PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
25882020-1	2015	Imatinib mesylate is a competitive inhibitor of BCR/ ABL tyrosine kinase and inhibits also several receptor tyrosin kinases.	Imatinib Mesylate	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 Mesylate	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-125
25179732-0	2015	Relapse of BCR-ABL1-like ALL mediated by the ABL1 kinase domain mutation T315I following initial response to dasatinib treatment.	Dasatinib	109-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-19
25179732-0	2015	Relapse of BCR-ABL1-like ALL mediated by the ABL1 kinase domain mutation T315I following initial response to dasatinib treatment.	Dasatinib	109-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-49
25465126-0	2015	Synergism between bosutinib (SKI-606) and the Chk1 inhibitor (PF-00477736) in highly imatinib-resistant BCR/ABL+ leukemia cells.	bosutinib	18-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
25465126-0	2015	Synergism between bosutinib (SKI-606) and the Chk1 inhibitor (PF-00477736) in highly imatinib-resistant BCR/ABL+ leukemia cells.	bosutinib	29-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
25465126-0	2015	Synergism between bosutinib (SKI-606) and the Chk1 inhibitor (PF-00477736) in highly imatinib-resistant BCR/ABL+ leukemia cells.	Imatinib Mesylate	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
25721903-0	2015	Persistent major molecular response to nilotinib therapy in a patient with chronic myeloid leukemia harboring ABL gene T315I mutation.	nilotinib	39-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-113
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 Mesylate	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
25319658-0	2015	Targeting bcr-abl transcripts with siRNAs in an imatinib-resistant chronic myeloid leukemia patient: challenges and future directions.	Imatinib Mesylate	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 Mesylate	217-225	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
25348715-4	2015	We identified a selected number of Phe mutations in a small group of kinases that included BRAF, ABL1, and the epidermal growth factor receptor.	Phenylalanine	35-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-101
27182477-5	2015	Bosutinib, an orally bioavailable Src/Abl tyrosine kinase inhibitor, has proved to be effective in vitro against resistant chronic myeloid leukemia cells that do not harbor the T315I or V299L ABL kinase domain mutations.	bosutinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-41
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 Mesylate	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 Mesylate	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 Mesylate	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	250-257
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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
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 Mesylate	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 Mesylate	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	180-187
27182477-5	2015	Bosutinib, an orally bioavailable Src/Abl tyrosine kinase inhibitor, has proved to be effective in vitro against resistant chronic myeloid leukemia cells that do not harbor the T315I or V299L ABL kinase domain mutations.	bosutinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	192-195
25527332-0	2015	The BCR-ABL inhibitor ponatinib inhibits platelet immunoreceptor tyrosine-based activation motif (ITAM) signaling, platelet activation and aggregate formation under shear.	ponatinib	22-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
25527332-0	2015	The BCR-ABL inhibitor ponatinib inhibits platelet immunoreceptor tyrosine-based activation motif (ITAM) signaling, platelet activation and aggregate formation under shear.	Tyrosine	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
25527332-1	2015	BACKGROUND: Treatment of chronic myelogenous leukemia (CML) with the BCR-ABL tyrosine kinase inhibitor (TKI) imatinib significantly improves patient outcomes.	Imatinib Mesylate	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.	nilotinib	90-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
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 Mesylate	143-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
25527332-9	2015	As our results indicate that pobatinib inhibits platelet function, the adverse cardiovascular events observed in patients taking ponatinib may be the result of the effect of ponatinib on other organs or cell types, or disease-specific processes, such as BCR-ABL+cells undergoing apoptosis in response to chemotherapy, or drug-induced adverse effects on the integrity of the vascular endothelium in ponatinib-treated patients.	pobatinib	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	254-261
25527332-9	2015	As our results indicate that pobatinib inhibits platelet function, the adverse cardiovascular events observed in patients taking ponatinib may be the result of the effect of ponatinib on other organs or cell types, or disease-specific processes, such as BCR-ABL+cells undergoing apoptosis in response to chemotherapy, or drug-induced adverse effects on the integrity of the vascular endothelium in ponatinib-treated patients.	ponatinib	129-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	254-261
25304212-1	2015	Ponatinib, a multi-targeted TKI and potent pan-ABL inhibitor, approved for the treatment of Ph + ALL and CML, was temporarily withdrawn from the U.S. market due to severe vascular adverse events.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
25464886-0	2014	Discovery of novel Bcr-Abl inhibitors targeting myristoyl pocket and ATP site.	Adenosine Triphosphate	69-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
25464886-3	2014	In order to obtain novel and potent Bcr-Abl inhibitors, twenty seven 4,6-disubstituted pyrimidines were synthesized and evaluated herein.	4,6-disubstituted pyrimidines	69-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
25464886-6	2014	The results suggested that these 4,6-disubstituted pyrimidines could serve as promising leads for further optimization of Bcr-Abl inhibitors.	4,6-disubstituted pyrimidines	33-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
25490448-2	2014	Activity of the proto-oncogene ABL1 is upregulated in FH-deficient kidney tumors and drives a metabolic and survival signaling network necessary to cope with impaired mitochondrial function and abnormal accumulation of intracellular fumarate.	Fumarates	233-241	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-35
25490448-3	2014	Excess fumarate indirectly stimulates ABL1 activity, while restoration of wild-type FH abrogates both ABL1 activation and the cytotoxicity caused by ABL1 inhibition or knockdown.	Fumarates	7-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-42
25490448-4	2014	ABL1 upregulates aerobic glycolysis via the mTOR/HIF1alpha pathway and neutralizes fumarate-induced proteotoxic stress by promoting nuclear localization of the antioxidant response transcription factor NRF2.	Fumarates	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-4
25465127-2	2014	Despite a high level of sequence homology in the ATP-binding site, the majority of reported inhibitors are selective for the FGFR1-3 isoforms and display much reduced potency toward FGFR4, an exception being the Bcr-Abl inhibitor ponatinib.	ponatinib	230-239	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	212-219
25200837-0	2014	Tyrosine kinase inhibitor Thiotanib targets Bcr-Abl and induces apoptosis and autophagy in human chronic myeloid leukemia cells.	Thiotanib	26-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
25331939-0	2014	Combination therapy with nilotinib for drug-sensitive and drug-resistant BCR-ABL-positive leukemia and other malignancies.	nilotinib	25-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
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 Mesylate	102-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
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.	nilotinib	153-162	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
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.	Dasatinib	166-175	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
25331939-4	2014	Here, we present an overview of the use of nilotinib in combination with other agents against BCR-ABL-positive leukemia, as well as solid tumors, for the purpose of increasing clinical efficacy and overriding drug resistance.	nilotinib	43-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
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 Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-81
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 Mesylate	206-223	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
25435721-8	2014	In first case, dual color dual fusion (DCDF)-FISH studies revealed 1 Red (R) 2 Green (G) 1 Fusion (F) signal pattern in 80 % of cells indicating BCR/ABL fusion signals on chromosomes 9 instead of Ph and 2G2F signal pattern in 20 % of cells indicating two BCR/ABL fusions on both chromosomes 9q34 on presentation.	dcdf	39-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-152
25435722-3	2014	The development of the BCR-ABL-targeted imatinib mesylate represents a paradigm shift in the treatment of CML.	Imatinib Mesylate	40-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
25281405-1	2014	Imatinib resistance in chronic myeloid leukemia (CML) is commonly due to BCR-ABL kinase domain mutations (KDMs).	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
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 Mesylate	120-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
25420054-6	2014	However, the Bland-Altman plot revealed that there was closer agreement between ABL-80 machines for tHbmass than for the OSM-3.	thbmass	100-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
25420054-9	2014	Previously, five replicates were required to achieve a low error using the OSM-3; however, three replicates are sufficient with the ABL-80 model to produce an error of <= 1% in tHbmass.	thbmass	180-187	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-135
25526032-10	2014	Furthermore, inhibition of c-Abl with STI571 also abrogated the effect on apoptosis caused by MLH1.	Imatinib Mesylate	38-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-32
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 Mesylate	167-184	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
25621010-6	2014	The ratio of BCR-ABL/ABL expression in post nilotinib treatment was 0.07% on international scale.	nilotinib	44-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
25621010-6	2014	The ratio of BCR-ABL/ABL expression in post nilotinib treatment was 0.07% on international scale.	nilotinib	44-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-20
25290090-1	2014	BACKGROUND: This phase 1 study evaluated the maximum tolerated dose (MTD), safety, and efficacy of bosutinib (competitive Src/Abl tyrosine kinase inhibitor) plus capecitabine.	bosutinib	99-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-129
25426931-0	2014	Inhibition of Aurora kinase B is important for biologic activity of the dual inhibitors of BCR-ABL and Aurora kinases R763/AS703569 and PHA-739358 in BCR-ABL transformed cells.	MSC1992371A	123-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
25426931-1	2014	ABL tyrosine kinase inhibitors (TKI) like Imatinib, Dasatinib and Nilotinib are the gold standard in conventional treatment of CML.	Imatinib Mesylate	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
25426931-1	2014	ABL tyrosine kinase inhibitors (TKI) like Imatinib, Dasatinib and Nilotinib are the gold standard in conventional treatment of CML.	Dasatinib	52-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
25426931-1	2014	ABL tyrosine kinase inhibitors (TKI) like Imatinib, Dasatinib and Nilotinib are the gold standard in conventional treatment of CML.	nilotinib	66-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
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 Mesylate	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 Mesylate	135-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-179
25382104-4	2014	Drugs that are currently available, such as imatinib and ponatinib, were also docked against BCR-ABL protein to set a cutoff value for our screening.	ponatinib	57-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
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 Mesylate	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 Mesylate	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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-148
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	165-172
25264277-6	2014	We demonstrate that the mechanism of p27(KIP1) stabilization relied on inhibition of p27(KIP1) phosphorylation on tyrosine residues by c-Abl.	Tyrosine	114-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-140
25264277-7	2014	We provide evidence that in neuroblastoma cell lines a significant fraction of cellular c-Abl is phosphorylated on Tyr-245, consistent with an open and active conformation.	Tyrosine	115-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-93
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 Mesylate	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 Mesylate	120-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-38
25429298-6	2014	Two specific inhibitors (ATP-competitive or allosteric compounds) regulate the c-Abl kinase through different mechanisms.	Adenosine Triphosphate	25-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-84
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 Mesylate	181-189	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
25193854-0	2014	Anti-rheumatic agent auranofin induced apoptosis in chronic myeloid leukemia cells resistant to imatinib through both Bcr/Abl-dependent and -independent mechanisms.	Auranofin	21-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-125
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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
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 Mesylate	109-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
25189629-9	2014	RT-qPCR indicated that virosecurinine upregulated the gene expression of PTEN and downregulated the expression of mTOR, SHIP-2 and BCR/ABL in K562 cells.	virosecurinine	23-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
