out of 16 patients became BCR/ABL negative, including 3 patients already subjected to HSCT.	imatinib	36-44	BCR activator of RhoGEF and GTPase	Homo sapiens	82-85
30998137-11	2019	Within the 17 patients treated with imatinib at induction stage,2 of which became BCR/ABLnegative.At consolidation chemotherapy stage, 9 out of 16 patients became BCR/ABL negative, including 3 patients already subjected to HSCT.	imatinib	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
31037149-2	2019	At present, imatinib is the only targeted drug for KIT-mutation-bearing melanomas that is recommended by the National Comprehensive Cancer Network (NCCN) Clinical Practice guidelines.	imatinib	12-20	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	51-54
31037149-3	2019	Patients with KIT mutations, however, are either insensitive or rapidly progress to imatinib insensitivity, which restricts its clinical use.	imatinib	84-92	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-17
31037149-6	2019	Results: Ponatinib was more potent than imatinib against cells bearing KIT mutations.	imatinib	40-48	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	71-74
30956759-0	2019	Potentiation of imatinib by cilostazol in sensitive and resistant gastrointestinal stromal tumor cell lines involves YAP inhibition.	imatinib	16-24	Yes1 associated transcriptional regulator	Homo sapiens	117-120
30792533-0	2019	Complementary activity of tyrosine kinase inhibitors against secondary kit mutations in imatinib-resistant gastrointestinal stromal tumours.	imatinib	88-96	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	71-74
30543306-4	2019	Selective inhibition of PDGFR-beta or SFKs with imatinib or A-419259, respectively, on one hand, or with specific small-interfering RNAs (siRNAs) on the other hand, aborted PDGF-induced phosphorylation of GluN2B, thus validating the pathway.	imatinib	48-56	platelet derived growth factor receptor beta	Homo sapiens	24-34
30956965-0	2019	ABCB1 and BMI1 mRNA expression in patients with chronic myeloid leukemia: impact on imatinib efficacy.	imatinib	84-92	ATP binding cassette subfamily B member 1	Homo sapiens	0-5
30956965-0	2019	ABCB1 and BMI1 mRNA expression in patients with chronic myeloid leukemia: impact on imatinib efficacy.	imatinib	84-92	BMI1 proto-oncogene, polycomb ring finger	Homo sapiens	10-14
30956965-2	2019	ABCB1 displays a high affinity for imatinib.	imatinib	35-43	ATP binding cassette subfamily B member 1	Homo sapiens	0-5
30792533-1	2019	BACKGROUND: Most patients with KIT-mutant gastrointestinal stromal tumours (GISTs) benefit from imatinib, but treatment resistance results from outgrowth of heterogeneous subclones with KIT secondary mutations.	imatinib	96-104	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	31-34
30956965-13	2019	Conclusion: ABCB1 mRNA expression may serve as a predictor of the optimal response to imatinib treatment in patients with CML.	imatinib	86-94	ATP binding cassette subfamily B member 1	Homo sapiens	12-17
30792533-8	2019	CONCLUSIONS: Our data highlight that heterogeneity of KIT secondary mutations is the main mechanism of tumour progression to KIT inhibitors in imatinib-resistant GIST patients.	imatinib	143-151	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	54-57
30792533-8	2019	CONCLUSIONS: Our data highlight that heterogeneity of KIT secondary mutations is the main mechanism of tumour progression to KIT inhibitors in imatinib-resistant GIST patients.	imatinib	143-151	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	125-128
30530703-2	2019	Imatinib, an inhibitor of KIT, platelet-derived growth factor receptor alpha (PDGFRA), and a few other tyrosine kinases, is highly effective for GIST, but advanced GISTs frequently progress on imatinib and other approved tyrosine kinase inhibitors.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	26-29
30693663-9	2019	PFS with imatinib (P = 0.002) and OS (P = 0.019) were significantly longer in period 2.	imatinib	9-17	period circadian regulator 2	Homo sapiens	78-86
30530703-2	2019	Imatinib, an inhibitor of KIT, platelet-derived growth factor receptor alpha (PDGFRA), and a few other tyrosine kinases, is highly effective for GIST, but advanced GISTs frequently progress on imatinib and other approved tyrosine kinase inhibitors.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	31-76
30530703-2	2019	Imatinib, an inhibitor of KIT, platelet-derived growth factor receptor alpha (PDGFRA), and a few other tyrosine kinases, is highly effective for GIST, but advanced GISTs frequently progress on imatinib and other approved tyrosine kinase inhibitors.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	78-84
30880826-5	2019	The benefit of radio- and chemotherapies is not clear and a small number of treatment attempts with imatinib have been made in cases of CD117 positivity or treatment attempts on an endocrine basis.	imatinib	100-108	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	136-141
30547682-1	2019	Nilotinib, a second-generation tyrosine kinase inhibitor, was designed to overcome resistance of a wide range of BCR-ABL mutants to imatinib.	imatinib	132-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
30993099-0	2019	Erratum: Anti-growth Effects of Imatinib and GNF5 via Regulation of Skp2 in Human Hepatocellular Carcinoma Cells.	imatinib	32-40	S-phase kinase associated protein 2	Homo sapiens	68-72
30459357-6	2019	Treating mice with dasatinib or imatinib, which target c-Kit, resulted in complete tumor regression, indicating that c-Kit activity is crucial in the oncogenic process.	imatinib	32-40	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	55-60
30199578-0	2019	Successful treatment of metastatic mucosal melanoma with a Del579 c-KIT mutation by imatinib after treatment of anti-PD-1 antibody.	imatinib	84-92	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	68-71
30569109-1	2019	Imatinib is a powerful tyrosine kinase inhibitor that specifically targets BCR-ABL, c-KIT, and PDGFR kinases, and is used in the treatment of chronic myelogenous leukemia, gastrointestinal stromal tumors, and other types of cancers.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
30569109-1	2019	Imatinib is a powerful tyrosine kinase inhibitor that specifically targets BCR-ABL, c-KIT, and PDGFR kinases, and is used in the treatment of chronic myelogenous leukemia, gastrointestinal stromal tumors, and other types of cancers.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	84-89
30569109-1	2019	Imatinib is a powerful tyrosine kinase inhibitor that specifically targets BCR-ABL, c-KIT, and PDGFR kinases, and is used in the treatment of chronic myelogenous leukemia, gastrointestinal stromal tumors, and other types of cancers.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	95-100
30569109-4	2019	We determined that imatinib induced mitochondria-mediated apoptosis of gastric cancer cells by involving endoplasmic reticulum (ER) stress-associated activation of c-Jun NH2-terminal kinase (JNK).	imatinib	19-27	mitogen-activated protein kinase 8	Homo sapiens	164-189
30459357-6	2019	Treating mice with dasatinib or imatinib, which target c-Kit, resulted in complete tumor regression, indicating that c-Kit activity is crucial in the oncogenic process.	imatinib	32-40	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	117-122
30569109-4	2019	We determined that imatinib induced mitochondria-mediated apoptosis of gastric cancer cells by involving endoplasmic reticulum (ER) stress-associated activation of c-Jun NH2-terminal kinase (JNK).	imatinib	19-27	mitogen-activated protein kinase 8	Homo sapiens	191-194
30569109-7	2019	Moreover, imatinib-treated cells exhibited increased levels of phosphorylated JNK, and of the transcription factor C/EBP homologous protein, an ER stress-associated apoptotic molecule.	imatinib	10-18	mitogen-activated protein kinase 8	Homo sapiens	78-81
30251267-6	2019	In conclusion, we documented the anti-CML effects of EGCG in imatinib-sensitive and imatinib-resistant Bcr/Abl+ cells, especially T315I-mutated cells.	imatinib	84-92	BCR activator of RhoGEF and GTPase	Homo sapiens	103-106
30569109-9	2019	These data indicated that imatinib exerted cytotoxic effects on gastric cancer cells by inducing apoptosis mediated by reactive oxygen species generation and ER stress-associated JNK activation.	imatinib	26-34	mitogen-activated protein kinase 8	Homo sapiens	179-182
30882001-6	2019	24 hours after the imatinib mesylate injection, we observed significant Kras downregulation in the bone marrow and lung of the DMBA-treated mice.	imatinib	19-36	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	72-76
30418193-0	2019	Hydroxychavicol sensitizes imatinib-resistant chronic myelogenous leukemia cells to TRAIL-induced apoptosis by ROS-mediated IAP downregulation.	imatinib	27-35	TNF superfamily member 10	Homo sapiens	84-89
30418193-4	2019	When imatinib-resistant K562 cells were treated with HCH, it made these K562 cells sensitive to TRAIL.	imatinib	5-13	TNF superfamily member 10	Homo sapiens	96-101
30418193-8	2019	In conclusion, this study demonstrates the combinatorial treatment of TRAIL and HCH as promising alternative therapeutic approach to treat the imatinib-resistant leukemia, which are also resistant to TRAIL.	imatinib	143-151	TNF superfamily member 10	Homo sapiens	70-75
30422832-6	2019	F-B1 was found to inhibit the growth of myelogenous leukemia cell lines, that is, K562 cells bearing wild-type Bcr/Abl and imatinib-resistant K562G cells.	imatinib	123-131	TCF3 fusion partner	Homo sapiens	0-4
30422832-9	2019	Experimental validation results together demonstrated that F-B1 can inhibit Bcr/Abl fusion proteins in K562 and K562G cells, implying that F-B1 might be a promising drug to treat CML, especially the imatinib-resistant CML.	imatinib	199-207	TCF3 fusion partner	Homo sapiens	59-63
30422832-9	2019	Experimental validation results together demonstrated that F-B1 can inhibit Bcr/Abl fusion proteins in K562 and K562G cells, implying that F-B1 might be a promising drug to treat CML, especially the imatinib-resistant CML.	imatinib	199-207	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
30422832-9	2019	Experimental validation results together demonstrated that F-B1 can inhibit Bcr/Abl fusion proteins in K562 and K562G cells, implying that F-B1 might be a promising drug to treat CML, especially the imatinib-resistant CML.	imatinib	199-207	TCF3 fusion partner	Homo sapiens	139-143
30787317-0	2019	Novel mutations in the kinase domain of BCR-ABL gene causing imatinib resistance in chronic myeloid leukemia patients.	imatinib	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
30787317-1	2019	Mutations in the drug binding region of BCR-ABL lead to imatinib resistance during the management of chronic myeloid leukemia (CML).	imatinib	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
30787317-2	2019	In our study, 62 Philadelphia positive (Ph+) CML patients showing conspicuous expression of BCR-ABL gene were treated with imatinib.	imatinib	123-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
30787317-4	2019	In all the imatinib-resistant patients BCR-ABL gene was PCR amplified and sequenced.	imatinib	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
30787317-7	2019	The primary intention of the study was to find out the mutations in the BCR-ABL gene causing imatinib resistance.	imatinib	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
30778083-2	2019	Over half of all PDGFRA mutations are represented by the substitution at position 842 in the A-loop of an aspartic acid (D) with a valine (V), recognized as D842V, conferring primary resistance to imatinib in vitro and in clinical observations due to the conformation of the kinase domain, which negatively affects imatinib binding.	imatinib	197-205	platelet derived growth factor receptor alpha	Homo sapiens	17-23
30778083-2	2019	Over half of all PDGFRA mutations are represented by the substitution at position 842 in the A-loop of an aspartic acid (D) with a valine (V), recognized as D842V, conferring primary resistance to imatinib in vitro and in clinical observations due to the conformation of the kinase domain, which negatively affects imatinib binding.	imatinib	315-323	platelet derived growth factor receptor alpha	Homo sapiens	17-23
30281780-0	2019	Imatinib inhibits CSF1R that stimulates proliferation of rheumatoid arthritis fibroblast-like synoviocytes.	imatinib	0-8	macrophage colony-stimulating factor 1 receptor	Oryctolagus cuniculus	18-23
30281780-1	2019	In this study, we aimed to explore the effects of imatinib on the proliferation of rheumatoid arthritis synovial cell (RA-FLS) and inflammatory responses by regulating CSF1R.	imatinib	50-58	macrophage colony-stimulating factor 1 receptor	Oryctolagus cuniculus	168-173
30281780-9	2019	The targeting relationship between imatinib and CSF1R was also validated in this study.	imatinib	35-43	macrophage colony-stimulating factor 1 receptor	Oryctolagus cuniculus	48-53
30281780-13	2019	Conversely, imatinib could significantly restrain the cell cycle and viability of RA-FLS and accelerated apoptosis via suppression of CSF1R expression.	imatinib	12-20	macrophage colony-stimulating factor 1 receptor	Oryctolagus cuniculus	134-139
30712551-9	2019	The animal model showed that bowel anastomosis healing was weakened by imatinib through the downregulation of Col1A1, Col3A1, and MMPs.	imatinib	71-79	collagen type I alpha 1 chain	Homo sapiens	110-116
30712551-9	2019	The animal model showed that bowel anastomosis healing was weakened by imatinib through the downregulation of Col1A1, Col3A1, and MMPs.	imatinib	71-79	collagen type III alpha 1 chain	Homo sapiens	118-124
30605651-0	2019	Tyrosine kinase inhibitor imatinib modulates the viability and apoptosis of castrate-resistant prostate cancer cells dependently on the glycolytic environment.	imatinib	26-34	TXK tyrosine kinase	Homo sapiens	0-15
30273596-2	2019	Because tyrosine kinases like c-Abl kinase are important for fibroblast activation and fibrosis development in SSc, the c-Abl inhibitor imatinib was proposed for SSc treatment.	imatinib	136-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-35
30273596-2	2019	Because tyrosine kinases like c-Abl kinase are important for fibroblast activation and fibrosis development in SSc, the c-Abl inhibitor imatinib was proposed for SSc treatment.	imatinib	136-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-125
30273596-8	2019	In small interfering RNA experiments, MATE1 was identified as key transporter for imatinib uptake and biological effect in dermal fibroblasts.	imatinib	82-90	solute carrier family 47 member 1	Homo sapiens	38-43
30273596-9	2019	Furthermore, PDGF reduced imatinib uptake by decreasing MATE1 expression in SSc fibroblasts, but not in healthy fibroblasts.	imatinib	26-34	solute carrier family 47 member 1	Homo sapiens	56-61
30273596-11	2019	In conclusion, MATE1-mediated transport governs therapeutic efficacy of imatinib in SSc.	imatinib	72-80	solute carrier family 47 member 1	Homo sapiens	15-20
30605651-1	2019	AIMS: The tyrosine kinase inhibitor imatinib has been used in prostate cancer treatment with outcomes that did not follow the in vitro findings.	imatinib	36-44	TXK tyrosine kinase	Homo sapiens	10-25
30612056-0	2019	Molecular response to imatinib in KIT F522C-mutated systemic mastocytosis.	imatinib	22-30	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	34-37
31043947-0	2019	Lack of Response to Imatinib in Melanoma Carrying Rare KIT Mutation p.T632I.	imatinib	20-28	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	55-58
30738487-4	2019	Besides, the high expression of C-Myc may lead to the decrease of the sensitivity of chronic myelogenous leukemia cells to imatinib.	imatinib	123-131	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	32-37
30738487-5	2019	Therefore, C-Myc has been concerned in the study of imatinib drug resistance.	imatinib	52-60	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	11-16
30450754-0	2019	The combined treatment of brassinin and imatinib synergistically downregulated the expression of MMP-9 in SW480 colon cancer cells.	imatinib	40-48	matrix metallopeptidase 9	Homo sapiens	97-102
30370673-1	2019	BACKGROUND: The tyrosine kinase inhibitors (TKI), imatinib and nilotinib, are used to treat chronic myelogenous leukemia (CML).	imatinib	50-58	TXK tyrosine kinase	Homo sapiens	16-31
30370673-12	2019	Nilotinib and imatinib both decreased AR and PSA expression in PCa cell lines with the nilotinib effect evident at lower doses.	imatinib	14-22	kallikrein related peptidase 3	Homo sapiens	45-48
30738443-3	2019	RESULTS: 80.0% of the patients in dasatinib group, 16.6% of the patients in nilotinib group and 27.5% of the patients in imatinib group respectively had a Th1 proportion in the peripheral blood (Th1/CD4+ T) above the upper limit of normal.	imatinib	121-129	negative elongation factor complex member C/D	Homo sapiens	155-158
30738443-4	2019	More specifically, the Th1 proportion in dasatinib group (30.86%+-9.75%) was significantly higher than that in nilotinib group(17.37%+-9.35%) (P&lt;0.001) and that in imatinib group (20.79%+-9.01%) (P&lt;0.001).	imatinib	167-175	negative elongation factor complex member C/D	Homo sapiens	23-26
30691103-10	2019	Also, anti-cancer agents, including IL-2 + imatinib mesylate (three studies) and anti-CD22 monoclinal antibodies (mAb) (four studies), showed a dose-dependent increase in the incidence of CLS.	imatinib	43-60	interleukin 2	Homo sapiens	36-40
31043947-2	2019	There is a diversity of spectrum of KIT mutations, with some of them rendering tumors responsive to imatinib, while others being imatinib-resistant or not studied yet.	imatinib	100-108	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	36-39
31043947-2	2019	There is a diversity of spectrum of KIT mutations, with some of them rendering tumors responsive to imatinib, while others being imatinib-resistant or not studied yet.	imatinib	129-137	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	36-39
30705677-10	2018	In line with dasatinib-specific down-regulation of NKG2A, NK cytotoxicity evaluated by the killing assay was also significantly higher in patients treated with dasatinib than in those treated with imatinib or nilotinib.	imatinib	197-205	killer cell lectin like receptor C1	Homo sapiens	51-56
30705677-2	2018	ABL tyrosine kinase inhibitors (TKIs), such as imatinib, nilotinib, and dasatinib, are currently the front-line treatment options for CML.	imatinib	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
30705677-11	2018	The lower NK cytotoxicity from imatinib or nilotinib treatments could be reverted by NKG2A blockade using anti-NKG2A antibody.	imatinib	31-39	killer cell lectin like receptor C1	Homo sapiens	85-90
30705677-11	2018	The lower NK cytotoxicity from imatinib or nilotinib treatments could be reverted by NKG2A blockade using anti-NKG2A antibody.	imatinib	31-39	killer cell lectin like receptor C1	Homo sapiens	111-116
30687103-0	2018	A Novel Naphthoquinone-Coumarin Hybrid That Inhibits BCR-ABL1-STAT5 Oncogenic Pathway and Reduces Survival in Imatinib-Resistant Chronic Myelogenous Leukemia Cells.	imatinib	110-118	BCR activator of RhoGEF and GTPase	Homo sapiens	53-61
30687103-0	2018	A Novel Naphthoquinone-Coumarin Hybrid That Inhibits BCR-ABL1-STAT5 Oncogenic Pathway and Reduces Survival in Imatinib-Resistant Chronic Myelogenous Leukemia Cells.	imatinib	110-118	signal transducer and activator of transcription 5A	Homo sapiens	62-67
30687103-11	2018	Notably, NPQ-C6 maintained its activity on BCR-ABL1/STAT5/c-MYC/PIM-1 oncogenic pathway in imatinib-resistant cells.	imatinib	91-99	BCR activator of RhoGEF and GTPase	Homo sapiens	43-51
30687103-11	2018	Notably, NPQ-C6 maintained its activity on BCR-ABL1/STAT5/c-MYC/PIM-1 oncogenic pathway in imatinib-resistant cells.	imatinib	91-99	signal transducer and activator of transcription 5A	Homo sapiens	52-57
30687103-11	2018	Notably, NPQ-C6 maintained its activity on BCR-ABL1/STAT5/c-MYC/PIM-1 oncogenic pathway in imatinib-resistant cells.	imatinib	91-99	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	58-63
30687103-11	2018	Notably, NPQ-C6 maintained its activity on BCR-ABL1/STAT5/c-MYC/PIM-1 oncogenic pathway in imatinib-resistant cells.	imatinib	91-99	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	64-69
30894066-5	2019	Here we report a novel type II BCR-ABL kinase inhibitor, CHMFL-ABL-039, which not only displayed great potency (IC50: 7.9 nM) and selectivity (S score (1) = 0.02) against native ABL kinase among other kinases in the kinome, but also exhibited great potency (IC50: 27.9 nM) and selectivity against Imatinib-resistant V299L mutant among other frequently observed ABL kinase mutants.	imatinib	297-305	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
30713559-2	2019	Imatinib inhibits BCR-ABL tyrosine kinase produced due to reciprocal translocation t(9;22) in neoplastic CML cells.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
30359545-0	2019	Identification of a novel PDGFRA point mutation at p.P6L as a potential molecular target of imatinib in an eosinophilia patient showing genetic heterogeneity.	imatinib	92-100	platelet derived growth factor receptor alpha	Homo sapiens	26-32
30359545-3	2019	Another significant genetic biomarker is the PDGFRA gene alone as some of its mutations are targets of imatinib.	imatinib	103-111	platelet derived growth factor receptor alpha	Homo sapiens	45-51
30359545-8	2019	The patient then received imatinib therapy, leading to the complete disappearance of FIP1L1-PDGFRA fusion gene and mutated MYOM2.	imatinib	26-34	factor interacting with PAPOLA and CPSF1	Homo sapiens	85-91
30359545-8	2019	The patient then received imatinib therapy, leading to the complete disappearance of FIP1L1-PDGFRA fusion gene and mutated MYOM2.	imatinib	26-34	platelet derived growth factor receptor alpha	Homo sapiens	92-98
30359545-8	2019	The patient then received imatinib therapy, leading to the complete disappearance of FIP1L1-PDGFRA fusion gene and mutated MYOM2.	imatinib	26-34	myomesin 2	Homo sapiens	123-128
30359545-11	2019	To the best of our knowledge, this is the first case in which the point mutation of PDGFRA has been identified at p.P6L in exon 2, likely making it sensitive to imatinib and thus should be further studied as a potential new molecular target of imatinib therapy.	imatinib	161-169	platelet derived growth factor receptor alpha	Homo sapiens	84-90
30359545-11	2019	To the best of our knowledge, this is the first case in which the point mutation of PDGFRA has been identified at p.P6L in exon 2, likely making it sensitive to imatinib and thus should be further studied as a potential new molecular target of imatinib therapy.	imatinib	244-252	platelet derived growth factor receptor alpha	Homo sapiens	84-90
30726835-0	2019	Sustained Response to Imatinib in a Pediatric Patient with Concurrent Myeloproliferative Disease and Lymphoblastic Lymphoma Associated with a CCDC88C-PDGFRB Fusion Gene.	imatinib	22-30	coiled-coil domain containing 88C	Homo sapiens	142-149
30726835-0	2019	Sustained Response to Imatinib in a Pediatric Patient with Concurrent Myeloproliferative Disease and Lymphoblastic Lymphoma Associated with a CCDC88C-PDGFRB Fusion Gene.	imatinib	22-30	platelet derived growth factor receptor beta	Homo sapiens	150-156
30726835-2	2019	PDGFRB-rearranged MLN sensitive to imatinib were described in adult patients.	imatinib	35-43	platelet derived growth factor receptor beta	Homo sapiens	0-6
30726835-3	2019	We report the first pediatric patient with PDGFRB-rearranged myeloproliferative disorder associated with T-lymphoblastic lymphoma bearing the t(5; 14)(q33;q32) translocation who was successfully treated with imatinib only.	imatinib	208-216	platelet derived growth factor receptor beta	Homo sapiens	43-49
31085913-0	2019	RNA Sequencing Analysis for the Identification of a PCM1/PDGFRB Fusion Gene Responsive to Imatinib.	imatinib	90-98	pericentriolar material 1	Homo sapiens	52-56
31085913-0	2019	RNA Sequencing Analysis for the Identification of a PCM1/PDGFRB Fusion Gene Responsive to Imatinib.	imatinib	90-98	platelet derived growth factor receptor beta	Homo sapiens	57-63
28777148-2	2019	KIT tyrosine kinase inhibitor, imatinib mesylate, has been successfully used for the treatment of primary, advanced, and disseminated GISTs.	imatinib	31-48	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
28777148-3	2019	Recently, activation of mTOR pathway independent of KIT signaling was demonstrated in imatinib mesylate naive malignant GISTs and treatment-resistant metastatic tumors.	imatinib	86-103	mechanistic target of rapamycin kinase	Homo sapiens	24-28
28777148-5	2019	In this study, mTOR pathway genes were evaluated in 14 imatinib mesylate naive, KIT-mutant, malignant small intestinal GISTs using next-generation sequencing.	imatinib	55-63	mechanistic target of rapamycin kinase	Homo sapiens	15-19
31166382-0	2019	Downregulation of lncRNA CCDC26 contributes to imatinib resistance in human gastrointestinal stromal tumors through IGF-1R upregulation.	imatinib	47-55	CCDC26 long non-coding RNA	Homo sapiens	25-31
31166382-0	2019	Downregulation of lncRNA CCDC26 contributes to imatinib resistance in human gastrointestinal stromal tumors through IGF-1R upregulation.	imatinib	47-55	insulin like growth factor 1 receptor	Homo sapiens	116-122
31166382-6	2019	The expression of a series of reported drug resistance-related lncRNAs, including CCDC26, ARF, H19, NBR2, NEAT1, and HOTAIR, in GIST cells treated with imatinib H19 was examined at various time-points by qRT-PCR.	imatinib	152-160	CCDC26 long non-coding RNA	Homo sapiens	82-88
31166382-7	2019	Based on our results and published literature, CCDC26, a strongly down-regulated lncRNA following imatinib treatment, was chosen as our research target.	imatinib	98-106	CCDC26 long non-coding RNA	Homo sapiens	47-53
31166382-8	2019	GIST cells with high expression of CCDC26 were sensitive to imatinib treatment while knockdown of CCDC26 significantly increased the resistance to imatinib.	imatinib	60-68	CCDC26 long non-coding RNA	Homo sapiens	35-41
31166382-8	2019	GIST cells with high expression of CCDC26 were sensitive to imatinib treatment while knockdown of CCDC26 significantly increased the resistance to imatinib.	imatinib	147-155	CCDC26 long non-coding RNA	Homo sapiens	98-104
31166382-10	2019	Moreover, IGF-1R inhibition reversed CCDC26 knockdown-mediated imatinib resistance in GIST.	imatinib	63-71	insulin like growth factor 1 receptor	Homo sapiens	10-16
31166382-10	2019	Moreover, IGF-1R inhibition reversed CCDC26 knockdown-mediated imatinib resistance in GIST.	imatinib	63-71	CCDC26 long non-coding RNA	Homo sapiens	37-43
31166382-11	2019	These results indicated that treatments targeting CCDC26-IGF-1R axis would be useful in increasing sensitivity to imatinib in GIST.	imatinib	114-122	CCDC26 long non-coding RNA	Homo sapiens	50-56
31166382-11	2019	These results indicated that treatments targeting CCDC26-IGF-1R axis would be useful in increasing sensitivity to imatinib in GIST.	imatinib	114-122	insulin like growth factor 1 receptor	Homo sapiens	57-63
30836770-6	2019	PDGF-D and its PDGF receptor beta (PDGFR-beta) are expressed in colorectal cancer and blockage of PDGF-D/PDGFR-beta signaling using tyrosine kinase inhibitors, such as imatinib, might be important in inhibiting tumor-promoting actions.	imatinib	168-176	platelet derived growth factor D	Homo sapiens	0-6
30894066-5	2019	Here we report a novel type II BCR-ABL kinase inhibitor, CHMFL-ABL-039, which not only displayed great potency (IC50: 7.9 nM) and selectivity (S score (1) = 0.02) against native ABL kinase among other kinases in the kinome, but also exhibited great potency (IC50: 27.9 nM) and selectivity against Imatinib-resistant V299L mutant among other frequently observed ABL kinase mutants.	imatinib	297-305	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
30836770-6	2019	PDGF-D and its PDGF receptor beta (PDGFR-beta) are expressed in colorectal cancer and blockage of PDGF-D/PDGFR-beta signaling using tyrosine kinase inhibitors, such as imatinib, might be important in inhibiting tumor-promoting actions.	imatinib	168-176	platelet derived growth factor receptor beta	Homo sapiens	35-45
30836770-6	2019	PDGF-D and its PDGF receptor beta (PDGFR-beta) are expressed in colorectal cancer and blockage of PDGF-D/PDGFR-beta signaling using tyrosine kinase inhibitors, such as imatinib, might be important in inhibiting tumor-promoting actions.	imatinib	168-176	platelet derived growth factor D	Homo sapiens	98-104
30894066-5	2019	Here we report a novel type II BCR-ABL kinase inhibitor, CHMFL-ABL-039, which not only displayed great potency (IC50: 7.9 nM) and selectivity (S score (1) = 0.02) against native ABL kinase among other kinases in the kinome, but also exhibited great potency (IC50: 27.9 nM) and selectivity against Imatinib-resistant V299L mutant among other frequently observed ABL kinase mutants.	imatinib	297-305	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-66
30836770-6	2019	PDGF-D and its PDGF receptor beta (PDGFR-beta) are expressed in colorectal cancer and blockage of PDGF-D/PDGFR-beta signaling using tyrosine kinase inhibitors, such as imatinib, might be important in inhibiting tumor-promoting actions.	imatinib	168-176	platelet derived growth factor receptor beta	Homo sapiens	105-115
30894066-5	2019	Here we report a novel type II BCR-ABL kinase inhibitor, CHMFL-ABL-039, which not only displayed great potency (IC50: 7.9 nM) and selectivity (S score (1) = 0.02) against native ABL kinase among other kinases in the kinome, but also exhibited great potency (IC50: 27.9 nM) and selectivity against Imatinib-resistant V299L mutant among other frequently observed ABL kinase mutants.	imatinib	297-305	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-66
30971653-2	2019	The specific BCR-ABL inhibitors including imatinib, nilotinib, and dasatinib, are clinically utilized in the treatment with CML and ALL patients.	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
30734690-2	2019	Whether the influxorganic cation transporter 1 (OCT1) encoded by the gene SLC221A1 is implicated in the cellularuptake of imatinib is still controversial.	imatinib	122-130	solute carrier family 22 member 1	Homo sapiens	48-52
30734690-8	2019	In OCT1- and OCT2-HEK cells at pH 6, imatinib accumulation was reduced by 2-3-fold regardless of OCTs expressions.	imatinib	37-45	solute carrier family 22 member 1	Homo sapiens	3-7
30734690-8	2019	In OCT1- and OCT2-HEK cells at pH 6, imatinib accumulation was reduced by 2-3-fold regardless of OCTs expressions.	imatinib	37-45	POU class 2 homeobox 2	Homo sapiens	13-17
30614229-7	2019	The HDAC2 inhibitor, valproate (VPA) and the c-Abl inhibitor, imatinib, lowered the expression level of cyclin D1/CDK4, and increased the expression level of p21, leading to an inhibitory effect on IFN-gamma-induced malignant cell growth.	imatinib	62-70	histone deacetylase 2	Bos taurus	4-9
30614229-7	2019	The HDAC2 inhibitor, valproate (VPA) and the c-Abl inhibitor, imatinib, lowered the expression level of cyclin D1/CDK4, and increased the expression level of p21, leading to an inhibitory effect on IFN-gamma-induced malignant cell growth.	imatinib	62-70	cyclin D1	Bos taurus	104-113
30614229-7	2019	The HDAC2 inhibitor, valproate (VPA) and the c-Abl inhibitor, imatinib, lowered the expression level of cyclin D1/CDK4, and increased the expression level of p21, leading to an inhibitory effect on IFN-gamma-induced malignant cell growth.	imatinib	62-70	cyclin-dependent kinase 4	Bos taurus	114-118
30614229-7	2019	The HDAC2 inhibitor, valproate (VPA) and the c-Abl inhibitor, imatinib, lowered the expression level of cyclin D1/CDK4, and increased the expression level of p21, leading to an inhibitory effect on IFN-gamma-induced malignant cell growth.	imatinib	62-70	cyclin dependent kinase inhibitor 1A	Bos taurus	158-161
30614229-7	2019	The HDAC2 inhibitor, valproate (VPA) and the c-Abl inhibitor, imatinib, lowered the expression level of cyclin D1/CDK4, and increased the expression level of p21, leading to an inhibitory effect on IFN-gamma-induced malignant cell growth.	imatinib	62-70	interferon gamma	Bos taurus	198-207
30332954-2	2019	Bcr-Abl fusion protein has constitutively activated Abl tyrosine kinase activity which is responsible for the uncontrolled proliferation in CML The tyrosine kinase inhibitors (TKIs) such as Imatinib, Dasatinib, and Nilotinib are the current first-line treatments approved by the United States Food and Drug Administration (US FDA) for the treatment of the disease.	imatinib	190-198	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
29741432-6	2019	However, higher trough levels were observed in two homozygous carriers of CYP2C8*2 while diminished imatinib levels were seen in two homozygous carriers of CYP3A5*7.	imatinib	100-108	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	156-162
29916288-0	2019	BIM deletion polymorphism profiling complements prognostic values of risk scores in imatinib-treated Asian chronic myeloid leukemia patients.	imatinib	84-92	BCL2 like 11	Homo sapiens	0-3
29932782-0	2019	PARP1 inhibitor eliminated imatinib-refractory chronic myeloid leukemia cells in bone marrow microenvironment conditions.	imatinib	27-35	poly(ADP-ribose) polymerase 1	Homo sapiens	0-5
30583336-0	2018	Prevalence of BCR-ABL T315I Mutation in Malaysian Patients with Imatinib-Resistant Chronic Myeloid Leukemia Objective: Chronic Myeloid Leukemia (CML) is caused by a reciprocal translocation between chromosomes 9and 22, t(9;22) (q34;q11) which encodes for the BCR-ABL fusion protein.	imatinib	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
30583835-5	2019	The characteristic translocation t(17;22)(q22;q13) leading to the formation of COL1A1/PDGFbeta fusion transcripts is not only of diagnostic value but also enables an alternative imatinib-based therapy in inoperable or metastatic cases.	imatinib	178-186	collagen type I alpha 1 chain	Homo sapiens	79-85
30583835-5	2019	The characteristic translocation t(17;22)(q22;q13) leading to the formation of COL1A1/PDGFbeta fusion transcripts is not only of diagnostic value but also enables an alternative imatinib-based therapy in inoperable or metastatic cases.	imatinib	178-186	platelet derived growth factor subunit A	Homo sapiens	86-94
31593970-3	2019	CS late chronic anemia was defined as the presence of persistent (>6 months) and otherwise unexplained Hb levels <=10 g/dL, which occurred >6 months from imatinib start.	imatinib	154-162	citrate synthase	Homo sapiens	0-2
31593970-4	2019	RESULTS: A condition of CS late chronic anemia occurred in 22 out of 81 patients (27.2%) at different intervals from imatinib start.	imatinib	117-125	citrate synthase	Homo sapiens	24-26
31593970-9	2019	CONCLUSIONS: CS late chronic anemia during long-term treatment with imatinib is a common complication in responsive elderly patients, with worse EFS if untreated.	imatinib	68-76	citrate synthase	Homo sapiens	13-15
30583336-0	2018	Prevalence of BCR-ABL T315I Mutation in Malaysian Patients with Imatinib-Resistant Chronic Myeloid Leukemia Objective: Chronic Myeloid Leukemia (CML) is caused by a reciprocal translocation between chromosomes 9and 22, t(9;22) (q34;q11) which encodes for the BCR-ABL fusion protein.	imatinib	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	259-266
30366670-0	2018	LncRNA MALAT1 promotes cell proliferation and imatinib resistance by sponging miR-328 in chronic myelogenous leukemia.	imatinib	46-54	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	7-13
30366670-0	2018	LncRNA MALAT1 promotes cell proliferation and imatinib resistance by sponging miR-328 in chronic myelogenous leukemia.	imatinib	46-54	microRNA 328	Homo sapiens	78-85
30366670-11	2018	Moreover, MALAT1 knockdown enhanced imatinib sensitivity of K562 cells, while silencing of miR-328 abolished this effect.	imatinib	36-44	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	10-16
30366670-12	2018	CONCLUSIONS: These findings indicate that lncRNA MALAT1/miR-328 axis promotes the proliferation and imatinib resistance of CML cells, providing new perspectives for the future study of MALAT1 as a therapeutic target for CML.	imatinib	100-108	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	49-55
30366670-12	2018	CONCLUSIONS: These findings indicate that lncRNA MALAT1/miR-328 axis promotes the proliferation and imatinib resistance of CML cells, providing new perspectives for the future study of MALAT1 as a therapeutic target for CML.	imatinib	100-108	microRNA 328	Homo sapiens	56-63
30366670-12	2018	CONCLUSIONS: These findings indicate that lncRNA MALAT1/miR-328 axis promotes the proliferation and imatinib resistance of CML cells, providing new perspectives for the future study of MALAT1 as a therapeutic target for CML.	imatinib	100-108	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	185-191
30311036-0	2018	A phase II study of imatinib mesylate and letrozole in patients with hormone receptor-positive metastatic breast cancer expressing c-kit or PDGFR-beta.	imatinib	20-37	platelet derived growth factor receptor beta	Homo sapiens	140-150
30526517-2	2018	p230 CML is associated with various clinical presentations and courses with variable responses to first-line imatinib.	imatinib	109-117	golgin A4	Homo sapiens	0-4
30574454-5	2018	To begin we measured, by flow cytometry, the proportion of CD34+/CD26+ cells in 31 bone marrow samples from 20 CML patients, at diagnosis and during treatment with imatinib.	imatinib	164-172	CD34 molecule	Homo sapiens	59-63
30574454-8	2018	At diagnosis, CD34+/CD26+ cells median value/muL was 0.48; this number increased from diagnosis to the third month of therapy and then reduced during treatment with imatinib.	imatinib	165-173	CD34 molecule	Homo sapiens	14-18
30574454-8	2018	At diagnosis, CD34+/CD26+ cells median value/muL was 0.48; this number increased from diagnosis to the third month of therapy and then reduced during treatment with imatinib.	imatinib	165-173	dipeptidyl peptidase 4	Homo sapiens	20-24
30317026-1	2018	There is still a great demand in the clinic for the drugs which can overcome a variety of imatinib resistant ABL mutants.	imatinib	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-112
30317026-2	2018	Starting from a type I inhibitor axitinib, which has been reported to overcome ABL-T315I mutant induced resistance, through a structure guided drug design approach and binding mode switch strategy, we have discovered a novel type II ABL inhibitor 24 (CHMFL-ABL-121), which significantly improved the inhibitory activity against ABL wt and a broad spectrum of mutants including the most prevalent imatinib-resistant gatekeeper mutant T315I.	imatinib	396-404	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-82
30317026-2	2018	Starting from a type I inhibitor axitinib, which has been reported to overcome ABL-T315I mutant induced resistance, through a structure guided drug design approach and binding mode switch strategy, we have discovered a novel type II ABL inhibitor 24 (CHMFL-ABL-121), which significantly improved the inhibitory activity against ABL wt and a broad spectrum of mutants including the most prevalent imatinib-resistant gatekeeper mutant T315I.	imatinib	396-404	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	233-236
30317026-2	2018	Starting from a type I inhibitor axitinib, which has been reported to overcome ABL-T315I mutant induced resistance, through a structure guided drug design approach and binding mode switch strategy, we have discovered a novel type II ABL inhibitor 24 (CHMFL-ABL-121), which significantly improved the inhibitory activity against ABL wt and a broad spectrum of mutants including the most prevalent imatinib-resistant gatekeeper mutant T315I.	imatinib	396-404	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	233-236
30317026-2	2018	Starting from a type I inhibitor axitinib, which has been reported to overcome ABL-T315I mutant induced resistance, through a structure guided drug design approach and binding mode switch strategy, we have discovered a novel type II ABL inhibitor 24 (CHMFL-ABL-121), which significantly improved the inhibitory activity against ABL wt and a broad spectrum of mutants including the most prevalent imatinib-resistant gatekeeper mutant T315I.	imatinib	396-404	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	233-236
30205168-5	2018	Furthermore, OT-55 synergized with omacetaxine in imatinib-resistant KBM-5 R cells to inhibit the expression of Mcl-1, triggering apoptosis.	imatinib	50-58	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	112-117
29945498-0	2018	Expression analysis of Akirin-2, NFkappaB-p65 and beta-catenin proteins in imatinib resistance of chronic myeloid leukemia.	imatinib	75-83	akirin 2	Homo sapiens	23-31
29945498-0	2018	Expression analysis of Akirin-2, NFkappaB-p65 and beta-catenin proteins in imatinib resistance of chronic myeloid leukemia.	imatinib	75-83	RELA proto-oncogene, NF-kB subunit	Homo sapiens	33-45
29945498-0	2018	Expression analysis of Akirin-2, NFkappaB-p65 and beta-catenin proteins in imatinib resistance of chronic myeloid leukemia.	imatinib	75-83	catenin beta 1	Homo sapiens	50-62
29945498-2	2018	Constitutive activation of NFkappaB and beta-catenin signaling promotes cellular proliferation and survival and resistance to Imatinib therapy in CML.	imatinib	126-134	nuclear factor kappa B subunit 1	Homo sapiens	27-35
29945498-2	2018	Constitutive activation of NFkappaB and beta-catenin signaling promotes cellular proliferation and survival and resistance to Imatinib therapy in CML.	imatinib	126-134	catenin beta 1	Homo sapiens	40-52
29945498-6	2018	RESULTS: beta-catenin and NFkappaB-p65 proteins bound to DNA promoter regions of MDR1 in imatinib-sensitive and resistant CML cells, whereas any direct protein-protein interaction could not be found between NFkappaB-p65 and Akirin-2 or beta-catenin proteins.	imatinib	89-97	catenin beta 1	Homo sapiens	9-21
29945498-6	2018	RESULTS: beta-catenin and NFkappaB-p65 proteins bound to DNA promoter regions of MDR1 in imatinib-sensitive and resistant CML cells, whereas any direct protein-protein interaction could not be found between NFkappaB-p65 and Akirin-2 or beta-catenin proteins.	imatinib	89-97	nuclear factor kappa B subunit 1	Homo sapiens	26-34
29945498-6	2018	RESULTS: beta-catenin and NFkappaB-p65 proteins bound to DNA promoter regions of MDR1 in imatinib-sensitive and resistant CML cells, whereas any direct protein-protein interaction could not be found between NFkappaB-p65 and Akirin-2 or beta-catenin proteins.	imatinib	89-97	ATP binding cassette subfamily B member 1	Homo sapiens	81-85
29945498-6	2018	RESULTS: beta-catenin and NFkappaB-p65 proteins bound to DNA promoter regions of MDR1 in imatinib-sensitive and resistant CML cells, whereas any direct protein-protein interaction could not be found between NFkappaB-p65 and Akirin-2 or beta-catenin proteins.	imatinib	89-97	RELA proto-oncogene, NF-kB subunit	Homo sapiens	26-38
29945498-7	2018	Nuclear beta-catenin and NFkappaB-p65 levels increased in imatinib resistance.	imatinib	58-66	catenin beta 1	Homo sapiens	8-20
29945498-7	2018	Nuclear beta-catenin and NFkappaB-p65 levels increased in imatinib resistance.	imatinib	58-66	RELA proto-oncogene, NF-kB subunit	Homo sapiens	25-37
29945498-8	2018	Moreover, increased Akirin-2 protein accumulation in the nucleus was shown for the first time in imatinib resistant CML cells.	imatinib	97-105	akirin 2	Homo sapiens	20-28
29945498-9	2018	DISCUSSION: We show for the first time that Akirin-2 can be a novel biomarker in imatinib resistance.	imatinib	81-89	akirin 2	Homo sapiens	44-52
29945498-10	2018	Targeting Akirin-2, NFkappaB and beta-catenin genes may provide an opportunity to overcome imatinib resistance in CML.	imatinib	91-99	akirin 2	Homo sapiens	10-18
29945498-10	2018	Targeting Akirin-2, NFkappaB and beta-catenin genes may provide an opportunity to overcome imatinib resistance in CML.	imatinib	91-99	nuclear factor kappa B subunit 1	Homo sapiens	20-28
29945498-10	2018	Targeting Akirin-2, NFkappaB and beta-catenin genes may provide an opportunity to overcome imatinib resistance in CML.	imatinib	91-99	catenin beta 1	Homo sapiens	33-45
30567202-1	2018	Imatinib is a specific tyrosine kinase inhibitor which has been approved for the treatment of Philadelphia chromosome-positive chronic myeloid leukaemia and c-KIT (CD117)-positive gastrointestinal stromal tumours.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	157-162
30567202-1	2018	Imatinib is a specific tyrosine kinase inhibitor which has been approved for the treatment of Philadelphia chromosome-positive chronic myeloid leukaemia and c-KIT (CD117)-positive gastrointestinal stromal tumours.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	164-169
30396570-0	2018	Imatinib mesylate elicits extracellular signal-related kinase (ERK) activation and enhances the survival of gamma-irradiated epithelial cells.	imatinib	0-17	mitogen-activated protein kinase 1	Homo sapiens	26-61
30396570-0	2018	Imatinib mesylate elicits extracellular signal-related kinase (ERK) activation and enhances the survival of gamma-irradiated epithelial cells.	imatinib	0-17	mitogen-activated protein kinase 1	Homo sapiens	63-66
30396570-1	2018	Imatinib mesylate, commercially known as Gleevec/Glivec, is the first targeted anticancer drug that inhibits activity of the tyrosine kinases, c-ABL, c-KIT, and PDGFR.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-148
30396570-1	2018	Imatinib mesylate, commercially known as Gleevec/Glivec, is the first targeted anticancer drug that inhibits activity of the tyrosine kinases, c-ABL, c-KIT, and PDGFR.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	150-155
30396570-1	2018	Imatinib mesylate, commercially known as Gleevec/Glivec, is the first targeted anticancer drug that inhibits activity of the tyrosine kinases, c-ABL, c-KIT, and PDGFR.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	161-166
30396570-2	2018	A number of studies have shown that treatment with imatinib mesylate elicits extracellular signal-related kinase (ERK) activation, which, in turn, has been shown to confer radioresistance.	imatinib	51-68	mitogen-activated protein kinase 1	Homo sapiens	77-112
30396570-2	2018	A number of studies have shown that treatment with imatinib mesylate elicits extracellular signal-related kinase (ERK) activation, which, in turn, has been shown to confer radioresistance.	imatinib	51-68	mitogen-activated protein kinase 1	Homo sapiens	114-117
30396570-4	2018	ERK activation was detected 30 min after imatinib mesylate treatment in all three cell lines.	imatinib	41-58	mitogen-activated protein kinase 1	Homo sapiens	0-3
30396570-5	2018	In cells exposed to gamma-irradiation in the presence of imatinib mesylate, this activation of ERK was associated with a reduction in radiation-induced apoptosis and enhanced cell survival.	imatinib	57-74	mitogen-activated protein kinase 1	Homo sapiens	95-98
29976745-0	2018	BCR-ABL1 genomic DNA PCR response kinetics during first-line imatinib treatment of chronic myeloid leukemia.	imatinib	61-69	BCR activator of RhoGEF and GTPase	Homo sapiens	0-8
30311036-0	2018	A phase II study of imatinib mesylate and letrozole in patients with hormone receptor-positive metastatic breast cancer expressing c-kit or PDGFR-beta.	imatinib	20-37	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	131-136
30311036-1	2018	Background Imatinib mesylate is a potent inhibitor of the Abl, KIT and platelet derived growth factor (PDGF) receptor tyrosine kinases.	imatinib	11-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-61
30311036-1	2018	Background Imatinib mesylate is a potent inhibitor of the Abl, KIT and platelet derived growth factor (PDGF) receptor tyrosine kinases.	imatinib	11-28	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	63-66
30383140-13	2018	Recurrence was noted in 7 patients: 1 had disease recur while receiving imatinib (PDGFRA D842V mutation) and died; 6 had disease recur after discontinuation of imatinib therapy.	imatinib	72-80	platelet derived growth factor receptor alpha	Homo sapiens	82-88
30545989-6	2018	The tumor harbored a KIT exon 11 deletion mutation in codon 558, which predicts a favorable response to imatinib.	imatinib	104-112	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	21-24
30541960-0	2018	Serum miR-518e-5p is a potential biomarker for secondary imatinib-resistant gastrointestinal stromal tumor.	imatinib	57-65	MLX interacting protein	Homo sapiens	6-9
30541960-5	2018	Serum miR- 518e-5p and miR-548e levels were higher in secondary imatinib-resistant GIST than imatinib-sensitive GIST patients or healthy controls (P less than 0.0001).	imatinib	64-72	MLX interacting protein	Homo sapiens	6-9
30541960-5	2018	Serum miR- 518e-5p and miR-548e levels were higher in secondary imatinib-resistant GIST than imatinib-sensitive GIST patients or healthy controls (P less than 0.0001).	imatinib	64-72	microRNA 548e	Homo sapiens	23-31
30541960-5	2018	Serum miR- 518e-5p and miR-548e levels were higher in secondary imatinib-resistant GIST than imatinib-sensitive GIST patients or healthy controls (P less than 0.0001).	imatinib	93-101	MLX interacting protein	Homo sapiens	6-9
30541960-7	2018	To discriminate imatinib-resistant from imatinib-sensitive GIST patients, the AUC for serum miR-518e-5p was 0.9938, with 99.8% sensitivity and 82.1% specificity.	imatinib	16-24	MLX interacting protein	Homo sapiens	92-95
30541960-7	2018	To discriminate imatinib-resistant from imatinib-sensitive GIST patients, the AUC for serum miR-518e-5p was 0.9938, with 99.8% sensitivity and 82.1% specificity.	imatinib	40-48	MLX interacting protein	Homo sapiens	92-95
30541960-8	2018	Serum miR-518e-5p could also discriminate imatinib-resistant GIST patients from healthy controls with 99.9% sensitivity and 97.4% specificity.	imatinib	42-50	MLX interacting protein	Homo sapiens	6-9
30541960-9	2018	These data indicate that serum miR-518e- 5p is a potentially promising non-invasive biomarker for early detection and diagnosis of secondary imatinib-resistant GIST.	imatinib	141-149	MLX interacting protein	Homo sapiens	31-34
30671399-0	2018	Anti-growth Effects of Imatinib and GNF5 via Regulation of Skp2 in Human Hepatocellular Carcinoma Cells.	imatinib	23-31	S-phase kinase associated protein 2	Homo sapiens	59-63
30671399-5	2018	Using immunoblot analysis, we assessed change of the activation of caspases, PARP, Akt, mitogen-activated protein kinases, and Skp2/p27/p21 pathway by imatinib and GNF5 in SK-HEP1 cells.	imatinib	151-159	collagen type XI alpha 2 chain	Homo sapiens	77-81
30671399-5	2018	Using immunoblot analysis, we assessed change of the activation of caspases, PARP, Akt, mitogen-activated protein kinases, and Skp2/p27/p21 pathway by imatinib and GNF5 in SK-HEP1 cells.	imatinib	151-159	AKT serine/threonine kinase 1	Homo sapiens	83-86
30671399-5	2018	Using immunoblot analysis, we assessed change of the activation of caspases, PARP, Akt, mitogen-activated protein kinases, and Skp2/p27/p21 pathway by imatinib and GNF5 in SK-HEP1 cells.	imatinib	151-159	S-phase kinase associated protein 2	Homo sapiens	127-131
30671399-5	2018	Using immunoblot analysis, we assessed change of the activation of caspases, PARP, Akt, mitogen-activated protein kinases, and Skp2/p27/p21 pathway by imatinib and GNF5 in SK-HEP1 cells.	imatinib	151-159	interferon alpha inducible protein 27	Homo sapiens	132-135
30671399-5	2018	Using immunoblot analysis, we assessed change of the activation of caspases, PARP, Akt, mitogen-activated protein kinases, and Skp2/p27/p21 pathway by imatinib and GNF5 in SK-HEP1 cells.	imatinib	151-159	H3 histone pseudogene 16	Homo sapiens	136-139
30671399-6	2018	Using sh-Skp2 HCC cells, the role of Skp2 in the effects of imatinib and GNF5 was evaluated.	imatinib	60-68	S-phase kinase associated protein 2	Homo sapiens	37-41
30671399-8	2018	Treatment of imatinib and GNF5 decreased Skp2 expression and Akt phosphorylation, and increased the expression of p27, p21, and active-caspases in SK-HEP1 cells.	imatinib	13-21	S-phase kinase associated protein 2	Homo sapiens	41-45
30671399-8	2018	Treatment of imatinib and GNF5 decreased Skp2 expression and Akt phosphorylation, and increased the expression of p27, p21, and active-caspases in SK-HEP1 cells.	imatinib	13-21	AKT serine/threonine kinase 1	Homo sapiens	61-64
30671399-8	2018	Treatment of imatinib and GNF5 decreased Skp2 expression and Akt phosphorylation, and increased the expression of p27, p21, and active-caspases in SK-HEP1 cells.	imatinib	13-21	interferon alpha inducible protein 27	Homo sapiens	114-117
30671399-8	2018	Treatment of imatinib and GNF5 decreased Skp2 expression and Akt phosphorylation, and increased the expression of p27, p21, and active-caspases in SK-HEP1 cells.	imatinib	13-21	H3 histone pseudogene 16	Homo sapiens	119-122
30671399-9	2018	In sh-Skp2 HCC cells, cell growth and the expression of Skp2 were inhibited by more than in the mock group treated with imatinib and GNF5.	imatinib	120-128	S-phase kinase associated protein 2	Homo sapiens	6-10
30671399-9	2018	In sh-Skp2 HCC cells, cell growth and the expression of Skp2 were inhibited by more than in the mock group treated with imatinib and GNF5.	imatinib	120-128	S-phase kinase associated protein 2	Homo sapiens	56-60
29616854-0	2018	The effectiveness of interferon-alpha combined with imatinib in patient with chronic myeloid leukemia harboring T315I BCR-ABL1 mutation.	imatinib	52-60	BCR activator of RhoGEF and GTPase	Homo sapiens	118-126
29909726-2	2018	Blockade of oncogenic BCR-ABL1 tyrosine kinase activity by imatinib translated into an impressive demonstration of clinical and biological control of the disease.	imatinib	59-67	BCR activator of RhoGEF and GTPase	Homo sapiens	22-30
30400842-1	2018	BACKGROUND: Chronic myeloid leukemia is associated with a BCR/ABL oncoprotein inhibited by imatinib mesylate, the first tyrosine kinase inhibitor.	imatinib	91-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
30282814-13	2018	Mutations of IL13 rs1800925 and CXCL14 rs7716492 may be the promising biomarkers to predict the ADRs of imatinib.	imatinib	104-112	interleukin 13	Homo sapiens	13-17