25189629-10	2014	Virosecurinine inhibited the growth and proliferation of the K562 cell lines and induced apoptosis in K562 cells by affecting the expression of mTOR, SHIP2, BCR/ABL and PTEN.	virosecurinine	0-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-164
24865355-0	2014	Growth inhibition effects of isoalantolactone on K562/A02 cells: caspase-dependent apoptotic pathways, S phase arrest, and downregulation of Bcr/Abl.	isoalantolactone	29-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-148
24865355-3	2014	The purposes of this study were to evaluate the effects of isoalantolactone on the human erythroleukemia drug-resistant cell line K562/A02 and to provide evidence of its function as a potent therapeutic agent in patients with chronic myelogenous leukemia with the Bcr/Abl phenotype.	isoalantolactone	59-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	264-271
24865355-4	2014	Our results showed that isoalantolactone significantly inhibited K562/A02 cell growth by downregulating Bcr/Abl expression.	isoalantolactone	24-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
24865355-7	2014	Taken together, all these findings support that growth inhibition effects of isoalantolactone on K562/A02 cells may be mediated through caspase-dependent apoptotic pathways, S phase arrest, and downregulation of Bcr/Abl.	isoalantolactone	77-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	212-219
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 Mesylate	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-147
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	60-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-26
25153794-5	2014	We also found that SB202190 has weak bindings to ABL1 with KD > 10 muM, which is not reported in the literature.	4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-53
25284075-0	2014	Reduced miR-3127-5p expression promotes NSCLC proliferation/invasion and contributes to dasatinib sensitivity via the c-Abl/Ras/ERK pathway.	Dasatinib	88-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-123
25201268-1	2014	Abelson tyrosine-protein kinase 1 (ABL1) catalysed phosphorylation involves the addition of a phosphate group from ATP to the tyrosine residue on the substrate abltide.	Phosphates	94-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-33
25201268-1	2014	Abelson tyrosine-protein kinase 1 (ABL1) catalysed phosphorylation involves the addition of a phosphate group from ATP to the tyrosine residue on the substrate abltide.	Phosphates	94-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-39
25201268-1	2014	Abelson tyrosine-protein kinase 1 (ABL1) catalysed phosphorylation involves the addition of a phosphate group from ATP to the tyrosine residue on the substrate abltide.	Adenosine Triphosphate	115-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-33
25284075-5	2014	Overexpression of miR-3127-5p in A549 or H292 cells resulted in enhanced resistance to dasatinib, an Abl/src tyrosine kinase inhibitor.	Dasatinib	87-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-104
25201268-1	2014	Abelson tyrosine-protein kinase 1 (ABL1) catalysed phosphorylation involves the addition of a phosphate group from ATP to the tyrosine residue on the substrate abltide.	Adenosine Triphosphate	115-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-39
24944159-1	2014	Bosutinib, an orally active, Src/Abl tyrosine kinase inhibitor, has demonstrated clinical activity and acceptable tolerability in chronic phase chronic myeloid leukemia (CP CML).	bosutinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-36
25201268-1	2014	Abelson tyrosine-protein kinase 1 (ABL1) catalysed phosphorylation involves the addition of a phosphate group from ATP to the tyrosine residue on the substrate abltide.	Tyrosine	8-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-39
25201268-5	2014	The influence of co-adsorption of ABL1, ATP and phosphorylated abltide was evaluated and the conditions for the electrochemical detection of ABL1-catalysed phosphorylation optimised.	Adenosine Triphosphate	40-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-145
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 Mesylate	26-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-22
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.	danusertib	48-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-22
25041880-7	2014	At 3 months, 58 patients (64.4% TPA) obtained a BCR-ABL transcripts level <10%.	Tetradecanoylphorbol Acetate	32-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
25536607-1	2014	PURPOSE: Ponatinib (P) has been used for the treatment of chronic myeloid leukemia (CML) and it is known that inhibition of BCR-ABL fusion protein by ponatinib induces apoptosis of CML cells.	ponatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
24928376-10	2014	Bcr-abl mRNA copies decreased, but no changes of phosphorylated Bcr-abl and Bcr-abl proteins were observed, after treatment with quercetin.	Quercetin	129-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
25536607-1	2014	PURPOSE: Ponatinib (P) has been used for the treatment of chronic myeloid leukemia (CML) and it is known that inhibition of BCR-ABL fusion protein by ponatinib induces apoptosis of CML cells.	ponatinib	150-159	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
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 Mesylate	164-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
25173530-5	2014	The effectiveness of an oral dual-specific (Src and Abl) multikinase inhibitors-dasatinib-was observed in different cell lines and in some NSCLC patients with identified DDR2 mutation.	Dasatinib	80-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-55
25114223-5	2014	This approach identified a number of kinase inhibitors that robustly up-regulate IL-10 production including the Food and Drug Administration (FDA)-approved drugs dasatinib, bosutinib, and saracatinib that target ABL, SRC-family, and numerous other kinases.	Dasatinib	162-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	212-215
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 Mesylate	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
24882272-4	2014	Here, we investigated whether the BCR-ABL/SRC inhibitor dasatinib would modulate the major effector functions of DCs, especially their migration, a prerequisite to interaction with lymphocytes in secondary lymphoid organs.	Dasatinib	56-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
25392452-5	2014	In this report, we use two small molecule inhibitors, PP242 (dual mTOR (mammalian target of rapamycin) kinase inhibitor) and hippuristanol (eIF4A inhibitor), to define IRES regulation via a Bcr-Abl-mTOR-eIF4A axis in CML cell lines and primary patient leukaemias.	PP242	54-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	190-197
25392452-5	2014	In this report, we use two small molecule inhibitors, PP242 (dual mTOR (mammalian target of rapamycin) kinase inhibitor) and hippuristanol (eIF4A inhibitor), to define IRES regulation via a Bcr-Abl-mTOR-eIF4A axis in CML cell lines and primary patient leukaemias.	hippuristanol	125-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	190-197
25193862-5	2014	The mesenchymal cells were more resistant to most tested agents; however, a small number of agents showed selective growth inhibitory activity against the mesenchymal cells, with the most potent being the Abl/Src inhibitor, dasatinib.	Dasatinib	224-233	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	205-208
25207766-8	2014	Cell lines and human leukemic cells expressing ABL1, ABL2, CSF1R, and PDGFRB fusions were sensitive in vitro to dasatinib, EPOR and JAK2 rearrangements were sensitive to ruxolitinib, and the ETV6-NTRK3 fusion was sensitive to crizotinib.	Dasatinib	112-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-51
25207766-8	2014	Cell lines and human leukemic cells expressing ABL1, ABL2, CSF1R, and PDGFRB fusions were sensitive in vitro to dasatinib, EPOR and JAK2 rearrangements were sensitive to ruxolitinib, and the ETV6-NTRK3 fusion was sensitive to crizotinib.	ruxolitinib	170-181	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-51
25207766-8	2014	Cell lines and human leukemic cells expressing ABL1, ABL2, CSF1R, and PDGFRB fusions were sensitive in vitro to dasatinib, EPOR and JAK2 rearrangements were sensitive to ruxolitinib, and the ETV6-NTRK3 fusion was sensitive to crizotinib.	Crizotinib	226-236	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-51
24961450-1	2014	We describe an ultrasensitive electrochemical nucleic acid assay amplified by carbon nanotubes (CNTs)-based labels for the detection of human acute lymphocytic leukemia (ALL)-related p185 BCR-ABL fusion transcript.	Carbon	78-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	188-195
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 Mesylate	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 Mesylate	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-90
25198091-9	2014	In the intracellular context, EC50 for BCR-ABL inhibition was in subnanomolar range for dasatinib and in submicromolar one for imatinib.	Dasatinib	88-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
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 Mesylate	127-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
24096484-6	2014	Importantly, the invasion- and metastasis-promoting activity of c-Abl/Arg is dependent on their ability to induce NM23-H1 degradation, and the pathway is clinically relevant as c-Abl/Arg activity and NM23-H1 expression are inversely correlated in primary breast cancers and melanomas.	Arginine	70-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-69
24096484-6	2014	Importantly, the invasion- and metastasis-promoting activity of c-Abl/Arg is dependent on their ability to induce NM23-H1 degradation, and the pathway is clinically relevant as c-Abl/Arg activity and NM23-H1 expression are inversely correlated in primary breast cancers and melanomas.	Arginine	70-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-69
24096484-6	2014	Importantly, the invasion- and metastasis-promoting activity of c-Abl/Arg is dependent on their ability to induce NM23-H1 degradation, and the pathway is clinically relevant as c-Abl/Arg activity and NM23-H1 expression are inversely correlated in primary breast cancers and melanomas.	Arginine	183-186	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-69
24096484-6	2014	Importantly, the invasion- and metastasis-promoting activity of c-Abl/Arg is dependent on their ability to induce NM23-H1 degradation, and the pathway is clinically relevant as c-Abl/Arg activity and NM23-H1 expression are inversely correlated in primary breast cancers and melanomas.	Arginine	183-186	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-69
25186176-0	2014	A therapeutically targetable mechanism of BCR-ABL-independent imatinib resistance in chronic myeloid leukemia.	Imatinib Mesylate	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 Mesylate	36-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
25186176-7	2014	Combined treatment with IM and trametinib, a U.S. Food and Drug Administration-approved MEK inhibitor, synergistically kills BCR-ABL(+) IMSG knockdown cells and prolongs survival in mouse models of BCR-ABL-independent IM-resistant CML.	trametinib	31-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
25186176-7	2014	Combined treatment with IM and trametinib, a U.S. Food and Drug Administration-approved MEK inhibitor, synergistically kills BCR-ABL(+) IMSG knockdown cells and prolongs survival in mouse models of BCR-ABL-independent IM-resistant CML.	trametinib	31-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	198-205
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
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 Mesylate	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 Mesylate	161-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
25202073-3	2014	MATERIALS AND METHODS: Proliferation of different BCR-ABL(+) leukemic cells was measured with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay; cell apoptosis with Annexin V/propidium iodide (PI) and flow cytometry.	monooxyethylene trimethylolpropane tristearate	156-159	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
25202073-3	2014	MATERIALS AND METHODS: Proliferation of different BCR-ABL(+) leukemic cells was measured with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay; cell apoptosis with Annexin V/propidium iodide (PI) and flow cytometry.	Propidium	198-214	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
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 Mesylate	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
25023728-8	2014	Addition of the Src/c-Abl inhibitor, dasatinib, completely blocks this feedback activation, confirming convergence between Src and the mTOR pathway.	Dasatinib	37-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-25
25213664-9	2014	Moreover, when K562 cells were treated with 5-aza-2"-deoxycytidine, a DNA methylation inhibitor, BCR/ABL expression was upregulated, which indicates epigenetic silencing of miR-23a in leukemic cells.	Decitabine	44-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
25114223-5	2014	This approach identified a number of kinase inhibitors that robustly up-regulate IL-10 production including the Food and Drug Administration (FDA)-approved drugs dasatinib, bosutinib, and saracatinib that target ABL, SRC-family, and numerous other kinases.	saracatinib	188-199	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	212-215
25148385-0	2014	Inhibition of c-Abl kinase activity renders cancer cells highly sensitive to mitoxantrone.	Mitoxantrone	77-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
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 Mesylate	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.	Mitoxantrone	161-173	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 Mesylate	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 Mesylate	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 Mesylate	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-102
25038611-7	2014	RESULTS: Treatment of imatinib-sensitive, BCR-ABL-positive K562 and LAMA84 cells with nilotinib in combination with mafosfamide, treosulfan, or busulfan resulted in synergistic (CI < 1), additive (CI ~ 1), and predominantly antagonistic (CI > 1) effects, respectively.	nilotinib	86-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
25119536-7	2014	With personalised medicine and curative treatment in view, blocking activation of HGF/Met could be a useful addition in the treatment of CML and MPNs for those patients with high HGF/MET expression not controlled by current treatments (Bcr-Abl inhibitors in CML; phlebotomy, hydroxurea, JAK inhibitors in MPNs).	hydroxurea	275-285	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	236-243
24686006-11	2014	In addition, levels of bcr-abl mRNA and protein in K562 cells decreased after treatment with either suberoylanilide hydroxamic acid or ZYJ-34c; moreover, ZYJ-34c had a higher inhibition activity.	Vorinostat	100-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
24686006-11	2014	In addition, levels of bcr-abl mRNA and protein in K562 cells decreased after treatment with either suberoylanilide hydroxamic acid or ZYJ-34c; moreover, ZYJ-34c had a higher inhibition activity.	2-(2-(3,3-dimethylbutanamido)-3-methylpentanoyl)-7-(2-(hydroxyamino)-2-oxoethoxy)-N-(4-methoxyphenyl)-1,2,3,4-tetrahydroisoquinoline-3-carboxamide	135-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
24686006-11	2014	In addition, levels of bcr-abl mRNA and protein in K562 cells decreased after treatment with either suberoylanilide hydroxamic acid or ZYJ-34c; moreover, ZYJ-34c had a higher inhibition activity.	2-(2-(3,3-dimethylbutanamido)-3-methylpentanoyl)-7-(2-(hydroxyamino)-2-oxoethoxy)-N-(4-methoxyphenyl)-1,2,3,4-tetrahydroisoquinoline-3-carboxamide	154-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
24833663-4	2014	Chronic myelogenous leukemia (CML) is triggered by the expression of BCR-ABL kinase, whose activity leads to increased ROS production, partly through NADPH oxidases.	Reactive Oxygen Species	119-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
23966360-0	2014	Effect of imatinib on male reproductive hormones in BCR-ABL positive CML patients: A preliminary report.	Imatinib Mesylate	10-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
25023053-7	2014	Suppressing BCR-ABL by imatinib mesylate (IM) significantly decreased CIP2A expression.	Imatinib Mesylate	23-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
25130811-8	2014	The mRNA expression of C-MYC, hTERT and BCR-ABL was reduced significantly by SU11248 in a time-dependent manner (P < 0.05).	Sunitinib	77-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
25130811-10	2014	It is concluded that SU11248 can inhibit the growth of K562 cells efficiently through inducing apoptosis, its mechanism may be closely relate with the expression down-regulation of C-MYC, hTERT, BCR-ABL and the inhibition of Akt phosphorylation.	Sunitinib	21-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	195-202
24865254-0	2014	Pharmacophore modeling of nilotinib as an inhibitor of ATP-binding cassette drug transporters and BCR-ABL kinase using a three-dimensional quantitative structure-activity relationship approach.	nilotinib	26-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
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 Mesylate	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-63
24913448-5	2014	We demonstrate that LASP1 is specifically phosphorylated by BCR-ABL at tyrosine-171 in CML patients, which is abolished by tyrosine kinase inhibitor therapy.	Tyrosine	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
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 Mesylate	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 Mesylate	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
25029499-0	2014	Identification of drug combinations containing imatinib for treatment of BCR-ABL+ leukemias.	Imatinib Mesylate	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
24865254-3	2014	The goal of this study was to identify pharmacophoric features of nilotinib in order to potentially develop specific inhibitors of BCR-ABL kinase with minimal interactions with ABC drug transporters.	nilotinib	66-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
24865254-4	2014	Three-dimensional pharmacophore modeling and quantitative structure-activity relationship (QSAR) studies were carried out on a series of nilotinib analogues to identify chemical features that contribute to inhibitory activity of nilotinib against BCR-ABL kinase activity, P-gp, and ABCG2.	nilotinib	229-238	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	247-254
24865254-5	2014	Twenty-five derivatives of nilotinib were synthesized and were then tested to measure their activity to inhibit BCR-ABL kinase and to inhibit the function of ABC drug transporters.	nilotinib	27-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
24759597-3	2014	S116836 at low concentrations used in the present study mildly downregulates auto-tyrosine phosphorylation of Bcr-Abl.	Tyrosine	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
24891505-1	2014	The closely related Abl family kinases, Arg and Abl, play important non-redundant roles in the regulation of cell morphogenesis and motility.	Arginine	40-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-23
24891505-4	2014	We report that the Arg Src homology (SH) 2 domain binds two specific phosphotyrosines on cortactin, a known Abl/Arg substrate, with over 10-fold higher affinity than the Abl SH2 domain.	Arginine	19-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-111
24891505-4	2014	We report that the Arg Src homology (SH) 2 domain binds two specific phosphotyrosines on cortactin, a known Abl/Arg substrate, with over 10-fold higher affinity than the Abl SH2 domain.	Phosphotyrosine	69-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-111
24891505-4	2014	We report that the Arg Src homology (SH) 2 domain binds two specific phosphotyrosines on cortactin, a known Abl/Arg substrate, with over 10-fold higher affinity than the Abl SH2 domain.	Phosphotyrosine	69-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-173
24891505-5	2014	We show that this significant affinity difference is due to the substitution of arginine 161 and serine 187 in Abl to leucine 207 and threonine 233 in Arg, respectively.	Arginine	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-114
24891505-5	2014	We show that this significant affinity difference is due to the substitution of arginine 161 and serine 187 in Abl to leucine 207 and threonine 233 in Arg, respectively.	Serine	97-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-114
24891505-6	2014	We constructed Abl SH2 domains with R161L and S187T mutations alone and in combination and find that these substitutions are sufficient to convert the low affinity Abl SH2 domain to a higher affinity "Arg-like" SH2 domain in binding to a phospho-cortactin peptide.	Arginine	201-204	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-18
24891505-6	2014	We constructed Abl SH2 domains with R161L and S187T mutations alone and in combination and find that these substitutions are sufficient to convert the low affinity Abl SH2 domain to a higher affinity "Arg-like" SH2 domain in binding to a phospho-cortactin peptide.	Arginine	201-204	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	164-167
24891505-7	2014	We crystallized the Arg SH2 domain for structural comparison to existing crystal structures of the Abl SH2 domain.	Arginine	20-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-102
24891505-9	2014	Finally, we expressed Arg containing an "Abl-like" low affinity mutant Arg SH2 domain (L207R/T233S) and find that this mutant, although properly localized to the cell periphery, does not support wild type levels of cell edge protrusion.	Arginine	22-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-44
24891505-9	2014	Finally, we expressed Arg containing an "Abl-like" low affinity mutant Arg SH2 domain (L207R/T233S) and find that this mutant, although properly localized to the cell periphery, does not support wild type levels of cell edge protrusion.	Arginine	71-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-44
24711212-1	2014	Bosutinib is an orally active, dual Src/Abl tyrosine kinase inhibitor for treatment of chronic myeloid leukemia (CML) following resistance/intolerance to prior therapy.	bosutinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-43
24759597-5	2014	However, we found a synergistic interaction between SAHA and S116836 in Bcr-Abl-positive CML cells that were sensitive or resistant to IM.	Vorinostat	52-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
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 Mesylate	263-271	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-101
24143950-3	2014	RESULTS: Therapeutic options for front-line treatment have increased with the approval of two second-generation BCR-ABL inhibitors, dasatinib and nilotinib.	Dasatinib	132-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
24143950-3	2014	RESULTS: Therapeutic options for front-line treatment have increased with the approval of two second-generation BCR-ABL inhibitors, dasatinib and nilotinib.	nilotinib	146-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
24364873-0	2014	Uptake of imatinib-loaded polyelectrolyte complexes by BCR-ABL(+) cells: a long-acting drug-delivery strategy for targeting oncoprotein activity.	Imatinib Mesylate	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 Mesylate	21-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
24364873-6	2014	RESULTS & DISCUSSION: Polyelectrolyte complexes promoted a long-acting BCR-ABL kinase inactivation that was necessary to promote apoptosis at approximately twofold lower intracellular IM dose compared with the microscale formulation polyelectrolyte microcapsules.	Adenosine Monophosphate	9-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
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 Mesylate	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-133
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.	nilotinib	55-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-133
24715717-4	2014	Notably, the two most active compounds promoted the translocation of c-Abl and FOXO pro-apoptotic factors into the nucleus and sensitized multidrug-resistant cancer cells to apoptotic inducers such as doxorubicin and the pan-Akt inhibitor GSK690693, thus becoming valuable lead candidates for further optimization.	GSK690693	239-248	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-74
24967705-0	2014	ATRA-induced cellular differentiation and CD38 expression inhibits acquisition of BCR-ABL mutations for CML acquired resistance.	Tretinoin	0-4	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
24967705-4	2014	Forced myeloid differentiation by all-trans-retinoic acid (ATRA) effectively blocked acquisition of BCR-ABL mutations and resistance to the TKIs imatinib, nilotinib or dasatinib in our previously described in vitro models of acquired TKI resistance.	Tretinoin	34-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
24967705-4	2014	Forced myeloid differentiation by all-trans-retinoic acid (ATRA) effectively blocked acquisition of BCR-ABL mutations and resistance to the TKIs imatinib, nilotinib or dasatinib in our previously described in vitro models of acquired TKI resistance.	Tretinoin	59-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
24967705-7	2014	Consequently, ATRA treatment decreased DNA damage repair and suppressed acquisition of BCR-ABL mutations.	Tretinoin	14-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
24928687-6	2014	RESULTS: Total and protein specific pTyr levels on ABL, SHC, ERK2 and PI3K proteins were detected and samples of control and treated cells were distinguished at the pTyr level using this novel approach.	Phosphotyrosine	36-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-54
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 Mesylate	58-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-46
24863063-0	2014	Imatinib inhibits VEGF-independent angiogenesis by targeting neuropilin 1-dependent ABL1 activation in endothelial cells.	Imatinib Mesylate	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 Mesylate	109-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-153
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-24
24392933-10	2014	Treatment with the c-Abl pharmacological inhibitors, imatinib and GNF-5, had similar effects.	GNF-5	66-71	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.	n-morpholino	36-48	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 Mesylate	219-227	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
24629639-0	2014	ApoptomiRs expression modulated by BCR-ABL is linked to CML progression and imatinib resistance.	Imatinib Mesylate	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
24629639-4	2014	Phosphotyrosine and c-ABL expressions in HL-60.BCR-ABL cells treated with TKI were done by Western blot.	Phosphotyrosine	0-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
24726617-0	2014	Imatinib inhibits the expression of SCO2 and FRATAXIN genes that encode mitochondrial proteins in human Bcr-Abl+ leukemia cells.	Imatinib Mesylate	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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
24680705-0	2014	Down-regulation of miR-199b associated with imatinib drug resistance in 9q34.1 deleted BCR/ABL positive CML patients.	Imatinib Mesylate	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
24412932-6	2014	In vitro studies demonstrate that c-Abl directly interacts with alpha-syn and catalyzes its phosphorylation mainly at tyrosine 39 (pY39) and to a lesser extent at tyrosine 125 (pY125).	Tyrosine	118-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-39
24412932-6	2014	In vitro studies demonstrate that c-Abl directly interacts with alpha-syn and catalyzes its phosphorylation mainly at tyrosine 39 (pY39) and to a lesser extent at tyrosine 125 (pY125).	py39	131-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-39
24412932-6	2014	In vitro studies demonstrate that c-Abl directly interacts with alpha-syn and catalyzes its phosphorylation mainly at tyrosine 39 (pY39) and to a lesser extent at tyrosine 125 (pY125).	Tyrosine	163-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-39
24412932-6	2014	In vitro studies demonstrate that c-Abl directly interacts with alpha-syn and catalyzes its phosphorylation mainly at tyrosine 39 (pY39) and to a lesser extent at tyrosine 125 (pY125).	py125	177-182	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-39