30282814-13	2018	Mutations of IL13 rs1800925 and CXCL14 rs7716492 may be the promising biomarkers to predict the ADRs of imatinib.	imatinib	104-112	C-X-C motif chemokine ligand 14	Homo sapiens	32-38
30290167-0	2018	Inducible SHP-2 activation confers resistance to imatinib in drug-tolerant chronic myeloid leukemia cells.	imatinib	49-57	protein tyrosine phosphatase non-receptor type 11	Homo sapiens	10-15
30290167-1	2018	BCR-ABL kinase mutations, accounting for clinical resistance to tyrosine kinase inhibitor (TKI) such as imatinib, frequently occur in acquired resistance or in advanced phases of chronic myeloid leukemia (CML).	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
30290167-3	2018	Here, we utilized non-mutational imatinib-resistant K562/G cells to reveal SHP-2 as a resistance modulator of imatinib treatment response during the early phase.	imatinib	33-41	protein tyrosine phosphatase non-receptor type 11	Homo sapiens	75-80
30290167-3	2018	Here, we utilized non-mutational imatinib-resistant K562/G cells to reveal SHP-2 as a resistance modulator of imatinib treatment response during the early phase.	imatinib	110-118	protein tyrosine phosphatase non-receptor type 11	Homo sapiens	75-80
30290167-5	2018	In K562 cells, both short-term and long-term exposure to imatinib induced SHP-2 phosphorylation.	imatinib	57-65	protein tyrosine phosphatase non-receptor type 11	Homo sapiens	74-79
30290167-6	2018	Consistently, gain- and loss-of-function mutants in SHP-2 proved its regulation of imatinib resistance.	imatinib	83-91	protein tyrosine phosphatase non-receptor type 11	Homo sapiens	52-57
30290167-9	2018	In conclusion, our results highlight that SHP-2 could be exploited as a biomarker and therapeutic target during the early phase of imatinib resistance development in CML.	imatinib	131-139	protein tyrosine phosphatase non-receptor type 11	Homo sapiens	42-47
30396237-4	2018	The inhibition of SCF signaling via treatment with a c-KIT antagonist (imatinib) during hPSC-derived hematopoiesis resulted in reductions in the yield and multi-lineage potential of hematopoietic progenitors.	imatinib	71-79	KIT ligand	Homo sapiens	18-21
30396237-4	2018	The inhibition of SCF signaling via treatment with a c-KIT antagonist (imatinib) during hPSC-derived hematopoiesis resulted in reductions in the yield and multi-lineage potential of hematopoietic progenitors.	imatinib	71-79	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	53-58
30506540-1	2018	OBJECTIVE: To investigate the biological behavior characteristics of gastrointestinal stromal tumors (GIST) with PDGFRA mutation and the patients" survival, and elucidate the efficacy of imatinib therapy.	imatinib	187-195	platelet derived growth factor receptor alpha	Homo sapiens	113-119
30419548-0	2018	MXD1 regulates the imatinib resistance of chronic myeloid leukemia cells by repressing BCR-ABL1 expression.	imatinib	19-27	MAX dimerization protein 1	Homo sapiens	0-4
30419548-0	2018	MXD1 regulates the imatinib resistance of chronic myeloid leukemia cells by repressing BCR-ABL1 expression.	imatinib	19-27	BCR activator of RhoGEF and GTPase	Homo sapiens	87-95
30419548-4	2018	Overexpression of MXD1 markedly inhibited the proliferation of K562 cells and sensitized the imatinib-resistant K562/G01 cell line to imatinib, with decreased BCR-ABL1 mRNA and protein expression.	imatinib	93-101	MAX dimerization protein 1	Homo sapiens	18-22
30419548-4	2018	Overexpression of MXD1 markedly inhibited the proliferation of K562 cells and sensitized the imatinib-resistant K562/G01 cell line to imatinib, with decreased BCR-ABL1 mRNA and protein expression.	imatinib	134-142	MAX dimerization protein 1	Homo sapiens	18-22
30419548-6	2018	Taken together, these data show that MXD1 functions as a negative regulator of BCR-ABL1 expression and subsequently inhibits proliferation and sensitizes CML cells to imatinib treatment.	imatinib	167-175	MAX dimerization protein 1	Homo sapiens	37-41
30168245-5	2018	An adapted 3-probe FISH strategy identified two patients with ETV6-ABL1 fusion who received imatinib.	imatinib	92-100	ETS variant transcription factor 6	Homo sapiens	62-66
30168245-5	2018	An adapted 3-probe FISH strategy identified two patients with ETV6-ABL1 fusion who received imatinib.	imatinib	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-71
30253992-11	2018	Subsequent KIT-targeting tyrosine kinase inhibitor therapy with imatinib was administered for a short time.	imatinib	64-72	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	11-14
30500954-7	2018	Notably, upregulation of c-KIT expression by FUBP1 and RUNX1 promotes cell proliferation and renders cells more resistant to the c-KIT inhibitor imatinib mesylate, a common therapeutic drug.	imatinib	145-162	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	25-30
30500954-7	2018	Notably, upregulation of c-KIT expression by FUBP1 and RUNX1 promotes cell proliferation and renders cells more resistant to the c-KIT inhibitor imatinib mesylate, a common therapeutic drug.	imatinib	145-162	far upstream element binding protein 1	Homo sapiens	45-50
30500954-7	2018	Notably, upregulation of c-KIT expression by FUBP1 and RUNX1 promotes cell proliferation and renders cells more resistant to the c-KIT inhibitor imatinib mesylate, a common therapeutic drug.	imatinib	145-162	RUNX family transcription factor 1	Homo sapiens	55-60
30500954-7	2018	Notably, upregulation of c-KIT expression by FUBP1 and RUNX1 promotes cell proliferation and renders cells more resistant to the c-KIT inhibitor imatinib mesylate, a common therapeutic drug.	imatinib	145-162	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	129-134
30176265-4	2018	Interestingly, we also found that sensitivity to imatinib can be partly restored in imatinib-resistant chronic myelogenous leukemia cells by ZNF224 overexpression and the resulting suppression of Axl expression.	imatinib	49-57	zinc finger protein 224	Homo sapiens	141-147
30301525-1	2018	Chronic myeloid leukemia (CML) responds well to BCR-ABL tyrosine kinase inhibitors (TKI), such as imatinib and dasatinib.	imatinib	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
30176265-4	2018	Interestingly, we also found that sensitivity to imatinib can be partly restored in imatinib-resistant chronic myelogenous leukemia cells by ZNF224 overexpression and the resulting suppression of Axl expression.	imatinib	49-57	AXL receptor tyrosine kinase	Homo sapiens	196-199
30176265-4	2018	Interestingly, we also found that sensitivity to imatinib can be partly restored in imatinib-resistant chronic myelogenous leukemia cells by ZNF224 overexpression and the resulting suppression of Axl expression.	imatinib	84-92	zinc finger protein 224	Homo sapiens	141-147
30176265-4	2018	Interestingly, we also found that sensitivity to imatinib can be partly restored in imatinib-resistant chronic myelogenous leukemia cells by ZNF224 overexpression and the resulting suppression of Axl expression.	imatinib	84-92	AXL receptor tyrosine kinase	Homo sapiens	196-199
30176265-5	2018	These results, in accordance with our previous findings, support the role of ZNF224 in imatinib responsiveness and shed new insights into potential therapeutic use of ZNF224 in imatinib-resistant chronic myelogenous leukemia.	imatinib	87-95	zinc finger protein 224	Homo sapiens	77-83
30176265-5	2018	These results, in accordance with our previous findings, support the role of ZNF224 in imatinib responsiveness and shed new insights into potential therapeutic use of ZNF224 in imatinib-resistant chronic myelogenous leukemia.	imatinib	177-185	zinc finger protein 224	Homo sapiens	167-173
29623544-0	2018	SOCS1 gene therapy has antitumor effects in imatinib-resistant gastrointestinal stromal tumor cells through FAK/PI3 K signaling.	imatinib	44-52	suppressor of cytokine signaling 1	Homo sapiens	0-5
30297237-6	2018	Advanced stages not amenable to surgery or metastatic DFSP (with presence of COL1A1;PDGFB) are best treated with imatinib.	imatinib	113-121	collagen type I alpha 1 chain	Homo sapiens	77-83
30297237-6	2018	Advanced stages not amenable to surgery or metastatic DFSP (with presence of COL1A1;PDGFB) are best treated with imatinib.	imatinib	113-121	platelet derived growth factor subunit B	Homo sapiens	84-89
29623544-0	2018	SOCS1 gene therapy has antitumor effects in imatinib-resistant gastrointestinal stromal tumor cells through FAK/PI3 K signaling.	imatinib	44-52	protein tyrosine kinase 2	Homo sapiens	108-111
29623544-3	2018	Despite the revolutionary effects of imatinib, some patients are primarily resistant to imatinib and many become resistant because of acquisition of secondary mutations in KIT.	imatinib	37-45	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	172-175
29623544-11	2018	However, inhibition of the FAK signaling with an FAK inhibitor or RNA interference significantly showed inhibitory effect on cell growth and suppressed the phosphorylation of AKT, indicating a cross-talk between the AKT and FAK pathways in both the imatinib-sensitive and imatinib-resistant GIST cells.	imatinib	249-257	protein tyrosine kinase 2	Homo sapiens	27-30
29623544-11	2018	However, inhibition of the FAK signaling with an FAK inhibitor or RNA interference significantly showed inhibitory effect on cell growth and suppressed the phosphorylation of AKT, indicating a cross-talk between the AKT and FAK pathways in both the imatinib-sensitive and imatinib-resistant GIST cells.	imatinib	249-257	protein tyrosine kinase 2	Homo sapiens	49-52
29623544-11	2018	However, inhibition of the FAK signaling with an FAK inhibitor or RNA interference significantly showed inhibitory effect on cell growth and suppressed the phosphorylation of AKT, indicating a cross-talk between the AKT and FAK pathways in both the imatinib-sensitive and imatinib-resistant GIST cells.	imatinib	249-257	AKT serine/threonine kinase 1	Homo sapiens	175-178
29623544-11	2018	However, inhibition of the FAK signaling with an FAK inhibitor or RNA interference significantly showed inhibitory effect on cell growth and suppressed the phosphorylation of AKT, indicating a cross-talk between the AKT and FAK pathways in both the imatinib-sensitive and imatinib-resistant GIST cells.	imatinib	249-257	AKT serine/threonine kinase 1	Homo sapiens	216-219
29623544-11	2018	However, inhibition of the FAK signaling with an FAK inhibitor or RNA interference significantly showed inhibitory effect on cell growth and suppressed the phosphorylation of AKT, indicating a cross-talk between the AKT and FAK pathways in both the imatinib-sensitive and imatinib-resistant GIST cells.	imatinib	249-257	protein tyrosine kinase 2	Homo sapiens	49-52
29623544-11	2018	However, inhibition of the FAK signaling with an FAK inhibitor or RNA interference significantly showed inhibitory effect on cell growth and suppressed the phosphorylation of AKT, indicating a cross-talk between the AKT and FAK pathways in both the imatinib-sensitive and imatinib-resistant GIST cells.	imatinib	272-280	protein tyrosine kinase 2	Homo sapiens	27-30
29623544-11	2018	However, inhibition of the FAK signaling with an FAK inhibitor or RNA interference significantly showed inhibitory effect on cell growth and suppressed the phosphorylation of AKT, indicating a cross-talk between the AKT and FAK pathways in both the imatinib-sensitive and imatinib-resistant GIST cells.	imatinib	272-280	AKT serine/threonine kinase 1	Homo sapiens	175-178
29623544-11	2018	However, inhibition of the FAK signaling with an FAK inhibitor or RNA interference significantly showed inhibitory effect on cell growth and suppressed the phosphorylation of AKT, indicating a cross-talk between the AKT and FAK pathways in both the imatinib-sensitive and imatinib-resistant GIST cells.	imatinib	272-280	AKT serine/threonine kinase 1	Homo sapiens	216-219
29623544-12	2018	CONCLUSIONS: Our results indicate that the activation of FAK signaling is critical for proliferation of both imatinib-sensitive and -resistant GIST cells and the interference with FAK/AKT pathway might be beneficial for therapeutic target.	imatinib	109-117	protein tyrosine kinase 2	Homo sapiens	57-60
29623544-12	2018	CONCLUSIONS: Our results indicate that the activation of FAK signaling is critical for proliferation of both imatinib-sensitive and -resistant GIST cells and the interference with FAK/AKT pathway might be beneficial for therapeutic target.	imatinib	109-117	AKT serine/threonine kinase 1	Homo sapiens	184-187
30384441-6	2018	Crucially, the degradation of cleaved fragment of Lyn by the N-end rule counters imatinib resistance in these cells, implicating a possible linkage between the N-end rule degradation pathway and imatinib resistance.	imatinib	81-89	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	50-53
30384441-6	2018	Crucially, the degradation of cleaved fragment of Lyn by the N-end rule counters imatinib resistance in these cells, implicating a possible linkage between the N-end rule degradation pathway and imatinib resistance.	imatinib	195-203	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	50-53
30248347-0	2018	Synergistic activity of imatinib and AR-42 against chronic myeloid leukemia cells mainly through HDAC1 inhibition.	imatinib	24-32	histone deacetylase 1	Homo sapiens	97-102
30405627-4	2018	In particular, increased proportions of terminally differentiated CD56+CD16+CD57+ NK cells have been reported to be associated with successful Imatinib therapy discontinuation or with a deep molecular response in Dasatinib-treated patients.	imatinib	143-151	neural cell adhesion molecule 1	Homo sapiens	66-70
30405627-4	2018	In particular, increased proportions of terminally differentiated CD56+CD16+CD57+ NK cells have been reported to be associated with successful Imatinib therapy discontinuation or with a deep molecular response in Dasatinib-treated patients.	imatinib	143-151	Fc gamma receptor IIIa	Homo sapiens	71-75
30405627-4	2018	In particular, increased proportions of terminally differentiated CD56+CD16+CD57+ NK cells have been reported to be associated with successful Imatinib therapy discontinuation or with a deep molecular response in Dasatinib-treated patients.	imatinib	143-151	beta-1,3-glucuronyltransferase 1	Homo sapiens	76-80
30333571-6	2018	In obese mice, imatinib reduced TNFalpha-gene expression in peritoneal and liver macrophages and systemic lipid levels at one month.	imatinib	15-23	tumor necrosis factor	Mus musculus	32-40
30180991-4	2018	Our results indicated that PDGF phosphorylated Akt, stimulated PASMCs proliferation; while inhibition of PDGF receptor (PDGFR) by imatinib prevented these effects.	imatinib	130-138	platelet derived growth factor receptor beta	Homo sapiens	105-118
30180991-4	2018	Our results indicated that PDGF phosphorylated Akt, stimulated PASMCs proliferation; while inhibition of PDGF receptor (PDGFR) by imatinib prevented these effects.	imatinib	130-138	platelet derived growth factor receptor beta	Homo sapiens	120-125
30217442-4	2018	Treatment of CML-derived K562 cells with BCR-ABL tyrosine kinase inhibitors, including imatinib, dasatinib, nilotinib and ponatinib, prevented activation of eIF2alpha kinases, protein kinase-like endoplasmic reticulum kinase (PERK) and general control nonderepressible 2, and downstream ATF4 induction during metabolic stress.	imatinib	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
30217442-4	2018	Treatment of CML-derived K562 cells with BCR-ABL tyrosine kinase inhibitors, including imatinib, dasatinib, nilotinib and ponatinib, prevented activation of eIF2alpha kinases, protein kinase-like endoplasmic reticulum kinase (PERK) and general control nonderepressible 2, and downstream ATF4 induction during metabolic stress.	imatinib	87-95	eukaryotic translation initiation factor 2A	Homo sapiens	157-166
30217442-4	2018	Treatment of CML-derived K562 cells with BCR-ABL tyrosine kinase inhibitors, including imatinib, dasatinib, nilotinib and ponatinib, prevented activation of eIF2alpha kinases, protein kinase-like endoplasmic reticulum kinase (PERK) and general control nonderepressible 2, and downstream ATF4 induction during metabolic stress.	imatinib	87-95	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	176-224
30217442-4	2018	Treatment of CML-derived K562 cells with BCR-ABL tyrosine kinase inhibitors, including imatinib, dasatinib, nilotinib and ponatinib, prevented activation of eIF2alpha kinases, protein kinase-like endoplasmic reticulum kinase (PERK) and general control nonderepressible 2, and downstream ATF4 induction during metabolic stress.	imatinib	87-95	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	226-230
30217442-4	2018	Treatment of CML-derived K562 cells with BCR-ABL tyrosine kinase inhibitors, including imatinib, dasatinib, nilotinib and ponatinib, prevented activation of eIF2alpha kinases, protein kinase-like endoplasmic reticulum kinase (PERK) and general control nonderepressible 2, and downstream ATF4 induction during metabolic stress.	imatinib	87-95	eukaryotic translation initiation factor 2 alpha kinase 4	Homo sapiens	236-270
30217442-4	2018	Treatment of CML-derived K562 cells with BCR-ABL tyrosine kinase inhibitors, including imatinib, dasatinib, nilotinib and ponatinib, prevented activation of eIF2alpha kinases, protein kinase-like endoplasmic reticulum kinase (PERK) and general control nonderepressible 2, and downstream ATF4 induction during metabolic stress.	imatinib	87-95	activating transcription factor 4	Homo sapiens	287-291
30261468-0	2018	Targeting heme Oxygenase-1 with hybrid compounds to overcome Imatinib resistance in chronic myeloid leukemia cell lines.	imatinib	61-69	heme oxygenase 1	Homo sapiens	10-26
30261468-2	2018	Chronic myeloid leukemia (CML) is a blood cancer caused by pathological kinase activity of the BCR-ABL protein, currently treated with tyrosine kinase inhibitors (TKIs) such as Imatinib (IM).	imatinib	177-185	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
30410673-10	2018	Axl, a receptor tyrosine kinase, has previously been associated with imatinib and nilotinib resistance.	imatinib	69-77	AXL receptor tyrosine kinase	Homo sapiens	0-3
30138624-2	2018	The substrates and inhibitors of hOCT1 are structurally and physiochemically diverse and include some widely prescribed drugs (metformin and imatinib), vitamins (thiamine), and neurotransmitters (serotonin).	imatinib	141-149	solute carrier family 22 member 1	Homo sapiens	33-38
30291293-7	2018	Imatinib could inhibit ANKRD1 expression, resulting in restoration of the sensitivity to afatinib and osimertinib of EGFR-TKI-resistant cells.	imatinib	0-8	ankyrin repeat domain 1	Homo sapiens	23-29
30291293-7	2018	Imatinib could inhibit ANKRD1 expression, resulting in restoration of the sensitivity to afatinib and osimertinib of EGFR-TKI-resistant cells.	imatinib	0-8	epidermal growth factor receptor	Homo sapiens	117-121
30201265-13	2018	Biological assessment assays in two NKTCL cell lines revealed that a specific PDGFR antagonist, imatinib, inhibited cell viability, blocked cell cycle progression at G0/G1 stage and induced apoptosis.	imatinib	96-104	platelet derived growth factor receptor beta	Homo sapiens	78-83
30101284-2	2018	Mutations in these type III receptor tyrosine kinases (RTKs) account for over 85% of GIST cases, and the majority of KIT primary mutations respond to treatment with the tyrosine kinase inhibitor (TKI) imatinib.	imatinib	201-209	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	117-120
30082224-0	2018	Comparison of Frequency and Sensitivity of BCR-ABL1 Kinase Domain Mutations in Asian and White Patients With Imatinib-resistant Chronic-Phase Chronic Myeloid Leukemia.	imatinib	109-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-51
30086285-3	2018	Primary role of UGT2B17 in TG formation compared to UGT2B15 was confirmed by performing activity assays in UGT2B17 gene deletion samples and with a selective UGT2B17 inhibitor, imatinib.	imatinib	177-185	UDP glucuronosyltransferase family 2 member B17	Homo sapiens	16-23
30272826-8	2018	The tyrosine kinase inhibitors (TKIs) imatinib and dasatinib repressed SLC2A5 expression and the cell uptake of fructose.	imatinib	38-46	solute carrier family 2 (facilitated glucose transporter), member 5	Mus musculus	71-77
30268485-0	2018	Carving out another slice of the pie: Exceptional response to single agent imatinib in an asian female never-smoker with advanced NSCLC with a de-novo PDGFR-alpha N848 K mutation.	imatinib	75-83	platelet derived growth factor receptor alpha	Homo sapiens	151-162
30402857-4	2018	We detected the expression of HOXA11-AS in vascular smooth muscle cells (VSMCs) treated with platelet-derived growth factor (PDGF) or PDGF inhibitor imatinib, respectively.	imatinib	149-157	HOXA11 antisense RNA	Homo sapiens	30-39
30402857-13	2018	PDGF could upregulate HOXA11-AS expression in VSMCs, which was reversed by PDGF inhibitor imatinib.	imatinib	90-98	homeobox A11, opposite strand	Mus musculus	22-31
30149002-0	2018	miR-125a-5p regulation increases phosphorylation of FAK that contributes to imatinib resistance in gastrointestinal stromal tumors.	imatinib	76-84	protein tyrosine kinase 2	Homo sapiens	52-55
30149002-3	2018	We have previously shown that miR-125a-5p and its mRNA target PTPN18 modulate imatinib response in GIST cells.	imatinib	78-86	protein tyrosine phosphatase non-receptor type 18	Homo sapiens	62-68
30149002-4	2018	Herein, we evaluated phosphorylated FAK (pFAK) as a candidate downstream target of PTPN18 and the possible association of this regulation with imatinib resistance in GIST.	imatinib	143-151	protein tyrosine kinase 2	Homo sapiens	36-39
30149002-7	2018	Clinical associations of FAK and pFAK expression with imatinib resistance, KIT mutation and patient outcome were assessed by Fisher"s exact test or log-rank test.	imatinib	54-62	protein tyrosine kinase 2	Homo sapiens	25-28
30268485-4	2018	Amino acid sequence alignment confirmed homology to the imatinib-sensitive KIT N822 K activation loop mutation observed in GIST.	imatinib	56-64	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	75-78
30237472-1	2018	There is a controversy in literature as to whether c-Abl is crucial for the induction of TAp63-mediated apoptosis and whether that inhibition of c-Abl with imatinib, which was designed to inhibit the oncogenic kinase BCR-ABL and c-kit, protects oocytes from chemotherapy-induced apoptosis in mice.	imatinib	156-164	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	145-150
30111113-4	2018	At drug substance concentrations up to 250 muM, imatinib was mainly engulfed within the core of &gt;110 nm in diameter vesicles.	imatinib	48-56	latexin	Homo sapiens	43-46
30697609-5	2019	The tyrosine kinase inhibitor imatinib, which selectively inhibits tyrosine kinase KIT, has shown substantial clinical benefit for patients with GIST.	imatinib	30-38	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	83-86
30697609-6	2019	In clinical trials, imatinib treatment resulted in response rates of 40%-55% and longer progression-free survival for patients with a KIT-positive unresectable or metastatic GIST.	imatinib	20-28	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	134-137
29453608-9	2018	The pro-apoptotic proteins, Bax, Bad, Apaf-1, and Caspase-3 were highly diminished in DMBA and DMBA + LPS groups which were recovered with Imatinib treatment.	imatinib	139-147	apoptotic peptidase activating factor 1	Rattus norvegicus	38-44
29453608-9	2018	The pro-apoptotic proteins, Bax, Bad, Apaf-1, and Caspase-3 were highly diminished in DMBA and DMBA + LPS groups which were recovered with Imatinib treatment.	imatinib	139-147	caspase 3	Rattus norvegicus	50-59
30237472-3	2018	We therefore aimed to explore whether genomic damage induced by chemotherapy drug cisplatin activates c-Abl along with TAp63 and the inhibition of c-Abl with imatinib prevents cisplatin-induced oocyte death and follicle loss in human ovary.	imatinib	158-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-152
30298093-3	2018	Drug resistance to Imatinib Mesylate (c-KIT inhibitor) has emerged.	imatinib	19-36	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	38-43
29908887-2	2018	Indeed, successes of drugs targeting genetic alterations in tumors, such as imatinib that targets BCR-ABL in chronic myelogenous leukemia, have demonstrated the power of this approach.	imatinib	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
30249101-11	2018	Among the five miRNAs, the overexpression of hsa-miR-28-5p and hsa-miR-125a-5p had significant correlation to imatinib resistance or imatinib sensitivity in GIST patients.	imatinib	110-118	microRNA 28	Homo sapiens	45-55
30249101-11	2018	Among the five miRNAs, the overexpression of hsa-miR-28-5p and hsa-miR-125a-5p had significant correlation to imatinib resistance or imatinib sensitivity in GIST patients.	imatinib	133-141	microRNA 28	Homo sapiens	45-55
30249101-12	2018	Hsa-miR-28-5p and hsa-miR-125a-5p may be involved in the development and progression of GIST, and they may be able to serve as prognostic markers for imatinib-response in GIST patients.	imatinib	150-158	microRNA 28	Homo sapiens	0-10
28027118-0	2018	Gain of TP53 Mutation in Imatinib-treated SDH-Deficient Gastrointestinal Stromal Tumor and Clinical Utilization of Targeted Next-generation Sequencing Panel for Therapeutic Decision Support.	imatinib	25-33	tumor protein p53	Homo sapiens	8-12
29694642-1	2018	The Japan Adult Leukemia Study Group (JALSG) Ph+ALL202 study reported a high complete remission (CR) rate for Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ALL) patients treated with imatinib-combined chemotherapy.	imatinib	203-211	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	97-99
29694642-12	2018	The higher rate of CR upon imatinib use may have contributed to these improvements.	imatinib	27-35	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	19-21
29807053-4	2018	Pharmacological inhibition of c-Abl kinase by imatinib, nilotinib and GZD824, knock-down of c-Abl using siRNA, and the use of c-Abl kinase-dead drastically reduces tyrosine phosphorylation of YY1.	imatinib	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-35
29943365-2	2018	In this study, we investigated the effect of TKIs on the levels of plasma TPO concentration in patients with well-controlled chronic myeloid leukemia receiving imatinib or dasatinib and those in treatment-free remission (TFR).	imatinib	160-168	thrombopoietin	Homo sapiens	74-77
29809305-0	2018	Down-regulation of CD19 expression inhibits proliferation, adhesion, migration and invasion and promotes apoptosis and the efficacy of chemotherapeutic agents and imatinib in SUP-B15 cells.	imatinib	163-171	CD19 molecule	Homo sapiens	19-23
29809305-6	2018	Down-regulation of CD19 could inhibit cell proliferation, adhesion, migration and invasion, and increase cell apoptosis and the efficacy of chemotherapeutic agents and imatinib in SUP-B15 cells.	imatinib	168-176	CD19 molecule	Homo sapiens	19-23
29764854-2	2018	Treatment with the small-molecule inhibitors imatinib, sunitinib, and regorafenib resulted in resistance (c-KIT mutant tumors) or limited activity (c-KIT wild-type tumors).	imatinib	45-53	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	106-111
29764854-2	2018	Treatment with the small-molecule inhibitors imatinib, sunitinib, and regorafenib resulted in resistance (c-KIT mutant tumors) or limited activity (c-KIT wild-type tumors).	imatinib	45-53	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	148-153
29957833-0	2018	Inhibition of stromal-interacting molecule 1-mediated store-operated Ca2+ entry as a novel strategy for the treatment of acquired imatinib-resistant gastrointestinal stromal tumors.	imatinib	130-138	stromal interaction molecule 1	Homo sapiens	14-44
29957833-3	2018	In the present study, we reported a novel mechanism for the acquired resistance to imatinib, which was induced by enhanced Ca2+ influx via stromal-interacting molecule 1 (STIM1)-mediated store-operated Ca2+ entry (SOCE).	imatinib	83-91	stromal interaction molecule 1	Homo sapiens	139-169
29957833-3	2018	In the present study, we reported a novel mechanism for the acquired resistance to imatinib, which was induced by enhanced Ca2+ influx via stromal-interacting molecule 1 (STIM1)-mediated store-operated Ca2+ entry (SOCE).	imatinib	83-91	stromal interaction molecule 1	Homo sapiens	171-176
29957833-4	2018	We found that the STIM1 expression level was related to the acquired resistance to imatinib in our studied cohort.	imatinib	83-91	stromal interaction molecule 1	Homo sapiens	18-23
29957833-5	2018	The function of STIM1 in imatinib-resistant GIST cells was also confirmed both in vivo and in vitro.	imatinib	25-33	stromal interaction molecule 1	Homo sapiens	16-21
29957833-6	2018	The results showed that STIM1 overexpression contributed to SOCE and drug response in imatinib-sensitive GIST cells.	imatinib	86-94	stromal interaction molecule 1	Homo sapiens	24-29
29943365-7	2018	However, imatinib and dasatinib intake increased the levels of TPO in these patients (p = 0.0024, dasatinib; p = 0.0098, imatinib).	imatinib	9-17	thrombopoietin	Homo sapiens	63-66
29957833-7	2018	Blockage of SOCE by STIM1 knockdown suppressed the proliferation of imatinib-resistant GIST cell lines and xenografts.	imatinib	68-76	stromal interaction molecule 1	Homo sapiens	20-25
29943365-7	2018	However, imatinib and dasatinib intake increased the levels of TPO in these patients (p = 0.0024, dasatinib; p = 0.0098, imatinib).	imatinib	121-129	thrombopoietin	Homo sapiens	63-66
30191913-2	2018	There has been recent research into the neuroprotective role and modulation of dopaminergic neurones by imatinib through the abl pathway in Parkinson"s disease (PD).	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-128
29663362-0	2018	CD69 partially inhibits apoptosis and erythroid differentiation via CD24, and their knockdown increase imatinib sensitivity in BCR-ABL-positive cells.	imatinib	103-111	CD69 molecule	Homo sapiens	0-4
29663362-0	2018	CD69 partially inhibits apoptosis and erythroid differentiation via CD24, and their knockdown increase imatinib sensitivity in BCR-ABL-positive cells.	imatinib	103-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
29663362-6	2018	CD69 knockdown partially increased apoptosis and expression of erythroid differentiation markers, alpha-globin, zeta-globin, and glycophorin A, and increased imatinib sensitivity in K562 and KU812 CML cells.	imatinib	158-166	CD69 molecule	Homo sapiens	0-4
29663362-9	2018	CD24 knockdown also partially increased apoptosis, erythroid differentiation, and imatinib sensitivity in K562 cells, whereas its overexpression inhibited the effects of CD69 knockdown on apoptosis, erythroid differentiation, and imatinib sensitivity in K562 cells.	imatinib	82-90	CD24 molecule	Homo sapiens	0-4
29663362-9	2018	CD24 knockdown also partially increased apoptosis, erythroid differentiation, and imatinib sensitivity in K562 cells, whereas its overexpression inhibited the effects of CD69 knockdown on apoptosis, erythroid differentiation, and imatinib sensitivity in K562 cells.	imatinib	230-238	CD24 molecule	Homo sapiens	0-4
29663362-10	2018	Imatinib-induced apoptosis and erythroid differentiation were also inhibited by CD69 or CD24 overexpression in BCR-ABL-expressing CML cell lines and CD34+ cells.	imatinib	0-8	CD69 molecule	Homo sapiens	80-84
29663362-10	2018	Imatinib-induced apoptosis and erythroid differentiation were also inhibited by CD69 or CD24 overexpression in BCR-ABL-expressing CML cell lines and CD34+ cells.	imatinib	0-8	CD24 molecule	Homo sapiens	88-92
29663362-10	2018	Imatinib-induced apoptosis and erythroid differentiation were also inhibited by CD69 or CD24 overexpression in BCR-ABL-expressing CML cell lines and CD34+ cells.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
29663362-12	2018	CD69 and CD24 partially inhibit apoptosis and erythroid differentiation in CML cells; thus, they may be potential targets to increase imatinib sensitivity.	imatinib	134-142	CD69 molecule	Homo sapiens	0-4
29663362-12	2018	CD69 and CD24 partially inhibit apoptosis and erythroid differentiation in CML cells; thus, they may be potential targets to increase imatinib sensitivity.	imatinib	134-142	CD24 molecule	Homo sapiens	9-13
30186389-0	2018	Decreased expression of microRNA-214 contributes to imatinib mesylate resistance of chronic myeloid leukemia patients by upregulating ABCB1 gene expression.	imatinib	52-69	microRNA 214	Homo sapiens	24-36
30186389-0	2018	Decreased expression of microRNA-214 contributes to imatinib mesylate resistance of chronic myeloid leukemia patients by upregulating ABCB1 gene expression.	imatinib	52-69	ATP binding cassette subfamily B member 1	Homo sapiens	134-139
30186389-1	2018	The aim of the present study was to determine the expression of adenosine triphosphate binding cassette subfamily B member 1 (ABCB1) gene and its protein P-glycoprotein (PGP) in bone marrow mononuclear cells from chronic myeloid leukemia (CML) patients with imatinib mesylate (IM) resistance, or IM-resistant CML K562 cells.	imatinib	258-275	ATP binding cassette subfamily B member 1	Homo sapiens	64-124
30186389-1	2018	The aim of the present study was to determine the expression of adenosine triphosphate binding cassette subfamily B member 1 (ABCB1) gene and its protein P-glycoprotein (PGP) in bone marrow mononuclear cells from chronic myeloid leukemia (CML) patients with imatinib mesylate (IM) resistance, or IM-resistant CML K562 cells.	imatinib	258-275	ATP binding cassette subfamily B member 1	Homo sapiens	126-131
30186389-1	2018	The aim of the present study was to determine the expression of adenosine triphosphate binding cassette subfamily B member 1 (ABCB1) gene and its protein P-glycoprotein (PGP) in bone marrow mononuclear cells from chronic myeloid leukemia (CML) patients with imatinib mesylate (IM) resistance, or IM-resistant CML K562 cells.	imatinib	258-275	ATP binding cassette subfamily B member 1	Homo sapiens	170-173
30241197-0	2018	Imatinib-Associated Tumor Lysis Syndrome in a Patient With Myeloid Neoplasm With Eosinophilia and PDGFRA Rearrangement: A Case Report and Review of the Literature.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	98-104
30262695-0	2018	Genetic variations in influx transporter gene SLC22A1 are associated with clinical responses to imatinib mesylate among Malaysian chronic myeloid leukaemia patients.	imatinib	96-113	solute carrier family 22 member 1	Homo sapiens	46-53
32300425-4	2018	We report a case of p190 BCR-ABL CML characterized by moderate monocytosis, without deep molecular response (DMR) to an initial imatinib treatment.	imatinib	128-136	contactin associated protein 1	Homo sapiens	20-24
30210745-7	2018	Imatinib-responsive BCR-ABL1 negative HE/HES constitute 7.1% in our patients.	imatinib	0-8	BCR activator of RhoGEF and GTPase	Homo sapiens	20-28
30118898-0	2018	Imatinib resistance due to a novel and rare class of mutation at position S348 (1043nt C A) of Bcr/Abl gene in a chronic myeloid leukemia patient.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
29701267-0	2018	Costunolide promotes imatinib-induced apoptosis in chronic myeloid leukemia cells via the Bcr/Abl-Stat5 pathway.	imatinib	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
30055408-9	2018	Furthermore, inhibition of IRE1alpha/NLRP1 pathway sensitized CML cells to imatinib-mediated apoptosis.	imatinib	75-83	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	27-36
30055408-9	2018	Furthermore, inhibition of IRE1alpha/NLRP1 pathway sensitized CML cells to imatinib-mediated apoptosis.	imatinib	75-83	NLR family pyrin domain containing 1	Homo sapiens	37-42
30055408-12	2018	Collectively, this study demonstrated that the IRE1alpha/CREB/NLRP1 pathway contributes to the progression of CML and the development of imatinib resistance.	imatinib	137-145	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	47-56
30055408-12	2018	Collectively, this study demonstrated that the IRE1alpha/CREB/NLRP1 pathway contributes to the progression of CML and the development of imatinib resistance.	imatinib	137-145	cAMP responsive element binding protein 1	Homo sapiens	57-61
30055408-12	2018	Collectively, this study demonstrated that the IRE1alpha/CREB/NLRP1 pathway contributes to the progression of CML and the development of imatinib resistance.	imatinib	137-145	NLR family pyrin domain containing 1	Homo sapiens	62-67
29701267-5	2018	Costunolide promoted imatinib-induced apoptosis via the Bcr/Abl-signal transducer and activator of transcription 5 pathway.	imatinib	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
30054832-5	2018	Unexpectedly, imatinib activates rather than inhibits the phosphorylation of STAT3 in K562 cells.	imatinib	14-22	signal transducer and activator of transcription 3	Homo sapiens	77-82
30210447-1	2018	Background: Imatinib, a tyrosine kinase inhibitor, causes growth failure in children with chronic myeloid leukemia probably by targeting the growth hormone (GH)/insulin like growth factor-1 (IGF-1) axis.	imatinib	12-20	growth hormone 1	Homo sapiens	141-155
30165626-5	2018	In this study, STI-571, a c-Abl inhibitor, rescued the ALP function through facilitating the nuclear translocation of TFEB and protected against MPP+-induced neuronal cell death.	imatinib	15-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-31
30165626-5	2018	In this study, STI-571, a c-Abl inhibitor, rescued the ALP function through facilitating the nuclear translocation of TFEB and protected against MPP+-induced neuronal cell death.	imatinib	15-22	transcription factor EB	Homo sapiens	118-122
30153828-0	2018	The c-Myc-regulated lncRNA NEAT1 and paraspeckles modulate imatinib-induced apoptosis in CML cells.	imatinib	59-67	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	4-9
30153828-0	2018	The c-Myc-regulated lncRNA NEAT1 and paraspeckles modulate imatinib-induced apoptosis in CML cells.	imatinib	59-67	nuclear paraspeckle assembly transcript 1	Homo sapiens	27-32
30240612-6	2018	Preventing PDGFRalpha activation using imatinib, or through PDGF-A or PDGFRalpha deficiency, inhibits collagen expression in Nck1-deficient preadipocytes.	imatinib	39-47	platelet derived growth factor receptor alpha	Homo sapiens	11-21
30240612-6	2018	Preventing PDGFRalpha activation using imatinib, or through PDGF-A or PDGFRalpha deficiency, inhibits collagen expression in Nck1-deficient preadipocytes.	imatinib	39-47	NCK adaptor protein 1	Homo sapiens	125-129
30240612-7	2018	Finally, imatinib rescues differentiation of Nck1-deficient preadipocytes.	imatinib	9-17	NCK adaptor protein 1	Homo sapiens	45-49
30154435-0	2018	Novel AF1q/MLLT11 favorably affects imatinib resistance and cell survival in chronic myeloid leukemia.	imatinib	36-44	MLLT11 transcription factor 7 cofactor	Homo sapiens	6-10
30154435-0	2018	Novel AF1q/MLLT11 favorably affects imatinib resistance and cell survival in chronic myeloid leukemia.	imatinib	36-44	MLLT11 transcription factor 7 cofactor	Homo sapiens	11-17
30154435-6	2018	Knockdown of AF1q enhanced imatinib sensitivity, induced apoptosis, and suppressed growth in CML cells.	imatinib	27-35	MLLT11 transcription factor 7 cofactor	Homo sapiens	13-17
30154435-7	2018	Moreover, AF1q deficiency sensitized CD34+ CML cells to imatinib.	imatinib	56-64	MLLT11 transcription factor 7 cofactor	Homo sapiens	10-14
30154435-8	2018	In contrast, upregulation of AF1q promoted cell survival, protected CML cells from imatinib-induced apoptosis, and increased engraftment of CML cells in vivo.	imatinib	83-91	MLLT11 transcription factor 7 cofactor	Homo sapiens	29-33
30154435-10	2018	Importantly, AF1q contributes to imatinib-resistance in CML by regulating the expression of CD44.	imatinib	33-41	MLLT11 transcription factor 7 cofactor	Homo sapiens	13-17
30154435-11	2018	These findings reveal a novel BCR-ABL-independent pathway, AF1q/CD44, involves imatinib resistance in CML, thus representing a potential therapeutic target for imatinib-resistant CML patients.	imatinib	79-87	MLLT11 transcription factor 7 cofactor	Homo sapiens	59-63
30154435-11	2018	These findings reveal a novel BCR-ABL-independent pathway, AF1q/CD44, involves imatinib resistance in CML, thus representing a potential therapeutic target for imatinib-resistant CML patients.	imatinib	160-168	MLLT11 transcription factor 7 cofactor	Homo sapiens	59-63
30210447-1	2018	Background: Imatinib, a tyrosine kinase inhibitor, causes growth failure in children with chronic myeloid leukemia probably by targeting the growth hormone (GH)/insulin like growth factor-1 (IGF-1) axis.	imatinib	12-20	insulin like growth factor 1	Homo sapiens	161-189
30210447-1	2018	Background: Imatinib, a tyrosine kinase inhibitor, causes growth failure in children with chronic myeloid leukemia probably by targeting the growth hormone (GH)/insulin like growth factor-1 (IGF-1) axis.	imatinib	12-20	insulin like growth factor 1	Homo sapiens	191-196
30210447-3	2018	Materials and Methods: The expression pattern of imatinib"s targets (c-kit, VEGF, and PDGFR-alpha/beta) was studied using immunohistochemistry and immunoblotting 157 giant (&gt;=4 cm) pituitary adenomas (121 non-functioning pituitary adenomas, 32 somatotropinomas, and four prolactinomas) and compared to normal pituitary (n = 4) obtained at autopsy.	imatinib	49-57	vascular endothelial growth factor A	Rattus norvegicus	76-80
30210447-3	2018	Materials and Methods: The expression pattern of imatinib"s targets (c-kit, VEGF, and PDGFR-alpha/beta) was studied using immunohistochemistry and immunoblotting 157 giant (&gt;=4 cm) pituitary adenomas (121 non-functioning pituitary adenomas, 32 somatotropinomas, and four prolactinomas) and compared to normal pituitary (n = 4) obtained at autopsy.	imatinib	49-57	platelet derived growth factor receptor alpha	Rattus norvegicus	86-97
30210447-8	2018	The receptor tyrosine kinase array showed that imatinib inhibits GH signaling via PDGFR-beta pathway.	imatinib	47-55	platelet derived growth factor receptor beta	Rattus norvegicus	82-92
30024740-6	2018	Moreover, the inactivation of both Abl and Src by the inhibitor imatinib, dasatinib, and ponatinib was simultaneously traced, giving a whole picture of the competition behavior between the kinases for binding therapeutic molecules.	imatinib	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
30224936-1	2018	Objectives: Sunitinib (a second-line chemotherapeutic agent that inhibits multiple kinases, including KIT and PDGFR) is widely used in imatinib-resistant patients with gastrointestinal stromal tumors (GISTs).	imatinib	135-143	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	102-105
30153828-7	2018	Knockdown of NEAT1 could promote imatinib (IM)-induced apoptosis, and we demonstrated that the NEAT1-binding paraspeckle protein splicing factor proline/glutamine-rich (SFPQ) is required for NEAT1-mediated apoptosis in K562 cells.	imatinib	33-41	nuclear paraspeckle assembly transcript 1	Homo sapiens	13-18
30153828-7	2018	Knockdown of NEAT1 could promote imatinib (IM)-induced apoptosis, and we demonstrated that the NEAT1-binding paraspeckle protein splicing factor proline/glutamine-rich (SFPQ) is required for NEAT1-mediated apoptosis in K562 cells.	imatinib	33-41	nuclear paraspeckle assembly transcript 1	Homo sapiens	95-100
30153828-7	2018	Knockdown of NEAT1 could promote imatinib (IM)-induced apoptosis, and we demonstrated that the NEAT1-binding paraspeckle protein splicing factor proline/glutamine-rich (SFPQ) is required for NEAT1-mediated apoptosis in K562 cells.	imatinib	33-41	splicing factor proline and glutamine rich	Homo sapiens	169-173
30153828-7	2018	Knockdown of NEAT1 could promote imatinib (IM)-induced apoptosis, and we demonstrated that the NEAT1-binding paraspeckle protein splicing factor proline/glutamine-rich (SFPQ) is required for NEAT1-mediated apoptosis in K562 cells.	imatinib	33-41	nuclear paraspeckle assembly transcript 1	Homo sapiens	95-100
30024740-6	2018	Moreover, the inactivation of both Abl and Src by the inhibitor imatinib, dasatinib, and ponatinib was simultaneously traced, giving a whole picture of the competition behavior between the kinases for binding therapeutic molecules.	imatinib	64-72	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	43-46
30103756-3	2018	Our study has finally revealed 9 genes (DBP, NR3C1, TCF12, TP53, ZNF12, SOCS6, ZFP36, ACYP1, and DRD1) involved in imatinib-resistant GIST-T1 cells.	imatinib	115-123	D-box binding PAR bZIP transcription factor	Homo sapiens	40-43
30103756-3	2018	Our study has finally revealed 9 genes (DBP, NR3C1, TCF12, TP53, ZNF12, SOCS6, ZFP36, ACYP1, and DRD1) involved in imatinib-resistant GIST-T1 cells.	imatinib	115-123	nuclear receptor subfamily 3 group C member 1	Homo sapiens	45-50
30103756-3	2018	Our study has finally revealed 9 genes (DBP, NR3C1, TCF12, TP53, ZNF12, SOCS6, ZFP36, ACYP1, and DRD1) involved in imatinib-resistant GIST-T1 cells.	imatinib	115-123	transcription factor 12	Homo sapiens	52-57
30103756-3	2018	Our study has finally revealed 9 genes (DBP, NR3C1, TCF12, TP53, ZNF12, SOCS6, ZFP36, ACYP1, and DRD1) involved in imatinib-resistant GIST-T1 cells.	imatinib	115-123	tumor protein p53	Homo sapiens	59-63
30103756-3	2018	Our study has finally revealed 9 genes (DBP, NR3C1, TCF12, TP53, ZNF12, SOCS6, ZFP36, ACYP1, and DRD1) involved in imatinib-resistant GIST-T1 cells.	imatinib	115-123	zinc finger protein 12	Homo sapiens	65-70
30103756-3	2018	Our study has finally revealed 9 genes (DBP, NR3C1, TCF12, TP53, ZNF12, SOCS6, ZFP36, ACYP1, and DRD1) involved in imatinib-resistant GIST-T1 cells.	imatinib	115-123	suppressor of cytokine signaling 6	Homo sapiens	72-77
30103756-3	2018	Our study has finally revealed 9 genes (DBP, NR3C1, TCF12, TP53, ZNF12, SOCS6, ZFP36, ACYP1, and DRD1) involved in imatinib-resistant GIST-T1 cells.	imatinib	115-123	ZFP36 ring finger protein	Homo sapiens	79-84
30103756-3	2018	Our study has finally revealed 9 genes (DBP, NR3C1, TCF12, TP53, ZNF12, SOCS6, ZFP36, ACYP1, and DRD1) involved in imatinib-resistant GIST-T1 cells.	imatinib	115-123	acylphosphatase 1	Homo sapiens	86-91
30103756-3	2018	Our study has finally revealed 9 genes (DBP, NR3C1, TCF12, TP53, ZNF12, SOCS6, ZFP36, ACYP1, and DRD1) involved in imatinib-resistant GIST-T1 cells.	imatinib	115-123	dopamine receptor D1	Homo sapiens	97-101
30103756-4	2018	TP53 and SOCS6 may be the most promising candidate genes for imatinib-resistance due to the possible signaling pathway, such as apoptosis pathway and Wnt signaling pathway, JAK-STAT signaling pathway.	imatinib	61-69	tumor protein p53	Homo sapiens	0-4
30103756-4	2018	TP53 and SOCS6 may be the most promising candidate genes for imatinib-resistance due to the possible signaling pathway, such as apoptosis pathway and Wnt signaling pathway, JAK-STAT signaling pathway.	imatinib	61-69	suppressor of cytokine signaling 6	Homo sapiens	9-14
30279723-7	2018	Results: The layer-by-layer hybrid nanoparticles, which were pH-sensitive, enabled the release of IR-780 dye for NIR-induced photothermal and photodynamic effects, and the release of imatinib-loaded glucocorticoid-induced TNF receptor family-related protein/poly(lactic-co-glycolic acid) (GITR-PLGA) nanoparticles to initiate antitumor immunotherapy.	imatinib	183-191	tumor necrosis factor receptor superfamily, member 18	Mus musculus	289-293
30103756-5	2018	It is necessary to perform more studies to discover novel targets in imatinib-resistant GIST, including DBP, NR3C1, TCF12, ZNF12, ZFP36, ACYP1 and DRD1.	imatinib	69-77	D-box binding PAR bZIP transcription factor	Homo sapiens	104-107
29890129-0	2018	microRNA-199a/b-5p enhance imatinib efficacy via repressing WNT2 signaling-mediated protective autophagy in imatinib-resistant chronic myeloid leukemia cells.	imatinib	27-35	glycoprotein hormone subunit beta 5	Homo sapiens	14-18
30091999-10	2018	Moreover, a 4-day FICZ treatment was sufficient to significantly reduce the clonogenic potential of CML CD34+ cells and this effect was synergized by Imatinib and Dasatinib treatments.	imatinib	150-158	CD34 molecule	Homo sapiens	104-108
29859988-2	2018	Although direct BCR-ABL inhibitors, such as imatinib, were initially successful in the treatment of leukemia, many patients developed drug resistance over time due to the gatekeeper mutation of BCR-ABL T315I.	imatinib	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
30159192-5	2018	In addition, histological analysis of the tumor for macroscopic and microscopic characteristics including mitotic index and c-Kit/CD117 status should be obtained to guide adjuvant therapy with imatinib mesylate.	imatinib	193-210	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	124-129
30159192-5	2018	In addition, histological analysis of the tumor for macroscopic and microscopic characteristics including mitotic index and c-Kit/CD117 status should be obtained to guide adjuvant therapy with imatinib mesylate.	imatinib	193-210	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	130-135
28448384-8	2018	For patients on imatinib before surgery, radiographic response was predictive of PFS from time of surgery (RD 36 months, SD 30 months, UPD 11 months, MPD 6 months; P &lt; 0.001) and from imatinib initiation (RD 71 months, SD 51 months, UPD 47 months, MPD 33 months; P &lt; 0.001).	imatinib	16-24	leucine zipper protein 6	Homo sapiens	150-155
29890129-0	2018	microRNA-199a/b-5p enhance imatinib efficacy via repressing WNT2 signaling-mediated protective autophagy in imatinib-resistant chronic myeloid leukemia cells.	imatinib	27-35	Wnt family member 2	Homo sapiens	60-64
29890129-0	2018	microRNA-199a/b-5p enhance imatinib efficacy via repressing WNT2 signaling-mediated protective autophagy in imatinib-resistant chronic myeloid leukemia cells.	imatinib	108-116	glycoprotein hormone subunit beta 5	Homo sapiens	14-18
29890129-0	2018	microRNA-199a/b-5p enhance imatinib efficacy via repressing WNT2 signaling-mediated protective autophagy in imatinib-resistant chronic myeloid leukemia cells.	imatinib	108-116	Wnt family member 2	Homo sapiens	60-64
32721103-0	2018	Aberrant DNA methylation at HOXA4 and HOXA5 genes are associated with resistance to imatinib mesylate among chronic myeloid leukemia patients.	imatinib	84-92	homeobox A4	Homo sapiens	28-33
30007460-4	2018	The discovery of KIT mutations as central to the pathobiology of mastocytosis has prompted development of KIT-targeted agents, including imatinib and midostaurin (approved medications for patients with advanced systemic mastocytosis), and drugs in development, like KIT D816V-specific inhibitor avapritinib.	imatinib	137-145	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	17-20
32721103-0	2018	Aberrant DNA methylation at HOXA4 and HOXA5 genes are associated with resistance to imatinib mesylate among chronic myeloid leukemia patients.	imatinib	84-92	homeobox A5	Homo sapiens	38-43
32721103-3	2018	However, development of resistance to imatinib mesylate as a result of BCR-ABL dependent and BCR-ABL independent mechanisms has emerged as a daunting problem in the management of CML patients.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
32721103-3	2018	However, development of resistance to imatinib mesylate as a result of BCR-ABL dependent and BCR-ABL independent mechanisms has emerged as a daunting problem in the management of CML patients.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
32721103-5	2018	AIM: To investigate the correlation of HOXA4 and HOXA5 promoter DNA hypermethylation with imatinib resistance among CML patients.	imatinib	90-98	homeobox A4	Homo sapiens	39-44
32721103-5	2018	AIM: To investigate the correlation of HOXA4 and HOXA5 promoter DNA hypermethylation with imatinib resistance among CML patients.	imatinib	90-98	homeobox A5	Homo sapiens	49-54
32721103-10	2018	Chronic myeloid leukemia patients with >=63% HOXA4 and HOXA5 methylation level were shown to have 3.78 and 3.95 times the odds, respectively, to acquire resistance to imatinib.	imatinib	167-175	homeobox A4	Homo sapiens	45-50
32721103-10	2018	Chronic myeloid leukemia patients with >=63% HOXA4 and HOXA5 methylation level were shown to have 3.78 and 3.95 times the odds, respectively, to acquire resistance to imatinib.	imatinib	167-175	homeobox A5	Homo sapiens	55-60
32721103-12	2018	CONCLUSION: Hypermethylation of the HOXA4 and HOXA5 promoter is correlated with imatinib resistance and with further investigation, it could be a potential epigenetic biomarker in supplement to the BCR-ABL gene mutation in predicting imatinib treatment response among CML patients but could not be considered as a prognostic marker.	imatinib	80-88	homeobox A4	Homo sapiens	36-41
32721103-12	2018	CONCLUSION: Hypermethylation of the HOXA4 and HOXA5 promoter is correlated with imatinib resistance and with further investigation, it could be a potential epigenetic biomarker in supplement to the BCR-ABL gene mutation in predicting imatinib treatment response among CML patients but could not be considered as a prognostic marker.	imatinib	80-88	homeobox A5	Homo sapiens	46-51
32721103-12	2018	CONCLUSION: Hypermethylation of the HOXA4 and HOXA5 promoter is correlated with imatinib resistance and with further investigation, it could be a potential epigenetic biomarker in supplement to the BCR-ABL gene mutation in predicting imatinib treatment response among CML patients but could not be considered as a prognostic marker.	imatinib	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	198-205
32721103-12	2018	CONCLUSION: Hypermethylation of the HOXA4 and HOXA5 promoter is correlated with imatinib resistance and with further investigation, it could be a potential epigenetic biomarker in supplement to the BCR-ABL gene mutation in predicting imatinib treatment response among CML patients but could not be considered as a prognostic marker.	imatinib	234-242	homeobox A4	Homo sapiens	36-41
32721103-12	2018	CONCLUSION: Hypermethylation of the HOXA4 and HOXA5 promoter is correlated with imatinib resistance and with further investigation, it could be a potential epigenetic biomarker in supplement to the BCR-ABL gene mutation in predicting imatinib treatment response among CML patients but could not be considered as a prognostic marker.	imatinib	234-242	homeobox A5	Homo sapiens	46-51