24412932-9	2014	Interestingly, nilotinib, a specific inhibitor of c-Abl kinase activity, induces alpha-syn protein degradation via the autophagy and proteasome pathways, whereas the overexpression of alpha-syn in the rat midbrains enhances c-Abl expression.	nilotinib	15-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-55
24412932-9	2014	Interestingly, nilotinib, a specific inhibitor of c-Abl kinase activity, induces alpha-syn protein degradation via the autophagy and proteasome pathways, whereas the overexpression of alpha-syn in the rat midbrains enhances c-Abl expression.	nilotinib	15-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	224-229
24317448-5	2014	We further demonstrate that BCR-ABL physically interacts with and phosphorylates HAUSP on tyrosine residues to trigger its activity.	Tyrosine	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
24975338-0	2014	[Successful treatment with dasatinib for polycythemia vera patient emerging BCR-ABL positive clone during 13 years of treatment].	Dasatinib	27-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
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 Mesylate	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
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 Mesylate	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
24836440-5	2014	Although BCR-ABL induces STAT5-tyrosine phosphorylation independent of JAK2-kinase activity, BCR-ABL is less efficient in inducing active STAT5A:STAT5B-heterodimerization than IL-3, leaving constitutive STAT5A and STAT5B-homodimerization unaffected.	Tyrosine	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
24836440-8	2014	Finally, RNAi targeting STAT5B but not STAT5A sensitizes human BCR-ABL-positive cell lines to imatinib-treatment.	Imatinib Mesylate	94-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
24657894-2	2014	Myeloid progenitors express the fusion oncogene BCR-ABL, which has uncontrollable activity in malignant cells and prevents the cell apoptosis caused by some antineoplastic agents, such as paclitaxel.	Paclitaxel	188-198	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
24657894-7	2014	KEY FINDINGS: The effects of the tyrosine kinase inhibitor AG1024 were evaluated with regard to the regulation of BCR-ABL expression, inhibition of cell proliferation, and enhanced paclitaxel-induced apoptosis in BCR-ABL-expressing K562 cell lines.	tyrphostin AG 1024	59-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
24657894-7	2014	KEY FINDINGS: The effects of the tyrosine kinase inhibitor AG1024 were evaluated with regard to the regulation of BCR-ABL expression, inhibition of cell proliferation, and enhanced paclitaxel-induced apoptosis in BCR-ABL-expressing K562 cell lines.	tyrphostin AG 1024	59-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	213-220
24657894-7	2014	KEY FINDINGS: The effects of the tyrosine kinase inhibitor AG1024 were evaluated with regard to the regulation of BCR-ABL expression, inhibition of cell proliferation, and enhanced paclitaxel-induced apoptosis in BCR-ABL-expressing K562 cell lines.	Paclitaxel	181-191	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	213-220
24786396-0	2014	The c-Abl inhibitor, nilotinib, protects dopaminergic neurons in a preclinical animal model of Parkinson"s disease.	nilotinib	21-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-9
24786396-1	2014	c-Abl is activated in the brain of Parkinson"s disease (PD) patients and in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-intoxicated mice where it inhibits parkin through tyrosine phosphorylation leading to the accumulation of parkin substrates, and neuronal cell death.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	76-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
24786396-1	2014	c-Abl is activated in the brain of Parkinson"s disease (PD) patients and in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-intoxicated mice where it inhibits parkin through tyrosine phosphorylation leading to the accumulation of parkin substrates, and neuronal cell death.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	122-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
24786396-1	2014	c-Abl is activated in the brain of Parkinson"s disease (PD) patients and in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-intoxicated mice where it inhibits parkin through tyrosine phosphorylation leading to the accumulation of parkin substrates, and neuronal cell death.	Tyrosine	178-186	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
24330598-0	2014	Design, synthesis and biological evaluation of pyridin-3-yl pyrimidines as potent Bcr-Abl inhibitors.	pyridin-3-yl pyrimidines	47-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
24330598-1	2014	A series of pyridin-3-yl pyrimidines was synthesized and evaluated for their Bcr-Abl inhibitory and anticancer activity.	pyridin-3-yl pyrimidines	12-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
24330598-3	2014	Compounds A2, A8, and A9 exhibited potent Bcr-Abl inhibitory activity, suggesting that aniline containing halogen substituents might be important for biological activity.	aniline	87-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
24330598-3	2014	Compounds A2, A8, and A9 exhibited potent Bcr-Abl inhibitory activity, suggesting that aniline containing halogen substituents might be important for biological activity.	Halogens	106-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
24552773-3	2014	The purpose of this investigation was aimed at exploring whether ponatinib (AP24534), a novel effective TKI against T315I Bcr-Abl, was active against D816V KIT.	ponatinib	65-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
24552773-3	2014	The purpose of this investigation was aimed at exploring whether ponatinib (AP24534), a novel effective TKI against T315I Bcr-Abl, was active against D816V KIT.	ponatinib	76-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
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 Mesylate	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
24855825-2	2014	The BCR-ABL tyrosine kinase inhibitor imatinib is the standard treatment for CML.	Imatinib Mesylate	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
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 Mesylate	109-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
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 Mesylate	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.	nilotinib	59-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-16
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 Mesylate	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-180
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.	nilotonib	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-180
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 Mesylate	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
24775308-0	2014	Combination of the ABL kinase inhibitor imatinib with the Janus kinase 2 inhibitor TG101348 for targeting residual BCR-ABL-positive cells.	Fedratinib	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
24597676-0	2014	Exploring the chemical space around the privileged pyrazolo[3,4-d]pyrimidine scaffold: toward novel allosteric inhibitors of T315I-mutated Abl.	pyrazolo(3,4-d)pyrimidine	51-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-142
24569990-4	2014	We identify the damage-inducible kinase, c-Abl, as the PKCdelta Tyr-155 kinase and c-Src as the Tyr-64 kinase.	Tyrosine	64-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-46
24569990-4	2014	We identify the damage-inducible kinase, c-Abl, as the PKCdelta Tyr-155 kinase and c-Src as the Tyr-64 kinase.	Tyrosine	96-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-46
24569990-5	2014	Depletion of c-Abl or c-Src with shRNA decreased irradiation- and etoposide-induced apoptosis, suggesting that inhibitors of these kinases may be useful therapeutically.	Etoposide	66-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-18
24569990-7	2014	Expression of "gate-keeper" mutants of c-Abl or c-Src that are active in the presence of dasatinib restored phosphorylation of PKCdelta at Tyr-155 and Tyr-64, respectively.	Dasatinib	89-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-44
24569990-7	2014	Expression of "gate-keeper" mutants of c-Abl or c-Src that are active in the presence of dasatinib restored phosphorylation of PKCdelta at Tyr-155 and Tyr-64, respectively.	Tyrosine	139-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-44
24569990-7	2014	Expression of "gate-keeper" mutants of c-Abl or c-Src that are active in the presence of dasatinib restored phosphorylation of PKCdelta at Tyr-155 and Tyr-64, respectively.	Tyrosine	151-154	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-44
24569990-8	2014	Imatinib, a c-Abl-selective inhibitor, also specifically blocked PKCdelta Tyr-155 phosphorylation.	Imatinib Mesylate	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.	Tyrosine	74-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-17
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
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.	Dasatinib	90-99	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 Mesylate	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
24674874-2	2014	We evaluated bosutinib, a dual Src/Abl tyrosine kinase inhibitor that has previously demonstrated some antitumor activity in BC, plus letrozole as first-line endocrine therapy in locally advanced or metastatic HR+/HER2- BC.	bosutinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
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 Mesylate	153-170	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
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 Mesylate	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.	Sirolimus	64-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	164-171
24651611-8	2014	Furthermore, nilotinib was less effective in blocking the phosphorylation of Bcr-Abl and CrkL (a substrate of Bcr-Abl kinase) in CD34+CD38- cells.	nilotinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
24651611-8	2014	Furthermore, nilotinib was less effective in blocking the phosphorylation of Bcr-Abl and CrkL (a substrate of Bcr-Abl kinase) in CD34+CD38- cells.	nilotinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
23542172-0	2014	The Ron receptor tyrosine kinase activates c-Abl to promote cell proliferation through tyrosine phosphorylation of PCNA in breast cancer.	Tyrosine	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-48
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 Mesylate	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-94
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 Mesylate	170-178	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
24408322-5	2014	Resistance could be overcome with ponatinib, a multikinase inhibitor that targets BCR-ABL and FGF receptor.	ponatinib	34-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
24487968-0	2014	Curcumin derivative C817 inhibits proliferation of imatinib-resistant chronic myeloid leukemia cells with wild-type or mutant Bcr-Abl in vitro.	Curcumin	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
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 Mesylate	51-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
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 Mesylate	125-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
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 Mesylate	120-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
24346354-6	2014	We also found that BCR/ABL transcript leads to higher levels of ROS in accelerated and blastic CML phases.	Reactive Oxygen Species	64-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
24500518-2	2014	Inhibition of BCR-ABL using Abl-specific kinase inhibitors (TKI) such as imatinib induces remarkable clinical responses.	Imatinib Mesylate	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
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 Mesylate	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
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.	nilotinib	46-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
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.	Dasatinib	60-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
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 Mesylate	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 Mesylate	141-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
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 Mesylate	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
24297701-0	2014	BCR-ABL residues interacting with ponatinib are critical to preserve the tumorigenic potential of the oncoprotein.	ponatinib	34-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
24297701-6	2014	Molecular dynamics simulations of BCR-ABL(I360T) revealed differences in both helix alphaC dynamics and protein-correlated motions, consistent with a modified ATP-binding pocket.	Adenosine Triphosphate	159-162	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
24623669-6	2014	In the temporal neocortex of pilocarpine-treated rats, upregulation of total and phosphorylated c-Abl began 6 hours after seizures, with relatively high expression for 60 days.	Pilocarpine	29-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-101
24763825-0	2014	Incidence of Bcr-Abl kinase domain mutations in imatinib refractory chronic myeloid leukemia patients from South India.	Imatinib Mesylate	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 Mesylate	89-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
24657654-0	2014	HS-438, a new inhibitor of imatinib-resistant BCR-ABL T315I mutation in chronic myeloid leukemia.	1-(2-hydroxyethyl)-3-(6-(2-methoxyphenyl)benzo(d)thiazol-2-yl)urea	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
24657654-0	2014	HS-438, a new inhibitor of imatinib-resistant BCR-ABL T315I mutation in chronic myeloid leukemia.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	99-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
24657654-3	2014	In the present study, we synthesized a novel BCR-ABL inhibitor, HS-438, and identified its anti-leukemic effects in vitro and in vivo.	1-(2-hydroxyethyl)-3-(6-(2-methoxyphenyl)benzo(d)thiazol-2-yl)urea	64-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
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.	1-(2-hydroxyethyl)-3-(6-(2-methoxyphenyl)benzo(d)thiazol-2-yl)urea	14-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
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.	1-(2-hydroxyethyl)-3-(6-(2-methoxyphenyl)benzo(d)thiazol-2-yl)urea	14-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
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.	1-(2-hydroxyethyl)-3-(6-(2-methoxyphenyl)benzo(d)thiazol-2-yl)urea	14-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
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 Mesylate	193-201	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
24657654-7	2014	In summary, we suggest that HS-438 may be a novel drug candidate with the therapeutic potential to target BCR-ABL and overcome imatinib resistance in patients with CML.	1-(2-hydroxyethyl)-3-(6-(2-methoxyphenyl)benzo(d)thiazol-2-yl)urea	28-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
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 Mesylate	139-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-56
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.	Dasatinib	152-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-56
24768818-7	2014	P-loop residues in DDR1 that confer drug resistance in ABL are therefore accommodated outside the ATP pocket.	Adenosine Triphosphate	98-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-58
24768818-8	2014	Whereas imatinib and ponatinib bind potently to both the DDR and ABL kinases, the hydrophobic interactions of the ABL P-loop appear poorly satisfied by DDR1-IN-1 suggesting a structural basis for its DDR1 selectivity.	ponatinib	21-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-68
24691568-6	2014	With subsequent molecular dynamic (MD) simulation and MM/GBSA binding free energy calculation and energy decomposition, we identified chlorhexidine and sorafenib as potential "new use" drugs targeting wild-type ABL1, while nicergoline and plerixafor targeted T315I ABL1.	Chlorhexidine	134-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	211-215
24691568-6	2014	With subsequent molecular dynamic (MD) simulation and MM/GBSA binding free energy calculation and energy decomposition, we identified chlorhexidine and sorafenib as potential "new use" drugs targeting wild-type ABL1, while nicergoline and plerixafor targeted T315I ABL1.	Chlorhexidine	134-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	265-269
24691568-6	2014	With subsequent molecular dynamic (MD) simulation and MM/GBSA binding free energy calculation and energy decomposition, we identified chlorhexidine and sorafenib as potential "new use" drugs targeting wild-type ABL1, while nicergoline and plerixafor targeted T315I ABL1.	Sorafenib	152-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	211-215
24691568-6	2014	With subsequent molecular dynamic (MD) simulation and MM/GBSA binding free energy calculation and energy decomposition, we identified chlorhexidine and sorafenib as potential "new use" drugs targeting wild-type ABL1, while nicergoline and plerixafor targeted T315I ABL1.	Sorafenib	152-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	265-269
24691568-7	2014	Meanwhile, we also found that residues located in the ATP-binding site and A-loop motif played key roles in drug discovery towards ABL1.	Adenosine Triphosphate	54-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-135
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 Mesylate	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
24835010-2	2014	Imatinib specifically inhibits the tyrosine kinase, c-Abl.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-57
24835010-7	2014	Unexpectedly, high concentrations of glucose significantly induced c-Abl expression, suggesting c-Abl may play a role in balancing insulin production during glucose stimulation.	Glucose	37-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-72
24835010-7	2014	Unexpectedly, high concentrations of glucose significantly induced c-Abl expression, suggesting c-Abl may play a role in balancing insulin production during glucose stimulation.	Glucose	37-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-101
24835010-7	2014	Unexpectedly, high concentrations of glucose significantly induced c-Abl expression, suggesting c-Abl may play a role in balancing insulin production during glucose stimulation.	Glucose	157-164	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-101
24445143-4	2014	We report that IRF5 is expressed in CML cells, where it interacts with the BCR-ABL kinase that modulates its expression and induces its tyrosine phosphorylation.	Tyrosine	136-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
24445143-6	2014	Interestingly, a mutant devoid of a BCR-ABL consensus site (IRF5(Y104F)) still presented significant tyrosine phosphorylation.	Tyrosine	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
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 Mesylate	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 Mesylate	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 Mesylate	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
24378532-4	2014	Furthermore, using a high-throughput src homology 2 (SH2) domain binding assay, the SH2 domain of ABL1 and the PI 3-kinse regulator subunit (PIK3R3) were identified as candidates for the binding partner of tyrosine-phosphorylated PLEKHG2.	Tyrosine	206-214	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-102
24464935-2	2014	We previously found that H2O2-induced death of astrocytes is mediated by cAbl in a metallothionein-3 (Mt3)-dependent manner.	Hydrogen Peroxide	25-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-77
24464935-6	2014	STI571, an inhibitor of cAbl, blocked induction/activation of Mst1 and H2O2-induced cell death.	Imatinib Mesylate	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.	Hydrogen Peroxide	71-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-28
24464935-8	2014	The zinc chelator TPEN blocked induction/activation of cAbl and Mst1, indicating that these phenomena are dependent on the rise of intracellular zinc.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	18-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-59
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 Mesylate	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 Mesylate	13-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
24566825-10	2014	Bufalin may also induce K562 cell apoptosis via downregulating BCR/ABL expression levels, and this pathway may be independent of the BMI-1 pathway.	bufalin	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
24481648-4	2014	Ponatinib, a multi-targeted TKI, inhibits the activity of BCR-ABL with very high potency and broad specificity, including the T315I mutation which confers resistance to other TKIs.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
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 Mesylate	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-37
24658113-6	2014	More interestingly, we demonstrate EphA4/c-Abl activation is a key-signalling event that mediates the synaptic damage induced by AbetaOs.	abetaos	129-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-46
24550450-5	2014	ADP treatment promoted the H2O2-dependent phosphorylation of c-Abl, a nonreceptor tyrosine kinase that modulates the actin cytoskeleton.	Adenosine Diphosphate	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-66
24550450-5	2014	ADP treatment promoted the H2O2-dependent phosphorylation of c-Abl, a nonreceptor tyrosine kinase that modulates the actin cytoskeleton.	Hydrogen Peroxide	27-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-66
24550450-7	2014	However, Rac1-dependent activation of AMP-activated protein kinase, the signaling phospholipid phosphatidylinositol-(4, 5)-bisphosphate, and the c-Abl-interacting protein CrkII are mediated by H2O2.	Hydrogen Peroxide	193-197	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-150
24119291-1	2014	A novel series of pazopanib derivatives were designed, synthesized, and evaluated for their inhibitory activity against a series of kinases including VEGFR-2, EGFR, AKT1, ALK1, and ABL1.	pazopanib	18-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	181-185
24480037-0	2014	Serine and proline-rich ligands enriched via phage-display technology show preferential binding to BCR/ABL expressing cells.	Serine	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
24480037-0	2014	Serine and proline-rich ligands enriched via phage-display technology show preferential binding to BCR/ABL expressing cells.	Proline	11-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
24480037-7	2014	These peptides contained either multiple proline residues or serine/threonine-proline pairs and showed a confirmed binding preference for BCR/ABL+ fibroblasts.	Serine	61-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
24480037-7	2014	These peptides contained either multiple proline residues or serine/threonine-proline pairs and showed a confirmed binding preference for BCR/ABL+ fibroblasts.	Threonine	68-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
24480037-7	2014	These peptides contained either multiple proline residues or serine/threonine-proline pairs and showed a confirmed binding preference for BCR/ABL+ fibroblasts.	Proline	78-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
24333114-0	2014	Nilotinib 300 mg BID as frontline treatment of CML: prospective analysis of the Xpert BCR-ABL monitor system and significance of 3-month molecular response.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
24333704-3	2014	Among the reagents tested, D-gluconic acid sodium salt gave the best overall signal to noise (S/N) values for the indirect detection of p-Abltide, the product of Abl1 enzymatic reaction.	SODIUM GLUCONATE	27-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-166
24333704-3	2014	Among the reagents tested, D-gluconic acid sodium salt gave the best overall signal to noise (S/N) values for the indirect detection of p-Abltide, the product of Abl1 enzymatic reaction.	p-abltide	136-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-166
23734655-3	2014	This study was carried out to investigate how to improve the anticancer effects of alpha-mangostin in chronic myeloid leukemia (CML) cell lines bearing wild-type BCR-ABL or BCR-ABL-T315I mutation.	mangostin	83-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-169
23734655-3	2014	This study was carried out to investigate how to improve the anticancer effects of alpha-mangostin in chronic myeloid leukemia (CML) cell lines bearing wild-type BCR-ABL or BCR-ABL-T315I mutation.	mangostin	83-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	173-180
24263804-0	2014	PAK-dependent STAT5 serine phosphorylation is required for BCR-ABL-induced leukemogenesis.	Serine	20-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
24263804-3	2014	We have investigated the importance of STAT5 serine phosphorylation for BCR-ABL-induced leukemogenesis.	Serine	45-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
24345751-1	2014	Bosutinib is an oral, dual SRC/ABL tyrosine kinase inhibitor (TKI) with clinical activity in Philadelphia chromosome-positive (Ph(+)) leukemia.	bosutinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-34
27485688-0	2014	Theoretical Studies on Pyrazolo[3,4-d]pyrimidine Derivatives as Potent Dual c-Src/Abl Inhibitors Using 3D-QSAR and Docking Approaches.	pyrazolo(3,4-d)pyrimidine	23-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-85
27485688-2	2014	In this paper, three-dimensional quantitative structure-activity relationship and docking studies were performed on 87 pyrazolo[3,4-d]pyrimidines as dual Src/Abl inhibitors.	pyrazolo(3,4-d)pyrimidine	119-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-161
24527087-8	2014	Western blot analysis and protein tyrosine kinase activity assays showed that imatinib inhibited BCR-ABL protein tyrosine kinase activity.	Imatinib Mesylate	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
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 Mesylate	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-124
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 Mesylate	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
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 Mesylate	143-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
24100660-0	2014	Efficacy of the dual PI3K and mTOR inhibitor NVP-BEZ235 in combination with nilotinib against BCR-ABL-positive leukemia cells involves the ABL kinase domain mutation.	nilotinib	76-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
24420842-1	2014	Bosutinib (Bosulif ) is an orally administered small molecule tyrosine kinase inhibitor (TKI) of BCR-ABL and SRC family kinases.	bosutinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
24420842-1	2014	Bosutinib (Bosulif ) is an orally administered small molecule tyrosine kinase inhibitor (TKI) of BCR-ABL and SRC family kinases.	bosutinib	11-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
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 Mesylate	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.	dactolisib	23-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
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.	Doxorubicin	121-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-94
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.	Doxorubicin	72-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-160
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 Mesylate	178-184	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-160
24490604-1	2014	The SRC-ABL inhibitor bosutinib is one of the five tyrosine kinase inhibitors currently approved for the treatment of Philadelphia chromosome-positive leukemias.	bosutinib	22-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-11
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 Mesylate	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 Mesylate	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 Mesylate	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-30
24258348-4	2014	To overcome this resistance, four second-generation ATP competitive ABL TKIs, dasatinib, nilotinib, bosutinib and bafetinib, have been developed.	Adenosine Triphosphate	52-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-71
24258348-4	2014	To overcome this resistance, four second-generation ATP competitive ABL TKIs, dasatinib, nilotinib, bosutinib and bafetinib, have been developed.	Dasatinib	78-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-71
24258348-4	2014	To overcome this resistance, four second-generation ATP competitive ABL TKIs, dasatinib, nilotinib, bosutinib and bafetinib, have been developed.	nilotinib	89-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-71