29733872-10	2018	The messenger RNA expression of two of these genes (DNM3 and LIMS1) was found to be associated with the absence of major cytogenetic response after 1 year of imatinib therapy.	imatinib	158-166	dynamin 3	Homo sapiens	52-56
29733872-10	2018	The messenger RNA expression of two of these genes (DNM3 and LIMS1) was found to be associated with the absence of major cytogenetic response after 1 year of imatinib therapy.	imatinib	158-166	LIM zinc finger domain containing 1	Homo sapiens	61-66
30357053-10	2018	However, after Imatinib treatment NKp30 isoform mRNA levels significantly increase in BM samples, indicating that Imatinib mesylate exerted an off-target effect on NK cells in vivo.	imatinib	15-23	natural cytotoxicity triggering receptor 3	Homo sapiens	34-39
29885053-5	2018	Our current study shows that SH3BP2 is expressed in primary tumors and cell lines from GIST patients and that SH3BP2 silencing leads to a downregulation of oncogenic KIT and PDGFRA expression and an increase in apoptosis in imatinib-sensitive and imatinib-resistant GIST cells.	imatinib	224-232	SH3 domain binding protein 2	Homo sapiens	29-35
29885053-5	2018	Our current study shows that SH3BP2 is expressed in primary tumors and cell lines from GIST patients and that SH3BP2 silencing leads to a downregulation of oncogenic KIT and PDGFRA expression and an increase in apoptosis in imatinib-sensitive and imatinib-resistant GIST cells.	imatinib	224-232	SH3 domain binding protein 2	Homo sapiens	110-116
29885053-5	2018	Our current study shows that SH3BP2 is expressed in primary tumors and cell lines from GIST patients and that SH3BP2 silencing leads to a downregulation of oncogenic KIT and PDGFRA expression and an increase in apoptosis in imatinib-sensitive and imatinib-resistant GIST cells.	imatinib	247-255	SH3 domain binding protein 2	Homo sapiens	29-35
29885053-5	2018	Our current study shows that SH3BP2 is expressed in primary tumors and cell lines from GIST patients and that SH3BP2 silencing leads to a downregulation of oncogenic KIT and PDGFRA expression and an increase in apoptosis in imatinib-sensitive and imatinib-resistant GIST cells.	imatinib	247-255	SH3 domain binding protein 2	Homo sapiens	110-116
29885053-9	2018	Furthermore, SH3BP2 silencing significantly reduces cell migration and tumor growth of imatinib-sensitive and imatinib-resistant cells in vivo.	imatinib	87-95	SH3 domain binding protein 2	Homo sapiens	13-19
29885053-9	2018	Furthermore, SH3BP2 silencing significantly reduces cell migration and tumor growth of imatinib-sensitive and imatinib-resistant cells in vivo.	imatinib	110-118	SH3 domain binding protein 2	Homo sapiens	13-19
29885053-10	2018	Altogether, SH3BP2 regulates KIT and PDGFRA expression and cell viability, indicating a role as a potential target in imatinib-sensitive and imatinib-resistant GISTs.	imatinib	118-126	SH3 domain binding protein 2	Homo sapiens	12-18
29885053-10	2018	Altogether, SH3BP2 regulates KIT and PDGFRA expression and cell viability, indicating a role as a potential target in imatinib-sensitive and imatinib-resistant GISTs.	imatinib	141-149	SH3 domain binding protein 2	Homo sapiens	12-18
30357053-10	2018	However, after Imatinib treatment NKp30 isoform mRNA levels significantly increase in BM samples, indicating that Imatinib mesylate exerted an off-target effect on NK cells in vivo.	imatinib	114-131	natural cytotoxicity triggering receptor 3	Homo sapiens	34-39
30045750-2	2018	Imatinib (gleevec, STI-571) is a selective inhibitor of BCR-ABL activity highly effective in the treatment of CML.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
30045750-2	2018	Imatinib (gleevec, STI-571) is a selective inhibitor of BCR-ABL activity highly effective in the treatment of CML.	imatinib	19-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
29724653-0	2018	A naphthalene diimide G-quadruplex ligand inhibits cell growth and down-regulates BCL-2 expression in an imatinib-resistant gastrointestinal cancer cell line.	imatinib	105-113	BCL2 apoptosis regulator	Homo sapiens	82-87
29724897-0	2018	Targeting HSP90 dimerization via the C terminus is effective in imatinib-resistant CML and lacks the heat shock response.	imatinib	64-72	heat shock protein 90 alpha family class A member 1	Homo sapiens	10-15
29724653-2	2018	They can be effectively treated by the kinase inhibitor imatinib, which locks the c-KIT kinase domain into an inactive conformation.	imatinib	56-64	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	82-87
29724653-3	2018	However resistance to imatinib, driven by active-site mutations, is a recurrent clinical challenge, which has been only partly met by the subsequent development of second and third-generation c-KIT inhibitors.	imatinib	22-30	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	192-197
30073206-0	2018	BCL2 inhibitor ABT-199 and JNK inhibitor SP600125 exhibit synergistic cytotoxicity against imatinib-resistant Ph+ ALL cells.	imatinib	91-99	BCL2 apoptosis regulator	Homo sapiens	0-4
30073206-0	2018	BCL2 inhibitor ABT-199 and JNK inhibitor SP600125 exhibit synergistic cytotoxicity against imatinib-resistant Ph+ ALL cells.	imatinib	91-99	mitogen-activated protein kinase 8	Homo sapiens	27-30
30038712-5	2018	Here, we demonstrate that forced expression of KLF5 in B-ALL cells bypasses the imatinib resistance which is not associated with mutations of BCR-ABL.	imatinib	80-88	Kruppel like factor 5	Homo sapiens	47-51
29777794-3	2018	The tLyp1 peptide-modified hybrid nanoparticles presented good stability and effective targeting to Treg cells, and they enhanced the effect of imatinib in downregulating Treg cell suppression through inhibition of STAT3 and STAT5 phosphorylation.	imatinib	144-152	signal transducer and activator of transcription 3	Homo sapiens	215-220
29777794-3	2018	The tLyp1 peptide-modified hybrid nanoparticles presented good stability and effective targeting to Treg cells, and they enhanced the effect of imatinib in downregulating Treg cell suppression through inhibition of STAT3 and STAT5 phosphorylation.	imatinib	144-152	signal transducer and activator of transcription 5A	Homo sapiens	225-230
29697413-2	2018	Our present data show that BGJ398, a selective fibroblast growth factor receptor (FGFR) inhibitor, sensitizes imatinib (IM)-resistant GIST cells with receptor tyrosine kinase (RTK) switch (loss of c-KIT/gain of pFGFR2a) to the low doses of topoisomerase II inhibitors - doxorubicin (Dox) and etoposide (Eto).	imatinib	110-118	ret proto-oncogene	Homo sapiens	150-174
29966518-2	2018	This can be accomplished by e.g. inhibiting TGF-beta1 and -beta3 or treating with Imatinib, which results in scarcer collagen fibril structure in xenografted human KAT-4/HT29 (KAT-4) colon adenocarcinoma.	imatinib	82-90	glutamic-oxaloacetic transaminase 2	Homo sapiens	164-169
29966518-2	2018	This can be accomplished by e.g. inhibiting TGF-beta1 and -beta3 or treating with Imatinib, which results in scarcer collagen fibril structure in xenografted human KAT-4/HT29 (KAT-4) colon adenocarcinoma.	imatinib	82-90	glutamic-oxaloacetic transaminase 2	Homo sapiens	176-181
29967475-4	2018	Imatinib is a tyrosine kinase inhibitor for BCR-ABL1 in Philadelphia chromosome-positive (Ph+) leukemia, and development of resistance due to kinase domain mutation is an important issue.	imatinib	0-8	BCR activator of RhoGEF and GTPase	Homo sapiens	44-52
29697413-2	2018	Our present data show that BGJ398, a selective fibroblast growth factor receptor (FGFR) inhibitor, sensitizes imatinib (IM)-resistant GIST cells with receptor tyrosine kinase (RTK) switch (loss of c-KIT/gain of pFGFR2a) to the low doses of topoisomerase II inhibitors - doxorubicin (Dox) and etoposide (Eto).	imatinib	110-118	ret proto-oncogene	Homo sapiens	176-179
29494307-13	2018	Our cell death assay revealed that SpCC cell death was induced by the anticancer drug imatinib, which is known to inhibit protein tyrosine kinase activity of ABL, platelet-derived growth factor receptor alpha (PDGFRalpha), and KIT.	imatinib	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-161
29679908-8	2018	Some CSF-1R/c-FMS inhibitors such as ABT-869, Imatinib, AG013736, JNJ-40346527, PLX3397, DCC-3014 and Ki20227 have been successfully used in these disease conditions.	imatinib	46-54	colony stimulating factor 1 receptor	Homo sapiens	5-11
29969914-6	2018	CONCLUSION: Adjuvant imatinib improves RFS of GIST with intermediate risk of recurrence, particularly in GIST with intestinal and rectal location or c-kit gene exon 11 deletion mutation.	imatinib	21-29	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	149-154
29620139-9	2018	In addition, PDGFR-beta, PDGF-BB, c-Kit and SCF were expressed in both breast carcinoma cell lines; PDGFR-beta and c-Kit, as imatinib targets, were downregulated in response to imatinib mesylate treatment.	imatinib	125-133	platelet derived growth factor receptor beta	Homo sapiens	100-110
29620139-9	2018	In addition, PDGFR-beta, PDGF-BB, c-Kit and SCF were expressed in both breast carcinoma cell lines; PDGFR-beta and c-Kit, as imatinib targets, were downregulated in response to imatinib mesylate treatment.	imatinib	125-133	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	115-120
29620139-9	2018	In addition, PDGFR-beta, PDGF-BB, c-Kit and SCF were expressed in both breast carcinoma cell lines; PDGFR-beta and c-Kit, as imatinib targets, were downregulated in response to imatinib mesylate treatment.	imatinib	177-194	platelet derived growth factor receptor beta	Homo sapiens	13-23
29620139-9	2018	In addition, PDGFR-beta, PDGF-BB, c-Kit and SCF were expressed in both breast carcinoma cell lines; PDGFR-beta and c-Kit, as imatinib targets, were downregulated in response to imatinib mesylate treatment.	imatinib	177-194	platelet derived growth factor receptor beta	Homo sapiens	100-110
29620139-9	2018	In addition, PDGFR-beta, PDGF-BB, c-Kit and SCF were expressed in both breast carcinoma cell lines; PDGFR-beta and c-Kit, as imatinib targets, were downregulated in response to imatinib mesylate treatment.	imatinib	177-194	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	115-120
29620139-11	2018	In conclusion, the antiproliferative, cytostatic and proapoptotic effects of imatinib mesylate may be the result of a reduction in the expression of c-Kit and PDGFR tyrosine kinase receptors, thus resulting in suppression of the corresponding ligand PDGF-BB.	imatinib	77-94	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	149-154
29620139-11	2018	In conclusion, the antiproliferative, cytostatic and proapoptotic effects of imatinib mesylate may be the result of a reduction in the expression of c-Kit and PDGFR tyrosine kinase receptors, thus resulting in suppression of the corresponding ligand PDGF-BB.	imatinib	77-94	platelet derived growth factor receptor beta	Homo sapiens	159-164
29730267-2	2018	Here, we showed that Imatinib significantly prevented macrophage M2-like polarization induced by IL-13 or IL-4 in vitro, as illustrated by reduced expression of cell surface marker CD206 and M2-like genes, including Arg1, Mgl2, Mrc1, CDH1, and CCL2.	imatinib	21-29	interleukin 13	Homo sapiens	97-102
29730267-2	2018	Here, we showed that Imatinib significantly prevented macrophage M2-like polarization induced by IL-13 or IL-4 in vitro, as illustrated by reduced expression of cell surface marker CD206 and M2-like genes, including Arg1, Mgl2, Mrc1, CDH1, and CCL2.	imatinib	21-29	interleukin 4	Homo sapiens	106-110
29730267-2	2018	Here, we showed that Imatinib significantly prevented macrophage M2-like polarization induced by IL-13 or IL-4 in vitro, as illustrated by reduced expression of cell surface marker CD206 and M2-like genes, including Arg1, Mgl2, Mrc1, CDH1, and CCL2.	imatinib	21-29	arginase 1	Homo sapiens	216-220
29730267-2	2018	Here, we showed that Imatinib significantly prevented macrophage M2-like polarization induced by IL-13 or IL-4 in vitro, as illustrated by reduced expression of cell surface marker CD206 and M2-like genes, including Arg1, Mgl2, Mrc1, CDH1, and CCL2.	imatinib	21-29	mannose receptor C-type 1	Homo sapiens	228-232
29730267-2	2018	Here, we showed that Imatinib significantly prevented macrophage M2-like polarization induced by IL-13 or IL-4 in vitro, as illustrated by reduced expression of cell surface marker CD206 and M2-like genes, including Arg1, Mgl2, Mrc1, CDH1, and CCL2.	imatinib	21-29	cadherin 1	Homo sapiens	234-238
29730267-2	2018	Here, we showed that Imatinib significantly prevented macrophage M2-like polarization induced by IL-13 or IL-4 in vitro, as illustrated by reduced expression of cell surface marker CD206 and M2-like genes, including Arg1, Mgl2, Mrc1, CDH1, and CCL2.	imatinib	21-29	C-C motif chemokine ligand 2	Homo sapiens	244-248
29730267-4	2018	Mechanistically, Imatinib inhibited STAT6 phosphorylation and nuclear translocation, resulting in the macrophage M2-like polarization arrest.	imatinib	17-25	signal transducer and activator of transcription 6	Homo sapiens	36-41
29620139-0	2018	Antiproliferative effects of imatinib mesylate on ZR-75-1 and MDA-MB-231 cell lines via PDGFR-beta, PDGF-BB, c-Kit and SCF expression.	imatinib	29-46	platelet derived growth factor receptor beta	Homo sapiens	88-98
29620139-0	2018	Antiproliferative effects of imatinib mesylate on ZR-75-1 and MDA-MB-231 cell lines via PDGFR-beta, PDGF-BB, c-Kit and SCF expression.	imatinib	29-46	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	109-114
29620139-0	2018	Antiproliferative effects of imatinib mesylate on ZR-75-1 and MDA-MB-231 cell lines via PDGFR-beta, PDGF-BB, c-Kit and SCF expression.	imatinib	29-46	KIT ligand	Homo sapiens	119-122
29620139-1	2018	Imatinib mesylate is an anti-neoplastic targeted chemotherapeutic agent, which can inhibit tyrosine kinase receptors, including BCR-ABL, platelet-derived growth factor receptors (PDGFRs) and c-Kit.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
29620139-1	2018	Imatinib mesylate is an anti-neoplastic targeted chemotherapeutic agent, which can inhibit tyrosine kinase receptors, including BCR-ABL, platelet-derived growth factor receptors (PDGFRs) and c-Kit.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	191-196
29977537-0	2018	FIP1L1-PDGFRA fusion-negative hypereosinophilic syndrome with uncommon cardiac involvement responding to imatinib treatment: A case report.	imatinib	105-113	factor interacting with PAPOLA and CPSF1	Homo sapiens	0-6
29977537-0	2018	FIP1L1-PDGFRA fusion-negative hypereosinophilic syndrome with uncommon cardiac involvement responding to imatinib treatment: A case report.	imatinib	105-113	platelet derived growth factor receptor alpha	Homo sapiens	7-13
29704617-7	2018	An activation segment exon 17 D816V mutation is one of the more common resistance mutations in Kit and this mutant is resistant to imatinib and sorafenib.	imatinib	131-139	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	95-98
29704617-10	2018	Based upon the X-ray crystallographic structures, imatinib, sunitinib, and ponatinib are Type II Kit inhibitors.	imatinib	50-58	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	97-100
29494307-13	2018	Our cell death assay revealed that SpCC cell death was induced by the anticancer drug imatinib, which is known to inhibit protein tyrosine kinase activity of ABL, platelet-derived growth factor receptor alpha (PDGFRalpha), and KIT.	imatinib	86-94	platelet derived growth factor receptor alpha	Homo sapiens	163-208
29494307-13	2018	Our cell death assay revealed that SpCC cell death was induced by the anticancer drug imatinib, which is known to inhibit protein tyrosine kinase activity of ABL, platelet-derived growth factor receptor alpha (PDGFRalpha), and KIT.	imatinib	86-94	platelet derived growth factor receptor alpha	Homo sapiens	210-220
29494307-13	2018	Our cell death assay revealed that SpCC cell death was induced by the anticancer drug imatinib, which is known to inhibit protein tyrosine kinase activity of ABL, platelet-derived growth factor receptor alpha (PDGFRalpha), and KIT.	imatinib	86-94	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	227-230
29936718-0	2018	Prognostic Implication of BCR-ABL Fusion Transcript Variants in Chronic Myeloid Leukemia (CML) Treated with Imatinib.A First of Its Kind Study on CML Patients of Kashmir Background: The prognostic significance of the common BCR-ABL transcripts like e13a2 (b2a2) and e14a2(b3a2) in Chronic myeloid leukemia (CML) has been reported from patients treated with different tyrosine kinaseinhibitors but its impact on clinical response and overall survival remains still unexplored.	imatinib	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
29936783-8	2018	STAT3 was inactivated in K562-R+5-Aza cells which showedhigher sensitivity to imatinib.	imatinib	78-86	signal transducer and activator of transcription 3	Homo sapiens	0-5
29936718-0	2018	Prognostic Implication of BCR-ABL Fusion Transcript Variants in Chronic Myeloid Leukemia (CML) Treated with Imatinib.A First of Its Kind Study on CML Patients of Kashmir Background: The prognostic significance of the common BCR-ABL transcripts like e13a2 (b2a2) and e14a2(b3a2) in Chronic myeloid leukemia (CML) has been reported from patients treated with different tyrosine kinaseinhibitors but its impact on clinical response and overall survival remains still unexplored.	imatinib	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	224-231
30032569-8	2018	CRRLF2 P224L and PDGFRB R370C point mutations were detected separately in 2 patients with HES who treated with imatinib monotherapy and achieved hematologic remission.	imatinib	111-119	platelet derived growth factor receptor beta	Homo sapiens	17-23
30455790-7	2018	In December 2013, an increment in BCR-ABL/ABL transcript levels according to the International Scale (from 0.0471% to 1.4034%), indicating imatinib failure, was documented.	imatinib	139-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
30455790-7	2018	In December 2013, an increment in BCR-ABL/ABL transcript levels according to the International Scale (from 0.0471% to 1.4034%), indicating imatinib failure, was documented.	imatinib	139-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-41
29925402-2	2018	Imatinib was the first tyrosine kinase inhibitor to be discovered with high specificity for Bcr-Abl protein resulting from t(9, 22)-derived Philadelphia chromosome.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
29925402-3	2018	Although the specific targeting of that oncoprotein, several Bcr-Abl-dependent and Bcr-Abl-independent mechanisms of resistance to imatinib arose after becoming first-line therapy in chronic myelogenous leukemia (CML) treatment.Consequently, new specific drugs, namely dasatinib, nilotinib, bosutinib, and ponatinib, were rationally designed and approved for clinic to override resistances.	imatinib	131-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
29925402-3	2018	Although the specific targeting of that oncoprotein, several Bcr-Abl-dependent and Bcr-Abl-independent mechanisms of resistance to imatinib arose after becoming first-line therapy in chronic myelogenous leukemia (CML) treatment.Consequently, new specific drugs, namely dasatinib, nilotinib, bosutinib, and ponatinib, were rationally designed and approved for clinic to override resistances.	imatinib	131-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
29921306-2	2018	Recently, we showed that PDGF-BB contracts pulmonary veins (PVs) and that this contraction is prevented by inhibition of PDGFR-beta (imatinib/SU6668).	imatinib	133-141	platelet-derived growth factor receptor beta	Cavia porcellus	121-131
29915281-9	2018	In mouse xenograft models, combining PDGFR-alpha/beta inhibition (using shRNA or imatinib) with doxorubicin had a more-than-additive effect in blocking tumor growth, with enhanced apoptosis, especially in CD133(+) cells.	imatinib	81-89	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	37-48
29915281-9	2018	In mouse xenograft models, combining PDGFR-alpha/beta inhibition (using shRNA or imatinib) with doxorubicin had a more-than-additive effect in blocking tumor growth, with enhanced apoptosis, especially in CD133(+) cells.	imatinib	81-89	prominin 1	Mus musculus	205-210
29915248-8	2018	Gefitinib, imatinib, pazopanib, sorafenib, and sunitinib also inhibited MATE1-mediated creatinine uptake.	imatinib	11-19	solute carrier family 47 member 1	Rattus norvegicus	72-77
29915172-0	2018	Early BCR-ABL1 decline in imatinib-treated patients with chronic myeloid leukemia: results from a multicenter study of the Chinese CML alliance.	imatinib	26-34	BCR activator of RhoGEF and GTPase	Homo sapiens	6-14
30034943-6	2018	Inhibiting SCF/c-KIT signaling by Imatinib also resulted in weakened mucus secretion in WT mice.	imatinib	34-42	kit ligand	Mus musculus	11-14
30034943-6	2018	Inhibiting SCF/c-KIT signaling by Imatinib also resulted in weakened mucus secretion in WT mice.	imatinib	34-42	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	15-20
29678462-2	2018	Clinically used kinase inhibitors imatinib and sunitinib are potent inhibitors of wild-type PDGFR family members, but show reduced binding to mutant forms.	imatinib	34-42	platelet derived growth factor receptor beta	Homo sapiens	92-97
29665256-6	2018	The inhibition of BCR-ABL activity by imatinib in human ph+ ALL cells reduces the prolyl isomerase activity of Pin 1, further suggesting a key role of the newly identified BCR-ABL-Pin 1 axis in ph+ ALL progression.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
29793583-13	2018	Plasma neutrophil-gelatinase-associated-lipocalin concentrations were reduced by imatinib.	imatinib	81-89	lipocalin 2	Rattus norvegicus	7-49
29665256-6	2018	The inhibition of BCR-ABL activity by imatinib in human ph+ ALL cells reduces the prolyl isomerase activity of Pin 1, further suggesting a key role of the newly identified BCR-ABL-Pin 1 axis in ph+ ALL progression.	imatinib	38-46	peptidylprolyl cis/trans isomerase, NIMA-interacting 1	Homo sapiens	111-116
29665256-6	2018	The inhibition of BCR-ABL activity by imatinib in human ph+ ALL cells reduces the prolyl isomerase activity of Pin 1, further suggesting a key role of the newly identified BCR-ABL-Pin 1 axis in ph+ ALL progression.	imatinib	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-179
29665256-6	2018	The inhibition of BCR-ABL activity by imatinib in human ph+ ALL cells reduces the prolyl isomerase activity of Pin 1, further suggesting a key role of the newly identified BCR-ABL-Pin 1 axis in ph+ ALL progression.	imatinib	38-46	peptidylprolyl cis/trans isomerase, NIMA-interacting 1	Homo sapiens	180-185
29998023-3	2018	Advances in immunopathology have identified a mutation in the c-KIT proto-oncogene, leading to the development of the tyrosine-kinase inhibitor Imatinib as targeted therapy for advanced disease.	imatinib	144-152	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	62-67
29615437-5	2018	Human AO substrates identified contained unsubstituted diazanaphthalene moieties (A77-01, INCB 28060, ML-347, LDN-193189, and SB-525334), 4-aminoquinazoline cores (lapatinib, lapatinib M1, and CL-387785), and terminal pyridine and pyrimidine groups (imatinib, bafetinib, and AMG 900).	imatinib	250-258	aldehyde oxidase 1	Homo sapiens	6-8
29600692-4	2018	Imatinib was shown to achieve high response rates in c-kit mutated melanoma.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	53-58
29950205-3	2018	CCK-8 assay was performed to evaluate the VE-cadherin of chemotherapeutic (Imatinib) sensitivity of K562 cells.	imatinib	75-83	cadherin 5	Homo sapiens	42-53
29710216-16	2018	Objective tumor response was observed in 25%, including 1 patient with an imatinib-resistant mutation in PDGFRA exon 18.	imatinib	74-82	platelet derived growth factor receptor alpha	Homo sapiens	105-111
29570794-5	2018	Conditional deletion of the platelet-derived growth factor (PDGF) receptor-alpha (PDGFRA) gene (Pdgfra) and inhibition of PDGFRA by imatinib in leptin receptor+ stromal cells suppressed their expansion and ameliorated bone marrow fibrosis.	imatinib	132-140	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	122-128
28762371-0	2018	Imatinib-induced ophthalmological side-effects in GIST patients are associated with the variations of EGFR, SLC22A1, SLC22A5 and ABCB1.	imatinib	0-8	epidermal growth factor receptor	Homo sapiens	102-106
28762371-0	2018	Imatinib-induced ophthalmological side-effects in GIST patients are associated with the variations of EGFR, SLC22A1, SLC22A5 and ABCB1.	imatinib	0-8	solute carrier family 22 member 1	Homo sapiens	108-115
28762371-0	2018	Imatinib-induced ophthalmological side-effects in GIST patients are associated with the variations of EGFR, SLC22A1, SLC22A5 and ABCB1.	imatinib	0-8	solute carrier family 22 member 5	Homo sapiens	117-124
29786668-5	2018	Atoh1 was significantly elevated in colorectal cancer (CRC) cells stimulated by exogenous SCF or overexpressing c-KIT in vitro, while decreased by the blockage of SCF/c-KIT signaling with Imatinib.	imatinib	188-196	atonal bHLH transcription factor 1	Mus musculus	0-5
28762371-0	2018	Imatinib-induced ophthalmological side-effects in GIST patients are associated with the variations of EGFR, SLC22A1, SLC22A5 and ABCB1.	imatinib	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	129-134
29786668-5	2018	Atoh1 was significantly elevated in colorectal cancer (CRC) cells stimulated by exogenous SCF or overexpressing c-KIT in vitro, while decreased by the blockage of SCF/c-KIT signaling with Imatinib.	imatinib	188-196	kit ligand	Mus musculus	163-166
28762371-5	2018	These results indicated that variants in EGFR, SLC22A1, SLC22A5 and ABCB1 influenced the incidence of Imatinib-induced ophthalmological toxicities, and polymorphism analyses in associated genes might be beneficial to optimize Imatinib treatment.	imatinib	102-110	epidermal growth factor receptor	Homo sapiens	41-45
29786668-5	2018	Atoh1 was significantly elevated in colorectal cancer (CRC) cells stimulated by exogenous SCF or overexpressing c-KIT in vitro, while decreased by the blockage of SCF/c-KIT signaling with Imatinib.	imatinib	188-196	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	167-172
28762371-5	2018	These results indicated that variants in EGFR, SLC22A1, SLC22A5 and ABCB1 influenced the incidence of Imatinib-induced ophthalmological toxicities, and polymorphism analyses in associated genes might be beneficial to optimize Imatinib treatment.	imatinib	102-110	solute carrier family 22 member 1	Homo sapiens	47-54
28762371-5	2018	These results indicated that variants in EGFR, SLC22A1, SLC22A5 and ABCB1 influenced the incidence of Imatinib-induced ophthalmological toxicities, and polymorphism analyses in associated genes might be beneficial to optimize Imatinib treatment.	imatinib	102-110	solute carrier family 22 member 5	Homo sapiens	56-63
28762371-5	2018	These results indicated that variants in EGFR, SLC22A1, SLC22A5 and ABCB1 influenced the incidence of Imatinib-induced ophthalmological toxicities, and polymorphism analyses in associated genes might be beneficial to optimize Imatinib treatment.	imatinib	102-110	ATP binding cassette subfamily B member 1	Homo sapiens	68-73
28762371-5	2018	These results indicated that variants in EGFR, SLC22A1, SLC22A5 and ABCB1 influenced the incidence of Imatinib-induced ophthalmological toxicities, and polymorphism analyses in associated genes might be beneficial to optimize Imatinib treatment.	imatinib	226-234	epidermal growth factor receptor	Homo sapiens	41-45
28762371-5	2018	These results indicated that variants in EGFR, SLC22A1, SLC22A5 and ABCB1 influenced the incidence of Imatinib-induced ophthalmological toxicities, and polymorphism analyses in associated genes might be beneficial to optimize Imatinib treatment.	imatinib	226-234	ATP binding cassette subfamily B member 1	Homo sapiens	68-73
29808796-10	2018	The apoptotic effect of imatinib on CML cell lines was tested by flow cytometric Annexin V-PE staining and caspase activation assays.	imatinib	24-32	annexin A5	Homo sapiens	81-90
29808796-13	2018	Our results indicate that inhibition of apoptosis, induction of autophagy, overexpression of efflux gene MDR1 and down-regulation of influx gene OCT1 play crucial roles in the progression of imatinib resistance.	imatinib	191-199	ATP binding cassette subfamily B member 1	Homo sapiens	105-109
29808796-13	2018	Our results indicate that inhibition of apoptosis, induction of autophagy, overexpression of efflux gene MDR1 and down-regulation of influx gene OCT1 play crucial roles in the progression of imatinib resistance.	imatinib	191-199	solute carrier family 22 member 1	Homo sapiens	145-149
29559564-0	2018	Overexpression of miR-202 resensitizes imatinib resistant chronic myeloid leukemia cells through targetting Hexokinase 2.	imatinib	39-47	microRNA 202	Homo sapiens	18-25
29434033-1	2018	Philadelphia chromosome (Ph)-like acute lymphoblastic leukemia (ALL) comprises ~10% to 15% of childhood ALL cases, many of which respond exquisitely to tyrosine kinase inhibitors (TKIs), for example, imatinib in PDGFRB-rearranged ALL.	imatinib	200-208	platelet derived growth factor receptor beta	Homo sapiens	212-218
29434033-4	2018	Further genomic profiling of longitudinally collected samples during treatment revealed the emergence of a mutation, PDGFRBC843G , which directly conferred resistance to all generations of ABL TKIs, including imatinib, dasatinib, nilotinib, and ponatinib.	imatinib	209-217	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	189-192
29559564-7	2018	By establishing imatinib resistant cell lines originating from K562 and KU812 cells, we observed expressions of miR-202 were down-regulated by imatinib treatments and imatinib resistant CML cell lines exhibited lower level of miR-202 On the contrary, imatinib resistant CML cell lines displayed up-regulated glycolysis rate than sensitive cells with the evidence that glucose uptake, lactate production, and key glycolysis enzymes were elevated in imatinib resistant cells.	imatinib	16-24	microRNA 202	Homo sapiens	112-119
29559564-7	2018	By establishing imatinib resistant cell lines originating from K562 and KU812 cells, we observed expressions of miR-202 were down-regulated by imatinib treatments and imatinib resistant CML cell lines exhibited lower level of miR-202 On the contrary, imatinib resistant CML cell lines displayed up-regulated glycolysis rate than sensitive cells with the evidence that glucose uptake, lactate production, and key glycolysis enzymes were elevated in imatinib resistant cells.	imatinib	16-24	microRNA 202	Homo sapiens	226-233
29559564-7	2018	By establishing imatinib resistant cell lines originating from K562 and KU812 cells, we observed expressions of miR-202 were down-regulated by imatinib treatments and imatinib resistant CML cell lines exhibited lower level of miR-202 On the contrary, imatinib resistant CML cell lines displayed up-regulated glycolysis rate than sensitive cells with the evidence that glucose uptake, lactate production, and key glycolysis enzymes were elevated in imatinib resistant cells.	imatinib	143-151	microRNA 202	Homo sapiens	112-119
29559564-7	2018	By establishing imatinib resistant cell lines originating from K562 and KU812 cells, we observed expressions of miR-202 were down-regulated by imatinib treatments and imatinib resistant CML cell lines exhibited lower level of miR-202 On the contrary, imatinib resistant CML cell lines displayed up-regulated glycolysis rate than sensitive cells with the evidence that glucose uptake, lactate production, and key glycolysis enzymes were elevated in imatinib resistant cells.	imatinib	143-151	microRNA 202	Homo sapiens	112-119
29559564-7	2018	By establishing imatinib resistant cell lines originating from K562 and KU812 cells, we observed expressions of miR-202 were down-regulated by imatinib treatments and imatinib resistant CML cell lines exhibited lower level of miR-202 On the contrary, imatinib resistant CML cell lines displayed up-regulated glycolysis rate than sensitive cells with the evidence that glucose uptake, lactate production, and key glycolysis enzymes were elevated in imatinib resistant cells.	imatinib	143-151	microRNA 202	Homo sapiens	112-119
29559564-7	2018	By establishing imatinib resistant cell lines originating from K562 and KU812 cells, we observed expressions of miR-202 were down-regulated by imatinib treatments and imatinib resistant CML cell lines exhibited lower level of miR-202 On the contrary, imatinib resistant CML cell lines displayed up-regulated glycolysis rate than sensitive cells with the evidence that glucose uptake, lactate production, and key glycolysis enzymes were elevated in imatinib resistant cells.	imatinib	143-151	microRNA 202	Homo sapiens	112-119
29559564-10	2018	Overexpression of miR-202 sensitized imatinib resistant CML through the miR-202-mediated glycolysis inhibition by targetting HK2.	imatinib	37-45	microRNA 202	Homo sapiens	18-25
29559564-10	2018	Overexpression of miR-202 sensitized imatinib resistant CML through the miR-202-mediated glycolysis inhibition by targetting HK2.	imatinib	37-45	microRNA 202	Homo sapiens	72-79
29559564-0	2018	Overexpression of miR-202 resensitizes imatinib resistant chronic myeloid leukemia cells through targetting Hexokinase 2.	imatinib	39-47	hexokinase 2	Homo sapiens	108-120
29559564-10	2018	Overexpression of miR-202 sensitized imatinib resistant CML through the miR-202-mediated glycolysis inhibition by targetting HK2.	imatinib	37-45	hexokinase 2	Homo sapiens	125-128
29559564-2	2018	As a specific inhibitor of the BCR-ABL tyrosine kinase, imatinib becomes the first choice for the treatment of CML due to its high efficacy and low toxicity.	imatinib	56-64	BCR activator of RhoGEF and GTPase	Homo sapiens	31-34
29559564-2	2018	As a specific inhibitor of the BCR-ABL tyrosine kinase, imatinib becomes the first choice for the treatment of CML due to its high efficacy and low toxicity.	imatinib	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
29559564-4	2018	In the present study, we aimed to investigate the roles of miR-202 in the regulation of imatinib sensitivity in CML cell lines and the possible mechanisms involved in this process.	imatinib	88-96	microRNA 202	Homo sapiens	59-66
29468363-1	2018	In chronic myeloid leukemia (CML), the translocation t(9;22) results in the fusion protein BCR-ABL (breakpoint cluster region-abelson murine leukemia), a tyrosine kinase mediating oncogenic signaling which is successfully targeted by treatment with BCR-ABL inhibitors like imatinib.	imatinib	273-281	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
29468363-1	2018	In chronic myeloid leukemia (CML), the translocation t(9;22) results in the fusion protein BCR-ABL (breakpoint cluster region-abelson murine leukemia), a tyrosine kinase mediating oncogenic signaling which is successfully targeted by treatment with BCR-ABL inhibitors like imatinib.	imatinib	273-281	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-149
29468363-1	2018	In chronic myeloid leukemia (CML), the translocation t(9;22) results in the fusion protein BCR-ABL (breakpoint cluster region-abelson murine leukemia), a tyrosine kinase mediating oncogenic signaling which is successfully targeted by treatment with BCR-ABL inhibitors like imatinib.	imatinib	273-281	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	249-256
29427770-0	2018	Impact of SLC22A1 and CYP3A5 genotypes on imatinib response in chronic myeloid leukemia: A systematic review and meta-analysis.	imatinib	42-50	solute carrier family 22 member 1	Homo sapiens	10-17
29439183-2	2018	Most patients exhibit a D816V-mutated variant of KIT, which confers resistance against imatinib.	imatinib	87-95	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	49-52
29485707-0	2018	Overexpression of Tpl2 is linked to imatinib resistance and activation of MEK-ERK and NF-kappaB pathways in a model of chronic myeloid leukemia.	imatinib	36-44	mitogen-activated protein kinase kinase kinase 8	Homo sapiens	18-22
29427770-0	2018	Impact of SLC22A1 and CYP3A5 genotypes on imatinib response in chronic myeloid leukemia: A systematic review and meta-analysis.	imatinib	42-50	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	22-28
29427770-1	2018	Contrasting results have been reported on the role of rs628031 and rs683369 polymorphisms of SLC22A1 and rs776746 of CYP3A5 on imatinib treatment response in patients with chronic myeloid leukemia (CML).	imatinib	127-135	solute carrier family 22 member 1	Homo sapiens	93-100
29427770-1	2018	Contrasting results have been reported on the role of rs628031 and rs683369 polymorphisms of SLC22A1 and rs776746 of CYP3A5 on imatinib treatment response in patients with chronic myeloid leukemia (CML).	imatinib	127-135	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	117-123
29427770-7	2018	In conclusion, the present meta-analysis supports the association of SLC22A1 and CYP3A5 genotypes with clinical imatinib response rates of CML patients, nevertheless further large studies, particularly in Caucasians, are still warranted to provide conclusive evidences.	imatinib	112-120	solute carrier family 22 member 1	Homo sapiens	69-76
29427770-7	2018	In conclusion, the present meta-analysis supports the association of SLC22A1 and CYP3A5 genotypes with clinical imatinib response rates of CML patients, nevertheless further large studies, particularly in Caucasians, are still warranted to provide conclusive evidences.	imatinib	112-120	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	81-87
29717168-3	2018	Here we characterize imatinib as first-in-class allosteric FXR modulator and report the development of an optimized descendant that markedly promotes agonist induced FXR activation in a reporter gene assay and FXR target gene expression in HepG2 cells.	imatinib	21-29	nuclear receptor subfamily 1 group H member 4	Homo sapiens	59-62
29717168-3	2018	Here we characterize imatinib as first-in-class allosteric FXR modulator and report the development of an optimized descendant that markedly promotes agonist induced FXR activation in a reporter gene assay and FXR target gene expression in HepG2 cells.	imatinib	21-29	nuclear receptor subfamily 1 group H member 4	Homo sapiens	166-169
29717168-3	2018	Here we characterize imatinib as first-in-class allosteric FXR modulator and report the development of an optimized descendant that markedly promotes agonist induced FXR activation in a reporter gene assay and FXR target gene expression in HepG2 cells.	imatinib	21-29	nuclear receptor subfamily 1 group H member 4	Homo sapiens	166-169
29717168-4	2018	Differential effects of imatinib on agonist-induced bile salt export protein and small heterodimer partner expression suggest that allosteric FXR modulation could open a new avenue to gene-selective FXR modulators.	imatinib	24-32	nuclear receptor subfamily 1 group H member 4	Homo sapiens	142-145
29717168-4	2018	Differential effects of imatinib on agonist-induced bile salt export protein and small heterodimer partner expression suggest that allosteric FXR modulation could open a new avenue to gene-selective FXR modulators.	imatinib	24-32	nuclear receptor subfamily 1 group H member 4	Homo sapiens	199-202
29458040-0	2018	Pharmacological inhibition of JAK3 enhances the antitumor activity of imatinib in human chronic myeloid leukemia.	imatinib	70-78	Janus kinase 3	Homo sapiens	30-34
29774130-3	2018	Here, we show that the ABL kinase inhibitors imatinib, nilotinib, and GNF-5 impede invadopodium precursor formation and cortactin-phosphorylation dependent invadopodium maturation, leading to decreased actin polymerization in invadopodia, reduced extracellular matrix degradation, and impaired matrix proteolysis-dependent invasion.	imatinib	45-53	cortactin	Homo sapiens	120-129
29661222-8	2018	RESULTS: The proliferation was remarkably promoted in cells treated with either 1% PRP or 10 ng/ml PDGF-BB, and both imatinib and sorafenib inhibited this proliferation.	imatinib	117-125	complement component 4 binding protein alpha	Homo sapiens	83-86
29458040-7	2018	The pharmacological inhibition of JAK3 by tofacitinib synergistically enhanced the antitumor effects of IMA in CML cells.	imatinib	104-107	Janus kinase 3	Homo sapiens	34-38
29386476-1	2018	The discovery of the chimeric tyrosine kinase breakpoint cluster region kinase-Abelson kinase (BCR-ABL)-targeted drug imatinib conceptually changed the treatment of chronic myelogenous leukemia (CML).	imatinib	118-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
29522716-5	2018	MTT assay was first performed to detect the effect of inhibitors of c-ABL (imatinib) and EGFR (lapatinib) on FRBC cells.	imatinib	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-73
29707154-6	2018	This result is in contrast to the distinct expression signature of CD34+ chronic phase chronic myeloid leukemia patients failing to achieve a cytogenetic response on imatinib and suggests that deep molecular response to second-generation tyrosine kinase inhibitors is governed by the biology of more primitive chronic myeloid leukemia cells or extrinsic factors.	imatinib	166-174	CD34 molecule	Homo sapiens	67-71
29467128-0	2018	Macrophages and CD8+ T Cells Mediate the Antitumor Efficacy of Combined CD40 Ligation and Imatinib Therapy in Gastrointestinal Stromal Tumors.	imatinib	90-98	CD8a molecule	Homo sapiens	16-19
28736245-5	2018	Imatinib has the desirable effect of attacking multiple targets involved in the early hypoxic and inflammatory stages of FOP flare-ups, including HIF1-alpha, PDGFRalpha, c-KIT, and multiple MAP kinases.	imatinib	0-8	hypoxia inducible factor 1 subunit alpha	Homo sapiens	146-156
28736245-5	2018	Imatinib has the desirable effect of attacking multiple targets involved in the early hypoxic and inflammatory stages of FOP flare-ups, including HIF1-alpha, PDGFRalpha, c-KIT, and multiple MAP kinases.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	158-168
28736245-5	2018	Imatinib has the desirable effect of attacking multiple targets involved in the early hypoxic and inflammatory stages of FOP flare-ups, including HIF1-alpha, PDGFRalpha, c-KIT, and multiple MAP kinases.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	170-175
29467128-4	2018	Activated TAMs had greater TNFalpha production and NFkappaB signaling and directly inhibited tumor cells in vitro Anti-CD40 required concomitant therapy with imatinib for efficacy and depended on TAMs, and to a lesser extent CD8+ T cells, but not on CD4+ T cells or B cells.	imatinib	158-166	CD40 molecule	Homo sapiens	119-123
29467128-4	2018	Activated TAMs had greater TNFalpha production and NFkappaB signaling and directly inhibited tumor cells in vitro Anti-CD40 required concomitant therapy with imatinib for efficacy and depended on TAMs, and to a lesser extent CD8+ T cells, but not on CD4+ T cells or B cells.	imatinib	158-166	CD8a molecule	Homo sapiens	225-228
29467128-4	2018	Activated TAMs had greater TNFalpha production and NFkappaB signaling and directly inhibited tumor cells in vitro Anti-CD40 required concomitant therapy with imatinib for efficacy and depended on TAMs, and to a lesser extent CD8+ T cells, but not on CD4+ T cells or B cells.	imatinib	158-166	CD4 molecule	Homo sapiens	119-122
29467128-5	2018	In an analysis of 50 human GIST specimens by flow cytometry, we found that CD40 was expressed on human TAMs and tumor cells yet was downregulated after response to imatinib.	imatinib	164-172	CD40 molecule	Homo sapiens	75-79
29541231-6	2018	The present data suggest that BCR-ABL gene amplification may be associated with imatinib resistance, which can be overcome with dasatinib.	imatinib	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
28710566-0	2018	Remarkable effects of imatinib in a family with young onset gastrointestinal stromal tumors and cutaneous hyperpigmentation associated with a germline KIT-Trp557Arg mutation: case report and literature overview.	imatinib	22-30	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	151-154
28710566-5	2018	The effect of imatinib in patients harboring a germline KIT mutation has been rarely described.	imatinib	14-22	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	56-59
28710566-13	2018	Imatinib treatment in GIST patients harboring a germline KIT mutation shows favorable and long-term responses in both the tumor and the phenotypical hyperpigmentation.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	57-60
29742077-5	2018	Imatinib was the first TKI that targeted the BCR-ABL1 oncoprotein in Ph+ ALL.	imatinib	0-8	BCR activator of RhoGEF and GTPase	Homo sapiens	45-53
29569526-3	2018	Resistance to imatinib can be due to heterogeneous array of factors involving BCR/ABL-dependent and BCR/ABL-independent pathways.	imatinib	14-22	BCR activator of RhoGEF and GTPase	Homo sapiens	78-103
29567937-0	2018	Imatinib Affects the Expression of SLC22A1 in a Non-Linear Concentration-Dependent Manner Within 24 Hours.	imatinib	0-8	solute carrier family 22 member 1	Homo sapiens	35-42
29567937-1	2018	BACKGROUND Imatinib is actively transported into cells by the organic cation transporter (OCT1), encoded by SLC22A1.	imatinib	11-19	solute carrier family 22 member 1	Homo sapiens	90-94
29567937-1	2018	BACKGROUND Imatinib is actively transported into cells by the organic cation transporter (OCT1), encoded by SLC22A1.	imatinib	11-19	solute carrier family 22 member 1	Homo sapiens	108-115
29567937-2	2018	As a result, the expression of SLC22A1 is considered a prognostic marker for treatment with imatinib in patients with chronic myeloid leukemia (CML).	imatinib	92-100	solute carrier family 22 member 1	Homo sapiens	31-38
29567937-3	2018	Although limited, there is conflicting evidence indicating that imatinib may affect the expression of SLC22A1.	imatinib	64-72	solute carrier family 22 member 1	Homo sapiens	102-109
29567937-5	2018	Changes in the expression of SLC22A1 as a result of imatinib could potentially negate its usefulness as a prognostic marker.	imatinib	52-60	solute carrier family 22 member 1	Homo sapiens	29-36
29567937-7	2018	RESULTS Our findings suggest that imatinib affects the expression of SLC22A1 within 24 h in a non-linear concentration-dependent manner.	imatinib	34-42	solute carrier family 22 member 1	Homo sapiens	69-76
29567937-8	2018	CONCLUSIONS This is the first study to report on the short-term effect of imatinib on the expression of SLC22A1 in an imatinib-sensitive CML cell line.	imatinib	74-82	solute carrier family 22 member 1	Homo sapiens	104-111
29567937-8	2018	CONCLUSIONS This is the first study to report on the short-term effect of imatinib on the expression of SLC22A1 in an imatinib-sensitive CML cell line.	imatinib	118-126	solute carrier family 22 member 1	Homo sapiens	104-111
29567937-9	2018	Our results suggest that imatinib affects SLC22A1 mRNA expression in a non-linear dose-dependent manner and that the changes in the expression of SLC22A1 as a result of the concentration of imatinib occur within 24 h of exposure to imatinib and remain stable thereafter for up to 72 h.	imatinib	25-33	solute carrier family 22 member 1	Homo sapiens	42-49
29567937-9	2018	Our results suggest that imatinib affects SLC22A1 mRNA expression in a non-linear dose-dependent manner and that the changes in the expression of SLC22A1 as a result of the concentration of imatinib occur within 24 h of exposure to imatinib and remain stable thereafter for up to 72 h.	imatinib	190-198	solute carrier family 22 member 1	Homo sapiens	146-153
29567937-9	2018	Our results suggest that imatinib affects SLC22A1 mRNA expression in a non-linear dose-dependent manner and that the changes in the expression of SLC22A1 as a result of the concentration of imatinib occur within 24 h of exposure to imatinib and remain stable thereafter for up to 72 h.	imatinib	190-198	solute carrier family 22 member 1	Homo sapiens	146-153
29554925-0	2018	Induction of apoptosis in imatinib sensitive and resistant chronic myeloid leukemia cells by efficient disruption of bcr-abl oncogene with zinc finger nucleases.	imatinib	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
29554925-1	2018	BACKGROUND: The bcr-abl fusion gene is the pathological origin of chronic myeloid leukemia (CML) and plays a critical role in the resistance of imatinib.	imatinib	144-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
29554925-8	2018	RESULTS: The ZFNs skillfully mediated 8-base NotI enzyme cutting site addition in bcr-abl gene of imatinib sensitive and resistant CML cells by homology-directed repair (HDR), which led to a stop codon and terminated the translation of BCR-ABL protein.	imatinib	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
29554925-8	2018	RESULTS: The ZFNs skillfully mediated 8-base NotI enzyme cutting site addition in bcr-abl gene of imatinib sensitive and resistant CML cells by homology-directed repair (HDR), which led to a stop codon and terminated the translation of BCR-ABL protein.	imatinib	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	236-243
29554925-12	2018	CONCLUSION: These results reveal that the bcr-abl gene disruption based on ZFNs may provide a treatment choice for imatinib resistant or intolerant CML patients.	imatinib	115-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
29321163-3	2018	On the basis of the finding that the NEDD8-activating enzyme subunit NAE1 is overexpressed in CML cells, we hypothesized that the function of certain neddylation-dependent protein substrates might be targeted to therapeutic ends in imatinib-resistant CML cells and LSCs.	imatinib	232-240	neural precursor cell expressed, developmentally down-regulated gene 8	Mus musculus	37-42
29321163-3	2018	On the basis of the finding that the NEDD8-activating enzyme subunit NAE1 is overexpressed in CML cells, we hypothesized that the function of certain neddylation-dependent protein substrates might be targeted to therapeutic ends in imatinib-resistant CML cells and LSCs.	imatinib	232-240	NEDD8 activating enzyme E1 subunit 1	Mus musculus	69-73
29510530-6	2018	Molecular modeling of PDGFRA D842V suggests that the mutant protein binds imatinib with lower affinity with respect to wild-type structure, showing higher stability during the interaction with other type I TKIs (like crenolanib).	imatinib	74-82	platelet derived growth factor receptor alpha	Homo sapiens	22-28
29414416-1	2018	The introduction of BCR/Abl tyrosine kinase inhibitors (TKI), such as imatinib-mesylate (IM), has revolutioned the treatment of chronic myeloid leukemia (CML).	imatinib	70-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-27
29682621-1	2018	Although imatinib is a standard treatment for metastatic or recurrent gastrointestinal stromal tumors (GISTs), acquired c-kit mutations reportedly cause secondary resistance to imatinib.	imatinib	177-185	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	120-125
29549929-9	2018	Importantly, combination of ropivacaine with imatinib or dasatinib (Bcr-Abl tyrosine kinase inhibitors) is significantly more effective in targeting CML cell lines as well as blast phase-CML CD34 cells than imatinib or dasatinib alone.	imatinib	45-53	CD34 molecule	Homo sapiens	191-195
29549929-9	2018	Importantly, combination of ropivacaine with imatinib or dasatinib (Bcr-Abl tyrosine kinase inhibitors) is significantly more effective in targeting CML cell lines as well as blast phase-CML CD34 cells than imatinib or dasatinib alone.	imatinib	207-215	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
29196126-7	2018	Importantly, M-COPA can inhibit the activation of the Kit kinase domain mutant, resulting in suppression of imatinib-resistant GIST proliferation.	imatinib	108-116	COPI coat complex subunit alpha	Homo sapiens	15-19
29223619-9	2018	CYP3A4 has the major role in the intrinsic clearance of sorafenib but plays a secondary role to CYP2C8 in the intrinsic clearance of imatinib.	imatinib	133-141	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
29223619-9	2018	CYP3A4 has the major role in the intrinsic clearance of sorafenib but plays a secondary role to CYP2C8 in the intrinsic clearance of imatinib.	imatinib	133-141	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	96-102
29076384-1	2018	INTRODUCTION: The tyrosine kinase inhibitor (TKI) imatinib was rationally designed to target BCR-ABL1 which is constitutively activated in chronic myeloid leukemia (CML).	imatinib	50-58	BCR activator of RhoGEF and GTPase	Homo sapiens	93-101
29523662-2	2018	Adjuvant imatinib therapy, which targets the most common driver mutations in GIST (KIT and PDGFRA), is recommended for patients with high-risk GIST, but it has known teratogenicity in the first trimester.	imatinib	9-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	83-86
29523662-2	2018	Adjuvant imatinib therapy, which targets the most common driver mutations in GIST (KIT and PDGFRA), is recommended for patients with high-risk GIST, but it has known teratogenicity in the first trimester.	imatinib	9-17	platelet derived growth factor receptor alpha	Homo sapiens	91-97
29523662-9	2018	Because neoadjuvant/adjuvant imatinib has risks of teratogenicity, tumor molecular profiling is critical as we identified a previously unreported gene fusion of PRKAR1B with BRAF that is predicted to be imatinib-resistant.	imatinib	29-37	protein kinase cAMP-dependent type I regulatory subunit beta	Homo sapiens	161-168
29523662-9	2018	Because neoadjuvant/adjuvant imatinib has risks of teratogenicity, tumor molecular profiling is critical as we identified a previously unreported gene fusion of PRKAR1B with BRAF that is predicted to be imatinib-resistant.	imatinib	29-37	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	174-178
29523662-9	2018	Because neoadjuvant/adjuvant imatinib has risks of teratogenicity, tumor molecular profiling is critical as we identified a previously unreported gene fusion of PRKAR1B with BRAF that is predicted to be imatinib-resistant.	imatinib	203-211	protein kinase cAMP-dependent type I regulatory subunit beta	Homo sapiens	161-168