24258348-4	2014	To overcome this resistance, four second-generation ATP competitive ABL TKIs, dasatinib, nilotinib, bosutinib and bafetinib, have been developed.	bosutinib	100-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-71
24258348-4	2014	To overcome this resistance, four second-generation ATP competitive ABL TKIs, dasatinib, nilotinib, bosutinib and bafetinib, have been developed.	bafetinib	114-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-71
24258348-7	2014	Thus, a third-generation ABL TKI, ponatinib, was developed to inhibit all mutated BCR-ABL and showed clinical efficacy in CML cells harbouring T315I.	ponatinib	34-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-28
24258348-7	2014	Thus, a third-generation ABL TKI, ponatinib, was developed to inhibit all mutated BCR-ABL and showed clinical efficacy in CML cells harbouring T315I.	ponatinib	34-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
24280282-4	2014	Taken together, our data provide a rationale for the therapeutic combination of TKIs and Ruxolitinib with the aim to eradicate primary BCR-ABL+ cells homed in BM niches.	ruxolitinib	89-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
24100660-9	2014	Taken together, these results suggest that administration of the dual PI3K and mTOR inhibitor NVP-BEZ235 may be an effective strategy against BCR-ABL mutant cells and may enhance the cytotoxic effects of nilotinib in ABL TKI-resistant BCR-ABL mutant cells.	dactolisib	98-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
24100660-9	2014	Taken together, these results suggest that administration of the dual PI3K and mTOR inhibitor NVP-BEZ235 may be an effective strategy against BCR-ABL mutant cells and may enhance the cytotoxic effects of nilotinib in ABL TKI-resistant BCR-ABL mutant cells.	dactolisib	98-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	235-242
24100660-9	2014	Taken together, these results suggest that administration of the dual PI3K and mTOR inhibitor NVP-BEZ235 may be an effective strategy against BCR-ABL mutant cells and may enhance the cytotoxic effects of nilotinib in ABL TKI-resistant BCR-ABL mutant cells.	nilotinib	204-213	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	235-242
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 Mesylate	141-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
24374144-0	2014	p-Stat3 and bcr/abl gene expression in chronic myeloid leukemia and their relation to imatinib therapy.	Imatinib Mesylate	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
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 Mesylate	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 Mesylate	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	165-172
24516334-3	2014	Omacetaxine mepesuccinate has been recently approved by the US Food and Drug Administration to treat patients with chronic myeloid leukemia who failed to respond to multiple tyrosine kinase inhibitors and/or acquired the BCR-ABL-T315I mutation.	Homoharringtonine	0-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	221-228
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 Mesylate	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-166
24475245-3	2014	Tyrosine phosphorylation of ArgBP2, mediated by c-Abl kinase and counterbalanced by PTP-PEST phosphatase, regulates many of its interactions.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-53
24311723-5	2014	At 3 and 6 months, the proportion of patients with BCR-ABL transcript levels <=10% was higher in the dasatinib arm.	Dasatinib	104-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
27774462-8	2014	Accordingly, leukemia stem cells of CML selected in low oxygen are refractory to the Bcr/Abl inhibitor imatinib mesylate.	Imatinib Mesylate	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.	Glucose	70-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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.	Oxygen	118-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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 Mesylate	229-246	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
24482808-8	2014	The assay correlated well with Asuragen"s BCR/ABL1 Quant  kit over a 6 log concentration range (r=0.9967).	asuragen	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-50
23962707-0	2014	Graphene sheets, polyaniline and AuNPs based DNA sensor for electrochemical determination of BCR/ABL fusion gene with functional hairpin probe.	Graphite	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
23962707-0	2014	Graphene sheets, polyaniline and AuNPs based DNA sensor for electrochemical determination of BCR/ABL fusion gene with functional hairpin probe.	polyaniline	17-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
24161787-0	2014	Andrographolide downregulates the v-Src and Bcr-Abl oncoproteins and induces Hsp90 cleavage in the ROS-dependent suppression of cancer malignancy.	andrographolide	0-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
24161787-8	2014	Notably, Hsp90 cleavage, decreased levels of Bcr-Abl (another known Hsp90 client protein), and the induction of apoptosis were also observed in human K562 leukemia cells treated with andrographolide or its active derivatives.	andrographolide	183-198	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
23208504-5	2014	Moreover, overexpression of miR-138 led to the downregulation of BCR-ABL.	mir-138	28-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
23208504-7	2014	Furthermore, miR-138 binding to ABL was shown to localize to the coding region instead of 3"-untranslated regions (3"-UTR) of ABL mRNA.	mir-138	13-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-35
23208504-11	2014	miR-138 represses expression of both BCR-ABL and CCND3 via binding to the coding region and 3"-UTR, respectively.	mir-138	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
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 Mesylate	163-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
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.	Phosphates	72-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
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.	Tyrosine	91-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
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 Mesylate	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	148-155
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 Mesylate	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 Mesylate	258-266	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
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 Mesylate	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
23387973-8	2014	Among genes up-regulated by Y15 and temozolomide more significantly than by each agent alone were: COX7B; interferon, gamma-inducible transcript: IFI16; DDIT4; GADD45G and down-regulated: KIF3A, AKT1; ABL; JAK1, GLI3 and ALDH1A3.	Temozolomide	36-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	201-204
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
25244981-5	2014	BCR-ABL and TEL-AML1 were shown to be associated with increased constitutive DSBs in various model systems.	dsbs	77-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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 Mesylate	6-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
25025064-0	2014	Efficacy and pharmacologic data of second-generation tyrosine kinase inhibitor nilotinib in BCR-ABL-positive leukemia patients with central nervous system relapse after allogeneic stem cell transplantation.	nilotinib	79-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
25025064-2	2014	Although second-generation tyrosine-kinase inhibitors (TKI) such as nilotinib have shown activity in systemic BCR-ABL(+) disease, little data exists on their penetration and efficacy within the CNS.	nilotinib	68-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
25025064-7	2014	Despite poor csf penetration, nilotinib showed significant clinical activity in CNS relapse of BCR-ABL(+) leukemias.	nilotinib	30-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
24280068-0	2014	Imatinib analogs as potential agents for PET imaging of Bcr-Abl and c-KIT expression at a kinase level.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
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 Mesylate	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 Mesylate	29-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	187-194
24955955-4	2014	We further characterized bosutinib, an FDA-approved Src/Abl inhibitor approved for chronic myelogenous leukemia.	bosutinib	25-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-59
25485495-4	2014	We demonstrated that the interference with cell metabolism (oxygen/glucose shortage) enriches cells exhibiting the leukemia stem cell (LSC) phenotype and, at the same time, suppresses BCR/Abl protein expression.	Oxygen	60-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	184-191
25485495-4	2014	We demonstrated that the interference with cell metabolism (oxygen/glucose shortage) enriches cells exhibiting the leukemia stem cell (LSC) phenotype and, at the same time, suppresses BCR/Abl protein expression.	Glucose	67-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	184-191
24963404-4	2014	Imatinib, an oral targeted therapy, inhibits tyrosine kinases specifically BCR-ABL, c-KIT, and PDGFRA.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
24334603-0	2014	Gambogic acid induces apoptosis in imatinib-resistant chronic myeloid leukemia cells via inducing proteasome inhibition and caspase-dependent Bcr-Abl downregulation.	gambogic acid	0-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
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 Mesylate	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 Mesylate	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.	gambogic acid	9-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
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 Mesylate	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 Mesylate	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.	gambogic acid	156-169	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 Mesylate	217-225	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-112
24850316-1	2014	The aim of this study is to investigate the metabolic (cytochrome P450-dependent) behaviour of pyrazolo[3,4-d]pyrimidines 1-10 dual Abl/Src kinase inhibitors.	pyrazolo(3,4-d)pyrimidine	95-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-135
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 Mesylate	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	280-284
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 Mesylate	131-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
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 Mesylate	197-214	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-146
24598651-0	2014	[Early monitoring drug-resistance of patients with BCR/ABL(+) ALL by DCDF-FISH].	dcdf	69-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
24598651-7	2014	It is concluded that the BCR/ABL (+) leukemia patient with complex translocation has multiple tumor cell subsets, and the responses of different cell subsets to the treatment are different, therefore the response to therapy and drug resistance of patient can be monitored early by the signal model of DCDF-FISH and the observation of dynamical changes of different cell subset.	dcdf	301-305	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
24919837-1	2014	Bosutinib is an orally active, competitive inhibitor of Src/Abl tyrosine kinases.	bosutinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-63
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 Mesylate	104-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	148-155
25006277-2	2014	Shortly thereafter, more potent BCR-ABL inhibitors (dasatinib and nilotinib) were introduced for use in patients resistant to or intolerant of imatinib.	Dasatinib	52-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
25006277-2	2014	Shortly thereafter, more potent BCR-ABL inhibitors (dasatinib and nilotinib) were introduced for use in patients resistant to or intolerant of imatinib.	nilotinib	66-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
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 Mesylate	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 Mesylate	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
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 Mesylate	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 Mesylate	103-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
23989453-6	2014	Among the validated hits, the well-tolerated antimalarial drug dihydroartemisinin (DHA) displayed potent activity in vitro and modest in vivo monotherapy activity against engineered murine BCR-ABL-KI-resistant Ph+ ALL.	artenimol	63-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	189-196
23989453-7	2014	Strikingly, cotreatment with DHA and dasatinib in vivo strongly reduced primary leukemia burden and improved long-term survival in a murine model that faithfully captures the BCR-ABL-KI-resistant phenotype of human Ph+ ALL.	Dasatinib	37-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-182
25501110-1	2014	Dasatinib is a BCR-ABL kinase inhibitor with improved potency compared with imatinib, for which efficacy and safety in imatinib-resistant and imatinib-intolerant patients with chronic myelogenous leukemia (CML) have been established.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
25501110-8	2014	A lower level of BCR-ABL transcript at 1 or 3 months after the initiation of dasatinib treatment was more strongly correlated with the BCR-ABL transcript level at 12 and 18 months (p < 0.001) than a higher level of BCR-ABL.	Dasatinib	77-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
25501110-8	2014	A lower level of BCR-ABL transcript at 1 or 3 months after the initiation of dasatinib treatment was more strongly correlated with the BCR-ABL transcript level at 12 and 18 months (p < 0.001) than a higher level of BCR-ABL.	Dasatinib	77-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
25501110-8	2014	A lower level of BCR-ABL transcript at 1 or 3 months after the initiation of dasatinib treatment was more strongly correlated with the BCR-ABL transcript level at 12 and 18 months (p < 0.001) than a higher level of BCR-ABL.	Dasatinib	77-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