29523662-9	2018	Because neoadjuvant/adjuvant imatinib has risks of teratogenicity, tumor molecular profiling is critical as we identified a previously unreported gene fusion of PRKAR1B with BRAF that is predicted to be imatinib-resistant.	imatinib	203-211	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	174-178
27384439-0	2018	Two different KIT mutations may lead to different responses to imatinib in metastatic gastrointestinal stromal tumor.	imatinib	63-71	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-17
29491129-0	2018	Comment on "MEK inhibition with trametinib and tyrosine kinase inhibition with imatinib in multifocal histiocytic sarcoma".	imatinib	79-87	mitogen-activated protein kinase kinase 7	Homo sapiens	12-15
29507818-6	2018	In co-culture, Lrp1-deficient osteoblasts stimulated osteoclastogenesis in a PDGFRbeta-dependent manner and in vivo treatment with the PDGFR tyrosine kinase inhibitor imatinib mesylate limited RANKL production and led to complete remission of the osteoporotic phenotype.	imatinib	167-184	LDL receptor related protein 1	Homo sapiens	15-19
29507818-6	2018	In co-culture, Lrp1-deficient osteoblasts stimulated osteoclastogenesis in a PDGFRbeta-dependent manner and in vivo treatment with the PDGFR tyrosine kinase inhibitor imatinib mesylate limited RANKL production and led to complete remission of the osteoporotic phenotype.	imatinib	167-184	platelet derived growth factor receptor beta	Homo sapiens	77-86
29507818-6	2018	In co-culture, Lrp1-deficient osteoblasts stimulated osteoclastogenesis in a PDGFRbeta-dependent manner and in vivo treatment with the PDGFR tyrosine kinase inhibitor imatinib mesylate limited RANKL production and led to complete remission of the osteoporotic phenotype.	imatinib	167-184	TNF superfamily member 11	Homo sapiens	193-198
31249931-2	2018	Second- (dasatinib, nilotinib, and bosutinib) and third-generation (ponatinib) TKIs have been developed to be effective against BCR-ABL mutations making imatinib less effective.	imatinib	153-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
29483845-0	2018	MLL2/KMT2D and MLL3/KMT2C expression correlates with disease progression and response to imatinib mesylate in chronic myeloid leukemia.	imatinib	89-97	lysine methyltransferase 2D	Homo sapiens	0-4
29483845-0	2018	MLL2/KMT2D and MLL3/KMT2C expression correlates with disease progression and response to imatinib mesylate in chronic myeloid leukemia.	imatinib	89-97	lysine methyltransferase 2C	Homo sapiens	15-19
29483845-0	2018	MLL2/KMT2D and MLL3/KMT2C expression correlates with disease progression and response to imatinib mesylate in chronic myeloid leukemia.	imatinib	89-97	lysine methyltransferase 2C	Homo sapiens	20-25
31249931-1	2018	Imatinib, the first-in-class BCR-ABL tyrosine kinase inhibitor (TKI), had been a revolution for the treatment of chronic myeloid leukemia (CML) and had greatly enhanced patient survival.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
29451912-12	2018	In summary, mutation analysis in TP53 plays a minor role in the subgroup of high-risk GIST before adjuvant treatment with imatinib.	imatinib	122-130	tumor protein p53	Homo sapiens	33-37
31249931-5	2018	Imatinib is associated with very low rates of thrombosis, suggesting a potentially protecting cardiovascular effect of this treatment in patients with BCR-ABL CML.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-158
29400343-4	2018	MATERIAL AND METHODS The expression of Siah2 was detected in CML patients (CML-CP and CML-BC), K562 cells, and K562-imatinib-resistant cells (K562-R cells).	imatinib	116-124	siah E3 ubiquitin protein ligase 2	Homo sapiens	39-44
29400343-7	2018	Similarly, K562-imatinib-resistant cells (K562-R cells) showed a significantly higher expression of Siah2 as compared to K562 cells in a hypoxic microenvironment.	imatinib	16-24	siah E3 ubiquitin protein ligase 2	Homo sapiens	100-105
29400343-9	2018	Additionally, Vitamin K3 (an inhibitor of Siah2) reversed these changes and promoted a higher degree of leukemic sensitivity to imatinib.	imatinib	128-136	siah E3 ubiquitin protein ligase 2	Homo sapiens	42-47
29138287-8	2018	The UGT2B17 inhibitor imatinib and the UGT2B7 and UGT1A9 inhibitor mefenamic acid inhibited clopidogrel carboxylic acid glucuronidation in HIMs and HLMs, respectively.	imatinib	22-30	UDP glucuronosyltransferase family 2 member B17	Homo sapiens	4-11
29269240-0	2018	Exosomes from mesenchymal stromal cells enhance imatinib-induced apoptosis in human leukemia cells via activation of caspase signaling pathway.	imatinib	48-56	caspase 9	Homo sapiens	117-124
29269240-1	2018	BACKGROUND AIMS: Imatinib (IM), a tyrosine kinase inhibitor targeting the BCR-ABL oncoprotein, remains a major therapeutic strategy for patients with chronic myelogenous leukemia (CML).	imatinib	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
29370077-0	2018	p53 Gene (NY-CO-13) Levels in Patients with Chronic Myeloid Leukemia: The Role of Imatinib and Nilotinib.	imatinib	82-90	tumor protein p53	Homo sapiens	0-3
29552659-9	2018	Imatinib mesylate (IM) is indicated as first-line treatment of metastatic or unresectable GIST, and clinical outcomes are correlated with KIT mutation genotype.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	138-141
29552659-9	2018	Imatinib mesylate (IM) is indicated as first-line treatment of metastatic or unresectable GIST, and clinical outcomes are correlated with KIT mutation genotype.	imatinib	19-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	138-141
29449840-3	2018	Loss-of-function of c-Abl through Imatinib, in a mouse model of tuberculosis or RNA interference, identified bone morphogenesis protein (BMP) signaling as its cellular target.	imatinib	34-42	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	20-25
29434953-0	2018	Molecular screening and the clinical impacts of BCR-ABL KD mutations in patients with imatinib-resistant chronic myeloid leukemia.	imatinib	86-94	BCR activator of RhoGEF and GTPase	Homo sapiens	48-51
33177018-0	2018	[Effect of MDR1 and CYP3A5 gene polymorphisms on outcomes of patients receiving imatinib treatment for chronic myeloid leukemia].	imatinib	80-88	ATP binding cassette subfamily B member 1	Homo sapiens	11-15
33177018-0	2018	[Effect of MDR1 and CYP3A5 gene polymorphisms on outcomes of patients receiving imatinib treatment for chronic myeloid leukemia].	imatinib	80-88	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	20-26
33177018-1	2018	OBJECTIVE: To study the effect of MDR1 and CYP3A5 gene polymorphisms on the outcomes of imatinib treatment in patients with chronic myeloid leukemia (CML).	imatinib	88-96	ATP binding cassette subfamily B member 1	Homo sapiens	34-38
33177018-1	2018	OBJECTIVE: To study the effect of MDR1 and CYP3A5 gene polymorphisms on the outcomes of imatinib treatment in patients with chronic myeloid leukemia (CML).	imatinib	88-96	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	43-49
33177018-9	2018	CONCLUSIONS: The risk of cytogenetic relapse of CML was significantly affected by SNPs of C1236T and C3435T loci of MDR1 gene and blood imatinib concentration.	imatinib	136-144	ATP binding cassette subfamily B member 1	Homo sapiens	116-120
29370077-5	2018	The purpose of the present study was to evaluate the differential effect of imatinib and nilotinib on p53 gene serum levels in patients with CML.	imatinib	76-84	tumor protein p53	Homo sapiens	102-105
29370077-10	2018	Patients with CML that were treated with either imatinib or nilotinib showed insignificant differences in most of the hematological profile (p &gt; 0.05) whereas, p53 serum levels were high (3.22 +- 1.99 ng/mL) in nilotinib-treated patients and relatively low (1.18 +- 0.19 ng/mL) in imatinib-treated patients (p = 0.0001).	imatinib	48-56	tumor protein p53	Homo sapiens	163-166
29370077-11	2018	CONCLUSIONS: Nilotinib is more effective than imatinib in raising p53 serum levels in patients with chronic myeloid leukemia.	imatinib	46-54	tumor protein p53	Homo sapiens	66-69
28681330-0	2018	Antiproliferative Activity and VEGF Expression Reduction in MCF7 and PC-3 Cancer Cells by Paclitaxel and Imatinib Co-encapsulation in Folate-Targeted Liposomes.	imatinib	105-113	vascular endothelial growth factor A	Homo sapiens	31-35
29423012-0	2018	CCDC26 knockdown enhances resistance of gastrointestinal stromal tumor cells to imatinib by interacting with c-KIT.	imatinib	80-88	CCDC26 long non-coding RNA	Homo sapiens	0-6
29423012-0	2018	CCDC26 knockdown enhances resistance of gastrointestinal stromal tumor cells to imatinib by interacting with c-KIT.	imatinib	80-88	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	109-114
29423012-3	2018	In the present study, we explored the biological function of the lncRNA coiled-coil domain-containing 26 (CCDC26) in imatinib resistance of GIST.	imatinib	117-125	CCDC26 long non-coding RNA	Homo sapiens	106-112
29423012-4	2018	We found that human GIST-882 cells with lower CCDC26 expression were less sensitive to imatinib compared with GIST-T1 cells with higher CCDC26 expression.	imatinib	87-95	CCDC26 long non-coding RNA	Homo sapiens	46-52
29423012-5	2018	CCDC26 expression decreased in a time-dependent manner in the presence of imatinib.	imatinib	74-82	CCDC26 long non-coding RNA	Homo sapiens	0-6
29423012-6	2018	Moreover, small interfering RNA (siRNA) knockdown of CCDC26 increased GIST cell sensitivity to imatinib.	imatinib	95-103	CCDC26 long non-coding RNA	Homo sapiens	53-59
29423012-8	2018	We also found that inhibiting c-KIT induced resistance to imatinib.	imatinib	58-66	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	30-35
29423012-9	2018	Lastly, we proved that inhibiting c-KIT can reverse CCDC26 knockdown-mediated imatinib resistance in GIST.	imatinib	78-86	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	34-39
29423012-9	2018	Lastly, we proved that inhibiting c-KIT can reverse CCDC26 knockdown-mediated imatinib resistance in GIST.	imatinib	78-86	CCDC26 long non-coding RNA	Homo sapiens	52-58
29423012-10	2018	We suggest that CCDC26 knockdown can induce imatinib resistance in GIST cells by downregulating c-KIT expression.	imatinib	44-52	CCDC26 long non-coding RNA	Homo sapiens	16-22
29423012-10	2018	We suggest that CCDC26 knockdown can induce imatinib resistance in GIST cells by downregulating c-KIT expression.	imatinib	44-52	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	96-101
29297244-2	2018	Moreover, TWIST-1 protein is a prognostic factor of leukemogenesis, and its level is raised in CML patients with cytogenetic resistance to imatinib.	imatinib	139-147	twist family bHLH transcription factor 1	Homo sapiens	10-17
29316665-1	2018	Abstract: The introduction of imatinib (IM), a BCR-ABL1 tyrosine kinase inhibitor (TKI), has represented a significant advance in the first-line treatment of chronic myeloid leukemia (CML).	imatinib	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
29551130-6	2018	The first TK to be targeted, Bcr-Abl, led to the generation of several drugs including imatinib, dasatinib, and sunitinib that provided a rich understanding of this phenomenon.	imatinib	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
29334307-0	2018	Regorafenib regresses an imatinib-resistant recurrent gastrointestinal stromal tumor (GIST) with a mutation in exons 11 and 17 of c-kit in a patient-derived orthotopic xenograft (PDOX) nude mouse model.	imatinib	25-33	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	130-135
28943239-3	2018	BCR-ABL has become the prototype for rational drug design, and drugs like Imatinib and subsequently improved drugs have a great impact on cancer treatments.	imatinib	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
29298654-8	2018	Treatment of K562 cell lines with a combination of XT5 and imatinib-XT5 increased cytotoxicity, the Annexin V binding and caspase 3/7 activation.	imatinib	59-67	annexin A5	Homo sapiens	100-109
29298654-8	2018	Treatment of K562 cell lines with a combination of XT5 and imatinib-XT5 increased cytotoxicity, the Annexin V binding and caspase 3/7 activation.	imatinib	59-67	caspase 3	Homo sapiens	122-131
30488756-2	2018	However, approximately 10% of KIT-positive GIST metastases lose KIT expression at the time of clinical progression during imatinib therapy.	imatinib	122-130	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	30-33
29669505-1	2018	BACKGROUND: In exploring the cause of Imatinib Mesylate (IM) resistance among Chronic Myeloid Leukemia (CML) patients who do not harbor BCR-ABL dependent mechanism, BCR-ABL independent pathways are the most probable pathways that should be explored.	imatinib	38-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-143
29669505-1	2018	BACKGROUND: In exploring the cause of Imatinib Mesylate (IM) resistance among Chronic Myeloid Leukemia (CML) patients who do not harbor BCR-ABL dependent mechanism, BCR-ABL independent pathways are the most probable pathways that should be explored.	imatinib	38-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	165-172
30488756-2	2018	However, approximately 10% of KIT-positive GIST metastases lose KIT expression at the time of clinical progression during imatinib therapy.	imatinib	122-130	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	64-67
30488756-5	2018	AXL expression was strong in KIT-negative or -weak clinical GIST samples that were obtained from progressing metastases during imatinib therapy.	imatinib	127-135	AXL receptor tyrosine kinase	Homo sapiens	0-3
29143894-1	2018	Imatinib has revolutionized the treatment of GIST since this drug is able to inhibit tumoral growth by blocking the activity of receptor tyrosine kinases, KIT or PDGFRA, that in these tumors are constitutively activated because of the presence of mutations that alters their catalytic activity.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	155-158
30007969-7	2018	Moreover, the expression and activation of PDGFR-alpha and -beta were inhibited by imatinib.	imatinib	83-91	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	43-64
30007969-8	2018	The imatinib-treated OIR mice presented with reduced expression of other potent pro-angiogenic factors such as VEGF and FGF2.	imatinib	4-12	vascular endothelial growth factor A	Mus musculus	111-115
30007969-8	2018	The imatinib-treated OIR mice presented with reduced expression of other potent pro-angiogenic factors such as VEGF and FGF2.	imatinib	4-12	fibroblast growth factor 2	Mus musculus	120-124
28726812-0	2018	A patient with germ-line gain-of-function PDGFRB p.N666H mutation and marked clinical response to imatinib.	imatinib	98-106	platelet derived growth factor receptor beta	Homo sapiens	42-48
28726812-2	2018	We describe a 10-year-old child with a germ-line PDGFRB p.N666H mutation who responded to the tyrosine kinase inhibitor imatinib by inhibition of PDGFRB.MethodsThe impact of p.N666H on PDGFRB function and sensitivity to imatinib was studied in cell culture.ResultsCells expressing the p.N666H mutation showed constitutive PDGFRB tyrosine phosphorylation.	imatinib	120-128	platelet derived growth factor receptor beta	Homo sapiens	49-55
28726812-2	2018	We describe a 10-year-old child with a germ-line PDGFRB p.N666H mutation who responded to the tyrosine kinase inhibitor imatinib by inhibition of PDGFRB.MethodsThe impact of p.N666H on PDGFRB function and sensitivity to imatinib was studied in cell culture.ResultsCells expressing the p.N666H mutation showed constitutive PDGFRB tyrosine phosphorylation.	imatinib	120-128	platelet derived growth factor receptor beta	Homo sapiens	146-152
28726812-2	2018	We describe a 10-year-old child with a germ-line PDGFRB p.N666H mutation who responded to the tyrosine kinase inhibitor imatinib by inhibition of PDGFRB.MethodsThe impact of p.N666H on PDGFRB function and sensitivity to imatinib was studied in cell culture.ResultsCells expressing the p.N666H mutation showed constitutive PDGFRB tyrosine phosphorylation.	imatinib	120-128	platelet derived growth factor receptor beta	Homo sapiens	146-152
28726812-2	2018	We describe a 10-year-old child with a germ-line PDGFRB p.N666H mutation who responded to the tyrosine kinase inhibitor imatinib by inhibition of PDGFRB.MethodsThe impact of p.N666H on PDGFRB function and sensitivity to imatinib was studied in cell culture.ResultsCells expressing the p.N666H mutation showed constitutive PDGFRB tyrosine phosphorylation.	imatinib	120-128	platelet derived growth factor receptor beta	Homo sapiens	146-152
28726812-2	2018	We describe a 10-year-old child with a germ-line PDGFRB p.N666H mutation who responded to the tyrosine kinase inhibitor imatinib by inhibition of PDGFRB.MethodsThe impact of p.N666H on PDGFRB function and sensitivity to imatinib was studied in cell culture.ResultsCells expressing the p.N666H mutation showed constitutive PDGFRB tyrosine phosphorylation.	imatinib	220-228	platelet derived growth factor receptor beta	Homo sapiens	49-55
30007969-0	2018	Imatinib Ameliorated Retinal Neovascularization by Suppressing PDGFR-alpha and PDGFR-beta.	imatinib	0-8	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	63-74
30007969-0	2018	Imatinib Ameliorated Retinal Neovascularization by Suppressing PDGFR-alpha and PDGFR-beta.	imatinib	0-8	platelet derived growth factor receptor, beta polypeptide	Mus musculus	79-89
30007969-2	2018	Here we evaluated the anti-angiogenic effect of imatinib, an inhibitor of PDGF receptors alpha and beta (PDGFR-alpha and -beta), in retinal neovascularization using an oxygen-induced retinopathy (OIR) model.	imatinib	48-56	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	105-126
29143894-1	2018	Imatinib has revolutionized the treatment of GIST since this drug is able to inhibit tumoral growth by blocking the activity of receptor tyrosine kinases, KIT or PDGFRA, that in these tumors are constitutively activated because of the presence of mutations that alters their catalytic activity.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	162-168
29061656-4	2018	2-(Benzylsulfonyl)-1-(1H-indol-3-yl)-1,2-dihydroisoquinoline (IBR2) inhibits RAD51-mediated DNA double-strand break repair but also enhances cytotoxicity of the Bcr-Abl inhibitor imatinib.	imatinib	179-187	RAD51 recombinase	Homo sapiens	77-82
29115375-0	2018	Persistent STAT5-mediated ROS production and involvement of aberrant p53 apoptotic signaling in the resistance of chronic myeloid leukemia to imatinib.	imatinib	142-150	signal transducer and activator of transcription 5A	Homo sapiens	11-16
29115375-0	2018	Persistent STAT5-mediated ROS production and involvement of aberrant p53 apoptotic signaling in the resistance of chronic myeloid leukemia to imatinib.	imatinib	142-150	tumor protein p53	Homo sapiens	69-72
29115375-3	2018	In the present study, it was observed that the mRNA levels of STAT5A and STAT5B were upregulated in patients with imatinib-resistant CML and in the imatinib-resistant K562/G CML cell line.	imatinib	114-122	signal transducer and activator of transcription 5A	Homo sapiens	62-68
29115375-3	2018	In the present study, it was observed that the mRNA levels of STAT5A and STAT5B were upregulated in patients with imatinib-resistant CML and in the imatinib-resistant K562/G CML cell line.	imatinib	114-122	signal transducer and activator of transcription 5B	Homo sapiens	73-79
29115375-3	2018	In the present study, it was observed that the mRNA levels of STAT5A and STAT5B were upregulated in patients with imatinib-resistant CML and in the imatinib-resistant K562/G CML cell line.	imatinib	148-156	signal transducer and activator of transcription 5A	Homo sapiens	62-68
29115375-3	2018	In the present study, it was observed that the mRNA levels of STAT5A and STAT5B were upregulated in patients with imatinib-resistant CML and in the imatinib-resistant K562/G CML cell line.	imatinib	148-156	signal transducer and activator of transcription 5B	Homo sapiens	73-79
29115375-4	2018	In addition, increased expression of STAT5 was observed in the BCR-ABL1 mutation group, compared with that in the non-BCR-ABL1 mutation group, regardless of patient imatinib resistance state.	imatinib	165-173	signal transducer and activator of transcription 5A	Homo sapiens	37-42
29115375-10	2018	Taken together, these findings suggest that the resistance of CML to the tyrosine kinase inhibitor, imatinib, may be associated with persistent STAT5-mediated ROS production, and the abnormality of the p53 pathway.	imatinib	100-108	signal transducer and activator of transcription 5A	Homo sapiens	144-149
29115375-10	2018	Taken together, these findings suggest that the resistance of CML to the tyrosine kinase inhibitor, imatinib, may be associated with persistent STAT5-mediated ROS production, and the abnormality of the p53 pathway.	imatinib	100-108	tumor protein p53	Homo sapiens	202-205
30055547-4	2018	Among the study group analyzed, a significantly higher frequency of BCR/ABL1 gene rearrangements that is consistent with der(9) deletion were observed in the blast crisis (BC) phase at 41.67%, followed by the accelerated phase (AP) at 36.84%, the imatinib mesylate (IM)-resistant chronic phase (CP) at 23.08%, and the lowest incidence was found in de novo CP at 16.61%.	imatinib	247-264	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-76
29061656-9	2018	A vincristine-resistant squamous cell line was not cross resistant to imatinib, but IBR2 and another RAD51 inhibitor (B02) enhanced imatinib toxicity in this cell line, its HN-5a parent, and the colon cancer line HT-29 by up to 60% and much better than verapamil, a P-glycoprotein inhibitor (P &lt; 0.05).	imatinib	132-140	RAD51 recombinase	Homo sapiens	101-106
29149649-0	2018	Chk1 inhibitors overcome imatinib resistance in chronic myeloid leukemia cells.	imatinib	25-33	checkpoint kinase 1	Homo sapiens	0-4
28540759-0	2018	Baseline BCR-ABL1 transcript type of e13a2 and large spleen size are predictors of poor long-term outcomes in chronic phase chronic myeloid leukemia patients who failed to achieve an early molecular response after 3 months of imatinib therapy.	imatinib	226-234	BCR activator of RhoGEF and GTPase	Homo sapiens	9-17
29149649-3	2018	In our study, Chk1 inhibitors, AZD7762 and MK-8776, had strong antitumor effects on CML cell line KBM5 and imatinib-resistant form KBM5T315I.	imatinib	107-115	checkpoint kinase 1	Homo sapiens	14-18
29149649-4	2018	Moreover, Chk1 inhibitors showed a strong cytotoxic effect on leukemia cells from primary CML and imatinib-resistance CML patients, but low cytotoxic effect on normal human mononuclear cells.	imatinib	98-106	checkpoint kinase 1	Homo sapiens	10-14
30101875-13	2018	GISTs with PDGFRA D842V mutations are reportedly resistant to imatinib, and GISTs originating from the stomach are reportedly less malignant than others.	imatinib	62-70	platelet derived growth factor receptor alpha	Homo sapiens	11-17
29295963-1	2018	In an article published on September, 2017, in Molecular Cancer Therapeutics, Zeng and colleagues showed that the WNT/beta-catenin oncogenic pathway was activated in a subset of human gastrointestinal stromal tumors (GIST) and that inhibiting its signaling alone or in combination with imatinib has antitumor efficacy in vitro and in vivo in imatinib-sensitive and resistant preclinical models.	imatinib	286-294	catenin beta 1	Homo sapiens	118-130
29295963-1	2018	In an article published on September, 2017, in Molecular Cancer Therapeutics, Zeng and colleagues showed that the WNT/beta-catenin oncogenic pathway was activated in a subset of human gastrointestinal stromal tumors (GIST) and that inhibiting its signaling alone or in combination with imatinib has antitumor efficacy in vitro and in vivo in imatinib-sensitive and resistant preclinical models.	imatinib	342-350	catenin beta 1	Homo sapiens	118-130
30286478-10	2018	In 3 patients KIT mutations (e.g. pM541L, pV654A) known to be tissue-based biomarkers with level 1 evidence for the treatment with imatinib and sunitinib were found.	imatinib	131-139	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-17
29192326-8	2018	Notably, attenuation of EPS8 increased chemosensitivity both in imatinib-sensitive K562 cells and in the imatinib-resistant murine BCR-ABL+ 32D-p210BCR/ABL-T315I cells.	imatinib	64-72	epidermal growth factor receptor pathway substrate 8	Homo sapiens	24-28
29192326-8	2018	Notably, attenuation of EPS8 increased chemosensitivity both in imatinib-sensitive K562 cells and in the imatinib-resistant murine BCR-ABL+ 32D-p210BCR/ABL-T315I cells.	imatinib	105-113	epidermal growth factor receptor pathway substrate 8	Homo sapiens	24-28
30531135-2	2018	While undergoing induction therapy combined with imatinib, she experienced intense anal pain a day after the four-time administration of L-ASP.	imatinib	49-57	asparaginase and isoaspartyl peptidase 1	Homo sapiens	137-142
30069623-3	2018	Imatinib is a rationally designed oral signal transduction inhibitor that specifically targets several protein tyrosine kinases, Abl, Arg (Abl-related gene), the stem cell factor receptor (c-KIT), platelet-derived growth factor receptor (PDGF-R), and their oncogenic forms, most notably BCR-ABL.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-132
30069623-3	2018	Imatinib is a rationally designed oral signal transduction inhibitor that specifically targets several protein tyrosine kinases, Abl, Arg (Abl-related gene), the stem cell factor receptor (c-KIT), platelet-derived growth factor receptor (PDGF-R), and their oncogenic forms, most notably BCR-ABL.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-142
30069623-3	2018	Imatinib is a rationally designed oral signal transduction inhibitor that specifically targets several protein tyrosine kinases, Abl, Arg (Abl-related gene), the stem cell factor receptor (c-KIT), platelet-derived growth factor receptor (PDGF-R), and their oncogenic forms, most notably BCR-ABL.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	189-194
30069623-3	2018	Imatinib is a rationally designed oral signal transduction inhibitor that specifically targets several protein tyrosine kinases, Abl, Arg (Abl-related gene), the stem cell factor receptor (c-KIT), platelet-derived growth factor receptor (PDGF-R), and their oncogenic forms, most notably BCR-ABL.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	197-236
30069623-3	2018	Imatinib is a rationally designed oral signal transduction inhibitor that specifically targets several protein tyrosine kinases, Abl, Arg (Abl-related gene), the stem cell factor receptor (c-KIT), platelet-derived growth factor receptor (PDGF-R), and their oncogenic forms, most notably BCR-ABL.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	238-244
30069623-3	2018	Imatinib is a rationally designed oral signal transduction inhibitor that specifically targets several protein tyrosine kinases, Abl, Arg (Abl-related gene), the stem cell factor receptor (c-KIT), platelet-derived growth factor receptor (PDGF-R), and their oncogenic forms, most notably BCR-ABL.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	287-294
30305514-2	2018	In many clinical trials, beginning with the French Stop Imatinib (STIM1) trial, approximately 40%-60% patients with chronic CML who sustained a long DMR could discontinue TKI therapy and achieve long-term treatment-free remission (TFR).	imatinib	56-64	stromal interaction molecule 1	Homo sapiens	66-71
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	imatinib	16-24	microRNA 214	Homo sapiens	118-125
30504658-1	2018	Resistance to the breakpoint cluster region-abelson (BCR-ABL) tyrosine kinase inhibitor (TKI), imatinib, poses a major problem in the treatment of chronic myeloid leukemia (CML).	imatinib	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
30504658-2	2018	Imatinib resistance often results from a secondary mutation in BCR-ABL1.	imatinib	0-8	BCR activator of RhoGEF and GTPase	Homo sapiens	63-71
30069623-8	2018	Clonal evolution, amplification, or overexpression of BCR-ABL as well as mutations in the catalytic domain, P-loop, and other mutations have been demonstrated to play a role in primary and secondary resistance to imatinib, respectively.	imatinib	213-221	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
30504658-1	2018	Resistance to the breakpoint cluster region-abelson (BCR-ABL) tyrosine kinase inhibitor (TKI), imatinib, poses a major problem in the treatment of chronic myeloid leukemia (CML).	imatinib	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-51
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	imatinib	16-24	membrane associated ring-CH-type finger 8	Homo sapiens	58-61
30504658-5	2018	To gain insight into BCR-ABL1-independent imatinib resistance mechanisms, we performed an array-based comparative genomic hybridization.	imatinib	42-50	BCR activator of RhoGEF and GTPase	Homo sapiens	21-29
30504658-8	2018	A treatment combining imatinib and a MET inhibitor in K562/IR cells inhibited extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun N-terminal kinase (JNK) activation, but did not affect AKT activation.	imatinib	22-30	mitogen-activated protein kinase 1	Homo sapiens	78-119
30504658-8	2018	A treatment combining imatinib and a MET inhibitor in K562/IR cells inhibited extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun N-terminal kinase (JNK) activation, but did not affect AKT activation.	imatinib	22-30	mitogen-activated protein kinase 3	Homo sapiens	121-127
30504658-8	2018	A treatment combining imatinib and a MET inhibitor in K562/IR cells inhibited extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun N-terminal kinase (JNK) activation, but did not affect AKT activation.	imatinib	22-30	mitogen-activated protein kinase 8	Homo sapiens	133-156
30504658-8	2018	A treatment combining imatinib and a MET inhibitor in K562/IR cells inhibited extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun N-terminal kinase (JNK) activation, but did not affect AKT activation.	imatinib	22-30	mitogen-activated protein kinase 8	Homo sapiens	158-161
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	imatinib	16-24	membrane associated ring-CH-type finger 8	Homo sapiens	118-121
30504658-11	2018	Our findings provide new and important information concerning the mechanisms of imatinib resistance in CML, and reveal new proteins potentially involved in BCR-ABL TKI resistance.	imatinib	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	imatinib	16-24	membrane associated ring-CH-type finger 8	Homo sapiens	118-121
29552859-8	2018	The results indicated that PD increased the sensitivity of drug-resistant cells to imatinib, and the inhibitory effect of PD combined with imatinib was significantly better than the single drug on cell proliferation, induction of apoptosis, inhibition of Bcr/abl protein and PI3K/AKT/mTOR signaling pathway.	imatinib	139-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	255-262
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	imatinib	16-24	microRNA 27b	Homo sapiens	166-173
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	imatinib	16-24	microRNA 23b	Homo sapiens	179-186
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	imatinib	16-24	microRNA 320e	Homo sapiens	192-200
29552859-8	2018	The results indicated that PD increased the sensitivity of drug-resistant cells to imatinib, and the inhibitory effect of PD combined with imatinib was significantly better than the single drug on cell proliferation, induction of apoptosis, inhibition of Bcr/abl protein and PI3K/AKT/mTOR signaling pathway.	imatinib	139-147	AKT serine/threonine kinase 1	Homo sapiens	280-283
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	imatinib	16-24	membrane associated ring-CH-type finger 8	Homo sapiens	118-121
29552859-8	2018	The results indicated that PD increased the sensitivity of drug-resistant cells to imatinib, and the inhibitory effect of PD combined with imatinib was significantly better than the single drug on cell proliferation, induction of apoptosis, inhibition of Bcr/abl protein and PI3K/AKT/mTOR signaling pathway.	imatinib	139-147	mechanistic target of rapamycin kinase	Homo sapiens	284-288
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	imatinib	16-24	membrane associated ring-CH-type finger 8	Homo sapiens	118-121
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	imatinib	16-24	microRNA 33a	Homo sapiens	228-234
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	imatinib	16-24	microRNA 766	Homo sapiens	243-250
29423045-6	2018	Furthermore, we showed that Ova alone or by enhancing the therapeutic potential of Imatinib, reduced the viability of CML cell lines, dose-dependently, irrespective of the cancer stemness, as well as markedly inhibit the Bcr-Abl, p-CrkL, Stat5, and MDR protein expression levels in CD34+ cells.	imatinib	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	221-228
29404396-2	2018	By simultaneously disrupting mitochondrial respiration and inhibiting BCR-ABL kinase activity using the antibiotic tigecycline and imatinib respectively, we effectively eradicated LSCs and prevented disease relapse in pre-clinical animal models.	imatinib	131-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
29423056-3	2018	Interestingly, Imatinib and second-generation tyrosine kinase inhibitors specifically increase ZNF224 expression.	imatinib	15-23	zinc finger protein 224	Homo sapiens	95-101
29423056-7	2018	We also show that ZNF224 induction by Imatinib and AG490, a specific JAK2 inhibitor, is responsible for the transcriptional repression of c-MYC, thus highlighting the crucial role of the ZNF224/c-Myc axis in Imatinib responsiveness.	imatinib	38-46	zinc finger protein 224	Homo sapiens	18-24
29423056-7	2018	We also show that ZNF224 induction by Imatinib and AG490, a specific JAK2 inhibitor, is responsible for the transcriptional repression of c-MYC, thus highlighting the crucial role of the ZNF224/c-Myc axis in Imatinib responsiveness.	imatinib	38-46	Janus kinase 2	Homo sapiens	69-73
29423056-7	2018	We also show that ZNF224 induction by Imatinib and AG490, a specific JAK2 inhibitor, is responsible for the transcriptional repression of c-MYC, thus highlighting the crucial role of the ZNF224/c-Myc axis in Imatinib responsiveness.	imatinib	38-46	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	138-143
29423056-7	2018	We also show that ZNF224 induction by Imatinib and AG490, a specific JAK2 inhibitor, is responsible for the transcriptional repression of c-MYC, thus highlighting the crucial role of the ZNF224/c-Myc axis in Imatinib responsiveness.	imatinib	38-46	zinc finger protein 224	Homo sapiens	187-193
29423056-7	2018	We also show that ZNF224 induction by Imatinib and AG490, a specific JAK2 inhibitor, is responsible for the transcriptional repression of c-MYC, thus highlighting the crucial role of the ZNF224/c-Myc axis in Imatinib responsiveness.	imatinib	38-46	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	194-199
29423056-7	2018	We also show that ZNF224 induction by Imatinib and AG490, a specific JAK2 inhibitor, is responsible for the transcriptional repression of c-MYC, thus highlighting the crucial role of the ZNF224/c-Myc axis in Imatinib responsiveness.	imatinib	208-216	zinc finger protein 224	Homo sapiens	18-24
29423056-7	2018	We also show that ZNF224 induction by Imatinib and AG490, a specific JAK2 inhibitor, is responsible for the transcriptional repression of c-MYC, thus highlighting the crucial role of the ZNF224/c-Myc axis in Imatinib responsiveness.	imatinib	208-216	Janus kinase 2	Homo sapiens	69-73
29423056-7	2018	We also show that ZNF224 induction by Imatinib and AG490, a specific JAK2 inhibitor, is responsible for the transcriptional repression of c-MYC, thus highlighting the crucial role of the ZNF224/c-Myc axis in Imatinib responsiveness.	imatinib	208-216	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	138-143
29423056-7	2018	We also show that ZNF224 induction by Imatinib and AG490, a specific JAK2 inhibitor, is responsible for the transcriptional repression of c-MYC, thus highlighting the crucial role of the ZNF224/c-Myc axis in Imatinib responsiveness.	imatinib	208-216	zinc finger protein 224	Homo sapiens	187-193
29423056-7	2018	We also show that ZNF224 induction by Imatinib and AG490, a specific JAK2 inhibitor, is responsible for the transcriptional repression of c-MYC, thus highlighting the crucial role of the ZNF224/c-Myc axis in Imatinib responsiveness.	imatinib	208-216	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	194-199
29423056-8	2018	Interestingly, we also report that ZNF224 is induced by AG490 in Imatinib-resistant CML cells, leading to c-Myc repression and apoptosis induction.	imatinib	65-73	zinc finger protein 224	Homo sapiens	35-41
29423056-8	2018	Interestingly, we also report that ZNF224 is induced by AG490 in Imatinib-resistant CML cells, leading to c-Myc repression and apoptosis induction.	imatinib	65-73	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	106-111
29423056-9	2018	These findings suggest that the development of molecular tools able to induce ZNF224 expression could provide promising means to bypass Imatinib resistance in CML.	imatinib	136-144	zinc finger protein 224	Homo sapiens	78-84
29423045-8	2018	Additionally, Ova alone or in combination with Imatinib suppressed the hCSC traits of the CD34+/CD38- cells, resulting in loss of their ability to form tumorspheres, enhanced apoptosis, increase in the Bax/Bcl-2 ratio, and dysregulation of the PI3K/AKT/mTOR signaling pathway.	imatinib	47-55	CD34 molecule	Homo sapiens	90-94
29423045-8	2018	Additionally, Ova alone or in combination with Imatinib suppressed the hCSC traits of the CD34+/CD38- cells, resulting in loss of their ability to form tumorspheres, enhanced apoptosis, increase in the Bax/Bcl-2 ratio, and dysregulation of the PI3K/AKT/mTOR signaling pathway.	imatinib	47-55	CD38 molecule	Homo sapiens	96-100
29423045-8	2018	Additionally, Ova alone or in combination with Imatinib suppressed the hCSC traits of the CD34+/CD38- cells, resulting in loss of their ability to form tumorspheres, enhanced apoptosis, increase in the Bax/Bcl-2 ratio, and dysregulation of the PI3K/AKT/mTOR signaling pathway.	imatinib	47-55	BCL2 associated X, apoptosis regulator	Homo sapiens	202-205
29423045-8	2018	Additionally, Ova alone or in combination with Imatinib suppressed the hCSC traits of the CD34+/CD38- cells, resulting in loss of their ability to form tumorspheres, enhanced apoptosis, increase in the Bax/Bcl-2 ratio, and dysregulation of the PI3K/AKT/mTOR signaling pathway.	imatinib	47-55	BCL2 apoptosis regulator	Homo sapiens	206-211
29423045-8	2018	Additionally, Ova alone or in combination with Imatinib suppressed the hCSC traits of the CD34+/CD38- cells, resulting in loss of their ability to form tumorspheres, enhanced apoptosis, increase in the Bax/Bcl-2 ratio, and dysregulation of the PI3K/AKT/mTOR signaling pathway.	imatinib	47-55	AKT serine/threonine kinase 1	Homo sapiens	249-252
29423045-8	2018	Additionally, Ova alone or in combination with Imatinib suppressed the hCSC traits of the CD34+/CD38- cells, resulting in loss of their ability to form tumorspheres, enhanced apoptosis, increase in the Bax/Bcl-2 ratio, and dysregulation of the PI3K/AKT/mTOR signaling pathway.	imatinib	47-55	mechanistic target of rapamycin kinase	Homo sapiens	253-257
29046392-5	2017	Here, we reported that nutlin-3 plus tanshinone IIA significantly potentiated the cytotoxic and apoptotic induction effects of imatinib by downregulation of the AKT/mTOR pathway and reactivating p53 pathway deeply in Ph+ acute lymphoblastic leukemia cell line.	imatinib	127-135	AKT serine/threonine kinase 1	Homo sapiens	161-164
28986256-9	2017	Taken together, our results showed that miR-7 inhibited proliferation and promoted apoptosis in K562 cells, and miR-7 might help to sensitize them to imatinib through BCR-ABL/PI3K/AKT signaling in chronic myeloid leukemia.	imatinib	150-158	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-174
28986256-9	2017	Taken together, our results showed that miR-7 inhibited proliferation and promoted apoptosis in K562 cells, and miR-7 might help to sensitize them to imatinib through BCR-ABL/PI3K/AKT signaling in chronic myeloid leukemia.	imatinib	150-158	AKT serine/threonine kinase 1	Homo sapiens	180-183
29046392-5	2017	Here, we reported that nutlin-3 plus tanshinone IIA significantly potentiated the cytotoxic and apoptotic induction effects of imatinib by downregulation of the AKT/mTOR pathway and reactivating p53 pathway deeply in Ph+ acute lymphoblastic leukemia cell line.	imatinib	127-135	mechanistic target of rapamycin kinase	Homo sapiens	165-169
29046392-5	2017	Here, we reported that nutlin-3 plus tanshinone IIA significantly potentiated the cytotoxic and apoptotic induction effects of imatinib by downregulation of the AKT/mTOR pathway and reactivating p53 pathway deeply in Ph+ acute lymphoblastic leukemia cell line.	imatinib	127-135	tumor protein p53	Homo sapiens	195-198
29230387-1	2017	Background: Imatinib mesylate is an inhibitor of the tyrosine kinase Bcr-Abl and a first-line treatment for Philadelphia chromosome-positive chronic myeloid leukaemia (CML).	imatinib	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
29032022-1	2017	The second-generation tyrosine kinase inhibitors (TKIs) (2G-TKIs) dasatinib (DAS) and nilotinib (NIL) yield faster responses in newly diagnosed chronic phase (CP) chronic myeloid leukemia (CML) as compared with imatinib (IM); however, long-term safety of these agents is a growing concern.	imatinib	211-219	TXK tyrosine kinase	Homo sapiens	22-37
28928163-0	2017	High BCR-ABL/GUSIS Levels at Diagnosis of Chronic Phase CML Are Associated with Unfavorable Responses to Standard-Dose Imatinib.	imatinib	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	5-12
28928163-7	2017	However, in internal validation experiments, GUS outperformed ABL in samples collected at diagnosis as the latter produced 80% misclassification rates.Conclusions: Our data suggest that high BCR-ABL transcripts at diagnosis measured using GUS as a reference gene identify patients with CML unlikely to benefit from standard-dose imatinib.	imatinib	329-337	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	191-198
28589317-8	2017	Regarding these results, it might be concluded that Bcl6 knockdown combined with PMA therapy could present a new therapeutical strategy for refractory CML patients to imatinib.	imatinib	167-175	BCL6 transcription repressor	Homo sapiens	52-56
29043985-11	2017	Lack of therapeutic response and absence of the KIT D816V mutation led to switch to imatinib, following the latest scientific recommendations.	imatinib	84-92	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	48-51
28988501-6	2017	The first effective systemic therapy in clinical practice in GIST and DFSP was imatinib - tyrosine kinase inhibitor acting on KIT and PDGFR alpha/beta.	imatinib	79-87	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	126-129
28988501-6	2017	The first effective systemic therapy in clinical practice in GIST and DFSP was imatinib - tyrosine kinase inhibitor acting on KIT and PDGFR alpha/beta.	imatinib	79-87	platelet derived growth factor receptor alpha	Homo sapiens	134-145
27698265-1	2017	The BCR-ABL kinase inhibitor, imatinib mesylate, is the front-line treatment for chronic myeloid leukemia, but the emergence of imatinib resistance has led to the search for alternative drug treatments.	imatinib	30-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
27698265-1	2017	The BCR-ABL kinase inhibitor, imatinib mesylate, is the front-line treatment for chronic myeloid leukemia, but the emergence of imatinib resistance has led to the search for alternative drug treatments.	imatinib	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
29152650-0	2017	Semi-random mutagenesis profile of BCR-ABL during imatinib resistance acquirement in K562 cells.	imatinib	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
28260399-4	2017	Thus, GZD856 may serve as a promising lead for the development of Bcr-Abl inhibitors overcoming acquired imatinib resistance.	imatinib	105-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
28882611-4	2017	Treatment of v-Abl/Bcl2 pro-B cells with the Abl kinase inhibitor Imatinib leads to G1 cell cycle arrest, the rapid induction of Rag1/2 gene expression and V(D)J recombination.	imatinib	66-74	B cell leukemia/lymphoma 2	Mus musculus	19-23
28882611-4	2017	Treatment of v-Abl/Bcl2 pro-B cells with the Abl kinase inhibitor Imatinib leads to G1 cell cycle arrest, the rapid induction of Rag1/2 gene expression and V(D)J recombination.	imatinib	66-74	recombination activating 1	Mus musculus	129-135
28882611-5	2017	In this system, the Bcl2 transgene alleviates Imatinib-induced apoptosis enabling the analysis of induced V(D)J recombination.	imatinib	46-54	B cell leukemia/lymphoma 2	Mus musculus	20-24
29245294-4	2017	However, imatinib mesylate, a specific inhibitor of KIT tyrosine kinase, frequently involves changes in the morphology and IHC staining of GIST, impeding the diagnosis.	imatinib	9-26	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	52-55
29245294-13	2017	However, ISH for ETV1 mRNA done for both biopsied and resected tumors was positive, even after imatinib treatment.	imatinib	95-103	ETS variant transcription factor 1	Homo sapiens	17-21
29245294-14	2017	A molecular analysis found a mutation in exon 11 of KIT gene before and after imatinib therapy in both patients, confirming the diagnosis of GIST.	imatinib	78-86	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	52-55
29245294-17	2017	LESSONS: ISH for ETV1 mRNA is a useful technique in diagnosing GIST when IHC with KIT, DOG1, or CD34 fail to stain positive after imatinib therapy.	imatinib	130-138	ETS variant transcription factor 1	Homo sapiens	17-21
29152650-4	2017	Clone sequencing of the BCR-ABL gene and other control genes was applied in two imatinib-resistant cell models.	imatinib	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
29152650-5	2017	The results have indicated that imatinib actively and selectively causes sporadic mutations in the BCR-ABL gene, however not in the control genes.	imatinib	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
29044676-9	2017	Identification of rearranged PDGFRA or PDGFRB is critical because of the exquisite responsiveness of these diseases to imatinib.	imatinib	119-127	platelet derived growth factor receptor alpha	Homo sapiens	29-35
29312652-4	2017	The most common mutation in PDGFRalpha, D842V, is known to be imatinib resistant.	imatinib	62-70	platelet derived growth factor receptor alpha	Homo sapiens	28-38
29312652-5	2017	Almost all other PDGFRalpha mutations are imatinib sensitive.	imatinib	42-50	platelet derived growth factor receptor alpha	Homo sapiens	17-27
29312652-9	2017	Computer 3D-modeling of the PDGFRalpha kinase domain of these two variants revealed no direct interference in imatinib or sunitinib binding and no effect in its activity in contrast to the reported structure of the imatinib resistant D842V mutation.	imatinib	215-223	platelet derived growth factor receptor alpha	Homo sapiens	28-38
28965860-2	2017	Imatinib inhibits two key profibrotic pathways; platelet-derived growth factor (PDGF) and transforming growth factor-beta (TGF-beta) and thus can be used to treat liver fibrosis.	imatinib	0-8	transforming growth factor, beta 1	Rattus norvegicus	123-131
29176653-9	2017	Subsequent studies found that inhibition of c-Kit activity using imatinib mesylate (Gleevec ) blocked estrogen mediated stimulation of BCK4 tumors and BCK4 cells in vitro as effectively as the anti-estrogen fulvestrant (Faslodex ).	imatinib	65-82	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	44-49
29176653-9	2017	Subsequent studies found that inhibition of c-Kit activity using imatinib mesylate (Gleevec ) blocked estrogen mediated stimulation of BCK4 tumors and BCK4 cells in vitro as effectively as the anti-estrogen fulvestrant (Faslodex ).	imatinib	84-91	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	44-49
29127277-3	2017	Masitinib, as well as other protein kinase inhibitors, such as imatinib, interact with dCK and provoke an unforeseen conformational-dependent activation of this nucleoside kinase, modulating phosphorylation of nucleoside analogue drugs.	imatinib	63-71	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	87-90
29044676-9	2017	Identification of rearranged PDGFRA or PDGFRB is critical because of the exquisite responsiveness of these diseases to imatinib.	imatinib	119-127	platelet derived growth factor receptor beta	Homo sapiens	39-45
28852787-0	2017	Exploring the binding of two potent anticancer drugs bosutinib and imatinib mesylate with bovine serum albumin: spectroscopic and molecular dynamic simulation studies.	imatinib	67-75	albumin	Homo sapiens	97-110
29075042-4	2017	However, Abl kinase inhibition by imatinib reduces rapid redistribution of the important cytoskeletal proteins to the periphery and their association with the cortical actin ring.	imatinib	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-12
28822797-0	2017	Influence of BCR-ABL Transcript Type on Outcome in Patients With Chronic-Phase Chronic Myeloid Leukemia Treated With Imatinib.	imatinib	117-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
29054076-10	2017	CONCLUSION: In addition to KIT exon 9 mutation and synchronous metastases, SNPs in KDR, VEGFA and SLCO1B3 appear to be associated with PFS in patients with advanced GIST receiving 400-mg imatinib.	imatinib	187-195	kinase insert domain receptor	Homo sapiens	83-86
29054076-10	2017	CONCLUSION: In addition to KIT exon 9 mutation and synchronous metastases, SNPs in KDR, VEGFA and SLCO1B3 appear to be associated with PFS in patients with advanced GIST receiving 400-mg imatinib.	imatinib	187-195	solute carrier organic anion transporter family member 1B3	Homo sapiens	98-105
29113157-3	2017	Gastrointestinal stromal tumor (GIST) development is associated with activating mutations of KIT proto-oncogene receptor tyrosine kinase (KIT) or platelet-derived growth factor receptor alpha (PDGFRA), which are oncogenes that predict the response to imatinib mesylate.	imatinib	251-268	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	93-136
29113157-3	2017	Gastrointestinal stromal tumor (GIST) development is associated with activating mutations of KIT proto-oncogene receptor tyrosine kinase (KIT) or platelet-derived growth factor receptor alpha (PDGFRA), which are oncogenes that predict the response to imatinib mesylate.	imatinib	251-268	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	93-96
29113157-3	2017	Gastrointestinal stromal tumor (GIST) development is associated with activating mutations of KIT proto-oncogene receptor tyrosine kinase (KIT) or platelet-derived growth factor receptor alpha (PDGFRA), which are oncogenes that predict the response to imatinib mesylate.	imatinib	251-268	platelet derived growth factor receptor alpha	Homo sapiens	146-191
29113157-3	2017	Gastrointestinal stromal tumor (GIST) development is associated with activating mutations of KIT proto-oncogene receptor tyrosine kinase (KIT) or platelet-derived growth factor receptor alpha (PDGFRA), which are oncogenes that predict the response to imatinib mesylate.	imatinib	251-268	platelet derived growth factor receptor alpha	Homo sapiens	193-199
28862704-0	2017	Sustained deep molecular responses in patients switched to nilotinib due to persistent BCR-ABL1 on imatinib: final ENESTcmr randomized trial results.	imatinib	99-107	BCR activator of RhoGEF and GTPase	Homo sapiens	87-95
28901467-10	2017	Following imatinib treatment, the expression of SOX4 was downregulated in the progression-free patients, but upregulated in the blastic phase patients, whereas the expression of C/EBPalpha showed the opposite trend.	imatinib	10-18	SRY-box transcription factor 4	Homo sapiens	48-52
28901467-10	2017	Following imatinib treatment, the expression of SOX4 was downregulated in the progression-free patients, but upregulated in the blastic phase patients, whereas the expression of C/EBPalpha showed the opposite trend.	imatinib	10-18	CCAAT enhancer binding protein alpha	Homo sapiens	178-188
28650474-4	2017	To address this issue, we established a TKI-resistant ETV6-ABL1-positive leukemic cell line through long-term exposure to imatinib.	imatinib	122-130	ETS variant transcription factor 6	Homo sapiens	54-58
28650474-4	2017	To address this issue, we established a TKI-resistant ETV6-ABL1-positive leukemic cell line through long-term exposure to imatinib.	imatinib	122-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-63
28803208-6	2017	In addition, UGT1A4 and UGT2B10 were primarily responsible for N-glucuronidation of many tertiary amines, including asenapine, loxapine, clozapine, chlorpromazine, dothiepin, doxepin, mirtazapine, mianserin, chlorcyclizine, cyclizine, promethazine, cyclobenzaprine, imatinib, retrorsine, strychnine and brucine.	imatinib	266-274	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	13-19
29187870-11	2017	Moreover, the presence of Snail or Twist1 partially blocked phorbol 12-myristate 13-acetate-induced megakaryocyte differentiation, while that of Twist significantly altered imatinib-induced erythroid differentiation.	imatinib	173-181	snail family transcriptional repressor 1	Homo sapiens	26-31
28803208-6	2017	In addition, UGT1A4 and UGT2B10 were primarily responsible for N-glucuronidation of many tertiary amines, including asenapine, loxapine, clozapine, chlorpromazine, dothiepin, doxepin, mirtazapine, mianserin, chlorcyclizine, cyclizine, promethazine, cyclobenzaprine, imatinib, retrorsine, strychnine and brucine.	imatinib	266-274	UDP glucuronosyltransferase family 2 member B10	Homo sapiens	24-31
28790106-2	2017	Imatinib treatment, which inhibits KIT signaling, depletes mast cells in vivo.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	35-38
28923937-7	2017	Moreover, combining PI3K and MEK inhibition was effective against imatinib-resistant KitV558Delta;T669I/+ tumors.	imatinib	66-74	midkine	Mus musculus	29-32
28982129-5	2017	Moreover, imatinib treatment also largely abolished the lower levels of inflammation which developed in IL-1R1-/- or KitW-sh/W-sh mice, indicating that this drug can inhibit IL-1-independent pathways, as well as mast cell-independent pathways, contributing to pathology in this model.	imatinib	10-18	interleukin 1 receptor, type I	Mus musculus	104-110
28829147-7	2017	Calorimetric experiments on two drugs, telmisartan and imatinib, revealed that L-PGDS forms a 1:2 complex with each drug, with dissociation constants of 0.4-40.0 muM.	imatinib	55-63	prostaglandin D2 synthase	Homo sapiens	79-85
28421416-1	2017	PURPOSE: The KIT inhibitor, imatinib, has shown promising efficacy in patients with KIT-mutated melanoma; however, acquisition of resistance to imatinib occurs rapidly in the majority of patients.	imatinib	28-36	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	13-16
28836054-0	2017	Molecular study of ABCB1 gene and its correlation with imatinib response in chronic myeloid leukemia.	imatinib	55-63	ATP binding cassette subfamily B member 1	Homo sapiens	19-24
28836054-3	2017	Three single-nucleotide polymorphisms (C1236T, G2677T/A, C3435T) and/or mRNA expression changes of ABCB1 gene were demonstrated to be associated with inter-individual variability of imatinib response in CML patients.	imatinib	182-190	ATP binding cassette subfamily B member 1	Homo sapiens	99-104
28421416-1	2017	PURPOSE: The KIT inhibitor, imatinib, has shown promising efficacy in patients with KIT-mutated melanoma; however, acquisition of resistance to imatinib occurs rapidly in the majority of patients.	imatinib	28-36	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	84-87
28421416-1	2017	PURPOSE: The KIT inhibitor, imatinib, has shown promising efficacy in patients with KIT-mutated melanoma; however, acquisition of resistance to imatinib occurs rapidly in the majority of patients.	imatinib	144-152	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	13-16
28421416-3	2017	METHODS: We analyzed biopsy samples from paired baseline and post-treatment tumor lesions in one patient with KIT-mutated melanoma who had had an initial objective tumor regression in response to imatinib treatment followed by disease progression 8 months later.	imatinib	196-204	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	110-113
28421416-7	2017	CONCLUSIONS: We report the first identification of the emergence of a CTNNB1 mutation that can confer acquired resistance to imatinib.	imatinib	125-133	catenin beta 1	Homo sapiens	70-76
28421416-8	2017	Further investigation into the causes of acquired resistance to imatinib will be essential to improve the prognosis for patients with KIT-mutated melanoma.	imatinib	64-72	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	134-137
28765927-0	2017	A decrease in ubiquitination and resulting prolonged life-span of KIT underlies the KIT overexpression-mediated imatinib resistance of KIT mutation-driven canine mast cell tumor cells.	imatinib	112-120	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	66-69
28836054-4	2017	In this study, we aimed to examine whether genetic variations and/or altered expression of ABCB1 gene may influence response to imatinib.	imatinib	128-136	ATP binding cassette subfamily B member 1	Homo sapiens	91-96
28836054-11	2017	However, haplotype analysis showed that the 1236C-2677A-3435C haplotype was observed only in imatinib non-responders" patients suggesting that CAC haplotype was linked to higher risk of imatinib resistance.	imatinib	93-101	carbonic anhydrase 2	Homo sapiens	143-146
28836054-11	2017	However, haplotype analysis showed that the 1236C-2677A-3435C haplotype was observed only in imatinib non-responders" patients suggesting that CAC haplotype was linked to higher risk of imatinib resistance.	imatinib	186-194	carbonic anhydrase 2	Homo sapiens	143-146
28836054-12	2017	CONCLUSION: Furthermore, analyses of ABCB1 haplotypes should be taken into account to study the relationship between ABCB1 genotypes and imatinib efficacy.	imatinib	137-145	ATP binding cassette subfamily B member 1	Homo sapiens	37-42
28836054-12	2017	CONCLUSION: Furthermore, analyses of ABCB1 haplotypes should be taken into account to study the relationship between ABCB1 genotypes and imatinib efficacy.	imatinib	137-145	ATP binding cassette subfamily B member 1	Homo sapiens	117-122
28550414-0	2017	Dasatinib rapidly induces deep molecular response in chronic-phase chronic myeloid leukemia patients who achieved major molecular response with detectable levels of BCR-ABL1 transcripts by imatinib therapy.	imatinib	189-197	BCR activator of RhoGEF and GTPase	Homo sapiens	165-173
28550414-1	2017	BACKGROUND: With the introduction of imatinib, a first-generation tyrosine kinase inhibitor (TKI) to inhibit BCR-ABL1 kinase, the outcome of chronic-phase chronic myeloid leukemia (CP-CML) has improved dramatically.	imatinib	37-45	BCR activator of RhoGEF and GTPase	Homo sapiens	109-117
28550414-3	2017	Dasatinib, a second-generation TKI, is more potent than imatinib in the inhibition of BCR-ABL1 tyrosine kinase in vitro and more effective in CP-CML patients who do not achieve an optimal response with imatinib treatment.	imatinib	56-64	BCR activator of RhoGEF and GTPase	Homo sapiens	86-94
28765927-0	2017	A decrease in ubiquitination and resulting prolonged life-span of KIT underlies the KIT overexpression-mediated imatinib resistance of KIT mutation-driven canine mast cell tumor cells.	imatinib	112-120	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	84-87
28765927-0	2017	A decrease in ubiquitination and resulting prolonged life-span of KIT underlies the KIT overexpression-mediated imatinib resistance of KIT mutation-driven canine mast cell tumor cells.	imatinib	112-120	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	84-87
28765927-1	2017	Overexpression of KIT is one of the mechanisms that contributes to imatinib resistance in KIT mutation-driven tumors.	imatinib	67-75	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	18-21
28765927-1	2017	Overexpression of KIT is one of the mechanisms that contributes to imatinib resistance in KIT mutation-driven tumors.	imatinib	67-75	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	90-93
28765927-2	2017	Here, the mechanism underlying this overexpression of KIT was investigated using an imatinib-sensitive canine mast cell tumor (MCT) line CoMS, which has an activating mutation in KIT exon 11.	imatinib	84-92	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	54-57
28765927-2	2017	Here, the mechanism underlying this overexpression of KIT was investigated using an imatinib-sensitive canine mast cell tumor (MCT) line CoMS, which has an activating mutation in KIT exon 11.	imatinib	84-92	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	179-182
28765927-3	2017	A KIT-overexpressing imatinib-resistant subline, rCoMS1, was generated from CoMS cells by their continuous exposure to increasing concentrations of imatinib.	imatinib	21-29	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	2-5
28765927-3	2017	A KIT-overexpressing imatinib-resistant subline, rCoMS1, was generated from CoMS cells by their continuous exposure to increasing concentrations of imatinib.	imatinib	148-156	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	2-5
28765927-7	2017	These findings suggest that imatinib elicited overexpression of KIT via suppression of its ubiquitination.	imatinib	28-36	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	64-67
28765927-8	2017	These results also indicated that imatinib-induced overexpression of KIT in rCoMS1 cells was not a permanently acquired feature but was a reversible response of the cells.	imatinib	34-42	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	69-72
28765927-9	2017	Moreover, the pan deubiquitinating enzyme inhibitor PR619 prevented imatinib induction of KIT overexpression, suggesting that the imatinib-induced decrease in KIT ubiquitination could be mediated by upregulation and/or activation of deubiquitinating enzyme(s).	imatinib	68-76	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	90-93
28765927-9	2017	Moreover, the pan deubiquitinating enzyme inhibitor PR619 prevented imatinib induction of KIT overexpression, suggesting that the imatinib-induced decrease in KIT ubiquitination could be mediated by upregulation and/or activation of deubiquitinating enzyme(s).	imatinib	68-76	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	159-162
28765927-9	2017	Moreover, the pan deubiquitinating enzyme inhibitor PR619 prevented imatinib induction of KIT overexpression, suggesting that the imatinib-induced decrease in KIT ubiquitination could be mediated by upregulation and/or activation of deubiquitinating enzyme(s).	imatinib	130-138	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	90-93
28765927-9	2017	Moreover, the pan deubiquitinating enzyme inhibitor PR619 prevented imatinib induction of KIT overexpression, suggesting that the imatinib-induced decrease in KIT ubiquitination could be mediated by upregulation and/or activation of deubiquitinating enzyme(s).	imatinib	130-138	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	159-162
28765927-10	2017	It may be possible that a similar mechanism of KIT overexpression underlies the acquisition of imatinib resistance in some human tumors that are driven by KIT mutation.	imatinib	95-103	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	47-50
28765927-10	2017	It may be possible that a similar mechanism of KIT overexpression underlies the acquisition of imatinib resistance in some human tumors that are driven by KIT mutation.	imatinib	95-103	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	155-158
28962554-9	2017	Interestingly, the levels of p-Akt, p-mTOR and p-S6 are lower in cells treated with combination of propofol and imatinib than cells treated with propofol or imatinib alone, suggesting that propofol augments BCR-ABL TKI"s inhibitory effect via suppressing Akt/mTOR pathway.	imatinib	112-120	AKT serine/threonine kinase 1	Homo sapiens	31-34
29019285-0	2017	PDGFRalpha promoter polymorphisms and expression patterns influence risk of development of imatinib-induced thrombocytopenia in chronic myeloid leukemia: A study from India.	imatinib	91-99	platelet derived growth factor receptor alpha	Homo sapiens	0-10
29019285-2	2017	Platelet-derived growth factor receptor-alpha is a tyrosine kinase and a side target for imatinib, a revolutionary drug for the treatment of chronic myeloid leukemia that has dramatically improved the survival of chronic myeloid leukemia patients.	imatinib	89-97	platelet derived growth factor receptor alpha	Homo sapiens	0-45
29019285-4	2017	We hypothesized that two known functional polymorphisms, +68GA insertion/deletion and -909C/A, in the promoter region of the platelet-derived growth factor receptor-alpha gene may affect the susceptibility of chronic myeloid leukemia patients receiving imatinib treatment to the development of thrombocytopenia.	imatinib	253-261	platelet derived growth factor receptor alpha	Homo sapiens	125-170
29019285-16	2017	Moreover, patients with imatinib-induced thrombocytopenia had a significantly lower platelet-derived growth factor receptor-alpha messenger RNA expression, compared to patients without thrombocytopenia (p = 0.01).	imatinib	24-32	platelet derived growth factor receptor alpha	Homo sapiens	84-129
29019285-19	2017	The platelet-derived growth factor receptor-alpha +68GA del/del, +68GA ins/del, and -909AA genotypes are associated with an increased risk of developing thrombocytopenia in imatinib-treated chronic myeloid leukemia patients.	imatinib	173-181	platelet derived growth factor receptor alpha	Homo sapiens	4-49
29019285-22	2017	The downregulation of platelet-derived growth factor receptor-alpha expression may play a causative role in imatinib-induced thrombocytopenia, a common side effect, in the subset of chronic myeloid leukemia patients with platelet-derived growth factor receptor-alpha +68 GA ins/del, +68 GA del/del, and -909C/A genotypes.	imatinib	108-116	platelet derived growth factor receptor alpha	Homo sapiens	22-67
29019285-22	2017	The downregulation of platelet-derived growth factor receptor-alpha expression may play a causative role in imatinib-induced thrombocytopenia, a common side effect, in the subset of chronic myeloid leukemia patients with platelet-derived growth factor receptor-alpha +68 GA ins/del, +68 GA del/del, and -909C/A genotypes.	imatinib	108-116	platelet derived growth factor receptor alpha	Homo sapiens	221-266
28962554-9	2017	Interestingly, the levels of p-Akt, p-mTOR and p-S6 are lower in cells treated with combination of propofol and imatinib than cells treated with propofol or imatinib alone, suggesting that propofol augments BCR-ABL TKI"s inhibitory effect via suppressing Akt/mTOR pathway.	imatinib	112-120	mechanistic target of rapamycin kinase	Homo sapiens	38-42
28962554-9	2017	Interestingly, the levels of p-Akt, p-mTOR and p-S6 are lower in cells treated with combination of propofol and imatinib than cells treated with propofol or imatinib alone, suggesting that propofol augments BCR-ABL TKI"s inhibitory effect via suppressing Akt/mTOR pathway.	imatinib	112-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	207-214
28767619-13	2017	Higher imatinib exposure in women may be a factor in the increased rate of long-term, stable, deep molecular response (undetectable breakpoint cluster-Abelson (BCR-ABL) transcript levels with a PCR sensitivity of 4.5 log, MR4.5) reported in women.	imatinib	7-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-158
28767619-13	2017	Higher imatinib exposure in women may be a factor in the increased rate of long-term, stable, deep molecular response (undetectable breakpoint cluster-Abelson (BCR-ABL) transcript levels with a PCR sensitivity of 4.5 log, MR4.5) reported in women.	imatinib	7-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-167
29070111-7	2017	CONCLUSION: Over-expression of p-Lyn may be involved in the mechanism of resistance to imatinib.	imatinib	87-95	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	33-36
29098070-0	2017	Imatinib response of gastrointestinal stromal tumor patients with germline mutation on KIT exon 13: A family report.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	87-90
28962554-9	2017	Interestingly, the levels of p-Akt, p-mTOR and p-S6 are lower in cells treated with combination of propofol and imatinib than cells treated with propofol or imatinib alone, suggesting that propofol augments BCR-ABL TKI"s inhibitory effect via suppressing Akt/mTOR pathway.	imatinib	112-120	AKT serine/threonine kinase 1	Homo sapiens	255-258
28962554-9	2017	Interestingly, the levels of p-Akt, p-mTOR and p-S6 are lower in cells treated with combination of propofol and imatinib than cells treated with propofol or imatinib alone, suggesting that propofol augments BCR-ABL TKI"s inhibitory effect via suppressing Akt/mTOR pathway.	imatinib	112-120	mechanistic target of rapamycin kinase	Homo sapiens	259-263
29098070-5	2017	We describe here clinical, imaging, pathological and genetic findings of a family with four affected members; grandmother, his son and two grand-sons having a germline gain-of-function mutation of KIT in exon 13 and discuss the imatinib mesylate treatment surveillance outcomes towards disease management.	imatinib	228-245	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	197-200
29100343-1	2017	Gastrointestinal stromal tumors (GISTs) with KIT or platelet-derived growth factor receptor alpha (PDGFRa) oncogenic driver gene mutations, respond to tyrosine kinase inhibitors (TKIs) including imatinib, sunitinib, and regorafenib.	imatinib	195-203	platelet derived growth factor receptor alpha	Homo sapiens	99-105
28760855-0	2017	Dual Targeting of Insulin Receptor and KIT in Imatinib-Resistant Gastrointestinal Stromal Tumors.	imatinib	46-54	insulin receptor	Homo sapiens	18-34
28760855-0	2017	Dual Targeting of Insulin Receptor and KIT in Imatinib-Resistant Gastrointestinal Stromal Tumors.	imatinib	46-54	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	39-42
28760855-1	2017	Oncogenic KIT or PDGFRA receptor tyrosine kinase (RTK) mutations are compelling therapeutic targets in gastrointestinal stromal tumors (GIST), and treatment with the KIT/PDGFRA inhibitor imatinib is the standard of care for patients with metastatic GIST.	imatinib	187-195	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	10-13
28760855-1	2017	Oncogenic KIT or PDGFRA receptor tyrosine kinase (RTK) mutations are compelling therapeutic targets in gastrointestinal stromal tumors (GIST), and treatment with the KIT/PDGFRA inhibitor imatinib is the standard of care for patients with metastatic GIST.	imatinib	187-195	platelet derived growth factor receptor alpha	Homo sapiens	17-23
28760855-1	2017	Oncogenic KIT or PDGFRA receptor tyrosine kinase (RTK) mutations are compelling therapeutic targets in gastrointestinal stromal tumors (GIST), and treatment with the KIT/PDGFRA inhibitor imatinib is the standard of care for patients with metastatic GIST.	imatinib	187-195	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	166-169
28760855-1	2017	Oncogenic KIT or PDGFRA receptor tyrosine kinase (RTK) mutations are compelling therapeutic targets in gastrointestinal stromal tumors (GIST), and treatment with the KIT/PDGFRA inhibitor imatinib is the standard of care for patients with metastatic GIST.	imatinib	187-195	platelet derived growth factor receptor alpha	Homo sapiens	170-176
28760855-3	2017	Using phospho-RTK and immunoblot assays, we demonstrate activation of KIT and insulin receptor (IR) in imatinib-resistant GIST cell lines (GIST430 and GIST48) and biopsies with acquisition of KIT secondary mutations, but not in imatinib-sensitive GIST cells (GIST882 and GIST-T1).	imatinib	103-111	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	70-73
28760855-3	2017	Using phospho-RTK and immunoblot assays, we demonstrate activation of KIT and insulin receptor (IR) in imatinib-resistant GIST cell lines (GIST430 and GIST48) and biopsies with acquisition of KIT secondary mutations, but not in imatinib-sensitive GIST cells (GIST882 and GIST-T1).	imatinib	103-111	insulin receptor	Homo sapiens	78-94
28760855-3	2017	Using phospho-RTK and immunoblot assays, we demonstrate activation of KIT and insulin receptor (IR) in imatinib-resistant GIST cell lines (GIST430 and GIST48) and biopsies with acquisition of KIT secondary mutations, but not in imatinib-sensitive GIST cells (GIST882 and GIST-T1).	imatinib	103-111	insulin receptor	Homo sapiens	96-98
28760855-3	2017	Using phospho-RTK and immunoblot assays, we demonstrate activation of KIT and insulin receptor (IR) in imatinib-resistant GIST cell lines (GIST430 and GIST48) and biopsies with acquisition of KIT secondary mutations, but not in imatinib-sensitive GIST cells (GIST882 and GIST-T1).	imatinib	228-236	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	70-73
28760855-3	2017	Using phospho-RTK and immunoblot assays, we demonstrate activation of KIT and insulin receptor (IR) in imatinib-resistant GIST cell lines (GIST430 and GIST48) and biopsies with acquisition of KIT secondary mutations, but not in imatinib-sensitive GIST cells (GIST882 and GIST-T1).	imatinib	228-236	insulin receptor	Homo sapiens	78-94
28760855-3	2017	Using phospho-RTK and immunoblot assays, we demonstrate activation of KIT and insulin receptor (IR) in imatinib-resistant GIST cell lines (GIST430 and GIST48) and biopsies with acquisition of KIT secondary mutations, but not in imatinib-sensitive GIST cells (GIST882 and GIST-T1).	imatinib	228-236	insulin receptor	Homo sapiens	96-98
28760855-5	2017	Additive effects showing increased apoptosis, antiproliferative effects, cell-cycle arrest, and decreased pAKT and pS6 expression, tumor growth, migration, and invasiveness were observed in imatinib-resistant GIST cells with IR activation after coordinated inhibition of IR and KIT by linsitinib (or IR shRNA) and imatinib, respectively, compared with either intervention alone.	imatinib	190-198	taste 2 receptor member 63 pseudogene	Homo sapiens	115-118
28760855-5	2017	Additive effects showing increased apoptosis, antiproliferative effects, cell-cycle arrest, and decreased pAKT and pS6 expression, tumor growth, migration, and invasiveness were observed in imatinib-resistant GIST cells with IR activation after coordinated inhibition of IR and KIT by linsitinib (or IR shRNA) and imatinib, respectively, compared with either intervention alone.	imatinib	190-198	insulin receptor	Homo sapiens	225-227
28760855-5	2017	Additive effects showing increased apoptosis, antiproliferative effects, cell-cycle arrest, and decreased pAKT and pS6 expression, tumor growth, migration, and invasiveness were observed in imatinib-resistant GIST cells with IR activation after coordinated inhibition of IR and KIT by linsitinib (or IR shRNA) and imatinib, respectively, compared with either intervention alone.	imatinib	190-198	insulin receptor	Homo sapiens	271-273
28760855-5	2017	Additive effects showing increased apoptosis, antiproliferative effects, cell-cycle arrest, and decreased pAKT and pS6 expression, tumor growth, migration, and invasiveness were observed in imatinib-resistant GIST cells with IR activation after coordinated inhibition of IR and KIT by linsitinib (or IR shRNA) and imatinib, respectively, compared with either intervention alone.	imatinib	190-198	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	278-281
28760855-5	2017	Additive effects showing increased apoptosis, antiproliferative effects, cell-cycle arrest, and decreased pAKT and pS6 expression, tumor growth, migration, and invasiveness were observed in imatinib-resistant GIST cells with IR activation after coordinated inhibition of IR and KIT by linsitinib (or IR shRNA) and imatinib, respectively, compared with either intervention alone.	imatinib	190-198	insulin receptor	Homo sapiens	271-273
29100343-6	2017	Imatinib inhibited the KIT pathway in imatinib-sensitive GIST-T1 but not GIST-RX1, RX2, and RX4.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	23-26
29100343-6	2017	Imatinib inhibited the KIT pathway in imatinib-sensitive GIST-T1 but not GIST-RX1, RX2, and RX4.	imatinib	38-46	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	23-26
28787270-3	2017	The application of LC-MS3 in imatinib quantification has not been discussed in the literature.	imatinib	29-37	MS3	Homo sapiens	22-25
28787270-4	2017	METHODS: An LC-MS3 imatinib quantification method was developed and validated in human serum.	imatinib	19-27	MS3	Homo sapiens	15-18
28787270-8	2017	It could be demonstrated that MS3 detection is a very effective way of sensitive imatinib quantification.	imatinib	81-89	MS3	Homo sapiens	30-33
29190894-0	2017	MicroRNA-212/ABCG2-axis contributes to development of imatinib-resistance in leukemic cells.	imatinib	54-62	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	13-18
29190894-6	2017	Under imatinib-treatment, miR-212 inhibition led to enhanced cell viability (p = 0.01), reduced apoptosis (p = 0.01) and cytotoxicity (p = 0.03).	imatinib	6-14	microRNA 212	Homo sapiens	26-33
29190894-10	2017	Taken together, the miR-212/ABCG2-axis influences imatinib-susceptibility contributing to development of imatinib-resistance.	imatinib	50-58	microRNA 212	Homo sapiens	20-27
29190894-10	2017	Taken together, the miR-212/ABCG2-axis influences imatinib-susceptibility contributing to development of imatinib-resistance.	imatinib	50-58	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	28-33
29190894-10	2017	Taken together, the miR-212/ABCG2-axis influences imatinib-susceptibility contributing to development of imatinib-resistance.	imatinib	105-113	microRNA 212	Homo sapiens	20-27
29190894-10	2017	Taken together, the miR-212/ABCG2-axis influences imatinib-susceptibility contributing to development of imatinib-resistance.	imatinib	105-113	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	28-33
29152155-7	2017	Accordingly, its induction by Imatinib (IM) and second generation TK inhibitors contributes to beta-catenin inactivation through multiple events encompassing the activation of endoplasmic reticulum (ER) stress-associated unfolded protein response (UPR) and autophagy, eventually leading to apoptotic death.	imatinib	30-38	catenin beta 1	Homo sapiens	95-107
28760855-5	2017	Additive effects showing increased apoptosis, antiproliferative effects, cell-cycle arrest, and decreased pAKT and pS6 expression, tumor growth, migration, and invasiveness were observed in imatinib-resistant GIST cells with IR activation after coordinated inhibition of IR and KIT by linsitinib (or IR shRNA) and imatinib, respectively, compared with either intervention alone.	imatinib	314-322	insulin receptor	Homo sapiens	225-227
28760855-6	2017	IGF2 overexpression was responsible for IR activation in imatinib-resistant GIST cells, whereas IR activation did not result from IR amplification, IR mutation, or KIT phosphorylation.	imatinib	57-65	insulin like growth factor 2	Homo sapiens	0-4
28760855-7	2017	Our findings suggest that combinatorial inhibition of IR and KIT warrants clinical evaluation as a novel therapeutic strategy in imatinib-resistant GISTs.	imatinib	129-137	insulin receptor	Homo sapiens	54-56
28760855-7	2017	Our findings suggest that combinatorial inhibition of IR and KIT warrants clinical evaluation as a novel therapeutic strategy in imatinib-resistant GISTs.	imatinib	129-137	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	61-64
28725989-0	2017	Imatinib in myeloid/lymphoid neoplasms with eosinophilia and rearrangement of PDGFRB in chronic or blast phase.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	78-84
28627443-0	2017	Impact of the BCR-ABL1 fusion transcripts on different responses to Imatinib and disease recurrence in Iranian patients with Chronic Myeloid Leukemia.	imatinib	68-76	BCR activator of RhoGEF and GTPase	Homo sapiens	14-22
28725989-1	2017	We evaluated clinical characteristics and outcome on imatinib of 22 patients with myeloid/lymphoid neoplasms with eosinophilia and rearrangement of PDGFRB.	imatinib	53-61	platelet derived growth factor receptor beta	Homo sapiens	148-154
28862699-6	2017	We detected CXorf48-specific CTLs in the peripheral blood mononuclear cells from CML patients who have discontinued imatinib after maintaining complete molecular remission for more than 2 years.	imatinib	116-124	cancer/testis antigen 55	Homo sapiens	12-19
27362495-6	2017	Comparing IMAB-AgNPs to AgNPs and Imatinib revealed the ability of IMAB-AgNPs to up-regulating Bax/Bcl-2 ratio.	imatinib	34-42	BCL2 associated X, apoptosis regulator	Homo sapiens	95-98
27362495-6	2017	Comparing IMAB-AgNPs to AgNPs and Imatinib revealed the ability of IMAB-AgNPs to up-regulating Bax/Bcl-2 ratio.	imatinib	34-42	BCL2 apoptosis regulator	Homo sapiens	99-104
28190319-0	2017	LncRNA MEG3 Regulates Imatinib Resistance in Chronic Myeloid Leukemia via Suppressing MicroRNA-21.	imatinib	22-30	maternally expressed 3	Homo sapiens	7-11
28190319-0	2017	LncRNA MEG3 Regulates Imatinib Resistance in Chronic Myeloid Leukemia via Suppressing MicroRNA-21.	imatinib	22-30	microRNA 21	Homo sapiens	86-97
28190319-2	2017	The aim of the present study was to investigate the involvement of MEG3, a lncRNA, in imatinib resistance and demonstrate its underlying mechanisms.	imatinib	86-94	maternally expressed 3	Homo sapiens	67-71
28190319-7	2017	Our results showed that MEG3 was significantly decreased in imatinib-resistant CML patients and imatinib-resistant K562 cells.	imatinib	60-68	maternally expressed 3	Homo sapiens	24-28
28190319-7	2017	Our results showed that MEG3 was significantly decreased in imatinib-resistant CML patients and imatinib-resistant K562 cells.	imatinib	96-104	maternally expressed 3	Homo sapiens	24-28
28190319-8	2017	Overexpression of MEG3 in imatinib-resistant K562 cells markedly decreased cell proliferation, increased cell apoptosis, reversed imatinib resistance, and reduced the expression of MRP1, MDR1, and ABCG2.	imatinib	26-34	maternally expressed 3	Homo sapiens	18-22
28190319-8	2017	Overexpression of MEG3 in imatinib-resistant K562 cells markedly decreased cell proliferation, increased cell apoptosis, reversed imatinib resistance, and reduced the expression of MRP1, MDR1, and ABCG2.	imatinib	26-34	mutS homolog 3	Homo sapiens	181-185
28190319-8	2017	Overexpression of MEG3 in imatinib-resistant K562 cells markedly decreased cell proliferation, increased cell apoptosis, reversed imatinib resistance, and reduced the expression of MRP1, MDR1, and ABCG2.	imatinib	26-34	ATP binding cassette subfamily B member 1	Homo sapiens	187-191
28190319-8	2017	Overexpression of MEG3 in imatinib-resistant K562 cells markedly decreased cell proliferation, increased cell apoptosis, reversed imatinib resistance, and reduced the expression of MRP1, MDR1, and ABCG2.	imatinib	26-34	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	197-202
28190319-8	2017	Overexpression of MEG3 in imatinib-resistant K562 cells markedly decreased cell proliferation, increased cell apoptosis, reversed imatinib resistance, and reduced the expression of MRP1, MDR1, and ABCG2.	imatinib	130-138	maternally expressed 3	Homo sapiens	18-22
28190319-11	2017	In addition, miR-21 mimics reversed the phenotype of MEG3-overexpression in imatinib-resistant K562 cells.	imatinib	76-84	microRNA 21	Homo sapiens	13-19
28190319-11	2017	In addition, miR-21 mimics reversed the phenotype of MEG3-overexpression in imatinib-resistant K562 cells.	imatinib	76-84	maternally expressed 3	Homo sapiens	53-57
28190319-12	2017	Taken together, MEG3 is involved in imatinib resistance in CML and possibly contributes to imatinib resistance through regulating miR-21, and subsequent cell proliferation, apoptosis and expression of multidrug resistant transporters.	imatinib	36-44	maternally expressed 3	Homo sapiens	16-20
28190319-12	2017	Taken together, MEG3 is involved in imatinib resistance in CML and possibly contributes to imatinib resistance through regulating miR-21, and subsequent cell proliferation, apoptosis and expression of multidrug resistant transporters.	imatinib	36-44	microRNA 21	Homo sapiens	130-136
28190319-12	2017	Taken together, MEG3 is involved in imatinib resistance in CML and possibly contributes to imatinib resistance through regulating miR-21, and subsequent cell proliferation, apoptosis and expression of multidrug resistant transporters.	imatinib	91-99	maternally expressed 3	Homo sapiens	16-20
28190319-12	2017	Taken together, MEG3 is involved in imatinib resistance in CML and possibly contributes to imatinib resistance through regulating miR-21, and subsequent cell proliferation, apoptosis and expression of multidrug resistant transporters.	imatinib	91-99	microRNA 21	Homo sapiens	130-136
28711648-11	2017	The Akt-mTOR pathway is thus a potential therapeutic target in imatinib-resistant DFSP/FS.	imatinib	63-71	mechanistic target of rapamycin kinase	Homo sapiens	8-12
28947711-0	2017	Association of GSTM1, GSTT1 and GSTP1 Ile105Val polymorphisms with clinical response to imatinib mesylate treatment among Malaysian chronic myeloid leukaemia patients.	imatinib	88-105	glutathione S-transferase mu 1	Homo sapiens	15-20
28947711-0	2017	Association of GSTM1, GSTT1 and GSTP1 Ile105Val polymorphisms with clinical response to imatinib mesylate treatment among Malaysian chronic myeloid leukaemia patients.	imatinib	88-105	glutathione S-transferase pi 1	Homo sapiens	32-37
28885361-0	2017	Angioimmunoblastic T-cell lymphoma and hypereosinophilic syndrome with FIP1L1/PDGFRA fusion gene effectively treated with imatinib: A case report.	imatinib	122-130	factor interacting with PAPOLA and CPSF1	Homo sapiens	71-77
28367681-0	2017	Do polymorphisms in MDR1 and CYP3A5 genes influence the risk of cytogenetic relapse in patients with chronic myeloid leukemia on imatinib therapy?	imatinib	129-137	ATP binding cassette subfamily B member 1	Homo sapiens	20-24
28367681-0	2017	Do polymorphisms in MDR1 and CYP3A5 genes influence the risk of cytogenetic relapse in patients with chronic myeloid leukemia on imatinib therapy?	imatinib	129-137	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	29-35
28885361-0	2017	Angioimmunoblastic T-cell lymphoma and hypereosinophilic syndrome with FIP1L1/PDGFRA fusion gene effectively treated with imatinib: A case report.	imatinib	122-130	platelet derived growth factor receptor alpha	Homo sapiens	78-84
28885361-2	2017	Some cases of HES are caused by the FIP1L1/PDGFRA fusion gene and respond to imatinib.	imatinib	77-85	factor interacting with PAPOLA and CPSF1	Homo sapiens	36-42
28885361-2	2017	Some cases of HES are caused by the FIP1L1/PDGFRA fusion gene and respond to imatinib.	imatinib	77-85	platelet derived growth factor receptor alpha	Homo sapiens	43-49
28885361-18	2017	Imatinib was very effective in treating both HES and lymphoma, suggesting that the FIP1L1/PDGFRA fusion gene plays a key role in the pathogenesis of both HES and lymphoma.	imatinib	0-8	factor interacting with PAPOLA and CPSF1	Homo sapiens	83-89
28885361-18	2017	Imatinib was very effective in treating both HES and lymphoma, suggesting that the FIP1L1/PDGFRA fusion gene plays a key role in the pathogenesis of both HES and lymphoma.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	90-96
28927158-0	2017	Regulation of HtrA2 on WT1 gene expression under imatinib stimulation and its effects on the cell biology of K562 cells.	imatinib	49-57	HtrA serine peptidase 2	Homo sapiens	14-19
28611108-9	2017	Collectively, our findings demonstrate that Wnt/beta-catenin signaling is a novel therapeutic target for selected untreated or imatinib-resistant GISTs.	imatinib	127-135	catenin beta 1	Homo sapiens	48-60
28637715-4	2017	Dasatinib, imatinib, and bosutinib all suppressed tyrosine phosphorylation of PKCdelta and inhibited IR-induced apoptosis in vitro To determine whether TKIs can provide radioprotection of salivary gland function in vivo, mice were treated with TKIs and a single or fractionated doses of irradiation.	imatinib	11-19	protein kinase C, delta	Mus musculus	78-86
28927158-13	2017	Imatinib inhibited the extracellular signal-related kinase (ERK1/2) pathway markedly and persistently, but UCF-101 exhibited no notable effect on the inhibition of the ERK1/2 pathway.	imatinib	0-8	mitogen-activated protein kinase 3	Homo sapiens	60-66
28927158-0	2017	Regulation of HtrA2 on WT1 gene expression under imatinib stimulation and its effects on the cell biology of K562 cells.	imatinib	49-57	WT1 transcription factor	Homo sapiens	23-26
28927158-3	2017	Expression of WT1 and HtrA2 mRNA, and proteins following imatinib and the HtrA2 inhibitor 5-[5-(2-nitrophenyl) furfuryl iodine]-1, 3-diphenyl-2-thiobarbituric acid (UCF-101) treatment was detected with reverse transcription-quantitative polymerase chain reaction and western blot analysis.	imatinib	57-65	WT1 transcription factor	Homo sapiens	14-17
28927158-3	2017	Expression of WT1 and HtrA2 mRNA, and proteins following imatinib and the HtrA2 inhibitor 5-[5-(2-nitrophenyl) furfuryl iodine]-1, 3-diphenyl-2-thiobarbituric acid (UCF-101) treatment was detected with reverse transcription-quantitative polymerase chain reaction and western blot analysis.	imatinib	57-65	HtrA serine peptidase 2	Homo sapiens	22-27
28927158-6	2017	In K562 cells, imatinib treatment activated HtrA2 gene at a transcription level, while the WT1 gene was simultaneously downregulated.	imatinib	15-23	HtrA serine peptidase 2	Homo sapiens	44-49
28927158-8	2017	At the protein level, imatinib induced the increase in HtrA2 protein level and concomitantly downregulated WT1 protein level.	imatinib	22-30	HtrA serine peptidase 2	Homo sapiens	55-60
28927158-8	2017	At the protein level, imatinib induced the increase in HtrA2 protein level and concomitantly downregulated WT1 protein level.	imatinib	22-30	WT1 transcription factor	Homo sapiens	107-110
28927158-10	2017	Imatinib induced apoptosis in K562 cells, but this effect was attenuated by the HtrA2 inhibitor UCF-101, resulting in the upregulation of the WT1 protein level.	imatinib	0-8	HtrA serine peptidase 2	Homo sapiens	80-85
28927158-10	2017	Imatinib induced apoptosis in K562 cells, but this effect was attenuated by the HtrA2 inhibitor UCF-101, resulting in the upregulation of the WT1 protein level.	imatinib	0-8	WT1 transcription factor	Homo sapiens	142-145
28927158-12	2017	Imatinib activated the p38 mitogen activated protein kinase (p38 MAPK) signaling pathway in K562 cells, and UCF-101 affected the activation of imatinib in the p38 MAPK signaling pathway.	imatinib	0-8	mitogen-activated protein kinase 14	Homo sapiens	23-59
28927158-12	2017	Imatinib activated the p38 mitogen activated protein kinase (p38 MAPK) signaling pathway in K562 cells, and UCF-101 affected the activation of imatinib in the p38 MAPK signaling pathway.	imatinib	0-8	mitogen-activated protein kinase 14	Homo sapiens	61-69
28927158-12	2017	Imatinib activated the p38 mitogen activated protein kinase (p38 MAPK) signaling pathway in K562 cells, and UCF-101 affected the activation of imatinib in the p38 MAPK signaling pathway.	imatinib	0-8	mitogen-activated protein kinase 1	Homo sapiens	23-26
28927158-12	2017	Imatinib activated the p38 mitogen activated protein kinase (p38 MAPK) signaling pathway in K562 cells, and UCF-101 affected the activation of imatinib in the p38 MAPK signaling pathway.	imatinib	0-8	mitogen-activated protein kinase 3	Homo sapiens	65-69
28578803-8	2017	Mechanistically, impairment of DNA repair seems to be associated with radiosensitization upon AIIB2/Imatinib and AIIB2/Imatinib-related radiosensitization could be reduced by exogenous overexpression of either wildtype or constitutively active c-Abl forms relative to controls.	imatinib	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	244-249
28578803-10	2017	For solid cancers, c-Abl phosphorylation status might be an indicator for reasonable Imatinib application as adjuvant for conventional radio(chemo)therapy.	imatinib	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-24
28512058-5	2017	By quantitative real time-PCR (qRT-PCR) and western blotting analysis we observed that imatinib resistant K562R cells exhibited marked high levels of CMP-N-acetylneuraminate-beta-galactosamide-alpha-2,3-sialyltransferase (ST3Gal IV) as compared to imatinib sensitive K562 cells.	imatinib	87-95	ST3 beta-galactoside alpha-2,3-sialyltransferase 4	Homo sapiens	222-231
28512058-6	2017	Further studies revealed that manipulated expression of ST3GAL IV led to the significant alterations of cell cycle distribution, apoptotic signal, cell proliferation and the effectiveness of imatinib treatment.	imatinib	191-199	ST3 beta-galactoside alpha-2,3-sialyltransferase 4	Homo sapiens	56-65
28666867-4	2017	The c-Abl inhibitor imatinib suppressed TGF-beta-induced expression of Smad3 targets as well as SKIP/Smad3 interaction.	imatinib	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-9
28666867-4	2017	The c-Abl inhibitor imatinib suppressed TGF-beta-induced expression of Smad3 targets as well as SKIP/Smad3 interaction.	imatinib	20-28	transforming growth factor beta 1	Homo sapiens	40-48
28843219-0	2017	Molecular Response to Imatinib and Its Correlation with mRNA Expression Levels of Imatinib Influx Transporter (OCT1) in Indian Chronic Myeloid Leukemia Patients Background and objectives: Imatinib mesylate is approved for the treatment of Chronic Myeloid Leukemia (CML).About 20% of patients with CML do not respond to treatment with Imatinib either initially or because of acquiredresistance.	imatinib	22-30	solute carrier family 22 member 1	Homo sapiens	111-115
28843219-0	2017	Molecular Response to Imatinib and Its Correlation with mRNA Expression Levels of Imatinib Influx Transporter (OCT1) in Indian Chronic Myeloid Leukemia Patients Background and objectives: Imatinib mesylate is approved for the treatment of Chronic Myeloid Leukemia (CML).About 20% of patients with CML do not respond to treatment with Imatinib either initially or because of acquiredresistance.	imatinib	188-205	solute carrier family 22 member 1	Homo sapiens	111-115
28666867-4	2017	The c-Abl inhibitor imatinib suppressed TGF-beta-induced expression of Smad3 targets as well as SKIP/Smad3 interaction.	imatinib	20-28	SMAD family member 3	Homo sapiens	71-76
28843219-0	2017	Molecular Response to Imatinib and Its Correlation with mRNA Expression Levels of Imatinib Influx Transporter (OCT1) in Indian Chronic Myeloid Leukemia Patients Background and objectives: Imatinib mesylate is approved for the treatment of Chronic Myeloid Leukemia (CML).About 20% of patients with CML do not respond to treatment with Imatinib either initially or because of acquiredresistance.	imatinib	82-90	solute carrier family 22 member 1	Homo sapiens	111-115
28843219-1	2017	In addition to mutated BCR-ABL1 kinase, the organic cation transporter1 (OCT1, encoded by SLC22A1) hasbeen considered to contribute to Imatinib resistance in patients with chronic myeloid leukemia (CML).	imatinib	135-143	solute carrier family 22 member 1	Homo sapiens	44-71
28666867-4	2017	The c-Abl inhibitor imatinib suppressed TGF-beta-induced expression of Smad3 targets as well as SKIP/Smad3 interaction.	imatinib	20-28	SMAD family member 3	Homo sapiens	101-106
28843219-1	2017	In addition to mutated BCR-ABL1 kinase, the organic cation transporter1 (OCT1, encoded by SLC22A1) hasbeen considered to contribute to Imatinib resistance in patients with chronic myeloid leukemia (CML).	imatinib	135-143	solute carrier family 22 member 1	Homo sapiens	73-77
28666867-5	2017	TGF-beta-stimulation induced tyrosine phosphorylation of SKIP, and this phosphorylation was suppressed by imatinib.	imatinib	106-114	transforming growth factor beta 1	Homo sapiens	0-8
28843219-1	2017	In addition to mutated BCR-ABL1 kinase, the organic cation transporter1 (OCT1, encoded by SLC22A1) hasbeen considered to contribute to Imatinib resistance in patients with chronic myeloid leukemia (CML).	imatinib	135-143	solute carrier family 22 member 1	Homo sapiens	90-97
28843219-2	2017	OCT1 has beenreported to be the main influx transporter involved in Imatinib uptake into CML cells.	imatinib	68-76	solute carrier family 22 member 1	Homo sapiens	0-4
28861326-0	2017	LncRNA SNHG5 regulates imatinib resistance in chronic myeloid leukemia via acting as a CeRNA against MiR-205-5p.	imatinib	23-31	small nucleolar RNA host gene 5	Homo sapiens	7-12
28843219-13	2017	Based on these findings, presentstudy believes that the pre-therapeutic higher expression of OCT1 may help to predict response to imatinib therapy inCML patients.	imatinib	130-138	solute carrier family 22 member 1	Homo sapiens	93-97
28442505-0	2017	Overexpressed Fatty Acid Synthase in Gastrointestinal Stromal Tumors: Targeting a Progression-Associated Metabolic Driver Enhances the Antitumor Effect of Imatinib.	imatinib	155-163	fatty acid synthase	Homo sapiens	14-33
28442505-3	2017	In imatinib-resistant FASN-overexpressing GIST cells, the roles of overexpressed FASN and FASN-targeting C75 in tumor phenotypes, apoptosis and autophagy, KIT transcription, PI3K/AKT/mTOR activation, and imatinib resistance were analyzed by RNAi or myristoylated-AKT transfection.	imatinib	3-11	fatty acid synthase	Homo sapiens	22-26
28442505-6	2017	In vitro, FASN knockdown inhibited cell growth and migration, inactivated the PI3K/AKT/mTOR pathway, and resensitized resistant GIST cells to imatinib.	imatinib	142-150	fatty acid synthase	Homo sapiens	10-14
28442505-8	2017	Compared with both monotherapies, the C75/imatinib combination more effectively suppressed the growth of xenografts, exhibiting decreased KIT phosphorylation, Ki-67, and phosphorylated PI3K/AKT/mTOR levels and increased TUNEL labeling.Conclusions: We have characterized the prognostic, biological, and therapeutic implications of overexpressed FASN in GISTs.	imatinib	42-50	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	138-141
28442505-8	2017	Compared with both monotherapies, the C75/imatinib combination more effectively suppressed the growth of xenografts, exhibiting decreased KIT phosphorylation, Ki-67, and phosphorylated PI3K/AKT/mTOR levels and increased TUNEL labeling.Conclusions: We have characterized the prognostic, biological, and therapeutic implications of overexpressed FASN in GISTs.	imatinib	42-50	AKT serine/threonine kinase 1	Homo sapiens	190-193
28442505-8	2017	Compared with both monotherapies, the C75/imatinib combination more effectively suppressed the growth of xenografts, exhibiting decreased KIT phosphorylation, Ki-67, and phosphorylated PI3K/AKT/mTOR levels and increased TUNEL labeling.Conclusions: We have characterized the prognostic, biological, and therapeutic implications of overexpressed FASN in GISTs.	imatinib	42-50	mechanistic target of rapamycin kinase	Homo sapiens	194-198
28442505-8	2017	Compared with both monotherapies, the C75/imatinib combination more effectively suppressed the growth of xenografts, exhibiting decreased KIT phosphorylation, Ki-67, and phosphorylated PI3K/AKT/mTOR levels and increased TUNEL labeling.Conclusions: We have characterized the prognostic, biological, and therapeutic implications of overexpressed FASN in GISTs.	imatinib	42-50	fatty acid synthase	Homo sapiens	344-348
28768491-2	2017	These GISTs generally respond well to therapy with the RTK inhibitor imatinib mesylate (IM), although initial response is genotype-dependent.	imatinib	69-86	ret proto-oncogene	Homo sapiens	55-58
28768491-2	2017	These GISTs generally respond well to therapy with the RTK inhibitor imatinib mesylate (IM), although initial response is genotype-dependent.	imatinib	88-90	ret proto-oncogene	Homo sapiens	55-58
28466557-0	2017	The BCR-ABL1 transcript type influences response and outcome in Philadelphia chromosome-positive chronic myeloid leukemia patients treated frontline with imatinib.	imatinib	154-162	BCR activator of RhoGEF and GTPase	Homo sapiens	4-12
28842696-0	2017	Adhesion to stromal cells mediates imatinib resistance in chronic myeloid leukemia through ERK and BMP signaling pathways.	imatinib	35-43	mitogen-activated protein kinase 1	Homo sapiens	91-94
28701512-8	2017	Acting at the transcriptional level, they increased the surface expression of CXCR4, an effect observed also in NK cells and monocytes of patients receiving imatinib for chronic myeloid leukemia.	imatinib	157-165	C-X-C motif chemokine receptor 4	Homo sapiens	78-83
28848440-1	2017	Imatinib (IM), as first inhibitor of the oncogenic tyrosine kinase BCR-ABL, has been widely used to treat chronic myeloid leukemia (CML) for decades in clinic.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
28848440-1	2017	Imatinib (IM), as first inhibitor of the oncogenic tyrosine kinase BCR-ABL, has been widely used to treat chronic myeloid leukemia (CML) for decades in clinic.	imatinib	10-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
28368400-0	2017	Interferon gamma is a STAT1-dependent direct inducer of BCL6 expression in imatinib-treated chronic myeloid leukemia cells.	imatinib	75-83	interferon gamma	Homo sapiens	0-16
28368400-0	2017	Interferon gamma is a STAT1-dependent direct inducer of BCL6 expression in imatinib-treated chronic myeloid leukemia cells.	imatinib	75-83	signal transducer and activator of transcription 1	Homo sapiens	22-27
28368400-0	2017	Interferon gamma is a STAT1-dependent direct inducer of BCL6 expression in imatinib-treated chronic myeloid leukemia cells.	imatinib	75-83	BCL6 transcription repressor	Homo sapiens	56-60
28368400-1	2017	B-cell CLL/lymphoma 6 (BCL6) exerts oncogenic effects in several human hematopoietic malignancies including chronic myeloid leukemia (CML), where BCL6 expression was shown to be essential for CML stem cell survival and self-renewal during imatinib mesylate (IM) treatment.	imatinib	239-256	BCL6 transcription repressor	Homo sapiens	0-21
28368400-1	2017	B-cell CLL/lymphoma 6 (BCL6) exerts oncogenic effects in several human hematopoietic malignancies including chronic myeloid leukemia (CML), where BCL6 expression was shown to be essential for CML stem cell survival and self-renewal during imatinib mesylate (IM) treatment.	imatinib	239-256	BCL6 transcription repressor	Homo sapiens	23-27
28368400-1	2017	B-cell CLL/lymphoma 6 (BCL6) exerts oncogenic effects in several human hematopoietic malignancies including chronic myeloid leukemia (CML), where BCL6 expression was shown to be essential for CML stem cell survival and self-renewal during imatinib mesylate (IM) treatment.	imatinib	239-256	BCL6 transcription repressor	Homo sapiens	146-150
28780584-9	2017	In addition, imatinib inhibited the activity of c-Kit in vivo and in vitro.	imatinib	13-21	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	48-53
28861326-0	2017	LncRNA SNHG5 regulates imatinib resistance in chronic myeloid leukemia via acting as a CeRNA against MiR-205-5p.	imatinib	23-31	microRNA 205	Homo sapiens	101-108
28861326-2	2017	The present study aimed to investigate the effects of the long non-coding RNA, SNHG5 on imatinib resistance in CML and explored the underlying mechanisms.	imatinib	88-96	small nucleolar RNA host gene 5	Homo sapiens	79-84
28861326-4	2017	In vitro studies showed that the expressions of SNHG5 and ABCC2 were up-regulated in imatinib resistant cells (K562-R) when compared to K562 cells.	imatinib	85-93	small nucleolar RNA host gene 5	Homo sapiens	48-53
28861326-4	2017	In vitro studies showed that the expressions of SNHG5 and ABCC2 were up-regulated in imatinib resistant cells (K562-R) when compared to K562 cells.	imatinib	85-93	ATP binding cassette subfamily C member 2	Homo sapiens	58-63
28861326-8	2017	In vitro functional assay showed that overexpression of SNHG5 in K562 cells increased imatinib resistance and knock-down of SNHG5 reduced the imatinib resistance in K562-R cells.	imatinib	86-94	small nucleolar RNA host gene 5	Homo sapiens	56-61
28861326-8	2017	In vitro functional assay showed that overexpression of SNHG5 in K562 cells increased imatinib resistance and knock-down of SNHG5 reduced the imatinib resistance in K562-R cells.	imatinib	142-150	small nucleolar RNA host gene 5	Homo sapiens	124-129
28861326-9	2017	Further experiments showed that SNHG5 promotes imatinib resistance through regulating ABCC2.	imatinib	47-55	small nucleolar RNA host gene 5	Homo sapiens	32-37
28861326-9	2017	Further experiments showed that SNHG5 promotes imatinib resistance through regulating ABCC2.	imatinib	47-55	ATP binding cassette subfamily C member 2	Homo sapiens	86-91
28861326-10	2017	Taken together, SNHG5 promotes imatinib resistance in CML via acting as a competing endogenous RNA against miR-205-5p.	imatinib	31-39	small nucleolar RNA host gene 5	Homo sapiens	16-21
28623111-0	2017	Reversal of ABCB1 mediated efflux by imatinib and nilotinib in cells expressing various transporter levels.	imatinib	37-45	ATP binding cassette subfamily B member 1	Homo sapiens	12-17
28556300-2	2017	Inhibitors of ABL tyrosine kinase, such as imatinib and dasatinib, exhibit remarkable therapeutic effects, although emergence of drug resistance hampers the therapy during long-term treatment.	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-17
28623111-1	2017	Recently, it has been suggested that imatinib (IM) and nilotinib (NIL) could be studied beyond their original application, as inhibitors of the drug efflux pump ABCB1 (P-glycoprotein, MDR1).	imatinib	37-45	ATP binding cassette subfamily B member 1	Homo sapiens	161-166
28623111-1	2017	Recently, it has been suggested that imatinib (IM) and nilotinib (NIL) could be studied beyond their original application, as inhibitors of the drug efflux pump ABCB1 (P-glycoprotein, MDR1).	imatinib	37-45	ATP binding cassette subfamily B member 1	Homo sapiens	168-182
28623111-1	2017	Recently, it has been suggested that imatinib (IM) and nilotinib (NIL) could be studied beyond their original application, as inhibitors of the drug efflux pump ABCB1 (P-glycoprotein, MDR1).	imatinib	37-45	ATP binding cassette subfamily B member 1	Homo sapiens	184-188
28654842-10	2017	Post-HSCT BCR-ABL transcript positivity was a significant factor for clinical relapse after allo-HSCT in the imatinib era.	imatinib	109-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
28093001-0	2017	miR-505-5p and miR-193b-3p: potential biomarkers of imatinib response in patients with chronic myeloid leukemia.	imatinib	52-60	microRNA 193b	Homo sapiens	15-23
27995529-0	2017	CYP2C8 Genotype Significantly Alters Imatinib Metabolism in Chronic Myeloid Leukaemia Patients.	imatinib	37-45	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	0-6
27995529-1	2017	OBJECTIVE: The aims of this study were to determine the effects of the CYP2C8*3 and *4 polymorphisms on imatinib metabolism and plasma imatinib concentrations in chronic myeloid leukaemia (CML) patients.	imatinib	104-112	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	71-77
27995529-5	2017	Plasma imatinib concentrations were consequently &gt; 50% higher for CYP2C8*1/*4 than for CYP2C8*1/*1 and CYP2C8*3 carriers (2.18 +- 0.66 vs. 1.45 +- 0.74 [P &lt; 0.05] and 1.36 +- 0.98 mug/mL [P &lt; 0.05], respectively).	imatinib	7-15	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	69-75
27995529-5	2017	Plasma imatinib concentrations were consequently &gt; 50% higher for CYP2C8*1/*4 than for CYP2C8*1/*1 and CYP2C8*3 carriers (2.18 +- 0.66 vs. 1.45 +- 0.74 [P &lt; 0.05] and 1.36 +- 0.98 mug/mL [P &lt; 0.05], respectively).	imatinib	7-15	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	90-96
27995529-5	2017	Plasma imatinib concentrations were consequently &gt; 50% higher for CYP2C8*1/*4 than for CYP2C8*1/*1 and CYP2C8*3 carriers (2.18 +- 0.66 vs. 1.45 +- 0.74 [P &lt; 0.05] and 1.36 +- 0.98 mug/mL [P &lt; 0.05], respectively).	imatinib	7-15	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	90-96
27995529-6	2017	CONCLUSIONS: CYP2C8 genotype significantly alters imatinib metabolism in patients through gain- and loss-of-function mechanisms.	imatinib	50-58	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	13-19
28349229-2	2017	The Bcr-Abl inhibitor imatinib and other second-generation tyrosine kinase inhibitors such as dasatinib and nilotinib have remarkable efficacy in CML treatment.	imatinib	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
28544907-0	2017	MicroRNAs that affect the Fanconi Anemia/BRCA pathway are downregulated in imatinib-resistant chronic myeloid leukemia patients without detectable BCR-ABL kinase domain mutations.	imatinib	75-83	BRCA1 DNA repair associated	Homo sapiens	41-45