25116401-1	2014	PURPOSE: Nilotinib is a selective tyrosine kinase inhibitor of c-Kit, Abl and platelet-derived growth factor receptor-alpha/beta.	nilotinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-73
25171229-1	2014	BACKGROUND: Imatinib is a tyrosine kinase inhibitor of BCR-ABL, ABL, PDGFR-alpha and -beta, KIT, and DDR.	Imatinib Mesylate	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
25171229-1	2014	BACKGROUND: Imatinib is a tyrosine kinase inhibitor of BCR-ABL, ABL, PDGFR-alpha and -beta, KIT, and DDR.	Imatinib Mesylate	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-62
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	287-294
24734217-1	2014	Dasatinib (DAS) is a potent inhibitor of the BCR-ABL, SRC, c-KIT, PDGFR, and ephrin tyrosine kinases that has demonstrated only modest clinical efficacy in melanoma patients.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
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 Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-142
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 Mesylate	213-221	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
24756784-1	2014	Dasatinib is an orally available short-acting dual ABL/SRC tyrosine kinase inhibitor (TKI).	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-54
24756784-5	2014	Dasatinib inhibits BCR-ABL with greater potency compared with other BCR-ABL inhibitors and is active in CML resistant or intolerant to imatinib.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
24756784-5	2014	Dasatinib inhibits BCR-ABL with greater potency compared with other BCR-ABL inhibitors and is active in CML resistant or intolerant to imatinib.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
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.	nilotinib	20-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
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 Mesylate	202-210	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
24756786-2	2014	In addition, the BCR-ABL fusion gene product, a constitutively activated tyrosine kinase which is crucial for the development of chronic myeloid leukemia (CML), is highly sensitive to bosutinib.	bosutinib	184-193	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
24756786-3	2014	Interestingly, distinctly lower concentrations of bosutinib are required to ablate BCR-ABL phosphorylation when compared to the first-generation tyrosine kinase inhibitor imatinib (IM).	bosutinib	50-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
24756786-5	2014	Remarkably, bosutinib has been found to be capable of overcoming the majority of IM-resistant BCR-ABL mutations.	bosutinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
24756787-9	2014	In conclusion, ponatinib has proved to be a powerful BCR-ABL inhibitor, which exhibits clinical activity both in BCR-ABL wild-type and mutant CML, including activity against the T315I mutation.	ponatinib	15-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
24756787-9	2014	In conclusion, ponatinib has proved to be a powerful BCR-ABL inhibitor, which exhibits clinical activity both in BCR-ABL wild-type and mutant CML, including activity against the T315I mutation.	ponatinib	15-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
24106839-0	2013	Conformation-selective inhibitors reveal differences in the activation and phosphate-binding loops of the tyrosine kinases Abl and Src.	Phosphates	75-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-126
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-77
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 Mesylate	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-77
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.	Adenosine Triphosphate	198-201	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.	Adenosine Triphosphate	72-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-212
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 Mesylate	166-174	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-212
24106839-8	2013	In attempting to explain this observation, we have uncovered an unexpected correlation between Abl"s activation loop and another flexible active site feature, called the phosphate-binding loop (p-loop).	Phosphates	170-179	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-98
24041959-5	2013	Adriamycin-induced DNA damage together with leptomycin B treatment accumulates c-Abl into the nucleus and increases the levels of nuclear F-actin.	Doxorubicin	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-84
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 Mesylate	208-216	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
24041959-5	2013	Adriamycin-induced DNA damage together with leptomycin B treatment accumulates c-Abl into the nucleus and increases the levels of nuclear F-actin.	leptomycin B	44-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-84
24041959-6	2013	Treatment of c-Abl-knockdown cells with Adriamycin and leptomycin B barely increases the nuclear F-actin levels.	Doxorubicin	40-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-18
24041959-6	2013	Treatment of c-Abl-knockdown cells with Adriamycin and leptomycin B barely increases the nuclear F-actin levels.	leptomycin B	55-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-18
24041959-7	2013	Expression of nuclear-targeted c-Abl (NLS-c-Abl) increases the levels of nuclear F-actin even without Adriamycin, and the increased levels of nuclear F-actin are not inhibited by inactivation of Abl kinase activity.	Doxorubicin	102-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-36
24041959-7	2013	Expression of nuclear-targeted c-Abl (NLS-c-Abl) increases the levels of nuclear F-actin even without Adriamycin, and the increased levels of nuclear F-actin are not inhibited by inactivation of Abl kinase activity.	Doxorubicin	102-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-47
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 Mesylate	181-189	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-163
24396109-5	2013	DATA SYNTHESIS: Bosutinib is a TKI of the breakpoint cluster region/Abelson murine leukemia (BCR-ABL) gene approved by the Food and Drug Administration on September 4, 2012, for second-line treatment of chronic phase, accelerated phase, and blast phase CML.	bosutinib	16-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
24396109-6	2013	In the second-line setting, bosutinib is effective in some patients with CML resistant or intolerant to imatinib, dasatinib, and/or nilotinib, but it is not effective in patients whose disease expresses the T315I point mutation in BCR-ABL.	bosutinib	28-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	231-238
24121479-0	2013	A novel antitumor piperazine alkyl compound causes apoptosis by inducing RhoB expression via ROS-mediated c-Abl/p38 MAPK signaling.	piperazine alkyl	18-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-111
24121479-0	2013	A novel antitumor piperazine alkyl compound causes apoptosis by inducing RhoB expression via ROS-mediated c-Abl/p38 MAPK signaling.	ros	93-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-111
24121479-5	2013	KR28 increased ROS production, leading to nuclear c-Abl expression, which in turn activated p38 mitogen-activated protein kinase (MAPK) to enhance the expression of RhoB, an apoptosis inducer.	ros	15-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-55
24121479-6	2013	The KR28-induced apoptosis was abrogated by the ROS scavenger N-acetylcysteine and by knockdown of c-Abl, p38 MAPK, or ATF2.	kr28	4-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-104
24121479-8	2013	CONCLUSION: The antitumor agent KR28 induces apoptosis of PC-3 cells by ROS-mediated RhoB expression via c-Abl upregulation and activation of p38 MAPK/ATF-2.	kr28	32-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-110
24121479-8	2013	CONCLUSION: The antitumor agent KR28 induces apoptosis of PC-3 cells by ROS-mediated RhoB expression via c-Abl upregulation and activation of p38 MAPK/ATF-2.	ros	72-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-110
24012954-2	2013	Here, we investigated the changes of protein profile in H2O2-induced DNA damage/repair in BaF3-MIGR1 and BaF3-BCR/ABL cells through a proteomic strategy consisting of two-dimensional gel electrophoresis (2-DE) coupled with MALDI-TOF mass spectrometry.	Hydrogen Peroxide	56-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
24012954-6	2013	We also proved that Apg-2 inhibition aggravated H2O2 induced damage in BCR/ABL positive cells, and enhanced the sensitivity of BaF3-BCR/ABL(T315I) to STI571.	Hydrogen Peroxide	48-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
24056763-6	2013	DNA damage-mediated tyrosine phosphorylation was required for MyoD recruitment to target genes, as the ABL phosphorylation-resistant MyoD mutant (MyoD Y30F) failed to bind the chromatin following DNA damage, while retaining the ability to activate transcription in response to differentiation signals.	Tyrosine	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-106
24012703-0	2013	Electrochemical determination of BCR/ABL fusion gene based on in situ synthesized gold nanoparticles and cerium dioxide nanoparticles.	ceric oxide	105-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
23701117-5	2013	BMS-354825 (dasatinib) and SKI-606 (bosutinib), second and third generation clinical SFK/ABL inhibitors, were found to be potent cytotoxic agents against tumorigenic cells with low toxicity to normal pediatric stem cells.	Dasatinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-92
23701117-5	2013	BMS-354825 (dasatinib) and SKI-606 (bosutinib), second and third generation clinical SFK/ABL inhibitors, were found to be potent cytotoxic agents against tumorigenic cells with low toxicity to normal pediatric stem cells.	bosutinib	27-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-92
23701117-5	2013	BMS-354825 (dasatinib) and SKI-606 (bosutinib), second and third generation clinical SFK/ABL inhibitors, were found to be potent cytotoxic agents against tumorigenic cells with low toxicity to normal pediatric stem cells.	bosutinib	36-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-92
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 Mesylate	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-13
24055812-7	2013	Phosporylations of the p85-bound Rho-GDP dissociation inhibitor-2 on 130 and 153 tyrosine residues by c-Abl and Src were required for the complex to be recruited to P-selectin glycoprotein ligand-1 and thereby regulate beta1 integrin-mediated T cell adhesion to vascular cell adhesion molecule-1.	Tyrosine	81-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-107
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).	nilotinib	36-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-13
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).	Dasatinib	51-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-13
23575252-1	2013	INTRODUCTION: ABL1 kinase mutations represent a major mechanism of imatinib resistance in Philadelphia-positive (Ph+) patients.	Imatinib Mesylate	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-18
23942795-1	2013	PURPOSE: Dasatinib is a dual Abl/Src tyrosine kinase inhibitor (TKI) designed as a prototypic short-acting BCR-ABL-targeted TKI that inhibits BCR-ABL with greater potency compared with imatinib, nilotinib, bosutinib, and ponatinib and has been shown to have potential immunomodulatory effects.	Dasatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-32
23942795-1	2013	PURPOSE: Dasatinib is a dual Abl/Src tyrosine kinase inhibitor (TKI) designed as a prototypic short-acting BCR-ABL-targeted TKI that inhibits BCR-ABL with greater potency compared with imatinib, nilotinib, bosutinib, and ponatinib and has been shown to have potential immunomodulatory effects.	Dasatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
23942795-1	2013	PURPOSE: Dasatinib is a dual Abl/Src tyrosine kinase inhibitor (TKI) designed as a prototypic short-acting BCR-ABL-targeted TKI that inhibits BCR-ABL with greater potency compared with imatinib, nilotinib, bosutinib, and ponatinib and has been shown to have potential immunomodulatory effects.	Dasatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
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.	Dasatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
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 Mesylate	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
23888935-1	2013	WHAT IS KNOWN AND OBJECTIVE: Ponatinib is a potent oral tyrosine kinase inhibitor with activity against BCR-ABL, the primary driver of chronic myeloid leukaemia and Philadelphia chromosome-positive acute lymphoblastic leukaemia.	ponatinib	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
24191057-1	2013	Successful treatment of chronic myelogenous leukemia is based on inhibitors binding to the ATP site of the deregulated breakpoint cluster region (Bcr)-Abelson tyrosine kinase (Abl) fusion protein.	Adenosine Triphosphate	91-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	176-179
24191057-2	2013	Recently, a new type of allosteric inhibitors targeting the Abl myristoyl pocket was shown in preclinical studies to overcome ATP-site inhibitor resistance arising in some patients.	Adenosine Triphosphate	126-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-63
24191057-3	2013	Using NMR and small-angle X-ray scattering, we have analyzed the solution conformations of apo Abelson tyrosine kinase (c-Abl) and c-Abl complexes with ATP-site and allosteric inhibitors.	Adenosine Triphosphate	152-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-125
24191057-3	2013	Using NMR and small-angle X-ray scattering, we have analyzed the solution conformations of apo Abelson tyrosine kinase (c-Abl) and c-Abl complexes with ATP-site and allosteric inhibitors.	Adenosine Triphosphate	152-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-136
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.	Adenosine Triphosphate	15-18	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.	Adenosine Triphosphate	15-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	181-188
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 Mesylate	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 Mesylate	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	181-188
24180494-1	2013	BACKGROUND: Ponatinib is a potent oral tyrosine kinase inhibitor of unmutated and mutated BCR-ABL, including BCR-ABL with the tyrosine kinase inhibitor-refractory threonine-to-isoleucine mutation at position 315 (T315I).	ponatinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