28410286-5	2017	We describe the sequential use of imatinib after nilotinib in a c-kit-mutated melanoma patient, who progressed on interferon, Allovectin, dacarbazine, nilotinib and ipilimumab, and was finally treated with the c-kit inhibitor imatinib.	imatinib	34-42	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	210-215
28410286-0	2017	Successful treatment with imatinib after nilotinib and ipilimumab in a c-kit-mutated advanced melanoma patient: a case report.	imatinib	26-34	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	71-76
28796048-10	2017	Four patients (33.3%) developed disease progression during imatinib treatment after initial resection, but all of these patients regained disease control when the treatment was altered to sunitinib targeted therapy.SDH-deficient GISTs arise exclusively in the stomach and account for approximately 7.4% (12/162) of gastric GISTs.	imatinib	59-67	succinate dehydrogenase complex iron sulfur subunit B	Homo sapiens	215-218
29296778-0	2017	ASXL1 and BIM germ line variants predict response and identify CML patients with the greatest risk of imatinib failure.	imatinib	102-110	ASXL transcriptional regulator 1	Homo sapiens	0-5
28866691-0	2017	Primary imatinib resistance in chronic myeloid leukemia patients in a developing country: BCR-ABL kinase domain mutations or BCR-ABL independent mechanisms?	imatinib	8-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
28866691-0	2017	Primary imatinib resistance in chronic myeloid leukemia patients in a developing country: BCR-ABL kinase domain mutations or BCR-ABL independent mechanisms?	imatinib	8-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
28410286-3	2017	Different trials show that imatinib or nilotinib lead to meaningful responses in c-kit-mutated melanoma patients.	imatinib	27-35	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	81-86
28410286-5	2017	We describe the sequential use of imatinib after nilotinib in a c-kit-mutated melanoma patient, who progressed on interferon, Allovectin, dacarbazine, nilotinib and ipilimumab, and was finally treated with the c-kit inhibitor imatinib.	imatinib	34-42	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	64-69
28808483-13	2017	Proliferation, suppression and expression of cytokines [interleukin (IL)-4, IL-10 and transforming growth factor (TGF)-beta] and molecules (FOXP3, GITR and CTLA-4) decreased significantly in treatment groups with imatinib and dasatinib.	imatinib	213-221	transforming growth factor beta 1	Homo sapiens	86-123
29137292-9	2017	The Kit inhibitor imatinib could benefit metastatic OMM patients with c-Kit mutations.	imatinib	18-26	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	70-75
29296778-0	2017	ASXL1 and BIM germ line variants predict response and identify CML patients with the greatest risk of imatinib failure.	imatinib	102-110	BCL2 like 11	Homo sapiens	10-13
29296778-8	2017	The Sokal risk score was combined with the ASXL1 and BIM variants in a classification tree model to predict imatinib response.	imatinib	108-116	ASXL transcriptional regulator 1	Homo sapiens	43-48
29296778-8	2017	The Sokal risk score was combined with the ASXL1 and BIM variants in a classification tree model to predict imatinib response.	imatinib	108-116	BCL2 like 11	Homo sapiens	53-56
28915580-0	2017	Molecular and functional characterization of a new 3" end KIT juxtamembrane deletion in a duodenal GIST treated with neoadjuvant Imatinib.	imatinib	129-137	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	58-61
28533480-1	2017	The development of Imatinib mesylate (IM), which targets the oncogenic BCR-ABL fusion protein, has greatly improved the outcome of Chronic Myeloid Leukemia (CML) patients.	imatinib	19-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
28719608-0	2017	Cholesterol esterification inhibition and imatinib treatment synergistically inhibit growth of BCR-ABL mutation-independent resistant chronic myelogenous leukemia.	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
28719608-7	2017	Blocking cholesterol esterification with avasimibe, a potent inhibitor of acyl-CoA cholesterol acyltransferase 1 (ACAT-1), significantly suppressed CML cell proliferation in Ba/F3 cells with the BCR-ABLT315I mutation and in K562 cells rendered imatinib resistant without mutations in the BCR-ABL kinase domain (K562R cells).	imatinib	244-252	acetyl-Coenzyme A acetyltransferase 1	Mus musculus	114-120
28719608-10	2017	Analysis of primary cells from a BCR-ABL mutation-independent imatinib resistant patient by mass cytometry suggested that the synergy may be due to downregulation of the MAPK pathway by avasimibe, which sensitized the CML cells to imatinib treatment.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
28753604-4	2017	Gene expression analyses of BCR-ABL positive ALL long-term cultured cells revealed strong reduction of SOCS mRNA expression after imatinib treatment, thereby demonstrating a strong inhibition of cytokine signaling.	imatinib	130-138	cytokine inducible SH2-containing protein	Mus musculus	103-107
28915580-6	2017	In line with these clinical evidences computer simulations, biophysical techniques and in vitro experiments demonstrated that the receptor tyrosine kinase KIT carrying the Delta574-580 mutation displays constitutive phosphorylation, which can be switched-off upon Imatinib treatment.	imatinib	264-272	ret proto-oncogene	Homo sapiens	130-154
28915580-6	2017	In line with these clinical evidences computer simulations, biophysical techniques and in vitro experiments demonstrated that the receptor tyrosine kinase KIT carrying the Delta574-580 mutation displays constitutive phosphorylation, which can be switched-off upon Imatinib treatment.	imatinib	264-272	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	155-158
28704552-0	2017	PTCH1 is a reliable marker for predicting imatinib response in chronic myeloid leukemia patients in chronic phase.	imatinib	42-50	patched 1	Homo sapiens	0-5
28334439-1	2017	BACKGROUND: KIT-directed tyrosine kinase inhibitors such as imatinib have demonstrated benefits in KIT-mutant (KIT+) mucosal, acral, vulvovaginal, and chronically sun-damaged (CSD) melanoma.	imatinib	60-68	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	12-15
28334439-1	2017	BACKGROUND: KIT-directed tyrosine kinase inhibitors such as imatinib have demonstrated benefits in KIT-mutant (KIT+) mucosal, acral, vulvovaginal, and chronically sun-damaged (CSD) melanoma.	imatinib	60-68	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	99-102
28334439-1	2017	BACKGROUND: KIT-directed tyrosine kinase inhibitors such as imatinib have demonstrated benefits in KIT-mutant (KIT+) mucosal, acral, vulvovaginal, and chronically sun-damaged (CSD) melanoma.	imatinib	60-68	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	99-102
28334439-19	2017	In view of its clinical activity, it is recommended that imatinib remain the KIT tyrosine kinase inhibitor of choice for unresectable KIT+ melanoma.	imatinib	57-65	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	77-80
28334439-19	2017	In view of its clinical activity, it is recommended that imatinib remain the KIT tyrosine kinase inhibitor of choice for unresectable KIT+ melanoma.	imatinib	57-65	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	134-137
28704552-1	2017	Patched homolog 1 gene (PTCH1) expression and the ratio of PTCH1 to Smoothened (SMO) expression have been proposed as prognostic markers of the response of chronic myeloid leukemia (CML) patients to imatinib.	imatinib	199-207	smoothened, frizzled class receptor	Homo sapiens	68-78
28704552-1	2017	Patched homolog 1 gene (PTCH1) expression and the ratio of PTCH1 to Smoothened (SMO) expression have been proposed as prognostic markers of the response of chronic myeloid leukemia (CML) patients to imatinib.	imatinib	199-207	smoothened, frizzled class receptor	Homo sapiens	80-83
28704552-6	2017	High and low PTCH1 expression groups had significantly different cumulative incidences of imatinib failure (IF), which was defined as discontinuation of imatinib due to lack of efficacy (5% vs. 25% at 4 years, P = 0.013), probabilities of achieving a major molecular response (81% vs. 53% at first year, P = 0.02), and proportions of early molecular failure (14% vs. 43%, P = 0.015).	imatinib	90-98	patched 1	Homo sapiens	13-18
28704552-6	2017	High and low PTCH1 expression groups had significantly different cumulative incidences of imatinib failure (IF), which was defined as discontinuation of imatinib due to lack of efficacy (5% vs. 25% at 4 years, P = 0.013), probabilities of achieving a major molecular response (81% vs. 53% at first year, P = 0.02), and proportions of early molecular failure (14% vs. 43%, P = 0.015).	imatinib	153-161	patched 1	Homo sapiens	13-18
28704552-10	2017	Therefore, we confirmed that PTCH1 expression can predict the imatinib response in CML patients in CP by applying a more rigorous statistical analysis.	imatinib	62-70	patched 1	Homo sapiens	29-34
28704552-11	2017	Thus, PTCH1 expression is a promising molecular marker for predicting the imatinib response in CML patients in CP.	imatinib	74-82	patched 1	Homo sapiens	6-11
28528977-0	2017	Imatinib induces autophagy via upregulating XIAP in GIST882 cells.	imatinib	0-8	X-linked inhibitor of apoptosis	Homo sapiens	44-48
28528977-7	2017	Here we report that XIAP is induced upon imatinb treatment in GIST882 cells, leading to imatinib-induced autophagy.	imatinib	88-96	X-linked inhibitor of apoptosis	Homo sapiens	20-24
28528977-8	2017	Imatinib-induced autophagy was impaired in XIAP-knockout cells generated by CRISPR/Cas9 system demonstrated by the decreasing of LC3 lipidation.	imatinib	0-8	X-linked inhibitor of apoptosis	Homo sapiens	43-47
28528977-8	2017	Imatinib-induced autophagy was impaired in XIAP-knockout cells generated by CRISPR/Cas9 system demonstrated by the decreasing of LC3 lipidation.	imatinib	0-8	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	129-132
28528977-9	2017	XIAP knockout sensitizes GIST882 cells to imatinib-induced apoptotic cell death, suggesting that XIAP protects GIST882 cells from imatinib-induced cell death by inducing autophagy.	imatinib	42-50	X-linked inhibitor of apoptosis	Homo sapiens	0-4
28528977-9	2017	XIAP knockout sensitizes GIST882 cells to imatinib-induced apoptotic cell death, suggesting that XIAP protects GIST882 cells from imatinib-induced cell death by inducing autophagy.	imatinib	42-50	X-linked inhibitor of apoptosis	Homo sapiens	97-101
28528977-9	2017	XIAP knockout sensitizes GIST882 cells to imatinib-induced apoptotic cell death, suggesting that XIAP protects GIST882 cells from imatinib-induced cell death by inducing autophagy.	imatinib	130-138	X-linked inhibitor of apoptosis	Homo sapiens	0-4
28528977-9	2017	XIAP knockout sensitizes GIST882 cells to imatinib-induced apoptotic cell death, suggesting that XIAP protects GIST882 cells from imatinib-induced cell death by inducing autophagy.	imatinib	130-138	X-linked inhibitor of apoptosis	Homo sapiens	97-101
28528977-10	2017	Thus, the resistance of the GIST882 cells to imatinib appears to be, in part, due to the increasing of XIAP and subsequent induction of autophagy.	imatinib	45-53	X-linked inhibitor of apoptosis	Homo sapiens	103-107
28682311-2	2017	T315I Bcr-Abl is the most notorious point mutation to elicit acquired resistance to imatinib (IM), leading to poor prognosis.	imatinib	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-13
28678800-1	2017	Targeted inhibition of the oncogenic BCR-ABL1 fusion protein using the ABL1 tyrosine kinase inhibitor imatinib has become standard therapy for chronic myelogenous leukemia (CML), with most patients reaching total and durable remission.	imatinib	102-110	BCR activator of RhoGEF and GTPase	Homo sapiens	37-45
28374041-0	2017	Imatinib Treatment of Lymphomatoid Papulosis Associated with Myeloproliferative Hypereosinophilic Syndrome Presenting the FIP1L1-PDGFRA Fusion Gene.	imatinib	0-8	factor interacting with PAPOLA and CPSF1	Homo sapiens	122-128
28374041-0	2017	Imatinib Treatment of Lymphomatoid Papulosis Associated with Myeloproliferative Hypereosinophilic Syndrome Presenting the FIP1L1-PDGFRA Fusion Gene.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	129-135
28678800-1	2017	Targeted inhibition of the oncogenic BCR-ABL1 fusion protein using the ABL1 tyrosine kinase inhibitor imatinib has become standard therapy for chronic myelogenous leukemia (CML), with most patients reaching total and durable remission.	imatinib	102-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-45
28445830-0	2017	Overexpression of heme oxygenase-1 in bone marrow stromal cells promotes microenvironment-mediated imatinib resistance in chronic myeloid leukemia.	imatinib	99-107	heme oxygenase 1	Homo sapiens	18-34
28487491-2	2017	Imatinib selectively inhibits KIT and PDGFR, leading to disease control for 80%-90% of patients with metastatic GIST.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	30-33
28487491-2	2017	Imatinib selectively inhibits KIT and PDGFR, leading to disease control for 80%-90% of patients with metastatic GIST.	imatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	38-43
28487491-3	2017	Imatinib resistance can occur within a median of 2-3 years due to secondary mutations in KIT.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	89-92
28445830-6	2017	Following co-culture of BMSCs and K562 cells, up-regulating HO-1 expression in bone marrow stromal cells increased the imatinib (IM) resistance of K562 cells, whereas the apoptosis of K562 cells was effectively promoted without BMSCs co-culture.	imatinib	119-127	heme oxygenase 1	Homo sapiens	60-64
28669127-6	2017	Moreover, the presence of SEW02675 in the allosteric site enhanced the binding of imatinib (DeltaG bind = -367.58 with wt and -294.56 kJ/mol with T334I) to the ATP sites of the wt and the mutant Bcr-Abl.	imatinib	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	195-202
28385785-0	2017	Imatinib and spironolactone suppress hepcidin expression.	imatinib	0-8	hepcidin antimicrobial peptide	Mus musculus	37-45
28385785-7	2017	Among these, imatinib and spironolactone further suppressed liver hepcidin expression in mice.	imatinib	13-21	hepcidin antimicrobial peptide	Mus musculus	66-74
28385785-8	2017	Our results demonstrate that a commonly used anti-hypertensive drug, spironolactone, which is prescribed for the treatment of heart failure, acne and female hirsutism, as well as imatinib, a first-line, lifelong therapeutic option for some frequent cancer types suppress hepcidin expression in cultured cells and in mice.	imatinib	179-187	hepcidin antimicrobial peptide	Mus musculus	271-279
29200684-1	2017	Introduction: BCR-ABL1 kinase domain mutations represent the most frequent mechanism of resistance to tyrosine kinase inhibitor (TKI) therapy, being detected in 40%-50% of imatinib-resistant patients with chronic myeloid leukemia in chronic phase (CML-CP).	imatinib	172-180	BCR activator of RhoGEF and GTPase	Homo sapiens	14-22
29200684-2	2017	Over 100 BCR-ABL1 single-point mutations have been reported in patients with imatinib-resistant CML.	imatinib	77-85	BCR activator of RhoGEF and GTPase	Homo sapiens	9-17
29200684-3	2017	There were few studies reported from India on BCR-ABL kinase mutations in imatinib failure patients.	imatinib	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
27830966-0	2017	A deletion polymorphism in the RIZ gene is associated with increased progression of imatinib treated chronic myeloid leukemia patients.	imatinib	84-92	PR/SET domain 2	Homo sapiens	31-34
28196207-1	2017	Importance: After identification of activating mutations of the KIT gene in gastrointestinal stromal tumor (GIST)-the most common sarcomaof the gastrointestinal tract-a phase 2 study demonstrated efficacy of imatinib mesylate in patients with metastatic GIST harboring a KIT exon 11 mutation.	imatinib	208-225	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	64-67
28196207-1	2017	Importance: After identification of activating mutations of the KIT gene in gastrointestinal stromal tumor (GIST)-the most common sarcomaof the gastrointestinal tract-a phase 2 study demonstrated efficacy of imatinib mesylate in patients with metastatic GIST harboring a KIT exon 11 mutation.	imatinib	208-225	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	271-274
28218239-9	2017	Consistent with prior reports of imatinib-treated patients, musculoskeletal pain-related events were reported in 24.7% of patients in the TFR phase (consolidation phase, 16.3%).	imatinib	33-41	transferrin receptor	Homo sapiens	138-141
28192400-2	2017	Most primary GIST patients respond to the Kit inhibitor imatinib, but this drug often becomes ineffective because of secondary mutations in the Kit kinase domain.	imatinib	56-64	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	42-45
28775967-2	2017	We describe the case of a 69-year old male with an EGFR- positive Imatinib refractory sacral chordoma with synchronous lung metastases, treated with erlotinib, a first-generation EGFR inhibitor.	imatinib	66-74	epidermal growth factor receptor	Homo sapiens	51-55
28192400-3	2017	The characteristic intracellular accumulation of imatinib-sensitive and -resistant Kit protein is well documented, but its relationship to oncogenic signaling remains unknown.	imatinib	49-57	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	83-86
28661474-9	2017	Moreover, we show that mutant p53 forms cytoplasmic complexes with c-Abl, thereby dictating the subcellular localization of c-Abl and the sensitivity of MDA-MB-231 cells to Imatinib.	imatinib	173-181	tumor protein p53	Homo sapiens	30-33
28661474-9	2017	Moreover, we show that mutant p53 forms cytoplasmic complexes with c-Abl, thereby dictating the subcellular localization of c-Abl and the sensitivity of MDA-MB-231 cells to Imatinib.	imatinib	173-181	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-72
28192400-5	2017	In imatinib-resistant GIST with a secondary Kit mutation, Kit localizes predominantly on the Golgi apparatus.	imatinib	3-11	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	44-47
28192400-5	2017	In imatinib-resistant GIST with a secondary Kit mutation, Kit localizes predominantly on the Golgi apparatus.	imatinib	3-11	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	58-61
28192400-6	2017	Both imatinib-sensitive and imatinib-resistant Kit (Kit(mut)) become fully auto-phosphorylated only on the Golgi and only if in a complex-glycosylated form.	imatinib	5-13	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	47-50
28192400-6	2017	Both imatinib-sensitive and imatinib-resistant Kit (Kit(mut)) become fully auto-phosphorylated only on the Golgi and only if in a complex-glycosylated form.	imatinib	5-13	methylmalonyl-CoA mutase	Homo sapiens	52-60
28192400-6	2017	Both imatinib-sensitive and imatinib-resistant Kit (Kit(mut)) become fully auto-phosphorylated only on the Golgi and only if in a complex-glycosylated form.	imatinib	28-36	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	47-50
28192400-6	2017	Both imatinib-sensitive and imatinib-resistant Kit (Kit(mut)) become fully auto-phosphorylated only on the Golgi and only if in a complex-glycosylated form.	imatinib	28-36	methylmalonyl-CoA mutase	Homo sapiens	52-60
28192400-14	2017	Our study demonstrates that Kit(mut)"s pathogenicity is related to its mis-localization, and may offer a new strategy for treating imatinib-resistant GISTs.	imatinib	131-139	methylmalonyl-CoA mutase	Homo sapiens	28-36
28978042-0	2017	Translocation of heme oxygenase-1 contributes to imatinib resistance in chronic myelogenous leukemia.	imatinib	49-57	heme oxygenase 1	Homo sapiens	17-33
28978042-8	2017	Cell viability tests with increasing concentrations of imatinib showed IC50-values for all six cell lines with ER localized HO-1 that were similar to control cells.	imatinib	55-63	heme oxygenase 1	Homo sapiens	124-128
28978042-9	2017	However, out of the seven cell lines with anchorless HO-1, two showed a statistically significant increase in the imatinib IC50 (19.76 muM and 12.35 muM versus 2.35 - 7.57 muM of sensitive cell lines) corresponding to plasma concentrations outside the therapeutic range.	imatinib	114-122	heme oxygenase 1	Homo sapiens	53-57
28978042-10	2017	We conclude that the presence of translocated HO-1 in the cytosol and nucleus supports imatinib resistance while it is not sufficient to cause imatinib resistance in every cell line.	imatinib	87-95	heme oxygenase 1	Homo sapiens	46-50
28454120-9	2017	Our results suggest a role for PDE3A during ICC development and open novel perspectives for PDE3A in targeted GIST therapy, on one hand by the synergism between imatinib and cilostazol, a PDE3 inhibitor already in clinical use for other indications, and, on the other hand, by the neomorphic, druggable, PDE3A-SLFN12 cytotoxic interplay.	imatinib	161-169	schlafen family member 12	Homo sapiens	310-316
28541695-0	2017	Discovery of Potent, Selective Stem Cell Factor Receptor/Platelet Derived Growth Factor Receptor Alpha (c-KIT/PDGFRalpha) Dual Inhibitor for the Treatment of Imatinib-Resistant Gastrointestinal Stromal Tumors (GISTs).	imatinib	158-166	platelet derived growth factor receptor alpha	Homo sapiens	57-102
28541695-0	2017	Discovery of Potent, Selective Stem Cell Factor Receptor/Platelet Derived Growth Factor Receptor Alpha (c-KIT/PDGFRalpha) Dual Inhibitor for the Treatment of Imatinib-Resistant Gastrointestinal Stromal Tumors (GISTs).	imatinib	158-166	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	104-109
28541695-0	2017	Discovery of Potent, Selective Stem Cell Factor Receptor/Platelet Derived Growth Factor Receptor Alpha (c-KIT/PDGFRalpha) Dual Inhibitor for the Treatment of Imatinib-Resistant Gastrointestinal Stromal Tumors (GISTs).	imatinib	158-166	platelet derived growth factor receptor alpha	Homo sapiens	110-120
28624216-2	2017	Considering the potential of nanotechnology in cancer treatment and the benefits of a combined therapy with imatinib, a nanoconjugate was designed to achieve BCR-ABL1 gene silencing.	imatinib	108-116	BCR activator of RhoGEF and GTPase	Homo sapiens	158-166
28674529-3	2017	Treatment of Abl tyrosine kinase-specific inhibitor, imatinib and dasatinib, also significantly decreased HCV RNA and protein levels in HCV-infected cells.	imatinib	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
28674529-4	2017	We showed that both imatinib and dasatinib selectively inhibited HCV infection at the entry step of HCV life cycle, suggesting that Abl kinase activity may be necessary for HCV entry.	imatinib	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-135
28615625-5	2017	However, the Az and imatinib hybrids have weak inhibitory activities towards Hsp70 and Abl, and display lower cytotoxicity against leukemia cells compared to those of the individual constituents.	imatinib	20-28	heat shock protein family A (Hsp70) member 4	Homo sapiens	77-82
28620185-8	2017	These results reveal a role for c-Abl-regulated smooth muscle proliferation in the pathogenesis of rectal prolapse, and imply that long-term use of imatinib mesylate may cause gastrointestinal problems in patients while ERK inhibitor may be effective in treating rectal prolapse.	imatinib	148-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-37
28620185-8	2017	These results reveal a role for c-Abl-regulated smooth muscle proliferation in the pathogenesis of rectal prolapse, and imply that long-term use of imatinib mesylate may cause gastrointestinal problems in patients while ERK inhibitor may be effective in treating rectal prolapse.	imatinib	148-165	EPH receptor B2	Homo sapiens	220-223
28615625-5	2017	However, the Az and imatinib hybrids have weak inhibitory activities towards Hsp70 and Abl, and display lower cytotoxicity against leukemia cells compared to those of the individual constituents.	imatinib	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-90
28410239-0	2017	Homoharringtonine suppresses imatinib resistance via the Bcl-6/p53 pathway in chronic myeloid leukemia cell lines.	imatinib	29-37	BCL6 transcription repressor	Homo sapiens	57-62
28418880-1	2017	Resistance to the breakpoint cluster region-abelson 1 (BCR-ABL1) tyrosine kinase inhibitor (TKI) imatinib poses a major problem when treating chronic myeloid leukemia (CML).	imatinib	97-105	BCR activator of RhoGEF and GTPase	Homo sapiens	55-63
28418880-2	2017	Imatinib resistance often results from a secondary mutation in BCR-ABL1.	imatinib	0-8	BCR activator of RhoGEF and GTPase	Homo sapiens	63-71
28418880-4	2017	To gain insight into the mechanisms of BCR-ABL1-independent imatinib resistance, we performed an array-based comparative genomic hybridization.	imatinib	60-68	BCR activator of RhoGEF and GTPase	Homo sapiens	39-47
28418880-7	2017	Combined treatment of K562/IR cells with imatinib and a MET inhibitor suppressed extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun N-terminal kinase (JNK) activation, but did not affect AKT activation.	imatinib	41-49	mitogen-activated protein kinase 1	Homo sapiens	81-122
28418880-7	2017	Combined treatment of K562/IR cells with imatinib and a MET inhibitor suppressed extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun N-terminal kinase (JNK) activation, but did not affect AKT activation.	imatinib	41-49	mitogen-activated protein kinase 3	Homo sapiens	124-130
28418880-7	2017	Combined treatment of K562/IR cells with imatinib and a MET inhibitor suppressed extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun N-terminal kinase (JNK) activation, but did not affect AKT activation.	imatinib	41-49	mitogen-activated protein kinase 8	Homo sapiens	136-159
28418880-7	2017	Combined treatment of K562/IR cells with imatinib and a MET inhibitor suppressed extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun N-terminal kinase (JNK) activation, but did not affect AKT activation.	imatinib	41-49	mitogen-activated protein kinase 8	Homo sapiens	161-164
28418880-8	2017	Our findings implicate the MET/ERK and MET/JNK pathways in conferring resistance to imatinib, providing new insights into the mechanisms of BCR-ABL1 TKI resistance in CML.	imatinib	84-92	mitogen-activated protein kinase 1	Homo sapiens	31-34
28418880-8	2017	Our findings implicate the MET/ERK and MET/JNK pathways in conferring resistance to imatinib, providing new insights into the mechanisms of BCR-ABL1 TKI resistance in CML.	imatinib	84-92	mitogen-activated protein kinase 8	Homo sapiens	43-46
28418880-8	2017	Our findings implicate the MET/ERK and MET/JNK pathways in conferring resistance to imatinib, providing new insights into the mechanisms of BCR-ABL1 TKI resistance in CML.	imatinib	84-92	BCR activator of RhoGEF and GTPase	Homo sapiens	140-148
28410239-0	2017	Homoharringtonine suppresses imatinib resistance via the Bcl-6/p53 pathway in chronic myeloid leukemia cell lines.	imatinib	29-37	tumor protein p53	Homo sapiens	63-66
28369812-0	2017	Treating Philadelphia chromosome/BCR-ABL1 positive patients with Glivec (Imatinib mesylate): 10 years" experience at Patan Hospital, Nepal.	imatinib	73-90	BCR activator of RhoGEF and GTPase	Homo sapiens	33-41
28969100-2	2017	Overexpression of lncRNA UCA1 correlates with resistance to chemotherapeutics such as cisplatin, gemcitabine, 5-FU, tamoxifen, imatinib and EGFR-TKIs, whereas lncRNA UCA1 knockdown restores drug sensitivity.	imatinib	127-135	urothelial cancer associated 1	Homo sapiens	25-29
28467002-0	2017	The use of Imatinib resistance mutation analysis to direct therapy in Philadelphia chromosome/BCR-ABL1 positive chronic myeloid leukaemia patients failing Imatinib treatment, in Patan Hospital, Nepal.	imatinib	11-19	BCR activator of RhoGEF and GTPase	Homo sapiens	94-102
28467002-1	2017	Philadelphia chromosome/BCR-ABL1 positive chronic myeloid leukaemia (CML) can be successfully treated with Glivec (Imatinib), which is available free of cost through the Glivec International Patient Assistance programme (GIPAP) to patients with proven CML without means to pay for the drug.	imatinib	107-113	BCR activator of RhoGEF and GTPase	Homo sapiens	24-32
28369812-1	2017	The Glivec International Patient Assistance Programme makes Glivec (Imatinib mesylate) available to Philadelphia chromosome/BCR-ABL1 positive patients with chronic myeloid leukaemia (CML) in Lower and Middle Income Countries (LMIC).	imatinib	68-85	BCR activator of RhoGEF and GTPase	Homo sapiens	124-132
28467002-1	2017	Philadelphia chromosome/BCR-ABL1 positive chronic myeloid leukaemia (CML) can be successfully treated with Glivec (Imatinib), which is available free of cost through the Glivec International Patient Assistance programme (GIPAP) to patients with proven CML without means to pay for the drug.	imatinib	115-123	BCR activator of RhoGEF and GTPase	Homo sapiens	24-32
28467002-2	2017	We review the acquired mutations in the tyrosine kinase encoded by the BCR-ABL1 gene underlying Glivec failure or resistance in a cohort of 388 imatinib-treated CML patients (149 Female and 239 male) registered between February 2003 and June 2016 in Nepal.	imatinib	144-152	BCR activator of RhoGEF and GTPase	Homo sapiens	71-79
28589771-1	2017	AIM: To investigate the possible role of imatinib, an inhibitor of the tyrosine kinase activity of PDGF-R, in desmoplastic small round cell tumor (DSRCT).	imatinib	41-49	platelet derived growth factor receptor beta	Homo sapiens	99-105
28596663-9	2017	Our Patient detected rare BCR-ABL fusion variant e8a2 was on imatinib 400 mg since last 3 months.	imatinib	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
28726645-4	2017	In order to find the clinical-hematologic indicators of the Chronic Myeloid Leukemia expected relapse, BCR-ABL gene quantitative determination using the PSR method after the Imatinib treatment was done in 64 patients with CML who had remission (duration 0,5-14 years).	imatinib	174-182	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
27883218-8	2017	In contrast, the c-Abl inhibitor imatinib reduced its activation.	imatinib	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-22
27353341-7	2017	More interestingly, gefitinib was found to enhance the ability of imatinib to bind at the ATP-binding site of Bcr-Abl kinase.	imatinib	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
28341918-5	2017	In patients who achieved BCR-ABL1 &lt;=10% at 3 months, 5-year progression-free survival and overall survival rates were high with dasatinib (96 and 96%) and imatinib (88 and 100%).	imatinib	158-166	BCR activator of RhoGEF and GTPase	Homo sapiens	25-33
28383355-2	2017	During chronic use of imatinib, CYP2C8 becomes an important metabolizing enzyme because of cytochrome P450 3A4 (CYP3A4) autoinhibition.	imatinib	22-30	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	91-110
28330783-0	2017	Influence of MDR1 and CYP3A5 genetic polymorphisms on trough levels and therapeutic response of imatinib in newly diagnosed patients with chronic myeloid leukemia.	imatinib	96-104	ATP binding cassette subfamily B member 1	Homo sapiens	13-17
28383355-2	2017	During chronic use of imatinib, CYP2C8 becomes an important metabolizing enzyme because of cytochrome P450 3A4 (CYP3A4) autoinhibition.	imatinib	22-30	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	112-118
28330783-0	2017	Influence of MDR1 and CYP3A5 genetic polymorphisms on trough levels and therapeutic response of imatinib in newly diagnosed patients with chronic myeloid leukemia.	imatinib	96-104	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	22-28
28363184-7	2017	ROCK inhibitor (fasudil) and PDGF inhibitor (imatinib) caused significant decreases in NGF mRNA and protein content when administered alone, with no further effects noted when used in combination.	imatinib	45-53	nerve growth factor	Rattus norvegicus	87-90
28383355-3	2017	Single nucleotide polymorphisms (SNPs) in CYP2C8 may affect imatinib trough levels.	imatinib	60-68	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	42-48
28383355-0	2017	Influence of CYP2C8 polymorphisms on imatinib steady-state trough level in chronic myeloid leukemia and gastrointestinal stromal tumor patients.	imatinib	37-45	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	13-19
28330783-2	2017	Aim of this study was to assess the influence of polymorphisms in MDR1 and CYP3A5 genes on imatinib trough levels, cytogenetic and molecular response in patients with CML.	imatinib	91-99	ATP binding cassette subfamily B member 1	Homo sapiens	66-70
28330783-2	2017	Aim of this study was to assess the influence of polymorphisms in MDR1 and CYP3A5 genes on imatinib trough levels, cytogenetic and molecular response in patients with CML.	imatinib	91-99	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	75-81
28383355-2	2017	During chronic use of imatinib, CYP2C8 becomes an important metabolizing enzyme because of cytochrome P450 3A4 (CYP3A4) autoinhibition.	imatinib	22-30	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	32-38
28330783-11	2017	Patients with GG genotype for CYP3A5-A6986G (P=0.016) and TT genotype for MDR1-C3435T (P=0.013) polymorphisms had significantly higher trough levels of imatinib.	imatinib	152-160	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	30-36
28615132-0	2017	Identification of a secondary mutation in the KIT kinase domain correlated with imatinib-resistance in a canine mast cell tumor.	imatinib	80-88	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	46-49
28330783-11	2017	Patients with GG genotype for CYP3A5-A6986G (P=0.016) and TT genotype for MDR1-C3435T (P=0.013) polymorphisms had significantly higher trough levels of imatinib.	imatinib	152-160	ATP binding cassette subfamily B member 1	Homo sapiens	74-78
28330783-13	2017	Patients with CGC haplotype for MDR1 polymorphisms had significantly lower imatinib trough levels and were at a higher risk of imatinib failure [RR=1.547, 95% CI (1.324, 1.808), P&lt;0.001].	imatinib	75-83	ATP binding cassette subfamily B member 1	Homo sapiens	32-36
28330783-13	2017	Patients with CGC haplotype for MDR1 polymorphisms had significantly lower imatinib trough levels and were at a higher risk of imatinib failure [RR=1.547, 95% CI (1.324, 1.808), P&lt;0.001].	imatinib	127-135	ATP binding cassette subfamily B member 1	Homo sapiens	32-36
28330783-15	2017	To conclude, MDR1 and CYP3A5 genetic polymorphisms significantly influence plasma trough levels and therapeutic response of imatinib in patients with CML.	imatinib	124-132	ATP binding cassette subfamily B member 1	Homo sapiens	13-17
28330783-15	2017	To conclude, MDR1 and CYP3A5 genetic polymorphisms significantly influence plasma trough levels and therapeutic response of imatinib in patients with CML.	imatinib	124-132	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	22-28
28478525-3	2017	Three tyrosine kinase inhibitors (TKIs) with KIT inhibitory activity - imatinib, sunitinib, and regorafenib - are approved to treat advanced GIST and have successfully exploited this addiction to KIT oncogenic signaling, demonstrating remarkable activity in a disease that historically had no successful systemic therapy options.	imatinib	71-79	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	45-48
28478525-3	2017	Three tyrosine kinase inhibitors (TKIs) with KIT inhibitory activity - imatinib, sunitinib, and regorafenib - are approved to treat advanced GIST and have successfully exploited this addiction to KIT oncogenic signaling, demonstrating remarkable activity in a disease that historically had no successful systemic therapy options.	imatinib	71-79	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	196-199
28615132-2	2017	In the present study, we identified the secondary mutation c.2006C&gt;T in c-KIT exon 14 in a mast cell tumor obtained from a dog carrying c.1663-1671del in exon 11 and showing resistance to imatinib.	imatinib	191-199	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	75-80
28615132-5	2017	The transfectant with mutant KIT encoded by c-KIT carrying c.1663-1671del showed constitutive ligand-independent phosphorylation that was suppressed by imatinib, indicating a gain-of-function mutation.	imatinib	152-160	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	29-32
28615132-5	2017	The transfectant with mutant KIT encoded by c-KIT carrying c.1663-1671del showed constitutive ligand-independent phosphorylation that was suppressed by imatinib, indicating a gain-of-function mutation.	imatinib	152-160	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	44-49
28615132-6	2017	Furthermore, the transfectant with mutant KIT encoded by c-KIT carrying both c.1663-1671del and c.2006C&gt;T caused ligand-independent phosphorylation, which was not suppressed by imatinib.	imatinib	180-188	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	42-45
28615132-6	2017	Furthermore, the transfectant with mutant KIT encoded by c-KIT carrying both c.1663-1671del and c.2006C&gt;T caused ligand-independent phosphorylation, which was not suppressed by imatinib.	imatinib	180-188	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	57-62
28615132-7	2017	From these results, we concluded that the mutation c.2006C&gt;T in c-KIT exon 14 was an imatinib-resistance mutation in a canine mast cell tumor.	imatinib	88-96	KIT proto-oncogene, receptor tyrosine kinase	Canis lupus familiaris	67-72
28533818-4	2017	The oncoprotein tyrosine kinase BCR-ABL1 is a constitutively active kinase involved in the activation of a number of signaling pathways, and it has been the therapeutic target for tyrosine kinase inhibitors (TKIs) such as imatinib.	imatinib	222-230	BCR activator of RhoGEF and GTPase	Homo sapiens	32-40
28520795-0	2017	BIRC6 mediates imatinib resistance independently of Mcl-1.	imatinib	15-23	baculoviral IAP repeat containing 6	Homo sapiens	0-5
28514613-0	2017	KIT Inhibition by Imatinib in Patients with Severe Refractory Asthma.	imatinib	18-26	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-3
28514613-3	2017	We conducted a proof-of-principle trial to evaluate the effect of imatinib, a KIT inhibitor, on airway hyperresponsiveness, a physiological marker of severe asthma, as well as on airway mast-cell numbers and activation in patients with severe asthma.	imatinib	66-74	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	78-81
28520795-3	2017	Our phosphoproteomic analysis of an imatinib-resistant chronic myelogenous leukemia (CML) cell line (MYL-R) identified increased amounts of a BIRC6 peptide phosphorylated at S480, S482, and S486 compared to imatinib-sensitive CML cells (MYL).	imatinib	36-44	baculoviral IAP repeat containing 6	Homo sapiens	142-147
28520795-3	2017	Our phosphoproteomic analysis of an imatinib-resistant chronic myelogenous leukemia (CML) cell line (MYL-R) identified increased amounts of a BIRC6 peptide phosphorylated at S480, S482, and S486 compared to imatinib-sensitive CML cells (MYL).	imatinib	207-215	baculoviral IAP repeat containing 6	Homo sapiens	142-147
28520795-4	2017	Thus we investigated the role of BIRC6 in mediating imatinib resistance and compared it to the well-characterized anti-apoptotic protein, Mcl-1.	imatinib	52-60	baculoviral IAP repeat containing 6	Homo sapiens	33-38
28520795-6	2017	Lentiviral shRNA knockdown of BIRC6 in MYL-R cells increased imatinib-stimulated caspase activation and resulted in a ~20-25-fold increase in imatinib sensitivity, without affecting Mcl-1.	imatinib	61-69	baculoviral IAP repeat containing 6	Homo sapiens	30-35
28520795-6	2017	Lentiviral shRNA knockdown of BIRC6 in MYL-R cells increased imatinib-stimulated caspase activation and resulted in a ~20-25-fold increase in imatinib sensitivity, without affecting Mcl-1.	imatinib	142-150	baculoviral IAP repeat containing 6	Homo sapiens	30-35
28520795-12	2017	In summary, our data show that BIRC6 stability is dependent on Lyn, and that BIRC6 mediates imatinib sensitivity independently of Mcl-1 or CDK9.	imatinib	92-100	baculoviral IAP repeat containing 6	Homo sapiens	77-82
28238945-11	2017	Furthermore, brain imatinib levels were increased by co-administration of the p-gp substrates, elacridar and pantoprazole, showing that both compounds were able to inhibit the elimination of imatinib from the brain.	imatinib	19-27	phosphoglycolate phosphatase	Homo sapiens	78-82
28365527-0	2017	Imatinib discontinuation in chronic myeloid leukaemia patients with undetectable BCR-ABL transcript level: A systematic review and a meta-analysis.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
28365527-14	2017	CONCLUSIONS: Our findings suggest that imatinib discontinuation is feasible for the majority of CML patients with stable undetectable BCR-ABL transcript level.	imatinib	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
27856601-6	2017	We show that Axl blockage decreased growth of BCR-ABL TKI-sensitive CML cells including CD34+ cells and exerts additive effects with imatinib via inhibition of Stat5 activation.	imatinib	133-141	AXL receptor tyrosine kinase	Homo sapiens	13-16
28315973-15	2017	Exposure to imatinib, a Kit receptor inhibitor, for 3 days from P4 phenocopied the effect of hypoxia on the neonatal pups that resulted in inhibited intestinal motilities and decreased Kit+ ICC numbers.	imatinib	12-20	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	24-27
28315973-15	2017	Exposure to imatinib, a Kit receptor inhibitor, for 3 days from P4 phenocopied the effect of hypoxia on the neonatal pups that resulted in inhibited intestinal motilities and decreased Kit+ ICC numbers.	imatinib	12-20	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	185-188
28238945-11	2017	Furthermore, brain imatinib levels were increased by co-administration of the p-gp substrates, elacridar and pantoprazole, showing that both compounds were able to inhibit the elimination of imatinib from the brain.	imatinib	191-199	phosphoglycolate phosphatase	Homo sapiens	78-82
27875938-0	2017	The role of long noncoding RNA HOTAIR in the acquired multidrug resistance to imatinib in chronic myeloid leukemia cells.	imatinib	78-86	HOX transcript antisense RNA	Homo sapiens	31-37
28154092-0	2017	Increased peroxisome proliferator-activated receptor gamma activity reduces imatinib uptake and efficacy in chronic myeloid leukemia mononuclear cells.	imatinib	76-84	peroxisome proliferator activated receptor gamma	Homo sapiens	10-58
28154092-1	2017	Imatinib is actively transported by organic cation transporter-1 (OCT-1) influx transporter, and low OCT-1 activity in diagnostic chronic myeloid leukemia blood mononuclear cells is significantly associated with poor molecular response to imatinib.	imatinib	0-8	solute carrier family 22 member 1	Homo sapiens	36-64
28154092-1	2017	Imatinib is actively transported by organic cation transporter-1 (OCT-1) influx transporter, and low OCT-1 activity in diagnostic chronic myeloid leukemia blood mononuclear cells is significantly associated with poor molecular response to imatinib.	imatinib	0-8	solute carrier family 22 member 1	Homo sapiens	66-71
28154092-1	2017	Imatinib is actively transported by organic cation transporter-1 (OCT-1) influx transporter, and low OCT-1 activity in diagnostic chronic myeloid leukemia blood mononuclear cells is significantly associated with poor molecular response to imatinib.	imatinib	0-8	solute carrier family 22 member 1	Homo sapiens	101-106
28154092-1	2017	Imatinib is actively transported by organic cation transporter-1 (OCT-1) influx transporter, and low OCT-1 activity in diagnostic chronic myeloid leukemia blood mononuclear cells is significantly associated with poor molecular response to imatinib.	imatinib	239-247	solute carrier family 22 member 1	Homo sapiens	36-64
28154092-1	2017	Imatinib is actively transported by organic cation transporter-1 (OCT-1) influx transporter, and low OCT-1 activity in diagnostic chronic myeloid leukemia blood mononuclear cells is significantly associated with poor molecular response to imatinib.	imatinib	239-247	solute carrier family 22 member 1	Homo sapiens	66-71
28154092-1	2017	Imatinib is actively transported by organic cation transporter-1 (OCT-1) influx transporter, and low OCT-1 activity in diagnostic chronic myeloid leukemia blood mononuclear cells is significantly associated with poor molecular response to imatinib.	imatinib	239-247	solute carrier family 22 member 1	Homo sapiens	101-106
28154092-5	2017	Furthermore, we identified a strong negative correlation between OCT-1 activity and peroxisome proliferator-activated receptor gamma transcriptional activity in diagnostic chronic myeloid leukemia patients (n=84; P&lt;0.0001), suggesting that peroxisome proliferator-activated receptor gamma activation has a negative impact on the intracellular uptake of imatinib and consequent BCR-ABL kinase inhibition.	imatinib	356-364	solute carrier family 22 member 1	Homo sapiens	65-70
28154092-5	2017	Furthermore, we identified a strong negative correlation between OCT-1 activity and peroxisome proliferator-activated receptor gamma transcriptional activity in diagnostic chronic myeloid leukemia patients (n=84; P&lt;0.0001), suggesting that peroxisome proliferator-activated receptor gamma activation has a negative impact on the intracellular uptake of imatinib and consequent BCR-ABL kinase inhibition.	imatinib	356-364	peroxisome proliferator activated receptor gamma	Homo sapiens	84-132
28154092-5	2017	Furthermore, we identified a strong negative correlation between OCT-1 activity and peroxisome proliferator-activated receptor gamma transcriptional activity in diagnostic chronic myeloid leukemia patients (n=84; P&lt;0.0001), suggesting that peroxisome proliferator-activated receptor gamma activation has a negative impact on the intracellular uptake of imatinib and consequent BCR-ABL kinase inhibition.	imatinib	356-364	peroxisome proliferator activated receptor gamma	Homo sapiens	243-291
28154092-7	2017	Recently, the peroxisome proliferator-activated receptor gamma agonist pioglitazone was reported to act synergistically with imatinib, targeting the residual chronic myeloid leukemia stem cell pool.	imatinib	125-133	peroxisome proliferator activated receptor gamma	Homo sapiens	14-62
28154092-9	2017	Since the effect of peroxisome proliferator-activated receptor gamma activation on imatinib uptake in mononuclear cells may counteract the clinical benefit of this activation in stem cells, caution should be applied when combining these therapies, especially in patients with high peroxisome proliferator-activated receptor gamma transcriptional activity.	imatinib	83-91	peroxisome proliferator activated receptor gamma	Homo sapiens	20-68
27638632-1	2017	Targeted therapy in the form of selective breakpoint cluster region-abelson (BCR/ABL) tyrosine kinase inhibitor (imatinib mesylate) has successfully been introduced in the treatment of the chronic myeloid leukemia (CML).	imatinib	113-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-75
27638632-1	2017	Targeted therapy in the form of selective breakpoint cluster region-abelson (BCR/ABL) tyrosine kinase inhibitor (imatinib mesylate) has successfully been introduced in the treatment of the chronic myeloid leukemia (CML).	imatinib	113-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
27825294-0	2017	Downregulation of miR-451 in Tunisian chronic myeloid leukemia patients: potential implication in imatinib resistance.	imatinib	98-106	microRNA 451a	Homo sapiens	18-25
27825294-3	2017	However, the role of miR-451 in imatinib resistance has not been investigated.	imatinib	32-40	microRNA 451a	Homo sapiens	21-28
27825294-4	2017	The present study was undertaken to determine the expression of miR-451 in order to find a possible association between the expression of this miRNA and imatinib resistance in Tunisian CML patients.	imatinib	153-161	microRNA 451a	Homo sapiens	64-71
27825294-5	2017	METHODS: First, real-time RT-PCR was performed to identify the expression of miR-451 in peripheral leukocytes of 59 CML patients treated with imatinib.	imatinib	142-150	microRNA 451a	Homo sapiens	77-84
27825294-6	2017	Then, bioinformatics analysis was carried out to understand the regulatory roles of miR-451 in imatinib-resistant process.	imatinib	95-103	microRNA 451a	Homo sapiens	84-91
27825294-7	2017	RESULTS: Downregulated miR-451 was observed in imatinib-resistant CML cases.	imatinib	47-55	microRNA 451a	Homo sapiens	23-30
27825294-10	2017	On the other hand, increased level of MYC was detected in imatinib-resistant CML cases which may explain the causative role of MYC in CML cases and the downregulation of miR-451.	imatinib	58-66	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	38-41
27825294-10	2017	On the other hand, increased level of MYC was detected in imatinib-resistant CML cases which may explain the causative role of MYC in CML cases and the downregulation of miR-451.	imatinib	58-66	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	127-130
27825294-10	2017	On the other hand, increased level of MYC was detected in imatinib-resistant CML cases which may explain the causative role of MYC in CML cases and the downregulation of miR-451.	imatinib	58-66	microRNA 451a	Homo sapiens	170-177
27875938-3	2017	In this study, we aimed to investigate the mechanisms of long noncoding RNA (lncRNA) HOTAIR in CML resistance to imatinib.	imatinib	113-121	HOX transcript antisense RNA	Homo sapiens	85-91
27875938-6	2017	An imatinib-resistant human CML cell line K562 (K562-R) was established, and western blot was used to detect the impact of lncRNA HOTAIR on the activation of PI3K/Akt signaling pathway.	imatinib	3-11	HOX transcript antisense RNA	Homo sapiens	130-136
27875938-6	2017	An imatinib-resistant human CML cell line K562 (K562-R) was established, and western blot was used to detect the impact of lncRNA HOTAIR on the activation of PI3K/Akt signaling pathway.	imatinib	3-11	AKT serine/threonine kinase 1	Homo sapiens	163-166
27875938-7	2017	RESULTS: Our results showed that lncRNA HOTAIR was greatly upregulated in the MRP1-high patients as well as in the K562-imatinib-resistant cells compared with control.	imatinib	120-128	HOX transcript antisense RNA	Homo sapiens	40-46
27875938-7	2017	RESULTS: Our results showed that lncRNA HOTAIR was greatly upregulated in the MRP1-high patients as well as in the K562-imatinib-resistant cells compared with control.	imatinib	120-128	ATP binding cassette subfamily B member 1	Homo sapiens	78-82
27875938-8	2017	Knockdown of HOTAIR expression downregulated the MRP1 expression levels in the K562-imatinib cells and resulted in higher sensitivity to the imatinib treatment.	imatinib	84-92	HOX transcript antisense RNA	Homo sapiens	13-19
27875938-8	2017	Knockdown of HOTAIR expression downregulated the MRP1 expression levels in the K562-imatinib cells and resulted in higher sensitivity to the imatinib treatment.	imatinib	84-92	ATP binding cassette subfamily B member 1	Homo sapiens	49-53
27875938-8	2017	Knockdown of HOTAIR expression downregulated the MRP1 expression levels in the K562-imatinib cells and resulted in higher sensitivity to the imatinib treatment.	imatinib	141-149	HOX transcript antisense RNA	Homo sapiens	13-19
27875938-8	2017	Knockdown of HOTAIR expression downregulated the MRP1 expression levels in the K562-imatinib cells and resulted in higher sensitivity to the imatinib treatment.	imatinib	141-149	ATP binding cassette subfamily B member 1	Homo sapiens	49-53
27875938-9	2017	In addition, the activation of PI3K/Akt was greatly attenuated when HOTAIR was knocked down in K562-imatinib cells.	imatinib	100-108	AKT serine/threonine kinase 1	Homo sapiens	36-39
27875938-9	2017	In addition, the activation of PI3K/Akt was greatly attenuated when HOTAIR was knocked down in K562-imatinib cells.	imatinib	100-108	HOX transcript antisense RNA	Homo sapiens	68-74
27875938-10	2017	DISCUSSIONS: These data suggest that the knockdown of HOTAIR may play a crucial role in improving acquired resistance to imatinib in CML K562-R cells via PI3K/Akt pathway.	imatinib	121-129	HOX transcript antisense RNA	Homo sapiens	54-60
27875938-10	2017	DISCUSSIONS: These data suggest that the knockdown of HOTAIR may play a crucial role in improving acquired resistance to imatinib in CML K562-R cells via PI3K/Akt pathway.	imatinib	121-129	AKT serine/threonine kinase 1	Homo sapiens	159-162
27701913-0	2017	The first case of acute T-cell lymphoblastic leukemia containing the e19a2 BCR-ABL1 transcript: a durable molecular response using imatinib-based chemotherapy.	imatinib	131-139	BCR activator of RhoGEF and GTPase	Homo sapiens	75-83
27650030-7	2017	HMGCoAR, LDL-R, and apobec1 expressions were significantly increased while CETP declined after 48-96 h. To conclude, imatinib produces an independent favorable lipid profile, which is not hindered by statins and is partly mediated via transcription regulation of genes involved in the clearance of plasma lipids.	imatinib	117-125	low density lipoprotein receptor	Homo sapiens	9-14
28000100-0	2017	Marked response to imatinib mesylate in a patient with platelet-derived growth factor receptor beta-associated acute myeloid leukemia.	imatinib	19-36	platelet derived growth factor receptor beta	Homo sapiens	55-94
28334365-16	2017	Conclusions and Relevance: Patients with KIT exon 11 deletion mutations benefit most from the longer duration of adjuvant imatinib.	imatinib	122-130	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	41-44
28334365-17	2017	The duration of adjuvant imatinib modifies the risk of GIST recurrence associated with some KIT mutations, including deletions that affect exon 11 codons 557 and/or 558.	imatinib	25-33	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	92-95
28319085-4	2017	These included the BCL2L1 and MCL1 combination, which was also effective in imatinib-resistant cells.	imatinib	76-84	BCL2 like 1	Homo sapiens	19-25
27650030-7	2017	HMGCoAR, LDL-R, and apobec1 expressions were significantly increased while CETP declined after 48-96 h. To conclude, imatinib produces an independent favorable lipid profile, which is not hindered by statins and is partly mediated via transcription regulation of genes involved in the clearance of plasma lipids.	imatinib	117-125	apolipoprotein B mRNA editing enzyme catalytic subunit 1	Homo sapiens	20-27
27650030-7	2017	HMGCoAR, LDL-R, and apobec1 expressions were significantly increased while CETP declined after 48-96 h. To conclude, imatinib produces an independent favorable lipid profile, which is not hindered by statins and is partly mediated via transcription regulation of genes involved in the clearance of plasma lipids.	imatinib	117-125	cholesteryl ester transfer protein	Homo sapiens	75-79
28319085-4	2017	These included the BCL2L1 and MCL1 combination, which was also effective in imatinib-resistant cells.	imatinib	76-84	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	30-34
28616912-0	2017	[The Roles of Glut5 in Imatinib Resistance in the Ph+ Acute Lymphoblastic Leukemia Cell].	imatinib	23-31	solute carrier family 2 member 5	Homo sapiens	14-19
28616912-1	2017	OBJECTIVES: To explore the possible roles of glucose transport 5 (Glut5) in imatinib resistance in the Ph+ acute lymphoblastic leukemia cell (Ph+ ALL).	imatinib	76-84	solute carrier family 2 member 5	Homo sapiens	45-64
28616912-1	2017	OBJECTIVES: To explore the possible roles of glucose transport 5 (Glut5) in imatinib resistance in the Ph+ acute lymphoblastic leukemia cell (Ph+ ALL).	imatinib	76-84	solute carrier family 2 member 5	Homo sapiens	66-71
28616912-2	2017	METHODS: The gene chip technique was used to detect different gene expression between Ph+ ALL cell line SUP-B15/R (imatinib resistant cell line) and SUP-B15/S (imatinib sensitive cell line), the gene of solute carrier family 2 member 5 (SLC2A5) and its coded protein Glut5 were screened out and were reconfirmed by qPCR and Western blot assay.	imatinib	115-123	solute carrier family 2 member 5	Homo sapiens	203-235
28103766-0	2017	Long-Term Exposure to Imatinib Mesylate Downregulates Hippo Pathway and Activates YAP in a Model of Chronic Myelogenous Leukemia.	imatinib	22-39	Yes1 associated transcriptional regulator	Homo sapiens	82-85
28616912-2	2017	METHODS: The gene chip technique was used to detect different gene expression between Ph+ ALL cell line SUP-B15/R (imatinib resistant cell line) and SUP-B15/S (imatinib sensitive cell line), the gene of solute carrier family 2 member 5 (SLC2A5) and its coded protein Glut5 were screened out and were reconfirmed by qPCR and Western blot assay.	imatinib	115-123	solute carrier family 2 member 5	Homo sapiens	237-243
28103766-3	2017	We have previously shown that prolonged exposure to imatinib mesylate (IM) results in dysregulation of Akt/Erk 1/2 signaling, upregulation of miR-181a, enhanced adhesiveness, and resistance to high IM.	imatinib	52-69	AKT serine/threonine kinase 1	Homo sapiens	103-106
28103766-3	2017	We have previously shown that prolonged exposure to imatinib mesylate (IM) results in dysregulation of Akt/Erk 1/2 signaling, upregulation of miR-181a, enhanced adhesiveness, and resistance to high IM.	imatinib	52-69	mitogen-activated protein kinase 3	Homo sapiens	107-114
28616912-2	2017	METHODS: The gene chip technique was used to detect different gene expression between Ph+ ALL cell line SUP-B15/R (imatinib resistant cell line) and SUP-B15/S (imatinib sensitive cell line), the gene of solute carrier family 2 member 5 (SLC2A5) and its coded protein Glut5 were screened out and were reconfirmed by qPCR and Western blot assay.	imatinib	115-123	solute carrier family 2 member 5	Homo sapiens	267-272
28616912-5	2017	IC50 values of imatinib to SUP-B15/S cells after treatment with 25 mumol/L fructose were increased from (44.50+-2.38) mumol/L to (64.71+-1.69) mumol/L, in the meanwhile, PI3K and AKT mRNA level also increased in fructose treated SUP-B15/S cells compared to the control.	imatinib	15-23	AKT serine/threonine kinase 1	Homo sapiens	179-182
28616912-6	2017	CONCLUSIONS: High expression of SLC2A5 and Glut5 protein in SUP-B15/R cells leads to increased fructose absorption, and further activates PI3K/AKT pathway which cause the SUP-B15 cell resistance to imatinib.	imatinib	198-206	solute carrier family 2 (facilitated glucose transporter), member 5	Mus musculus	32-38
28315715-0	2017	Sab mediates mitochondrial dysfunction involved in imatinib mesylate-induced cardiotoxicity.	imatinib	51-68	SH3-domain binding protein 5	Rattus norvegicus	0-3
28315715-5	2017	We examined the impact of Sab-mediated signaling on imatinib mesylate cardiotoxicity in H9c2 rat cardiomyocyte-like cells.	imatinib	52-60	SH3-domain binding protein 5	Rattus norvegicus	26-29
28616912-6	2017	CONCLUSIONS: High expression of SLC2A5 and Glut5 protein in SUP-B15/R cells leads to increased fructose absorption, and further activates PI3K/AKT pathway which cause the SUP-B15 cell resistance to imatinib.	imatinib	198-206	solute carrier family 2 (facilitated glucose transporter), member 5	Mus musculus	43-48
28315715-6	2017	Silencing Sab increased the LD50 of imatinib mesylate 4-fold in H9c2 cells.	imatinib	36-53	SH3-domain binding protein 5	Rattus norvegicus	10-13
28315715-7	2017	Disrupting Sab-mediated signaling prevented imatinib mesylate-induced apoptosis as well.	imatinib	44-61	SH3-domain binding protein 5	Rattus norvegicus	11-14
28616912-6	2017	CONCLUSIONS: High expression of SLC2A5 and Glut5 protein in SUP-B15/R cells leads to increased fructose absorption, and further activates PI3K/AKT pathway which cause the SUP-B15 cell resistance to imatinib.	imatinib	198-206	AKT serine/threonine kinase 1	Homo sapiens	143-146
28315715-9	2017	Further, inhibition of Sab-related signaling partially rescued deficits in mitochondrial respiration, ATP production, and membrane potential in imatinib mesylate-treated H9c2 cells.	imatinib	144-161	SH3-domain binding protein 5	Rattus norvegicus	23-26
28315715-10	2017	Conversely, over-expression of Sab in H9c2 cells increased the cardiotoxicity of imatinib mesylate in vitro decreasing the LD50 over 4-fold.	imatinib	81-98	SH3-domain binding protein 5	Rattus norvegicus	31-34
28502291-1	2017	Objective To investigate the effect of imatinib (IM) on the expressions of A20-binding inhibitor of NF-kappaB1 (ABIN1) and A20 in Jurkat T cells.	imatinib	39-47	TNFAIP3 interacting protein 1	Homo sapiens	75-110
28475010-1	2017	The ABL kinase inhibitor imatinib has been used as front-line therapy for Philadelphia-positive chronic myeloid leukemia.	imatinib	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
28475010-2	2017	However, a significant proportion of imatinib-treated patients relapse due to occurrence of mutations in the ABL kinase domain.	imatinib	37-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-112
28502291-1	2017	Objective To investigate the effect of imatinib (IM) on the expressions of A20-binding inhibitor of NF-kappaB1 (ABIN1) and A20 in Jurkat T cells.	imatinib	39-47	TNFAIP3 interacting protein 1	Homo sapiens	112-117
28502291-1	2017	Objective To investigate the effect of imatinib (IM) on the expressions of A20-binding inhibitor of NF-kappaB1 (ABIN1) and A20 in Jurkat T cells.	imatinib	39-47	immunoglobulin kappa variable 1-27	Homo sapiens	75-78
28484463-3	2017	TKIs such as imatinib, and more potent second-generation nilotinib and dasatinib induce a high rate of deep molecular response (DMR, BCR-ABL1 &lt;= 0.01%) in CML patients.	imatinib	13-21	BCR activator of RhoGEF and GTPase	Homo sapiens	133-141
28334729-5	2017	RESULTS: SLUG downregulation inhibited cell proliferation, induced cell death in both cell lines, and sensitised GIST882 cells to lower imatinib concentrations.	imatinib	136-144	snail family transcriptional repressor 2	Homo sapiens	9-13
28334729-7	2017	SLUG expression was associated with unfavourable RFS both when patients were treated with surgery alone (HR=3.40, 95% CI=1.67-6.89, P=0.001) and when treated with surgery plus adjuvant imatinib (HR=1.83, 95% CI=1.29-2.60, P=0.001).	imatinib	185-193	snail family transcriptional repressor 2	Homo sapiens	0-4
28437552-10	2017	In a subgroup of 44 patients, the molecular response to treatment with Imatinib was assessed by quantitative PCR at 3 months (BCR-ABL1 &lt;= 10%), 6 months (BCR-ABL1 &lt;= 1%), or 12 months (BCR-ABL1 &lt;= 0.1%).	imatinib	71-79	BCR activator of RhoGEF and GTPase	Homo sapiens	126-134
28437552-10	2017	In a subgroup of 44 patients, the molecular response to treatment with Imatinib was assessed by quantitative PCR at 3 months (BCR-ABL1 &lt;= 10%), 6 months (BCR-ABL1 &lt;= 1%), or 12 months (BCR-ABL1 &lt;= 0.1%).	imatinib	71-79	BCR activator of RhoGEF and GTPase	Homo sapiens	157-165
28437552-10	2017	In a subgroup of 44 patients, the molecular response to treatment with Imatinib was assessed by quantitative PCR at 3 months (BCR-ABL1 &lt;= 10%), 6 months (BCR-ABL1 &lt;= 1%), or 12 months (BCR-ABL1 &lt;= 0.1%).	imatinib	71-79	BCR activator of RhoGEF and GTPase	Homo sapiens	157-165
28445932-5	2017	CFTRinh-172, a classic CFTR inhibitor, down-regulated the expression of CFTR, p-BCR-ABL and classical Wnt/beta-catenin signaling in Ph+ acute leukemia cells, while imatinib had no effect on CFTR.	imatinib	164-172	CF transmembrane conductance regulator	Homo sapiens	0-4
28420426-0	2017	Genotypes of SLC22A4 and SLC22A5 regulatory loci are predictive of the response of chronic myeloid leukemia patients to imatinib treatment.	imatinib	120-128	solute carrier family 22 member 4	Homo sapiens	13-20
28420426-0	2017	Genotypes of SLC22A4 and SLC22A5 regulatory loci are predictive of the response of chronic myeloid leukemia patients to imatinib treatment.	imatinib	120-128	solute carrier family 22 member 5	Homo sapiens	25-32
28420426-8	2017	Genotype association analysis with the response to imatinib indicated that rs460089-GC carriers had a significantly higher probability of achieving a stable major molecular response (BCR-ABL1 transcript level below or equal to 0.1% in the international scale).	imatinib	51-59	BCR activator of RhoGEF and GTPase	Homo sapiens	183-191
28323047-4	2017	This chimeric protein is the target of a kinase inhibitor, imatinib, but the development of mutations in the ABL kinase domain resulting in drug resistance and several approaches to overcoming resistance have been study.	imatinib	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-112
28267438-0	2017	Nrf-2/Gst-alpha mediated imatinib resistance through rapid 4-HNE clearance.	imatinib	25-33	NFE2 like bZIP transcription factor 2	Homo sapiens	0-5
28403213-2	2017	The drug imatinib, a selective inhibitor of Kit, is used for treatment of mutant Kit-positive cancers.	imatinib	9-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	44-47
28403213-2	2017	The drug imatinib, a selective inhibitor of Kit, is used for treatment of mutant Kit-positive cancers.	imatinib	9-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	81-84
28403213-3	2017	However, mutations in the Kit kinase domain, which are frequently found in neoplastic mast cells, confer an imatinib resistance, and cancers expressing the mutants can proliferate in the presence of imatinib.	imatinib	108-116	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	26-29
28403213-3	2017	However, mutations in the Kit kinase domain, which are frequently found in neoplastic mast cells, confer an imatinib resistance, and cancers expressing the mutants can proliferate in the presence of imatinib.	imatinib	199-207	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	26-29
28403213-4	2017	Recently, we showed that in neoplastic mast cells that endogenously express an imatinib-resistant Kit mutant, Kit causes oncogenic activation of the phosphatidylinositol 3-kinase-Akt (PI3K-Akt) pathway and the signal transducer and activator of transcription 5 (STAT5) but only on endolysosomes and on the endoplasmic reticulum (ER), respectively.	imatinib	79-87	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	98-101
28403213-4	2017	Recently, we showed that in neoplastic mast cells that endogenously express an imatinib-resistant Kit mutant, Kit causes oncogenic activation of the phosphatidylinositol 3-kinase-Akt (PI3K-Akt) pathway and the signal transducer and activator of transcription 5 (STAT5) but only on endolysosomes and on the endoplasmic reticulum (ER), respectively.	imatinib	79-87	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	110-113
28403213-4	2017	Recently, we showed that in neoplastic mast cells that endogenously express an imatinib-resistant Kit mutant, Kit causes oncogenic activation of the phosphatidylinositol 3-kinase-Akt (PI3K-Akt) pathway and the signal transducer and activator of transcription 5 (STAT5) but only on endolysosomes and on the endoplasmic reticulum (ER), respectively.	imatinib	79-87	AKT serine/threonine kinase 1	Homo sapiens	179-182
28403213-4	2017	Recently, we showed that in neoplastic mast cells that endogenously express an imatinib-resistant Kit mutant, Kit causes oncogenic activation of the phosphatidylinositol 3-kinase-Akt (PI3K-Akt) pathway and the signal transducer and activator of transcription 5 (STAT5) but only on endolysosomes and on the endoplasmic reticulum (ER), respectively.	imatinib	79-87	AKT serine/threonine kinase 1	Homo sapiens	189-192
28403213-4	2017	Recently, we showed that in neoplastic mast cells that endogenously express an imatinib-resistant Kit mutant, Kit causes oncogenic activation of the phosphatidylinositol 3-kinase-Akt (PI3K-Akt) pathway and the signal transducer and activator of transcription 5 (STAT5) but only on endolysosomes and on the endoplasmic reticulum (ER), respectively.	imatinib	79-87	signal transducer and activator of transcription 5A	Homo sapiens	210-260
28403213-4	2017	Recently, we showed that in neoplastic mast cells that endogenously express an imatinib-resistant Kit mutant, Kit causes oncogenic activation of the phosphatidylinositol 3-kinase-Akt (PI3K-Akt) pathway and the signal transducer and activator of transcription 5 (STAT5) but only on endolysosomes and on the endoplasmic reticulum (ER), respectively.	imatinib	79-87	signal transducer and activator of transcription 5A	Homo sapiens	262-267
28445932-5	2017	CFTRinh-172, a classic CFTR inhibitor, down-regulated the expression of CFTR, p-BCR-ABL and classical Wnt/beta-catenin signaling in Ph+ acute leukemia cells, while imatinib had no effect on CFTR.	imatinib	164-172	CF transmembrane conductance regulator	Homo sapiens	23-27
28445932-5	2017	CFTRinh-172, a classic CFTR inhibitor, down-regulated the expression of CFTR, p-BCR-ABL and classical Wnt/beta-catenin signaling in Ph+ acute leukemia cells, while imatinib had no effect on CFTR.	imatinib	164-172	CF transmembrane conductance regulator	Homo sapiens	23-27
28469513-0	2017	BCR-ABL V280G Mutation, Potential Role in Imatinib Resistance: First Case Report.	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
28387753-0	2017	Imatinib mesylate inhibits STAT5 phosphorylation in response to IL-7 and promotes T cell lymphopenia in chronic myelogenous leukemia patients.	imatinib	0-17	signal transducer and activator of transcription 5A	Homo sapiens	27-32
28387753-0	2017	Imatinib mesylate inhibits STAT5 phosphorylation in response to IL-7 and promotes T cell lymphopenia in chronic myelogenous leukemia patients.	imatinib	0-17	interleukin 7	Homo sapiens	64-68
28469513-4	2017	DISCUSSION AND CONCLUSIONS: This is the first report describing a new BCR-ABL kinase domain mutation-V280G-that might be associated with resistance to imatinib.	imatinib	151-159	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
28278078-0	2017	Presence of novel compound BCR-ABL mutations in late chronic and advanced phase imatinib sensitive CML patients indicates their possible role in CML progression.	imatinib	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
28069548-6	2017	Furthermore, inhibition of HULC enhanced imatinib-induced apoptosis of CML cells.	imatinib	41-49	hepatocellular carcinoma up-regulated long non-coding RNA	Homo sapiens	27-31
28069548-7	2017	Further experiments demonstrated that HULC silencing markedly suppressed the phosphorylation of PI3K and AKT, indicating that enhancement of imatinib-induced apoptosis by HULC inhibition is related with the reduction of c-Myc expression and inhibition of PI3K/Akt pathway activity.	imatinib	141-149	hepatocellular carcinoma up-regulated long non-coding RNA	Homo sapiens	38-42
28069548-7	2017	Further experiments demonstrated that HULC silencing markedly suppressed the phosphorylation of PI3K and AKT, indicating that enhancement of imatinib-induced apoptosis by HULC inhibition is related with the reduction of c-Myc expression and inhibition of PI3K/Akt pathway activity.	imatinib	141-149	AKT serine/threonine kinase 1	Homo sapiens	105-108
28069548-7	2017	Further experiments demonstrated that HULC silencing markedly suppressed the phosphorylation of PI3K and AKT, indicating that enhancement of imatinib-induced apoptosis by HULC inhibition is related with the reduction of c-Myc expression and inhibition of PI3K/Akt pathway activity.	imatinib	141-149	hepatocellular carcinoma up-regulated long non-coding RNA	Homo sapiens	171-175
28069548-7	2017	Further experiments demonstrated that HULC silencing markedly suppressed the phosphorylation of PI3K and AKT, indicating that enhancement of imatinib-induced apoptosis by HULC inhibition is related with the reduction of c-Myc expression and inhibition of PI3K/Akt pathway activity.	imatinib	141-149	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	220-225
28069548-7	2017	Further experiments demonstrated that HULC silencing markedly suppressed the phosphorylation of PI3K and AKT, indicating that enhancement of imatinib-induced apoptosis by HULC inhibition is related with the reduction of c-Myc expression and inhibition of PI3K/Akt pathway activity.	imatinib	141-149	AKT serine/threonine kinase 1	Homo sapiens	260-263
28380378-4	2017	Imatinib-an anti-cancer tyrosine kinase inhibitor-antagonizes the ABL-IRE1alpha interaction, blunts IRE1alpha RNase hyperactivity, reduces pancreatic beta cell apoptosis, and reverses type 1 diabetes (T1D) in the non-obese diabetic (NOD) mouse model.	imatinib	0-8	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	66-69
28380378-4	2017	Imatinib-an anti-cancer tyrosine kinase inhibitor-antagonizes the ABL-IRE1alpha interaction, blunts IRE1alpha RNase hyperactivity, reduces pancreatic beta cell apoptosis, and reverses type 1 diabetes (T1D) in the non-obese diabetic (NOD) mouse model.	imatinib	0-8	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	70-79
28380378-4	2017	Imatinib-an anti-cancer tyrosine kinase inhibitor-antagonizes the ABL-IRE1alpha interaction, blunts IRE1alpha RNase hyperactivity, reduces pancreatic beta cell apoptosis, and reverses type 1 diabetes (T1D) in the non-obese diabetic (NOD) mouse model.	imatinib	0-8	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	100-109
30755950-5	2017	LEARNING POINTS: FIP1L1-PDGFRA fusion occurs in 10% of patients with idiopathic hypereosinophilia.Thromboembolism is a known cause of death in hypereosinophilia.The prognosis of FIP1L1-PDGFRA-associated chronic eosinophilic leukemia has been profoundly changed by imatinib treatment.	imatinib	264-272	factor interacting with PAPOLA and CPSF1	Homo sapiens	17-23
30755950-5	2017	LEARNING POINTS: FIP1L1-PDGFRA fusion occurs in 10% of patients with idiopathic hypereosinophilia.Thromboembolism is a known cause of death in hypereosinophilia.The prognosis of FIP1L1-PDGFRA-associated chronic eosinophilic leukemia has been profoundly changed by imatinib treatment.	imatinib	264-272	platelet derived growth factor receptor alpha	Homo sapiens	24-30
28278078-3	2017	However, there are limited reports about association of compound BCR-ABL mutations with disease progression in imatinib (IM) sensitive CML patients.	imatinib	111-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
28278078-13	2017	The compound missense mutations in BCR-ABL kinase domain responsible to elicit disease progression, drug resistance or disease relapse in CML, can be present in yet Imatinib sensitive patients.	imatinib	165-173	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
28103625-0	2017	Phase II study of imatinib-based chemotherapy for newly diagnosed BCR-ABL-positive acute lymphoblastic leukemia.	imatinib	18-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
28103625-2	2017	We conducted a phase II trial of imatinib-combined chemotherapy for newly diagnosed BCR-ABL-positive ALL in adults.	imatinib	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
28283735-8	2017	Similarly, in the pulmonary artery endothelial cells and smooth muscle cells co-culture model, imatinib and dasatinib increased NO and decreased endothelin-1 protein and mRNA.	imatinib	95-103	endothelin 1	Homo sapiens	145-157
28289867-0	2017	Association of the hOCT1/ABCB1 genotype with efficacy and tolerability of imatinib in patients affected by chronic myeloid leukemia.	imatinib	74-82	solute carrier family 22 member 1	Homo sapiens	19-24
28128444-0	2017	Suppression of carboxylesterases by imatinib mediated by the down-regulation of pregnane X receptor.	imatinib	36-44	nuclear receptor subfamily 1, group I, member 2	Mus musculus	80-99
28289867-0	2017	Association of the hOCT1/ABCB1 genotype with efficacy and tolerability of imatinib in patients affected by chronic myeloid leukemia.	imatinib	74-82	ATP binding cassette subfamily B member 1	Homo sapiens	25-30
28286932-0	2017	hOCT1 gene expression predict for optimal response to Imatinib in Tunisian patients with chronic myeloid leukemia.	imatinib	54-62	solute carrier family 22 member 1	Homo sapiens	0-5
28289867-4	2017	RESULTS: We found that a combination of two polymorphisms, namely hOCT1 c.480C&gt;G (rs683369) and ABCB1 c.3435C&gt;T (rs1045642), seems to play the role of predictor for imatinib in both efficacy and toxicity.	imatinib	171-179	solute carrier family 22 member 1	Homo sapiens	66-71
28289867-4	2017	RESULTS: We found that a combination of two polymorphisms, namely hOCT1 c.480C&gt;G (rs683369) and ABCB1 c.3435C&gt;T (rs1045642), seems to play the role of predictor for imatinib in both efficacy and toxicity.	imatinib	171-179	ATP binding cassette subfamily B member 1	Homo sapiens	99-104
28449810-0	2017	Novel t(5;11)(q32;q13.4) with NUMA1-PDGFRB fusion in a myeloid neoplasm with eosinophilia with response to imatinib mesylate.	imatinib	107-124	nuclear mitotic apparatus protein 1	Homo sapiens	30-35
28449810-0	2017	Novel t(5;11)(q32;q13.4) with NUMA1-PDGFRB fusion in a myeloid neoplasm with eosinophilia with response to imatinib mesylate.	imatinib	107-124	platelet derived growth factor receptor beta	Homo sapiens	36-42
28449810-1	2017	We report a NUMA1-PDGFRB fusion in a myeloproliferative neoplasm with eosinophilia in a 61-year old man, with response to imatinib mesylate therapy.	imatinib	122-139	nuclear mitotic apparatus protein 1	Homo sapiens	12-17
28449810-1	2017	We report a NUMA1-PDGFRB fusion in a myeloproliferative neoplasm with eosinophilia in a 61-year old man, with response to imatinib mesylate therapy.	imatinib	122-139	platelet derived growth factor receptor beta	Homo sapiens	18-24
28286932-10	2017	CONCLUSIONS: hOCT1 mRNA expression may serve as a clinical biomarker of response to imatinib and could be useful to predict IM therapy outcome of CML patients.	imatinib	84-92	solute carrier family 22 member 1	Homo sapiens	13-18
27997714-2	2017	Despite its proven benefits, half of the patients treated with imatinib show disease progression within 2 years due to secondary resistance mutations in KIT.	imatinib	63-71	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	153-156
28283298-1	2017	INTRODUCTION: Generics of imatinib mesylate, the first tyrosine kinase inhibitor targeting the BCR-ABL1 fusion protein, have recently been approved in many countries as the alternative, low-cost forms for the treatment of patients with chronic myeloid leukemia (CML).	imatinib	26-43	BCR activator of RhoGEF and GTPase	Homo sapiens	95-103
27997714-10	2017	Pre-existing cancer cells with genetic alterations promoting apoptosis resistance may serve as a basis whereby cancer cells with critical mutations, such as secondary KIT mutations, can establish full imatinib resistance.	imatinib	201-209	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	167-170
28435469-1	2017	Despite Imatinib (IM), a selective inhibitor of Bcr-Abl, having led to improved prognosis in Chronic Myeloid Leukemia (CML) patients, acquired resistance and long-term adverse effects is still being encountered.	imatinib	8-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
28367122-13	2017	When miR-20a ASODNs were combined with imatinib, the growth of K562 cells was significantly inhibited as compared to the ASODN treatment alone, imatinib alone, and SODN+imatinib groups (p &lt; 0.05).	imatinib	144-152	microRNA 20a	Homo sapiens	5-12
28367122-13	2017	When miR-20a ASODNs were combined with imatinib, the growth of K562 cells was significantly inhibited as compared to the ASODN treatment alone, imatinib alone, and SODN+imatinib groups (p &lt; 0.05).	imatinib	144-152	microRNA 20a	Homo sapiens	5-12
28446273-5	2017	The expression of gamma-H2AX was markedly enhanced and the phosphorylation of JNK up-regulated by quercetin in both imatinib-resistant and imatinib-sensitive cell lines.	imatinib	116-124	mitogen-activated protein kinase 8	Homo sapiens	78-81
28446273-5	2017	The expression of gamma-H2AX was markedly enhanced and the phosphorylation of JNK up-regulated by quercetin in both imatinib-resistant and imatinib-sensitive cell lines.	imatinib	139-147	mitogen-activated protein kinase 8	Homo sapiens	78-81
28329763-2	2017	ABL1 kinase inhibitors have improved the clinical outcomes for patients with CML, with over 80% of patients treated with imatinib surviving for more than 10 years.	imatinib	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-4
28329763-3	2017	Second-generation ABL1 kinase inhibitors induce more potent molecular responses in both previously untreated and imatinib-resistant patients with CML.	imatinib	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-22
28435469-1	2017	Despite Imatinib (IM), a selective inhibitor of Bcr-Abl, having led to improved prognosis in Chronic Myeloid Leukemia (CML) patients, acquired resistance and long-term adverse effects is still being encountered.	imatinib	18-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
28029010-0	2017	Concomitant AID Expression and BCL7A Loss Associates With Accelerated Phase Progression and Imatinib Resistance in Chronic Myeloid Leukemia.	imatinib	92-100	activation induced cytidine deaminase	Homo sapiens	12-15
28267803-0	2017	Correction: MicroRNA-1301-Mediated RanGAP1 Downregulation Induces BCR-ABL Nuclear Entrapment to Enhance Imatinib Efficacy in Chronic Myeloid Leukemia Cells.	imatinib	104-112	Ran GTPase activating protein 1	Homo sapiens	35-42
28267803-0	2017	Correction: MicroRNA-1301-Mediated RanGAP1 Downregulation Induces BCR-ABL Nuclear Entrapment to Enhance Imatinib Efficacy in Chronic Myeloid Leukemia Cells.	imatinib	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
28257089-7	2017	It was proven that nuclear located Bcr-Abl induced CML cell (including imatinib-resistant K562G01 cells) apoptosis by activation of p73 and its downstream molecules.	imatinib	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
28257089-7	2017	It was proven that nuclear located Bcr-Abl induced CML cell (including imatinib-resistant K562G01 cells) apoptosis by activation of p73 and its downstream molecules.	imatinib	71-79	tumor protein p73	Homo sapiens	132-135
28029010-0	2017	Concomitant AID Expression and BCL7A Loss Associates With Accelerated Phase Progression and Imatinib Resistance in Chronic Myeloid Leukemia.	imatinib	92-100	BAF chromatin remodeling complex subunit BCL7A	Homo sapiens	31-36
27533597-0	2017	Oroxylin A reverses the drug resistance of chronic myelogenous leukemia cells to imatinib through CXCL12/CXCR7 axis in bone marrow microenvironment.	imatinib	81-89	C-X-C motif chemokine ligand 12	Homo sapiens	98-104
27533597-0	2017	Oroxylin A reverses the drug resistance of chronic myelogenous leukemia cells to imatinib through CXCL12/CXCR7 axis in bone marrow microenvironment.	imatinib	81-89	atypical chemokine receptor 3	Homo sapiens	105-110
28454247-7	2017	In addition, AMPD3 depletion sensitized GIST-T1 cells to the tyrosine kinase inhibitor imatinib.	imatinib	87-95	adenosine monophosphate deaminase 3	Homo sapiens	13-18
28040471-7	2017	Imatinib treatment was associated with increased density of the multi-oocyte follicles (P&lt;0.01), oogonia (p&lt;0.01) and germline clusters (P&lt;0.05), decreased activation of primordial follicles, increased expression of c-Kit and AMH, and decreased protein expression of Kit-ligand and GDF9 when compared to age-matched controls.	imatinib	0-8	KIT ligand	Rattus norvegicus	276-286
28040471-7	2017	Imatinib treatment was associated with increased density of the multi-oocyte follicles (P&lt;0.01), oogonia (p&lt;0.01) and germline clusters (P&lt;0.05), decreased activation of primordial follicles, increased expression of c-Kit and AMH, and decreased protein expression of Kit-ligand and GDF9 when compared to age-matched controls.	imatinib	0-8	anti-Mullerian hormone	Rattus norvegicus	235-238
28040471-7	2017	Imatinib treatment was associated with increased density of the multi-oocyte follicles (P&lt;0.01), oogonia (p&lt;0.01) and germline clusters (P&lt;0.05), decreased activation of primordial follicles, increased expression of c-Kit and AMH, and decreased protein expression of Kit-ligand and GDF9 when compared to age-matched controls.	imatinib	0-8	growth differentiation factor 9	Rattus norvegicus	291-295
28028030-4	2017	The natural history of PDGFRA- and PDGFRB-rearranged neoplasms has been dramatically altered by imatinib.	imatinib	96-104	platelet derived growth factor receptor alpha	Homo sapiens	23-30
28260860-0	2017	Antiproliferation effect of imatinib mesylate on MCF7, T-47D tumorigenic and MCF 10A nontumorigenic breast cell lines via PDGFR-beta, PDGF-BB, c-Kit and SCF genes.	imatinib	28-45	platelet derived growth factor receptor beta	Homo sapiens	122-132
28260860-0	2017	Antiproliferation effect of imatinib mesylate on MCF7, T-47D tumorigenic and MCF 10A nontumorigenic breast cell lines via PDGFR-beta, PDGF-BB, c-Kit and SCF genes.	imatinib	28-45	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	143-148
28260860-0	2017	Antiproliferation effect of imatinib mesylate on MCF7, T-47D tumorigenic and MCF 10A nontumorigenic breast cell lines via PDGFR-beta, PDGF-BB, c-Kit and SCF genes.	imatinib	28-45	KIT ligand	Homo sapiens	153-156
28260860-3	2017	Imatinib mesylate is a selective inhibitor of receptor tyrosine kinase, including PDGFR-beta and c-Kit.	imatinib	0-17	platelet derived growth factor receptor beta	Homo sapiens	82-92
28260860-3	2017	Imatinib mesylate is a selective inhibitor of receptor tyrosine kinase, including PDGFR-beta and c-Kit.	imatinib	0-17	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	97-102
28260860-4	2017	In this research, we studied how imatinib mesylate would exert effect on MCF7 and T-47D breast cancer and MCF 10A epithelial cell lines, the gene and protein expression of PDGFR-beta, c-Kit and their relevant ligands platelet-derived growth factor (PDGF)-BB and stem cell factor (SCF).	imatinib	33-41	platelet derived growth factor receptor beta	Homo sapiens	172-182
28260860-4	2017	In this research, we studied how imatinib mesylate would exert effect on MCF7 and T-47D breast cancer and MCF 10A epithelial cell lines, the gene and protein expression of PDGFR-beta, c-Kit and their relevant ligands platelet-derived growth factor (PDGF)-BB and stem cell factor (SCF).	imatinib	33-41	KIT ligand	Homo sapiens	262-278
28260860-4	2017	In this research, we studied how imatinib mesylate would exert effect on MCF7 and T-47D breast cancer and MCF 10A epithelial cell lines, the gene and protein expression of PDGFR-beta, c-Kit and their relevant ligands platelet-derived growth factor (PDGF)-BB and stem cell factor (SCF).	imatinib	33-41	KIT ligand	Homo sapiens	280-283
28209946-10	2017	The recognition of this rare presentation as a manifestation of PDGFRbeta-gene translocation is important, and equally important that low-dose imatinib (100 mg/day) might have the same effect as higher dose imatinib (400 mg/day).	imatinib	143-151	platelet derived growth factor receptor beta	Homo sapiens	64-73
28186602-9	2017	CONCLUSION: The idic(Ph) chromosomes presented in CML-BLC may predict resistance to Imatinib and response to Dasatinib.	imatinib	84-92	C-X-C motif chemokine ligand 13	Homo sapiens	54-57
28186604-10	2017	Imatinib was initiated at a dosage of 200 mg, and after 10 months, the signal of the FIP1L1-PDGFRA fusion gene was undetectable in bone marrow sample.	imatinib	0-8	factor interacting with PAPOLA and CPSF1	Homo sapiens	85-91
28186604-10	2017	Imatinib was initiated at a dosage of 200 mg, and after 10 months, the signal of the FIP1L1-PDGFRA fusion gene was undetectable in bone marrow sample.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	92-98
28612529-6	2017	CONCLUSION: The combination of IM and PP242 could increase the inhibition of PI3K/Akt/mTOR signaling pathway and apoptosis mediated by bax and caspase-3 in SUP-B15 cell line.	imatinib	31-33	AKT serine/threonine kinase 1	Homo sapiens	82-85
28612529-6	2017	CONCLUSION: The combination of IM and PP242 could increase the inhibition of PI3K/Akt/mTOR signaling pathway and apoptosis mediated by bax and caspase-3 in SUP-B15 cell line.	imatinib	31-33	mechanistic target of rapamycin kinase	Homo sapiens	86-90
28612529-6	2017	CONCLUSION: The combination of IM and PP242 could increase the inhibition of PI3K/Akt/mTOR signaling pathway and apoptosis mediated by bax and caspase-3 in SUP-B15 cell line.	imatinib	31-33	BCL2 associated X, apoptosis regulator	Homo sapiens	135-138
28612529-6	2017	CONCLUSION: The combination of IM and PP242 could increase the inhibition of PI3K/Akt/mTOR signaling pathway and apoptosis mediated by bax and caspase-3 in SUP-B15 cell line.	imatinib	31-33	caspase 3	Homo sapiens	143-152
28231806-1	2017	BACKGROUND: Imatinib causes increased turnover of stromal collagen, reduces collagen fibril diameter, enhances extracellular fluid turnover and lowers interstitial fluid pressure (IFP) in the human colonic carcinoma KAT-4/HT-29 (KAT-4) xenograft model.	imatinib	12-20	glutamic-oxaloacetic transaminase 2	Homo sapiens	216-227
28231806-1	2017	BACKGROUND: Imatinib causes increased turnover of stromal collagen, reduces collagen fibril diameter, enhances extracellular fluid turnover and lowers interstitial fluid pressure (IFP) in the human colonic carcinoma KAT-4/HT-29 (KAT-4) xenograft model.	imatinib	12-20	glutamic-oxaloacetic transaminase 2	Homo sapiens	216-221
28231806-7	2017	Treatment with imatinib resulted in similar pO2-levels in all three tumor models but only in KAT-4 tumors did the increase reach statistical significance.	imatinib	15-23	glutamic-oxaloacetic transaminase 2	Homo sapiens	93-98
28231806-8	2017	It is likely that after imatinib treatment the increase in pO2 in KAT-4 tumors is caused by increased blood flow due to reduced vascular resistance.	imatinib	24-32	glutamic-oxaloacetic transaminase 2	Homo sapiens	66-71
28231806-9	2017	This notion is supported by the significant reduction observed in IFP in KAT-4 tumors after imatinib treatment.	imatinib	92-100	glutamic-oxaloacetic transaminase 2	Homo sapiens	73-78
28231806-12	2017	CONCLUSION: Our data suggest that the effects of imatinib on pO2-levels depend on a well-developed ECM and provide further support to the suggestion that imatinib acts by causing interstitial stroma cells to produce a less dense ECM, which would in turn allow for an increased blood flow.	imatinib	49-57	multimerin 1	Homo sapiens	99-102
28231806-12	2017	CONCLUSION: Our data suggest that the effects of imatinib on pO2-levels depend on a well-developed ECM and provide further support to the suggestion that imatinib acts by causing interstitial stroma cells to produce a less dense ECM, which would in turn allow for an increased blood flow.	imatinib	49-57	multimerin 1	Homo sapiens	229-232
28231806-12	2017	CONCLUSION: Our data suggest that the effects of imatinib on pO2-levels depend on a well-developed ECM and provide further support to the suggestion that imatinib acts by causing interstitial stroma cells to produce a less dense ECM, which would in turn allow for an increased blood flow.	imatinib	154-162	multimerin 1	Homo sapiens	229-232
27718450-0	2017	Interaction of imatinib mesylate with human serum transferrin: The comparative spectroscopic studies.	imatinib	15-32	transferrin	Homo sapiens	50-61
27718450-3	2017	In this study the mechanism of interactions between the imatinib mesylate and all states of transferrin (apo-Tf, Htf and holo-Tf) has been investigated by fluorescence, ultraviolet-visible (UV-vis), circular dichroism (CD) and zeta potential spectroscopic methods.	imatinib	56-73	transferrin	Homo sapiens	92-103
27718450-4	2017	Based on the experimental results it was proved that under physiological conditions the imatinib mesylate binds to the each form of transferrin with a binding constant c.a.	imatinib	88-105	transferrin	Homo sapiens	132-143
28028030-4	2017	The natural history of PDGFRA- and PDGFRB-rearranged neoplasms has been dramatically altered by imatinib.	imatinib	96-104	platelet derived growth factor receptor beta	Homo sapiens	35-41
27718039-14	2017	Moreover, 4MU, Imatinib and 4MU + Imatinib decreased pAkt/Akt ratio in both cell lines and reduced the pERK/ERK ratio only in K562 cells.	imatinib	34-42	EPH receptor B2	Homo sapiens	104-107
28178968-13	2017	In the IPL, perfusion or nebulization of imatinib reduced the ET-1-induced increase of the postcapillary resistance.	imatinib	41-49	endothelin-1	Cavia porcellus	62-66
28178968-17	2017	Perfused or nebulized imatinib significantly reduces the postcapillary resistance in the pre-constricted (ET-1) pulmonary venous bed.	imatinib	22-30	endothelin-1	Cavia porcellus	106-110
28178968-19	2017	Conversely, PDGF-BB contracts PVs by activation of PDGFR-beta suggesting that imatinib-induced relaxation depends on PDGFR-beta-antagonism.	imatinib	78-86	platelet-derived growth factor receptor beta	Cavia porcellus	51-61
28178968-19	2017	Conversely, PDGF-BB contracts PVs by activation of PDGFR-beta suggesting that imatinib-induced relaxation depends on PDGFR-beta-antagonism.	imatinib	78-86	platelet-derived growth factor receptor beta	Cavia porcellus	117-127
27450926-4	2017	The proposed methodology resulted in linear calibration plots with correlation coefficients values of r2  = 0.9995-0.9999 from concentration ranges of 2.5-100 ng mL-1 for imatinib, 5.0-100 ng mL-1 for sorafenib, tofacitinib and afatinib, and 1.0-100 ng mL-1 for cabozantinib.	imatinib	171-179	L1 cell adhesion molecule	Mus musculus	162-166
28074523-0	2017	Familial gastrointestinal stromal tumors, lentigines, and cafe-au-lait macules associated with germline c-kit mutation treated with imatinib.	imatinib	132-140	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	104-109
27718039-2	2017	The first line treatment for CML consists on BCR-ABL inhibitors such as Imatinib.	imatinib	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
27718039-13	2017	For both cell lines the mechanisms of tumor suppression involved was senescence, since the combination of 4MU and Imatinib arrested the cell cycle and increased senescence associated beta-galactosidase activity and senescence associated heterochromatin foci presence when compared to each drug alone.	imatinib	114-122	galactosidase beta 1	Homo sapiens	183-201
27718039-14	2017	Moreover, 4MU, Imatinib and 4MU + Imatinib decreased pAkt/Akt ratio in both cell lines and reduced the pERK/ERK ratio only in K562 cells.	imatinib	15-23	AKT serine/threonine kinase 1	Homo sapiens	54-57
27718039-14	2017	Moreover, 4MU, Imatinib and 4MU + Imatinib decreased pAkt/Akt ratio in both cell lines and reduced the pERK/ERK ratio only in K562 cells.	imatinib	34-42	AKT serine/threonine kinase 1	Homo sapiens	54-57
27718039-14	2017	Moreover, 4MU, Imatinib and 4MU + Imatinib decreased pAkt/Akt ratio in both cell lines and reduced the pERK/ERK ratio only in K562 cells.	imatinib	34-42	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	103-107
28384968-7	2017	We hereby, report a rare case of a 65-year-old female with intractable fasting hypoglycaemia due to overproduction of "big" insulin-like growth factor II diagnosed to have pelvic GIST and managed by Steroids and Imatinib.	imatinib	212-220	insulin	Canis lupus familiaris	124-131
27388852-11	2017	Imatinib also inhibited differentiation of fibrocytes via suppression of c-Abl activity that was essential for the differentiation of monocytes to fibrocytes.	imatinib	0-8	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	73-78
28139720-6	2017	Using this model, we found that platelet-derived growth factor receptor-alpha (PDGFRalpha)-positive mesenchymal stem cells are induced after this intervention and that inhibition of PDGFR signaling by imatinib treatment can significantly suppress fatty infiltration.	imatinib	201-209	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	32-77
28255316-6	2017	There was a significant up-regulation in caspase-3 enzyme activity and caspase-3 expression by imatinib and its half dose combination with DMC as compared to control.	imatinib	95-103	caspase 3	Homo sapiens	41-50
28255316-6	2017	There was a significant up-regulation in caspase-3 enzyme activity and caspase-3 expression by imatinib and its half dose combination with DMC as compared to control.	imatinib	95-103	caspase 3	Homo sapiens	71-80
27980106-4	2017	Aiming at simultaneously targeting prostate NE tumor cells and MCs, both expressing the cKit tyrosine kinase receptor, we have tested the therapeutic effect of imatinib in TRAMP mice.	imatinib	160-168	tumor necrosis factor receptor superfamily, member 25	Mus musculus	172-177
27980106-5	2017	Imatinib-treated TRAMP mice experience a partial benefit against prostate adenocarcinoma, because of inhibition of supportive MCs.	imatinib	0-8	tumor necrosis factor receptor superfamily, member 25	Mus musculus	17-22
27980106-9	2017	In both mice and in patients, these tumors are negative for cKit but express PDGFR-beta, another tyrosine kinase receptor specifically inhibited by imatinib.	imatinib	148-156	platelet derived growth factor receptor beta	Homo sapiens	77-87
27999193-2	2017	MDM2 (human homolog of the murine double minute-2) inhibitors such as Nutlin-3 have been shown to induce apoptosis in a p53-dependent manner in CML cells and sensitize cells to Imatinib.	imatinib	177-185	MDM2 proto-oncogene	Homo sapiens	0-4
28139720-6	2017	Using this model, we found that platelet-derived growth factor receptor-alpha (PDGFRalpha)-positive mesenchymal stem cells are induced after this intervention and that inhibition of PDGFR signaling by imatinib treatment can significantly suppress fatty infiltration.	imatinib	201-209	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	79-89
28139720-6	2017	Using this model, we found that platelet-derived growth factor receptor-alpha (PDGFRalpha)-positive mesenchymal stem cells are induced after this intervention and that inhibition of PDGFR signaling by imatinib treatment can significantly suppress fatty infiltration.	imatinib	201-209	platelet derived growth factor receptor, beta polypeptide	Mus musculus	79-84
28118844-6	2017	GATA high versus low cells express differential gene regulatory networks, differential sensitivity to the drug imatinib mesylate, and differential self-renewal capacity.	imatinib	111-119	glutaminyl-tRNA amidotransferase subunit QRSL1	Homo sapiens	0-4
27889611-6	2017	Upon overexpression in leukemic K562 cells, QPRT conferred partial resistance to the anti-leukemic drug imatinib, indicating possible anti-apoptotic functions, consistent with previous reports on glioma cells.	imatinib	104-112	quinolinate phosphoribosyltransferase	Homo sapiens	44-48
27854515-0	2017	lncRNA UCA1 Contributes to Imatinib Resistance by Acting as a ceRNA Against miR-16 in Chronic Myeloid Leukemia Cells.	imatinib	27-35	urothelial cancer associated 1	Homo sapiens	7-11
28095277-0	2017	Long-Term Follow-Up of the French Stop Imatinib (STIM1) Study in Patients With Chronic Myeloid Leukemia.	imatinib	39-47	stromal interaction molecule 1	Homo sapiens	49-54
28095277-2	2017	We report the final results of the Stop Imatinib (STIM1) study with a long follow-up.	imatinib	40-48	stromal interaction molecule 1	Homo sapiens	50-55
27470968-0	2017	PD-1/PD-L1 Blockade Enhances T-cell Activity and Antitumor Efficacy of Imatinib in Gastrointestinal Stromal Tumors.	imatinib	71-79	programmed cell death 1	Homo sapiens	0-4
27470968-0	2017	PD-1/PD-L1 Blockade Enhances T-cell Activity and Antitumor Efficacy of Imatinib in Gastrointestinal Stromal Tumors.	imatinib	71-79	CD274 molecule	Homo sapiens	5-10
27965460-0	2017	Opposing roles of KIT and ABL1 in the therapeutic response of gastrointestinal stromal tumor (GIST) cells to imatinib mesylate.	imatinib	109-126	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	18-21
27965460-0	2017	Opposing roles of KIT and ABL1 in the therapeutic response of gastrointestinal stromal tumor (GIST) cells to imatinib mesylate.	imatinib	109-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-30
27965460-2	2017	The small molecule inhibitor imatinib mesylate was initially developed to target the ABL1 kinase, which is constitutively activated through chromosomal translocation in BCR-ABL1-positive chronic myeloid leukemia.	imatinib	29-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-89
27965460-2	2017	The small molecule inhibitor imatinib mesylate was initially developed to target the ABL1 kinase, which is constitutively activated through chromosomal translocation in BCR-ABL1-positive chronic myeloid leukemia.	imatinib	29-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	173-177
27965460-3	2017	Because of cross-reactivity of imatinib against the KIT kinase, the drug is also successfully used for the treatment of GIST.	imatinib	31-39	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	52-55
27965460-4	2017	Although inhibition of KIT clearly has a major role in the therapeutic response of GIST to imatinib, the contribution of concomitant inhibition of ABL in this context has never been explored.	imatinib	91-99	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	23-26
27965460-6	2017	Using siRNA-mediated knockdown, we demonstrate that depletion of KIT in conjunction with ABL1 - hence mimicking imatinib treatment - leads to reduced apoptosis induction and attenuated inhibition of cellular proliferation when compared to depletion of KIT alone.	imatinib	112-120	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	65-68
27965460-6	2017	Using siRNA-mediated knockdown, we demonstrate that depletion of KIT in conjunction with ABL1 - hence mimicking imatinib treatment - leads to reduced apoptosis induction and attenuated inhibition of cellular proliferation when compared to depletion of KIT alone.	imatinib	112-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-93
27470968-7	2017	PD-1 expression on T cells was highest in imatinib-treated human GISTs.	imatinib	42-50	programmed cell death 1	Homo sapiens	0-4
27470968-9	2017	In human GIST cell lines, treatment with imatinib abrogated the IFNgamma-induced upregulation of PD-L1 via STAT1 inhibition.	imatinib	41-49	interferon gamma	Homo sapiens	64-72
27470968-9	2017	In human GIST cell lines, treatment with imatinib abrogated the IFNgamma-induced upregulation of PD-L1 via STAT1 inhibition.	imatinib	41-49	CD274 molecule	Homo sapiens	97-102
27470968-9	2017	In human GIST cell lines, treatment with imatinib abrogated the IFNgamma-induced upregulation of PD-L1 via STAT1 inhibition.	imatinib	41-49	signal transducer and activator of transcription 1	Homo sapiens	107-112
27470968-10	2017	In KitV558Delta/+ mice, imatinib downregulated IFNgamma-related genes and reduced PD-L1 expression on tumor cells.	imatinib	24-32	interferon gamma	Homo sapiens	47-55
27470968-10	2017	In KitV558Delta/+ mice, imatinib downregulated IFNgamma-related genes and reduced PD-L1 expression on tumor cells.	imatinib	24-32	CD274 antigen	Mus musculus	82-87
27470968-11	2017	PD-1 and PD-L1 blockade in vivo each had no efficacy alone but enhanced the antitumor effects of imatinib by increasing T-cell effector function in the presence of KIT and IDO inhibition.	imatinib	97-105	programmed cell death 1	Homo sapiens	0-4
27470968-11	2017	PD-1 and PD-L1 blockade in vivo each had no efficacy alone but enhanced the antitumor effects of imatinib by increasing T-cell effector function in the presence of KIT and IDO inhibition.	imatinib	97-105	CD274 molecule	Homo sapiens	9-14
27470968-11	2017	PD-1 and PD-L1 blockade in vivo each had no efficacy alone but enhanced the antitumor effects of imatinib by increasing T-cell effector function in the presence of KIT and IDO inhibition.	imatinib	97-105	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	164-167
27470968-11	2017	PD-1 and PD-L1 blockade in vivo each had no efficacy alone but enhanced the antitumor effects of imatinib by increasing T-cell effector function in the presence of KIT and IDO inhibition.	imatinib	97-105	indoleamine 2,3-dioxygenase 1	Homo sapiens	172-175
27687311-0	2017	Mutant KIT as imatinib-sensitive target in metastatic sinonasal carcinoma.	imatinib	14-22	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	7-10
27687311-6	2017	Results: Molecularly guided treatment with imatinib in analogy to the management of gastrointestinal stromal tumor (GIST) resulted in a dramatic and durable response with remission of nearly all tumor manifestations, indicating a dominant driver function of mutant KIT in this tumor.	imatinib	43-51	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	265-268
28403779-1	2017	BACKGROUND: Chronic myeloid leukemia (CML) is currently treated with imatinib, a Bcr-Abl inhibitor.	imatinib	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
28698872-6	2017	Pretreatment with the receptor tyrosine kinase inhibitor Imatinib prevented eNOS expression and ICs proliferation, as well as the increased voiding frequency and urinary tract weight provoked by CYP.	imatinib	57-65	nitric oxide synthase 3	Rattus norvegicus	76-80
28698872-6	2017	Pretreatment with the receptor tyrosine kinase inhibitor Imatinib prevented eNOS expression and ICs proliferation, as well as the increased voiding frequency and urinary tract weight provoked by CYP.	imatinib	57-65	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	195-198
29375916-0	2017	Late Emergence of an Imatinib-Resistant ABL1 Kinase Domain Mutation in a Patient with Chronic Myeloid Leukemia.	imatinib	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-44
29375916-1	2017	The introduction of the tyrosine kinase inhibitor (TKI) imatinib has revolutionised the outlook of chronic myeloid leukemia (CML); however, a significant proportion of patients develop resistance through several mechanisms, of which acquisition of ABL1 kinase domain mutations is prevalent.	imatinib	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	248-252
29375916-3	2017	A case is described of a chronic-phase CML patient who achieved a sustained, deep molecular response but who developed an Y253H ABL1 kinase domain mutation nearly nine years after commencing imatinib.	imatinib	191-199	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-132
29375916-6	2017	This case highlights the requirement for ABL1 kinase domain mutation analysis in those CML patients on long-term imatinib who lost their molecular response, regardless of whether nonadherence is suspected.	imatinib	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-45
27370604-4	2017	Recent studies have implicated the PI3K/AKT pathway in the survival of imatinib mesylate-resistant GIST cell lines and tumors.	imatinib	71-88	AKT serine/threonine kinase 1	Homo sapiens	40-43
27854515-0	2017	lncRNA UCA1 Contributes to Imatinib Resistance by Acting as a ceRNA Against miR-16 in Chronic Myeloid Leukemia Cells.	imatinib	27-35	glycerophosphodiester phosphodiesterase 1	Homo sapiens	76-82
27840977-2	2017	In the present study, we showed that in comparison with healthy controls, the expression of four centrosomal genes (AURKA, HMMR, PLK1 and ESPL1) in the peripheral blood of CML patients was significantly enhanced at diagnosis and decreased to the basal level in most patients treated with imatinib mesylate for three months.	imatinib	288-305	aurora kinase A	Homo sapiens	116-121
27550925-0	2017	Original Research: Featured Article: Imatinib mesylate (Gleevec) inhibits Notch and c-Myc signaling: Five-day treatment permanently rescues mammary development.	imatinib	37-54	notch receptor 4	Homo sapiens	74-79
27550925-0	2017	Original Research: Featured Article: Imatinib mesylate (Gleevec) inhibits Notch and c-Myc signaling: Five-day treatment permanently rescues mammary development.	imatinib	37-54	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	84-89
27550925-2	2017	Previously, we have shown that treatment of Wap-Int3 tumor bearing mice with Imatinib mesylate (Gleevec) is associated with complete regression of the tumor.	imatinib	77-94	whey acidic protein	Mus musculus	44-47
27550925-2	2017	Previously, we have shown that treatment of Wap-Int3 tumor bearing mice with Imatinib mesylate (Gleevec) is associated with complete regression of the tumor.	imatinib	77-94	notch 4	Mus musculus	48-52
28557709-2	2017	Therefore, the aim of our study was to investigate the possible correlation of selected P450, ABC and SLC polymorphic variants and the outcome of imatinib therapy.	imatinib	146-154	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	94-97
28557709-2	2017	Therefore, the aim of our study was to investigate the possible correlation of selected P450, ABC and SLC polymorphic variants and the outcome of imatinib therapy.	imatinib	146-154	C-C motif chemokine ligand 21	Homo sapiens	102-105
28331561-0	2017	Imatinib induces up-regulation of NM23, a metastasis suppressor gene, in human Hepatocarcinoma (HepG2) Cell Line.	imatinib	0-8	NME/NM23 nucleoside diphosphate kinase 1	Homo sapiens	34-38
28331561-1	2017	AIM: The present study investigated the anti-tumor activity of Imatinib mesylate through modulation of NM23 gene expression in human hepatocellular carcinoma (HepG2) cell line.	imatinib	63-80	NME/NM23 nucleoside diphosphate kinase 1	Homo sapiens	103-107
28331561-8	2017	The real time PCR results demonstrated that inhibitory effect of Imatinib mesylate on viability via up regulation of NM23 gene expression compared to GAPDH gene (internal control gene) in cancer cells.	imatinib	65-82	NME/NM23 nucleoside diphosphate kinase 1	Homo sapiens	117-121
28331561-8	2017	The real time PCR results demonstrated that inhibitory effect of Imatinib mesylate on viability via up regulation of NM23 gene expression compared to GAPDH gene (internal control gene) in cancer cells.	imatinib	65-82	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	150-155
28331561-9	2017	CONCLUSION: According to our findings, imatinib can modulate metastasis by enhancing Nm23 gene expression in human hepatocellular carcinoma (HepG2) cell line.	imatinib	39-47	NME/NM23 nucleoside diphosphate kinase 1	Homo sapiens	85-89
27416909-0	2017	The clinical significance of ABCB1 overexpression in predicting outcome of CML patients undergoing first-line imatinib treatment.	imatinib	110-118	ATP binding cassette subfamily B member 1	Homo sapiens	29-34
27416909-5	2017	Since the drug efflux transporter ABCB1 has previously been implicated in TKI resistance, we determined if early increases in ABCB1 mRNA expression (fold change from diagnosis to day 22 of imatinib therapy) predict for patient response.	imatinib	189-197	ATP binding cassette subfamily B member 1	Homo sapiens	34-39
27416909-5	2017	Since the drug efflux transporter ABCB1 has previously been implicated in TKI resistance, we determined if early increases in ABCB1 mRNA expression (fold change from diagnosis to day 22 of imatinib therapy) predict for patient response.	imatinib	189-197	ATP binding cassette subfamily B member 1	Homo sapiens	126-131
27852118-1	2017	BACKGROUND: A previous meta-analysis demonstrated that 3 of the new-generation BCR-ABL tyrosine kinase inhibitors (TKIs) (dasatinib, nilotinib and ponatinib) are associated with an increased risk of vascular occlusive events in patients with Ph+ chronic myeloid leukemia compared with imatinib.	imatinib	285-293	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
28435517-5	2017	The approaches employed included the use of gene silencing and the administration of small molecules, such as crenolanib and imatinib (PDGFR inhibitors) on MPM cell lines (IstMes2, Mero-14, Mero-25).	imatinib	125-133	platelet derived growth factor receptor beta	Homo sapiens	135-140
27840977-2	2017	In the present study, we showed that in comparison with healthy controls, the expression of four centrosomal genes (AURKA, HMMR, PLK1 and ESPL1) in the peripheral blood of CML patients was significantly enhanced at diagnosis and decreased to the basal level in most patients treated with imatinib mesylate for three months.	imatinib	288-305	hyaluronan mediated motility receptor	Homo sapiens	123-127
27840977-2	2017	In the present study, we showed that in comparison with healthy controls, the expression of four centrosomal genes (AURKA, HMMR, PLK1 and ESPL1) in the peripheral blood of CML patients was significantly enhanced at diagnosis and decreased to the basal level in most patients treated with imatinib mesylate for three months.	imatinib	288-305	extra spindle pole bodies like 1, separase	Homo sapiens	138-143
27863440-10	2016	The protein levels of NOTCH1 and platelet derived growth factor receptor alpha positively correlated with the responsiveness of GSCs to gamma-secretase inhibitor IX or imatinib, two compounds that inhibit these two proteins, respectively.	imatinib	168-176	notch receptor 1	Homo sapiens	22-28
27991849-0	2017	Trough concentration and ABCG2 polymorphism are better to predict imatinib response in chronic myeloid leukemia: a meta-analysis.	imatinib	66-74	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	25-30
28657534-4	2017	CASE REPORT: This is a report of a patient with BCR-ABL1 who initially achieved molecular response with imatinib therapy, relapsing after fifteen months.	imatinib	104-112	BCR activator of RhoGEF and GTPase	Homo sapiens	48-56
28830599-1	2017	BACKGROUND: Imatinib mesylate has revolutionized the treatment of chronic myeloid leukemia leading to significant reductions of BCR-ABL1 transcript levels in peripheral blood.	imatinib	12-29	BCR activator of RhoGEF and GTPase	Homo sapiens	128-136
27863440-10	2016	The protein levels of NOTCH1 and platelet derived growth factor receptor alpha positively correlated with the responsiveness of GSCs to gamma-secretase inhibitor IX or imatinib, two compounds that inhibit these two proteins, respectively.	imatinib	168-176	platelet derived growth factor receptor alpha	Homo sapiens	33-78
27942010-10	2016	In the severe scl-cGVHD model, imatinib-treated mice had significantly lower levels of PDGF-r phosphorylation than control mice on day 29 after transplantation (P = 0.008).	imatinib	31-39	platelet derived growth factor receptor, beta polypeptide	Mus musculus	87-93
30167550-2	2016	Imatinib and dasatinib are 2 BCR-ABL tyrosine kinase inhibitors (TKI) used in the treatment of CML.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
27797721-5	2016	The gene expression analysis revealed that UDP-Gal:betaGlcNAc beta 1,4-galactosyltransferase, polypeptide 1 (B4GALT1) was significantly down-regulated upon ZFX silencing, which is implicated in the response of K562 cells to the treatment of imatinib mesylate (IM).	imatinib	241-258	beta-1,4-galactosyltransferase 1	Homo sapiens	43-107
27797721-5	2016	The gene expression analysis revealed that UDP-Gal:betaGlcNAc beta 1,4-galactosyltransferase, polypeptide 1 (B4GALT1) was significantly down-regulated upon ZFX silencing, which is implicated in the response of K562 cells to the treatment of imatinib mesylate (IM).	imatinib	241-258	beta-1,4-galactosyltransferase 1	Homo sapiens	109-116
27797721-5	2016	The gene expression analysis revealed that UDP-Gal:betaGlcNAc beta 1,4-galactosyltransferase, polypeptide 1 (B4GALT1) was significantly down-regulated upon ZFX silencing, which is implicated in the response of K562 cells to the treatment of imatinib mesylate (IM).	imatinib	241-258	zinc finger protein X-linked	Homo sapiens	156-159
28028904-0	2016	Imatinib-sensitive myeloid neoplasm with low allele burden of FIP1L1-PDGFRA fusion gene in an elderly patient.	imatinib	0-8	factor interacting with PAPOLA and CPSF1	Homo sapiens	62-68
27806849-8	2016	Treatment options for systemic disease have been previously limited, but the PDGFbetaR, KIT, and ABL inhibitor imatinib is now an option for effective systemic therapy.	imatinib	111-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-100
27835591-7	2016	Treatment with celecoxib also restored GSK3beta function and led to down-regulation of beta-catenin activity through transcriptional and post-translational mechanisms, two effects likely to contribute to Ph+ cell growth suppression by celecoxib.Celecoxib inhibited colony formation of TKI-resistant Ph+ cell lines including those with the T315I BCR-ABL mutation and acted synergistically with imatinib in suppressing colony formation of TKI-sensitive Ph+ cell lines.	imatinib	393-401	catenin beta 1	Homo sapiens	87-99
28028904-0	2016	Imatinib-sensitive myeloid neoplasm with low allele burden of FIP1L1-PDGFRA fusion gene in an elderly patient.	imatinib	0-8	platelet derived growth factor receptor alpha	Homo sapiens	69-75
27562641-1	2016	With BCR-ABL1 tyrosine kinase inhibitors (TKIs), such as imatinib, nilotinib, dasatinib, bosutinib, and ponatinib, many patients with chronic myeloid leukemia in chronic phase (CML-CP) can expect to live near-normal life spans.	imatinib	57-65	BCR activator of RhoGEF and GTPase	Homo sapiens	5-13
27352262-0	2016	Sustained molecular response with nilotinib in imatinib-intolerant chronic myeloid leukaemia with an e19a2 BCR-ABL1 fusion.	imatinib	47-55	BCR activator of RhoGEF and GTPase	Homo sapiens	107-115
27989101-0	2016	Cantharidin Overcomes Imatinib Resistance by Depleting BCR-ABL in Chronic Myeloid Leukemia.	imatinib	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
27770655-0	2016	Low ABCB1 and high OCT1 levels play a favorable role in the molecular response to imatinib in CML patients in the community clinical practice.	imatinib	82-90	ATP binding cassette subfamily B member 1	Homo sapiens	4-9
27770655-0	2016	Low ABCB1 and high OCT1 levels play a favorable role in the molecular response to imatinib in CML patients in the community clinical practice.	imatinib	82-90	POU class 2 homeobox 1	Homo sapiens	19-23
27770655-6	2016	Our results suggest that ABCB1 and OCT1 mRNA expressions may present biological relevance to identify responder and non-responder patients to imatinib treatment.	imatinib	142-150	ATP binding cassette subfamily B member 1	Homo sapiens	25-30
27770655-6	2016	Our results suggest that ABCB1 and OCT1 mRNA expressions may present biological relevance to identify responder and non-responder patients to imatinib treatment.	imatinib	142-150	POU class 2 homeobox 1	Homo sapiens	35-39
27989101-10	2016	These findings indicated that CTD overcomes imatinib resistance through depletion of BCR-ABL.	imatinib	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
27793025-10	2016	Treatment with GLI1/2 inhibitors, including arsenic trioxide, significantly increased GLI3 binding to the KIT promoter, decreased KIT expression, and reduced viability in imatinib-sensitive and imatinib-resistant GIST cells.	imatinib	171-179	GLI family zinc finger 1	Homo sapiens	15-21
27748929-1	2016	Increasing resistance of imatinib, a BCR-ABL tyrosine kinase inhibitor, hinders its use in the therapy of chronic myeloid leukemia (CML).	imatinib	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
27864817-12	2016	Moreover, secondary mutations in the KIT gene, similar to those involved in resistance to imatinib, might be involved in resistance to nilotinib.	imatinib	90-98	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	37-40
27821800-5	2016	Cells were sensitive to anti BCR-ABL1 TKIs Imatinib, Nilotinib and GZD824, that specifically targeted the ABL1 fusion protein, but not the PI3K/Akt/mTOR axis.	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-37
27821800-5	2016	Cells were sensitive to anti BCR-ABL1 TKIs Imatinib, Nilotinib and GZD824, that specifically targeted the ABL1 fusion protein, but not the PI3K/Akt/mTOR axis.	imatinib	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-110
27884201-1	2016	BACKGROUND: Acquired imatinib (IM) resistance is frequently characterized by Bcr-Abl mutations that affect IM binding and kinase inhibition in patients with chronic myelogenous leukemia (CML).	imatinib	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
27723754-7	2016	By targeting BCR-ABL with dCas9-AIDx, we efficiently identified known and new mutations conferring imatinib resistance in chronic myeloid leukemia cells.	imatinib	99-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
27928798-13	2016	After 90 days of taking imatinib continuously, linear regression analysis revealed a negative correlation between imatinib plasma concentration in patients with 400 mg imatinib per day and white blood cell count (R2=0.103, P=0.013), and a positive correlation with serum alanine aminotransferase (ALT) concentration (R2=0.076, P=0.033).	imatinib	24-32	glutamic--pyruvic transaminase	Homo sapiens	271-295
27928798-13	2016	After 90 days of taking imatinib continuously, linear regression analysis revealed a negative correlation between imatinib plasma concentration in patients with 400 mg imatinib per day and white blood cell count (R2=0.103, P=0.013), and a positive correlation with serum alanine aminotransferase (ALT) concentration (R2=0.076, P=0.033).	imatinib	114-122	glutamic--pyruvic transaminase	Homo sapiens	271-295
27928798-13	2016	After 90 days of taking imatinib continuously, linear regression analysis revealed a negative correlation between imatinib plasma concentration in patients with 400 mg imatinib per day and white blood cell count (R2=0.103, P=0.013), and a positive correlation with serum alanine aminotransferase (ALT) concentration (R2=0.076, P=0.033).	imatinib	114-122	glutamic--pyruvic transaminase	Homo sapiens	271-295
27928806-6	2016	More than half of metastatic GISTs patients receiving imatinib treatment can develop to c-kit secondary mutations, which are responsible for secondary resistance.	imatinib	54-62	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	88-93
27793025-10	2016	Treatment with GLI1/2 inhibitors, including arsenic trioxide, significantly increased GLI3 binding to the KIT promoter, decreased KIT expression, and reduced viability in imatinib-sensitive and imatinib-resistant GIST cells.	imatinib	194-202	GLI family zinc finger 1	Homo sapiens	15-21
27793025-12	2016	Hedgehog signaling activates KIT expression irrespective of mutation status, offering a novel approach to treat imatinib-resistant GIST.	imatinib	112-120	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	29-32
27762455-10	2016	Imatinib has a therapeutic role in the presence of an imatinib-sensitive KIT mutation or in KITD816-unmutated patients.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
27680681-6	2016	Our data also revealed paradoxical tumor suppressor functions for Abl kinases in prostate cancer that may help to explain the failure of Abl kinase inhibitor imatinib in prostate cancer clinical trials.	imatinib	158-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-69
27762455-10	2016	Imatinib has a therapeutic role in the presence of an imatinib-sensitive KIT mutation or in KITD816-unmutated patients.	imatinib	54-62	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	73-76
27788881-6	2016	The percentages of CD4+CD25+CD134+ T cells present after incubating peripheral blood mononuclear cells with imatinib, at baseline and after successful desensitization, were analyzed using flow cytometric analysis.	imatinib	108-116	CD4 molecule	Homo sapiens	19-22
27788881-8	2016	The percentages of imatinib-induced CD4+CD25+CD134+ T cells decreased from a mean (SD) of 11.3% (6.5%) and 13.4% (7.3%) at baseline to 3.2% (0.7%) and 3.0% (1.1%) after successful desensitization, when stimulating peripheral blood mononuclear cells with 1 and 2 muM of imatinib, respectively.	imatinib	19-27	CD4 molecule	Homo sapiens	36-39
27788881-8	2016	The percentages of imatinib-induced CD4+CD25+CD134+ T cells decreased from a mean (SD) of 11.3% (6.5%) and 13.4% (7.3%) at baseline to 3.2% (0.7%) and 3.0% (1.1%) after successful desensitization, when stimulating peripheral blood mononuclear cells with 1 and 2 muM of imatinib, respectively.	imatinib	269-277	CD4 molecule	Homo sapiens	36-39
27788881-10	2016	The reduced percentages of imatinib-induced CD4+CD25+CD134+ T cells in these patients may be associated with immune tolerance.	imatinib	27-35	CD4 molecule	Homo sapiens	44-47
27793952-2	2016	Specifically, the consistent dependence of GISTs on proto-oncogene c-KIT signaling led to the development and successful implementation of imatinib, a small-molecule c-KIT inhibitor.	imatinib	139-147	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	52-72
27460916-12	2016	The imatinib group demonstrated maintained expression of VEC, inhibition of pCrkL, and a significantly higher level of interleukin (IL)-10.	imatinib	4-12	cadherin 5	Rattus norvegicus	57-60
27460916-12	2016	The imatinib group demonstrated maintained expression of VEC, inhibition of pCrkL, and a significantly higher level of interleukin (IL)-10.	imatinib	4-12	interleukin 10	Rattus norvegicus	119-138
27793952-2	2016	Specifically, the consistent dependence of GISTs on proto-oncogene c-KIT signaling led to the development and successful implementation of imatinib, a small-molecule c-KIT inhibitor.	imatinib	139-147	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	67-72
27793952-3	2016	Imatinib induces, rapid and sustained clinical benefit by blocking the signaling via c-KIT.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	85-90
27793952-5	2016	CASE SERIES: Herein, we report a case series of cutaneous squamous cell carcinoma (SCC) occurring secondary to imatinib in two patients treated for GISTs.	imatinib	111-119	serpin family B member 3	Homo sapiens	83-86
28030911-0	2016	Anti-Proliferative Effects of Dendrophthoe pentandra Methanol Extract on BCR/ABL-Positive and Imatinib-Resistant Leukemia Cell Lines Background: Imatinib mesylate, a tyrosine kinase inhibitor specifically targeting the BCR/ABL fusion protein,induces hematological remission in patients with chronic myeloid leukemia (CML).	imatinib	145-162	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	219-226
27793952-8	2016	Few cases of cutaneous SCC secondary to imatinib therapy were reported in patients with chronic myeloid leukemia.	imatinib	40-48	serpin family B member 3	Homo sapiens	23-26
27793952-10	2016	CONCLUSION: To our knowledge, the present report is the first to describe imatinib-related SCC in patients undergoing treatment for GISTs.	imatinib	74-82	serpin family B member 3	Homo sapiens	91-94
27565738-3	2016	We previously reported that the c-Abl tyrosine kinase is active in NPC neurons and in AD animal models and that Imatinib, a specific c-Abl inhibitor, decreased the amyloid burden in brains of the AD mouse model.	imatinib	112-120	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	32-37
27565738-3	2016	We previously reported that the c-Abl tyrosine kinase is active in NPC neurons and in AD animal models and that Imatinib, a specific c-Abl inhibitor, decreased the amyloid burden in brains of the AD mouse model.	imatinib	112-120	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	133-138
27565738-6	2016	Indeed, we found that levels of the Abeta oligomers and the carboxy-terminal fragment betaCTF were decreased when the cells were treated with Imatinib and upon shRNA-mediated c-Abl knockdown.	imatinib	142-150	amyloid beta (A4) precursor protein	Mus musculus	36-41
27565738-10	2016	More importantly, we found that c-Abl inhibition by Imatinib significantly inhibits the interaction between APP and BACE1.	imatinib	52-60	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	32-37
27565738-10	2016	More importantly, we found that c-Abl inhibition by Imatinib significantly inhibits the interaction between APP and BACE1.	imatinib	52-60	beta-site APP cleaving enzyme 1	Mus musculus	116-121
27548716-1	2016	INTRODUCTION: In Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL), the BCR-ABL translocation is the main transforming event; consequently, it is targeted by ABL-tyrosine kinase inhibitors (TKIs), the first of which to be identified was imatinib mesylate.	imatinib	261-278	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
27801322-0	2016	[Application of imatinib in BCR- ABL positive acute lymphoblastic leukemia treatment in the real world].	imatinib	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-36
27804783-1	2016	The use of imatinib in the treatment of BCR-ABL-positive chronic myeloid leukemia and gastrointestinal stromal tumors has significantly improved survival outcomes in patients afflicted by these malignancies.	imatinib	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
26416414-6	2016	In imatinib arm, KIT exon 11 deletions was associated with a shorter TTP (7 vs 17 months; P = 0.02), with a trend in OS (54 vs 71 months P = 0.063).	imatinib	3-11	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	17-20
26416414-7	2016	No difference was found in patients treated with sunitinib (P = 0.370).A second line with sunitinib was associated with an improved TTP in KIT exon 11 mutated patients progressing on imatinib 400 mg/die.	imatinib	183-191	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	139-142
27666635-0	2016	Development of BCR-ABL degradation inducers via the conjugation of an imatinib derivative and a cIAP1 ligand.	imatinib	70-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
27666635-3	2016	The designed molecules contained two biologically active scaffolds: one was an imatinib derivative that binds to BCL-ABL and the other was a methyl bestatin that binds to cellular IAP 1 (cIAP1).	imatinib	79-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-120
27812500-0	2016	An ETV6-ABL1 fusion in a patient with chronic myeloproliferative neoplasm: Initial response to Imatinib followed by rapid transformation into ALL.	imatinib	95-103	ETS variant transcription factor 6	Homo sapiens	3-7
27812500-0	2016	An ETV6-ABL1 fusion in a patient with chronic myeloproliferative neoplasm: Initial response to Imatinib followed by rapid transformation into ALL.	imatinib	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-12
28133332-6	2016	Mutational analysis revealed a PDGFRA mutation in exon 18, which causes resistance to both imatinib and sunitinib.	imatinib	91-99	platelet derived growth factor receptor alpha	Homo sapiens	31-37
27799652-5	2016	RESULTS Compared with the 0-muM imatinib-treated group, the apoptosis of 1.25-muM, 2.5-muM, and 5.0-muM treated groups was significantly induced (P&lt;0.05, all).	imatinib	32-40	latexin	Homo sapiens	78-81
27799652-5	2016	RESULTS Compared with the 0-muM imatinib-treated group, the apoptosis of 1.25-muM, 2.5-muM, and 5.0-muM treated groups was significantly induced (P&lt;0.05, all).	imatinib	32-40	latexin	Homo sapiens	78-81
27799652-5	2016	RESULTS Compared with the 0-muM imatinib-treated group, the apoptosis of 1.25-muM, 2.5-muM, and 5.0-muM treated groups was significantly induced (P&lt;0.05, all).	imatinib	32-40	latexin	Homo sapiens	78-81
27799652-8	2016	CONCLUSIONS Imatinib inhibits proliferation of colon cancer cells by reducing HGF and increasing p27 in a dose-dependent manner.	imatinib	12-20	hepatocyte growth factor	Homo sapiens	78-81
27799652-8	2016	CONCLUSIONS Imatinib inhibits proliferation of colon cancer cells by reducing HGF and increasing p27 in a dose-dependent manner.	imatinib	12-20	interferon alpha inducible protein 27	Homo sapiens	97-100
27726390-8	2016	Analogue 22 is the first derivative of a natural product identified as an inhibitor of wild-type and imatinib-resistant T315I mutant Abl kinases.	imatinib	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-136
27803915-2	2016	One of the best-characterized forms of HES is the one associated with FIP1L1-PDGFRA gene rearrangement, which was recently demonstrated as responsive to treatment with the small molecule kinase inhibitor drug, imatinib mesylate.	imatinib	210-227	factor interacting with PAPOLA and CPSF1	Homo sapiens	70-76
27803915-2	2016	One of the best-characterized forms of HES is the one associated with FIP1L1-PDGFRA gene rearrangement, which was recently demonstrated as responsive to treatment with the small molecule kinase inhibitor drug, imatinib mesylate.	imatinib	210-227	platelet derived growth factor receptor alpha	Homo sapiens	77-83
27567806-3	2016	Here, we investigated the therapeutic potential of inhibiting c-Abl using imatinib.	imatinib	74-82	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	62-67
27611742-1	2016	Patients with BCR-ABL1 fusion genes are potential candidates for targeted therapy with tyrosine kinase inhibitor (TKI) imatinib.	imatinib	119-127	BCR activator of RhoGEF and GTPase	Homo sapiens	14-22
27708529-0	2016	Imatinib-induced hyperbilirubinemia with UGT1A1 (*28) promoter polymorphism: first case series in patients with gastrointestinal stromal tumor.	imatinib	0-8	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	41-47
27708529-2	2016	Severe hepatotoxicity associated with imatinib is rare, and relationship to polymorphism of uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) expression and related frequency of hyperbilirubinemia or toxicity are not well known.	imatinib	38-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	141-147
27643437-1	2016	Imatinib-insensitive leukemia stem cells (LSCs) are believed to be responsible for resistance to BCR-ABL tyrosine kinase inhibitors and relapse of chronic myelogenous leukemia (CML).	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
27567806-5	2016	We found that imatinib reduces Abeta-oligomers in plasma, which correlates with a reduction of AD brain features such as plaques and oligomers accumulation, neuroinflammation, and cognitive deficits.	imatinib	14-22	amyloid beta (A4) precursor protein	Mus musculus	31-36
27567806-6	2016	Cells exposed to imatinib and c-Abl KO mice display decreased levels of beta-CTF fragments, suggesting that an altered processing of the amyloid-beta protein precursor is the most probable mechanism behind imatinib effects.	imatinib	206-214	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	30-35
27698808-0	2016	Increase of T and B cells and altered BACH2 expression patterns in bone marrow trephines of imatinib-treated patients with chronic myelogenous leukaemia.	imatinib	92-100	BTB domain and CNC homolog 2	Homo sapiens	38-43
27418107-8	2016	Further concentration dependent studies showed that imatinib, nilotinib and pazopanib were potent Pgp inhibitors with IC50 values of 2.42, 6.11 and 8.06 mum, respectively.	imatinib	52-60	ATP binding cassette subfamily B member 1	Homo sapiens	98-101
27418107-10	2016	Concentration dependent studies revealed that imatinib, erlotinib, nilotinib, axitinib and pazopanib were potent BCRP inhibitors with IC50 values of 0.94, 2.23, 2.50, 6.89 and 10.4 mum, respectively.	imatinib	46-54	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	113-117
27810077-9	2016	It may also contribute to the resistance to imatinib, as imatinib only targets on BCR-ABL fusion.	imatinib	57-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
27918111-10	2016	The expression of platelet-derived growth factor receptor beta, which is the major target of imatinib, was downregulated.	imatinib	93-101	platelet derived growth factor receptor, beta polypeptide	Mus musculus	18-62
27918111-13	2016	These results suggest that imatinib might promote the recovery of the liver following parenchymal injury through the inhibition of platelet-derived growth factor receptor beta.	imatinib	27-35	platelet derived growth factor receptor, beta polypeptide	Mus musculus	131-175
26479578-3	2016	Imatinib is considered as a first-generation drug that can inhibit the enzymatic action by inhibiting the ATP binding with BCR-ABL protein.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-130
26479578-4	2016	Later on, insensitivity of CML cells towards Imatinib has been observed may be due to mutation in tyrosine kinase domain of the ABL receptor.	imatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-131
26879808-6	2016	BCR/ABL persistent negativity at 6 and 9 months may have benefit to choose suitable patients for the imatinib/interferon-alpha maintenance strategy.	imatinib	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
26892479-4	2016	By direct sequencing, an ABL1 kinase mutation known to induce imatinib resistance was present at relapse in 13 of 20.	imatinib	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-29
27512117-4	2016	Tyrosine kinase inhibitors (TKI) targeting c-KIT, such as imatinib, has been used successfully to treat c-KIT driven gastrointestinal stromal tumors.	imatinib	58-66	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	43-48
27512117-4	2016	Tyrosine kinase inhibitors (TKI) targeting c-KIT, such as imatinib, has been used successfully to treat c-KIT driven gastrointestinal stromal tumors.	imatinib	58-66	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	104-109
27698886-8	2016	Furthermore, K562 cells treated with imatinib exhibited significantly enhanced PDCD4 expression.	imatinib	37-45	programmed cell death 4	Homo sapiens	79-84
27527414-4	2016	GISTs are known to be refractory to conventional therapies but the introduction of Imatinib, a selective inhibitor of tyrosine kinases Abl and Kit, significantly ameliorated the treatment options of GISTs patients.	imatinib	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-138
27527414-4	2016	GISTs are known to be refractory to conventional therapies but the introduction of Imatinib, a selective inhibitor of tyrosine kinases Abl and Kit, significantly ameliorated the treatment options of GISTs patients.	imatinib	83-91	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	143-146
27658269-0	2016	Resistance to imatinib in patients with chronic myelogenous leukemia and the splice variant BCR-ABL1(35INS).	imatinib	14-22	BCR activator of RhoGEF and GTPase	Homo sapiens	92-100
27658269-10	2016	CONCLUSIONS: The splice variant BCR-ABL1(35INS) is frequently found in patients who are resistant to imatinib.	imatinib	101-109	BCR activator of RhoGEF and GTPase	Homo sapiens	32-40
27474147-5	2016	We analyzed STI571-treated human colorectal KAT-4/HT-29 experimental carcinomas, known to have a well-developed stromal compartment, for solute exchange and glycosaminoglycan content, as well as collagen content, structure, and synthesis.	imatinib	12-18	glutamic-oxaloacetic transaminase 2	Homo sapiens	44-49
27474147-6	2016	MRI of STI571-treated KAT-4/HT-29 experimental carcinomas showed a significantly increased efficacy in dynamic exchanges of solutes between tumor interstitium and blood.	imatinib	7-13	glutamic-oxaloacetic transaminase 2	Homo sapiens	22-27
27698808-4	2016	Bone marrow trephines of CML patients in remission under imatinib therapy exhibited significantly higher numbers of CD3 and CD20 infiltrates (partly ordered in aggregates) compared with patients with newly diagnosed CML and control individuals.	imatinib	57-65	keratin 20	Homo sapiens	124-128
27698808-5	2016	Similarly, nuclear expression of BACH2 in granulopoietic cells was increased in CML patients treated with imatinib, which may represent the histological correlate of the positive treatment effect.	imatinib	106-114	BTB domain and CNC homolog 2	Homo sapiens	33-38
27698808-6	2016	Furthermore, since BACH2 is involved in B cell development, its altered expression patterns by imatinib may be one explanation for high B cell numbers, as revealed by CD20/BACH2 (nuclear)-positive cells.	imatinib	95-103	BTB domain and CNC homolog 2	Homo sapiens	19-24
27698808-6	2016	Furthermore, since BACH2 is involved in B cell development, its altered expression patterns by imatinib may be one explanation for high B cell numbers, as revealed by CD20/BACH2 (nuclear)-positive cells.	imatinib	95-103	keratin 20	Homo sapiens	167-171
27698808-6	2016	Furthermore, since BACH2 is involved in B cell development, its altered expression patterns by imatinib may be one explanation for high B cell numbers, as revealed by CD20/BACH2 (nuclear)-positive cells.	imatinib	95-103	BTB domain and CNC homolog 2	Homo sapiens	172-177
27432881-2	2016	BCR-ABL tyrosine kinase inhibitors (TKIs) imatinib and dasatinib inhibit fludarabine and cytarabine uptake.	imatinib	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
27517565-0	2016	miR-101 sensitizes K562 cell line to imatinib through Jak2 downregulation and inhibition of NF-kappaB target genes.	imatinib	37-45	Janus kinase 2	Homo sapiens	54-58
27472284-2	2016	For example, relapse of chronic myelogenous leukemia (CML) after inhibiting BCR-ABL fusion protein using tyrosine kinase inhibitors (TKI) (e.g., Imatinib) is of significant clinical concern.	imatinib	145-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
27320209-3	2016	Previous research in our lab has shown that imatinib methanesulfonate (IM) blocks the peripheral production of Abeta in response to LPS, thereby preventing the buildup of Abeta in the hippocampus, and rescuing the cognitive dysfunction that normally follows.	imatinib	44-69	histocompatibility 2, class II antigen A, beta 1	Mus musculus	111-116
27320209-3	2016	Previous research in our lab has shown that imatinib methanesulfonate (IM) blocks the peripheral production of Abeta in response to LPS, thereby preventing the buildup of Abeta in the hippocampus, and rescuing the cognitive dysfunction that normally follows.	imatinib	44-69	histocompatibility 2, class II antigen A, beta 1	Mus musculus	171-176
27599610-0	2016	Inhibition of YAP suppresses CML cell proliferation and enhances efficacy of imatinib in vitro and in vivo.	imatinib	77-85	yes-associated protein 1	Mus musculus	14-17
27349873-3	2016	Treatment of PDGFRA-mutated GIST with imatinib is successful in some cases, but the D842V mutation is imatinib-resistant.	imatinib	38-46	platelet derived growth factor receptor alpha	Homo sapiens	13-19
27349873-3	2016	Treatment of PDGFRA-mutated GIST with imatinib is successful in some cases, but the D842V mutation is imatinib-resistant.	imatinib	102-110	platelet derived growth factor receptor alpha	Homo sapiens	13-19
27349873-6	2016	The conserved residue Asp842 makes extensive contacts with several A-loop residues to maintain PDGFRA in the "DFG out" conformation, which stabilizes the kinase in the inactive state and facilitates the binding of imatinib.	imatinib	214-222	platelet derived growth factor receptor alpha	Homo sapiens	95-101
27566585-4	2016	In the present study, imatinib mesylate (IMA) was used to normalize the tumor microenvironment including platelet-derived growth factor receptor-beta expression inhibition, tumor vessel normalization, and tumor perfusion improvement as demonstrated by immunofluorescence staining.	imatinib	22-39	platelet derived growth factor receptor beta	Homo sapiens	105-149
27566585-4	2016	In the present study, imatinib mesylate (IMA) was used to normalize the tumor microenvironment including platelet-derived growth factor receptor-beta expression inhibition, tumor vessel normalization, and tumor perfusion improvement as demonstrated by immunofluorescence staining.	imatinib	41-44	platelet derived growth factor receptor beta	Homo sapiens	105-149
27635733-0	2016	MATE1 regulates cellular uptake and sensitivity to imatinib in CML patients.	imatinib	51-59	solute carrier family 47 member 1	Homo sapiens	0-5
27635733-4	2016	Here we found that the multidrug and toxin extrusion protein 1 (MATE1) transports imatinib with a manifold higher affinity.	imatinib	82-90	solute carrier family 47 member 1	Homo sapiens	23-62
27635733-4	2016	Here we found that the multidrug and toxin extrusion protein 1 (MATE1) transports imatinib with a manifold higher affinity.	imatinib	82-90	solute carrier family 47 member 1	Homo sapiens	64-69
27635733-5	2016	MATE1 mainly mediates the cellular uptake of imatinib into targeted cells and thereby controls the intracellular effectiveness of imatinib.	imatinib	45-53	solute carrier family 47 member 1	Homo sapiens	0-5
27635733-5	2016	MATE1 mainly mediates the cellular uptake of imatinib into targeted cells and thereby controls the intracellular effectiveness of imatinib.	imatinib	130-138	solute carrier family 47 member 1	Homo sapiens	0-5
27635733-6	2016	Importantly, MATE1 but not OCT1 expression is reduced in total bone marrow cells of imatinib-non-responding CML patients compared with imatinib-responding patients, indicating that MATE1 but not OCT1 determines the therapeutic success of imatinib.	imatinib	84-92	solute carrier family 47 member 1	Homo sapiens	13-18
27635733-7	2016	We thus propose that imatinib non-responders could be identified early before starting therapy by measuring MATE1 expression levels.	imatinib	21-29	solute carrier family 47 member 1	Homo sapiens	108-113
27725845-7	2016	ALL3 cells are very sensitive to potent tyrosine kinase inhibitors (TKIs) such as Dasatinib and PD166325, but less sensitive to AMN 107, Imatinib, and BMS 214662 (a farnesyl transferase inhibitor).	imatinib	137-145	paired box 5	Homo sapiens	0-4
27432881-4	2016	Imatinib inhibited hCNT2 with an IC50 value of 2.3 mum Ponatinib inhibited all five hNTs with the greatest effect seen for hENT1 (IC50 value, 9 mum).	imatinib	0-8	solute carrier family 28 member 2	Homo sapiens	19-24
27432881-4	2016	Imatinib inhibited hCNT2 with an IC50 value of 2.3 mum Ponatinib inhibited all five hNTs with the greatest effect seen for hENT1 (IC50 value, 9 mum).	imatinib	0-8	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	123-128
27036136-5	2016	Imatinib and Stattic were used to inhibit c-Abl and STAT3 activation, respectively.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-47
27344662-1	2016	Imatinib, a Bcr-Abl-specific inhibitor, is effective for treating chronic myeloid leukemia (CML), but drug resistance has emerged for this disease.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
27036136-5	2016	Imatinib and Stattic were used to inhibit c-Abl and STAT3 activation, respectively.	imatinib	0-8	signal transducer and activator of transcription 3	Homo sapiens	52-57
27036136-8	2016	Visfatin-promoted in vitro cell viability and metastatic capability were suppressed by imatinib (c-Abl inhibitor) and Stattic (STAT3 inhibitor).	imatinib	87-95	nicotinamide phosphoribosyltransferase	Homo sapiens	0-8
27036136-8	2016	Visfatin-promoted in vitro cell viability and metastatic capability were suppressed by imatinib (c-Abl inhibitor) and Stattic (STAT3 inhibitor).	imatinib	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-102
27036136-11	2016	Tail vein-injected mice with visfatin-pretreated breast cancer cells showed increased lung metastasis, which was suppressed by imatinib.	imatinib	127-135	nicotinamide phosphoribosyltransferase	Mus musculus	29-37
27649657-0	2016	miRNA-21 sensitizes gastrointestinal stromal tumors (GISTs) cells to Imatinib via targeting B-cell lymphoma 2 (Bcl-2).	imatinib	69-77	microRNA 21	Homo sapiens	0-8
27649657-3	2016	In this study, we investigated the regulation by miRNA-21 on the sensitivity of gastrointestinal stromal tumors (GISTs) cells to Imatinib.	imatinib	129-137	microRNA 21	Homo sapiens	49-57
27649657-0	2016	miRNA-21 sensitizes gastrointestinal stromal tumors (GISTs) cells to Imatinib via targeting B-cell lymphoma 2 (Bcl-2).	imatinib	69-77	BCL2 apoptosis regulator	Homo sapiens	92-109
27649657-6	2016	In addition, we examined the influence of miRNA-21 on the sensitivity to Imatinib of GIST-T1 cells with colony forming assay and apoptotic assay.	imatinib	73-81	microRNA 21	Homo sapiens	42-50
27649657-10	2016	Moreover, the miRNA-21 mimics transfection markedly aggravated the Imatinib-mediated growth inhibition and apoptosis induction in GIST-T1 cells.	imatinib	67-75	microRNA 21	Homo sapiens	14-22
27649657-0	2016	miRNA-21 sensitizes gastrointestinal stromal tumors (GISTs) cells to Imatinib via targeting B-cell lymphoma 2 (Bcl-2).	imatinib	69-77	BCL2 apoptosis regulator	Homo sapiens	111-116
27649657-12	2016	And the miRNA-21 promotion could sensitize GIST cells to Imatinib.	imatinib	57-65	microRNA 21	Homo sapiens	8-16
27738659-1	2016	BACKGROUND: The anticancer agent imatinib (IM) is a small molecular analog of ATP that inhibits tyrosine kinase activity of platelet derived growth factors (PDGFs) and stem cell factor (SCF) receptor in cancer cells.	imatinib	33-41	kit ligand	Mus musculus	186-189
27272942-0	2016	High IL-7 levels in the bone marrow microenvironment mediate imatinib resistance and predict disease progression in chronic myeloid leukemia.	imatinib	61-69	interleukin 7	Homo sapiens	5-9
27272942-6	2016	The increased IL-7 was secreted by mesenchymal stem cells (MSC) in the bone marrow, which may protect leukemic cells from apoptosis induced by imatinib through JAK1/STAT5 signaling pathway.	imatinib	143-151	interleukin 7	Homo sapiens	14-18
27272942-6	2016	The increased IL-7 was secreted by mesenchymal stem cells (MSC) in the bone marrow, which may protect leukemic cells from apoptosis induced by imatinib through JAK1/STAT5 signaling pathway.	imatinib	143-151	Janus kinase 1	Homo sapiens	160-164
27272942-6	2016	The increased IL-7 was secreted by mesenchymal stem cells (MSC) in the bone marrow, which may protect leukemic cells from apoptosis induced by imatinib through JAK1/STAT5 signaling pathway.	imatinib	143-151	signal transducer and activator of transcription 5A	Homo sapiens	165-170
26854822-0	2016	Metabolic characterization of imatinib-resistant BCR-ABL T315I chronic myeloid leukemia cells indicates down-regulation of glycolytic pathway and low ROS production.	imatinib	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
27444277-0	2016	Sensitivity of imatinib-resistant T315I BCR-ABL CML to a synergistic combination of ponatinib and forskolin treatment.	imatinib	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
27602125-3	2016	Imatinib mesylate is the first line breakpoint cluster region-Abelson gene (BCR/ABL)-targeted oral therapy for CML, and may produce a complete response in 70-80% of CML patients in the chronic phase.	imatinib	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
28195260-2	2016	The discovery of the occurrence of activating KIT mutations and KIT expression in GISTs opened the way to the unequivocal diagnosis of these tumors and to their successful treatment with imatinib, a tyrosin kinase inhibitor.	imatinib	187-195	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	46-49
28195260-2	2016	The discovery of the occurrence of activating KIT mutations and KIT expression in GISTs opened the way to the unequivocal diagnosis of these tumors and to their successful treatment with imatinib, a tyrosin kinase inhibitor.	imatinib	187-195	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	64-67
27444277-4	2016	To better understand the mechanism of drug resistance in TKI-resistant CML patients, the BCR-ABL transformed cell line KCL22 was grown with increasing concentrations of imatinib for a period of 6 weeks.	imatinib	169-177	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
27494773-5	2016	In vitro studies demonstrated that dasatinib and imatinib but not nilotinib inhibited ADP, CRP, and collagen-induced platelet aggregation and moreover, that nilotinib potentiated PAR-1-mediated alpha granule release.	imatinib	49-57	Prader Willi/Angelman region RNA 1	Homo sapiens	179-184
27572504-7	2016	Furthermore, oral administration of imatinib, an inhibitor of c-Kit and an anticancer agent for gastrointestinal stromal tumors, markedly induced appearance of ectopic neurons after BAC treatment, even in wildtype mice.	imatinib	36-44	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	62-67
27430982-2	2016	However, a subset of patients develops resistance to imatinib and other tyrosine kinase inhibitors (TKIs), mainly due to point mutations in the region encoding the kinase domain of the fused BCR-ABL oncogene.	imatinib	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	191-198
27430982-3	2016	To identify potential therapeutic targets in imatinib-resistant CML cells, we derived imatinib-resistant CML-T1 human cell line clone (CML-T1/IR) by prolonged exposure to imatinib in growth media.	imatinib	86-94	CD5 molecule	Homo sapiens	139-144
27430982-3	2016	To identify potential therapeutic targets in imatinib-resistant CML cells, we derived imatinib-resistant CML-T1 human cell line clone (CML-T1/IR) by prolonged exposure to imatinib in growth media.	imatinib	86-94	CD5 molecule	Homo sapiens	139-144
27430982-4	2016	Mutational analysis revealed that the Y235H mutation in BCR-ABL is probably the main cause of CML-T1/IR resistance to imatinib.	imatinib	118-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
27430982-4	2016	Mutational analysis revealed that the Y235H mutation in BCR-ABL is probably the main cause of CML-T1/IR resistance to imatinib.	imatinib	118-126	CD5 molecule	Homo sapiens	98-103
27430982-5	2016	To identify alternative therapeutic targets for selective elimination of imatinib-resistant cells, we compared the proteome profiles of CML-T1 and CML-T1/IR cells using 2-DE-MS. We identified eight differentially expressed proteins, with strongly upregulated Na+/H+ exchanger regulatory factor 1 (NHERF1) in the resistant cells, suggesting that this protein may influence cytosolic pH, Ca2+ concentration or signaling pathways such as Wnt in CML-T1/IR cells.	imatinib	73-81	CD5 molecule	Homo sapiens	151-156
27430982-5	2016	To identify alternative therapeutic targets for selective elimination of imatinib-resistant cells, we compared the proteome profiles of CML-T1 and CML-T1/IR cells using 2-DE-MS. We identified eight differentially expressed proteins, with strongly upregulated Na+/H+ exchanger regulatory factor 1 (NHERF1) in the resistant cells, suggesting that this protein may influence cytosolic pH, Ca2+ concentration or signaling pathways such as Wnt in CML-T1/IR cells.	imatinib	73-81	SLC9A3 regulator 1	Homo sapiens	259-295
27430982-5	2016	To identify alternative therapeutic targets for selective elimination of imatinib-resistant cells, we compared the proteome profiles of CML-T1 and CML-T1/IR cells using 2-DE-MS. We identified eight differentially expressed proteins, with strongly upregulated Na+/H+ exchanger regulatory factor 1 (NHERF1) in the resistant cells, suggesting that this protein may influence cytosolic pH, Ca2+ concentration or signaling pathways such as Wnt in CML-T1/IR cells.	imatinib	73-81	SLC9A3 regulator 1	Homo sapiens	297-303
27430982-5	2016	To identify alternative therapeutic targets for selective elimination of imatinib-resistant cells, we compared the proteome profiles of CML-T1 and CML-T1/IR cells using 2-DE-MS. We identified eight differentially expressed proteins, with strongly upregulated Na+/H+ exchanger regulatory factor 1 (NHERF1) in the resistant cells, suggesting that this protein may influence cytosolic pH, Ca2+ concentration or signaling pathways such as Wnt in CML-T1/IR cells.	imatinib	73-81	CD5 molecule	Homo sapiens	446-451
29029406-7	2017	We identified the FIP1L1-PDGFRA/JAK2/Lyn/Akt complex in the F/P-expressing cells which can be disrupted by dual inhibition of JAK2 and Lyn, repressing cell proliferation in both EOL-1(F/P-positive human eosinophilic cell line) and imatinib-resistance (IR) cells.	imatinib	231-239	factor interacting with PAPOLA and CPSF1	Homo sapiens	18-24
27382024-6	2016	We observed that CagA phosphorylation was strongly inhibited upon treatment with an Src inhibitor and slightly diminished when the Abl kinase inhibitor imatinib mesylate (Gleevec) was applied.	imatinib	152-169	S100 calcium binding protein A8 (calgranulin A)	Mus musculus	17-21
27382024-6	2016	We observed that CagA phosphorylation was strongly inhibited upon treatment with an Src inhibitor and slightly diminished when the Abl kinase inhibitor imatinib mesylate (Gleevec) was applied.	imatinib	171-178	S100 calcium binding protein A8 (calgranulin A)	Mus musculus	17-21
29029406-7	2017	We identified the FIP1L1-PDGFRA/JAK2/Lyn/Akt complex in the F/P-expressing cells which can be disrupted by dual inhibition of JAK2 and Lyn, repressing cell proliferation in both EOL-1(F/P-positive human eosinophilic cell line) and imatinib-resistance (IR) cells.	imatinib	231-239	platelet derived growth factor receptor alpha	Homo sapiens	25-31
29029406-7	2017	We identified the FIP1L1-PDGFRA/JAK2/Lyn/Akt complex in the F/P-expressing cells which can be disrupted by dual inhibition of JAK2 and Lyn, repressing cell proliferation in both EOL-1(F/P-positive human eosinophilic cell line) and imatinib-resistance (IR) cells.	imatinib	231-239	Janus kinase 2	Homo sapiens	32-36
29029406-7	2017	We identified the FIP1L1-PDGFRA/JAK2/Lyn/Akt complex in the F/P-expressing cells which can be disrupted by dual inhibition of JAK2 and Lyn, repressing cell proliferation in both EOL-1(F/P-positive human eosinophilic cell line) and imatinib-resistance (IR) cells.	imatinib	231-239	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	37-40
29029406-7	2017	We identified the FIP1L1-PDGFRA/JAK2/Lyn/Akt complex in the F/P-expressing cells which can be disrupted by dual inhibition of JAK2 and Lyn, repressing cell proliferation in both EOL-1(F/P-positive human eosinophilic cell line) and imatinib-resistance (IR) cells.	imatinib	231-239	AKT serine/threonine kinase 1	Homo sapiens	41-44
27482095-5	2016	A second class of KIT mutants, including a mutant resistant to imatinib treatment, responded well to a combination of TKI with anti-KIT antibodies or to anti-KIT toxin conjugates, respectively.	imatinib	63-71	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	18-21
27447561-7	2016	Furthermore, primary CD34+ leukemic cells derived from IK6-positive patients shown poor responses to imatinib in comparison with wild-type (IK1) patients, suggesting that the expression of IK6 resisted to imatinib in adult BCR-ABL1-positive B-ALL.	imatinib	101-109	CD34 molecule	Homo sapiens	21-25
27447561-7	2016	Furthermore, primary CD34+ leukemic cells derived from IK6-positive patients shown poor responses to imatinib in comparison with wild-type (IK1) patients, suggesting that the expression of IK6 resisted to imatinib in adult BCR-ABL1-positive B-ALL.	imatinib	205-213	CD34 molecule	Homo sapiens	21-25
27447561-7	2016	Furthermore, primary CD34+ leukemic cells derived from IK6-positive patients shown poor responses to imatinib in comparison with wild-type (IK1) patients, suggesting that the expression of IK6 resisted to imatinib in adult BCR-ABL1-positive B-ALL.	imatinib	205-213	BCR activator of RhoGEF and GTPase	Homo sapiens	223-231
27536777-6	2016	ABCB1 overexpression was also observed in cell lines as an intermediate step during development of resistance to imatinib and dasatinib in vitro.	imatinib	113-121	ATP binding cassette subfamily B member 1	Homo sapiens	0-5
27226592-8	2016	Surprisingly, immunofluorescence microscopy of imatinib-treated cells revealed a marked colocalization of internalized TfR1 with late endosomes/lysosomes, whereas attenuating the lysosome function with several inhibitors reduced this receptor loss.	imatinib	47-55	transferrin receptor	Homo sapiens	119-123
27570562-0	2016	Depletion of gamma-catenin by Histone Deacetylase Inhibition Confers Elimination of CML Stem Cells in Combination with Imatinib.	imatinib	119-127	junction plakoglobin	Mus musculus	13-26
27506146-0	2016	CCBE1 promotes GIST development through enhancing angiogenesis and mediating resistance to imatinib.	imatinib	91-99	collagen and calcium binding EGF domains 1	Homo sapiens	0-5
27506146-5	2016	In vitro experiments showed that recombinant CCBE1 protein can enhance angiogenesis and neutralize partial effect of imatinib on the GIST-T1 cells.	imatinib	117-125	collagen and calcium binding EGF domains 1	Homo sapiens	45-50
27583255-4	2016	Then, several stop studies of first-generation (imatinib) and second-generation ABL TKIs (dasatinib, nilotinib), which induce earlier response than imatinib, have also been started.	imatinib	148-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
27480221-0	2016	Imatinib binding to human c-Src is coupled to inter-domain allostery and suggests a novel kinase inhibition strategy.	imatinib	0-8	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	26-31
27485109-1	2016	BACKGROUND: Imatinib-resistant chronic myeloid leukemia (CML) patients receiving second-line tyrosine kinase inhibitor (TKI) therapy with dasatinib or nilotinib have a higher risk of disease relapse and progression and not infrequently BCR-ABL1 kinase domain (KD) mutations are implicated in therapeutic failure.	imatinib	12-20	BCR activator of RhoGEF and GTPase	Homo sapiens	236-244
27366945-6	2016	Both imatinib-sensitive (GIST882) and -resistant (GIST48 and GIST430) cell lines exhibited increased MGLL expression.	imatinib	5-13	monoglyceride lipase	Homo sapiens	101-105
27481339-5	2016	Accordingly, CML cells placed on FGF2-treated stromal layers were more sensitive to imatinib.	imatinib	84-92	fibroblast growth factor 2	Mus musculus	33-37
27480221-3	2016	We present a detailed study of the conformational dynamics, in the presence and absence of bound imatinib, for full-length human c-Src using hydrogen-deuterium exchange and mass spectrometry.	imatinib	97-105	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	129-134
27480221-4	2016	Our results demonstrate that imatinib binding to the kinase domain effects dynamics of proline-rich or phosphorylated peptide ligand binding sites in distal c-Src SH3 and SH2 domains.	imatinib	29-37	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	157-162
27480221-7	2016	Thus, the current study identifies novel c-Src allosteric sites associated with imatinib binding and kinase activation and provide a framework for follow-on development of TKI binding modulators.	imatinib	80-88	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	41-46
27515884-0	2016	Successful treatment of c-kit-positive metastatic Adenoid Cystic Carcinoma (ACC) with a combination of curcumin plus imatinib: A case report.	imatinib	117-125	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	24-29
27515884-5	2016	Imatinib is monoclonal antibody with specific activity against c-kit but has not been found to be effective in treating patients with ACC in which c-kit is overexpressed and activated.	imatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	63-68
27515884-15	2016	To our knowledge, this is the first report of a patient with a c-kit-positive ACC that is successfully treated with the combination of imatinib and curcumin in an integrative approach.	imatinib	135-143	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	63-68
27015352-5	2016	The expression of MT-1G messenger RNA and protein is remarkably induced by sorafenib but not other clinically relevant kinase inhibitors (e.g., erlotinib, gefitinib, tivantinib, vemurafenib, selumetinib, imatinib, masitinib, and ponatinib).	imatinib	204-212	metallothionein 1G	Homo sapiens	18-23
27297623-9	2016	Imatinib, the drug of choice for CML, abrogates MEF2C expression and reverses CEBPA repression both in the cell line and the primary cells.	imatinib	0-8	myocyte enhancer factor 2C	Homo sapiens	48-53
27297623-9	2016	Imatinib, the drug of choice for CML, abrogates MEF2C expression and reverses CEBPA repression both in the cell line and the primary cells.	imatinib	0-8	CCAAT enhancer binding protein alpha	Homo sapiens	78-83
27125982-0	2016	Imatinib-induced long-term remission in a relapsed RCSD1-ABL1-positive acute lymphoblastic leukemia.	imatinib	0-8	RCSD domain containing 1	Homo sapiens	51-56
27125982-0	2016	Imatinib-induced long-term remission in a relapsed RCSD1-ABL1-positive acute lymphoblastic leukemia.	imatinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-61