24180494-1	2013	BACKGROUND: Ponatinib is a potent oral tyrosine kinase inhibitor of unmutated and mutated BCR-ABL, including BCR-ABL with the tyrosine kinase inhibitor-refractory threonine-to-isoleucine mutation at position 315 (T315I).	ponatinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
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 Mesylate	89-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
24091918-8	2014	These results suggested that CTP-OD1 and CTP-OD2 may be an attractive therapeutic option to inhibit the activation of Bcr-Abl kinase in CML.	Cytidine Triphosphate	29-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
24091918-8	2014	These results suggested that CTP-OD1 and CTP-OD2 may be an attractive therapeutic option to inhibit the activation of Bcr-Abl kinase in CML.	Cytidine Triphosphate	41-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
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 Mesylate	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
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 Mesylate	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-15
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.	Glycerol	160-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-15
24012109-8	2013	Cell treatment with CX-4945, a CK2 inhibitor currently in clinical trials, counteracts CK2/Bcr-Abl interaction and causes cell death by apoptosis.	silmitasertib	20-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
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 Mesylate	144-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
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 Mesylate	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
24260231-4	2013	In cells expressing BCR/ABL, FLT3-ITD, or Jak2-V617F, etoposide induced a sustained activation of Chk1, thus leading to the G2/M arrest of cells.	Etoposide	54-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
24260231-6	2013	The PI3K inhibitor GD-0941 or the Akt inhibitor MK-2206 showed similar effects with imatinib on etoposide-treated BCR/ABL-expressing cells, including those expressing the imatinib-resistant T315I mutant, while expression of the constitutively activated Akt1-myr mutant conferred resistance to the combined treatment of etoposide and imatinib.	gd-0941	19-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
24260231-6	2013	The PI3K inhibitor GD-0941 or the Akt inhibitor MK-2206 showed similar effects with imatinib on etoposide-treated BCR/ABL-expressing cells, including those expressing the imatinib-resistant T315I mutant, while expression of the constitutively activated Akt1-myr mutant conferred resistance to the combined treatment of etoposide and imatinib.	MK 2206	48-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
24260231-6	2013	The PI3K inhibitor GD-0941 or the Akt inhibitor MK-2206 showed similar effects with imatinib on etoposide-treated BCR/ABL-expressing cells, including those expressing the imatinib-resistant T315I mutant, while expression of the constitutively activated Akt1-myr mutant conferred resistance to the combined treatment of etoposide and imatinib.	Etoposide	96-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
24236021-0	2013	Ponatinib is a pan-BCR-ABL kinase inhibitor: MD simulations and SIE study.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
24236021-2	2013	The inhibitors such as imatinib, dasatinib and nilotinib are effective drugs but are resistant to some BCR-ABL mutations.	Imatinib Mesylate	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
24236021-2	2013	The inhibitors such as imatinib, dasatinib and nilotinib are effective drugs but are resistant to some BCR-ABL mutations.	Dasatinib	33-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
24236021-2	2013	The inhibitors such as imatinib, dasatinib and nilotinib are effective drugs but are resistant to some BCR-ABL mutations.	nilotinib	47-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
24236021-3	2013	The pan-BCR-ABL kinase inhibitor ponatinib exhibits potent activity against native, T315I, and all other clinically relevant mutants, and showed better inhibition than the previously known inhibitors.	ponatinib	33-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-15
24236021-4	2013	We have studied the molecular dynamics simulations and calculated solvated interaction energies of native and fourteen mutant BCR-ABL kinases (M244V, G250E, Q252H, Y253F, Y253H, E255K, E255V, T315A, T315I, F317L, F317V, M351T, F359V and H396P) complexed with ponatinib.	ponatinib	259-268	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
24236021-5	2013	These studies revealed that the interactions between ponatinib and individual residues in BCR-ABL kinase are also affected due to the remote residue mutations.	ponatinib	53-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
24236021-7	2013	Our work provides the molecular mechanisms of native and mutant BCR-ABL kinases inhibition by ponatinib at atomic level that has not been studied before.	ponatinib	94-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
23318434-5	2013	On one hand, Abl indirectly enhanced phosphorylation of Myc on Ser 62 and Thr 58, its association with Pin1 and p300 and its acetylation by p300.	Serine	63-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
23318434-5	2013	On one hand, Abl indirectly enhanced phosphorylation of Myc on Ser 62 and Thr 58, its association with Pin1 and p300 and its acetylation by p300.	Threonine	74-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
23318434-7	2013	On the other hand, Abl interacted with the C-terminal domain of Myc and phosphorylated up to five tyrosine residues in its N-terminus, the principal of which was Y74.	Tyrosine	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-22
23318434-10	2013	Thus, our data unravel two potential effects of Abl on Myc: first, Abl signaling can indirectly augment acetylation of Myc by p300, and most likely also its transcriptional activity in the nucleus; second, Abl can directly phosphorylate Myc on tyrosine: the resulting form of Myc appears to be cytoplasmic, and its presence correlates with Abl activation in cancer.	Tyrosine	244-252	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-51
23318434-10	2013	Thus, our data unravel two potential effects of Abl on Myc: first, Abl signaling can indirectly augment acetylation of Myc by p300, and most likely also its transcriptional activity in the nucleus; second, Abl can directly phosphorylate Myc on tyrosine: the resulting form of Myc appears to be cytoplasmic, and its presence correlates with Abl activation in cancer.	Tyrosine	244-252	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-70
23318434-10	2013	Thus, our data unravel two potential effects of Abl on Myc: first, Abl signaling can indirectly augment acetylation of Myc by p300, and most likely also its transcriptional activity in the nucleus; second, Abl can directly phosphorylate Myc on tyrosine: the resulting form of Myc appears to be cytoplasmic, and its presence correlates with Abl activation in cancer.	Tyrosine	244-252	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-70
23318434-10	2013	Thus, our data unravel two potential effects of Abl on Myc: first, Abl signaling can indirectly augment acetylation of Myc by p300, and most likely also its transcriptional activity in the nucleus; second, Abl can directly phosphorylate Myc on tyrosine: the resulting form of Myc appears to be cytoplasmic, and its presence correlates with Abl activation in cancer.	Tyrosine	244-252	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-70
23676790-0	2013	Detection of BCR-ABL kinase domain mutations in patients with chronic myeloid leukemia on imatinib.	Imatinib Mesylate	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 Mesylate	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 Mesylate	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
24129092-0	2013	VEGF depletion enhances bcr-abl-specific sensitivity of arsenic trioxide in chronic myelogenous leukemia.	Arsenic Trioxide	56-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
24129092-1	2013	The development of resistance to imatinib mesylate may partly depend on high bcr-abl expression levels or point mutation(s).	Imatinib Mesylate	33-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
24129092-2	2013	Arsenic trioxide (ATO) has bcr-abl suppressing activity in vitro, without cross-resistance to imatinib.	Arsenic Trioxide	0-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
24129092-2	2013	Arsenic trioxide (ATO) has bcr-abl suppressing activity in vitro, without cross-resistance to imatinib.	Arsenic Trioxide	18-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
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 Mesylate	74-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
23811288-0	2013	Polyphenol tri-vanillic ester 13c inhibits P-JAK2V617F and Bcr-Abl oncokinase expression in correlation with STAT3/STAT5 inactivation and apoptosis induction in human leukemia cells.	Polyphenols	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
23811288-0	2013	Polyphenol tri-vanillic ester 13c inhibits P-JAK2V617F and Bcr-Abl oncokinase expression in correlation with STAT3/STAT5 inactivation and apoptosis induction in human leukemia cells.	tri-vanillic ester	11-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
23811288-0	2013	Polyphenol tri-vanillic ester 13c inhibits P-JAK2V617F and Bcr-Abl oncokinase expression in correlation with STAT3/STAT5 inactivation and apoptosis induction in human leukemia cells.	13c	30-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
23811288-3	2013	P-JAK2, P-Src and P-PI3Kp85 inhibition occurred independently of phosphatase involvement in JAK2V617F expressing HEL cells while 13c inhibited Bcr-Abl expression without inhibition of phosphorylation in chronic myelogenous leukemia cell lines (K562, MEG-01).	13c	129-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-150
24159169-0	2013	Activity of omacetaxine mepesuccinate against ponatinib-resistant BCR-ABL-positive cells.	Homoharringtonine	12-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
24159169-0	2013	Activity of omacetaxine mepesuccinate against ponatinib-resistant BCR-ABL-positive cells.	ponatinib	46-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
24147007-0	2013	Persistent inhibition of ABL tyrosine kinase causes enhanced apoptotic response to TRAIL and disrupts the pro-apoptotic effect of chloroquine.	Chloroquine	130-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-28
24155950-0	2013	Combination of bortezomib and mitotic inhibitors down-modulate Bcr-Abl and efficiently eliminates tyrosine-kinase inhibitor sensitive and resistant Bcr-Abl-positive leukemic cells.	Bortezomib	15-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
24155950-0	2013	Combination of bortezomib and mitotic inhibitors down-modulate Bcr-Abl and efficiently eliminates tyrosine-kinase inhibitor sensitive and resistant Bcr-Abl-positive leukemic cells.	Bortezomib	15-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	148-155
24155950-3	2013	Here we show that the combined regimens of bortezomib with mitotic inhibitors, such as the microtubule-stabilizing agent Paclitaxel and the PLK1 inhibitor BI2536, efficiently kill TKIs-resistant and -sensitive Bcr-Abl-positive leukemic cells.	Bortezomib	43-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	210-217
24155950-3	2013	Here we show that the combined regimens of bortezomib with mitotic inhibitors, such as the microtubule-stabilizing agent Paclitaxel and the PLK1 inhibitor BI2536, efficiently kill TKIs-resistant and -sensitive Bcr-Abl-positive leukemic cells.	Paclitaxel	121-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	210-217
24155950-7	2013	Moreover, we found that other mitotic inhibitors (Vincristine and Docetaxel), in combination with bortezomib, also suppress the Bcr-Abl-induced pro-survival signals and result in caspase 3 activation.	Vincristine	50-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
24155950-7	2013	Moreover, we found that other mitotic inhibitors (Vincristine and Docetaxel), in combination with bortezomib, also suppress the Bcr-Abl-induced pro-survival signals and result in caspase 3 activation.	Docetaxel	66-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
24155950-7	2013	Moreover, we found that other mitotic inhibitors (Vincristine and Docetaxel), in combination with bortezomib, also suppress the Bcr-Abl-induced pro-survival signals and result in caspase 3 activation.	Bortezomib	98-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
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 Mesylate	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
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.	Dasatinib	116-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
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.	nilotinib	130-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
24147007-8	2013	However, this pro-apoptotic effect of CQ was lost in the ABL-knockdown cells but restored by Abl re-expression.	Chloroquine	38-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-60
24147007-8	2013	However, this pro-apoptotic effect of CQ was lost in the ABL-knockdown cells but restored by Abl re-expression.	Chloroquine	38-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-96
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 Mesylate	52-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-68
24130846-4	2013	Here, we applied an integrated experimental and computational approach that allowed us to estimate the differential impact of the bcr-abl inhibitors nilotinib, dasatinib, Bosutinib and Bafetinib.	nilotinib	149-158	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
24130846-4	2013	Here, we applied an integrated experimental and computational approach that allowed us to estimate the differential impact of the bcr-abl inhibitors nilotinib, dasatinib, Bosutinib and Bafetinib.	Dasatinib	160-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
24130846-4	2013	Here, we applied an integrated experimental and computational approach that allowed us to estimate the differential impact of the bcr-abl inhibitors nilotinib, dasatinib, Bosutinib and Bafetinib.	bosutinib	171-180	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
24130846-4	2013	Here, we applied an integrated experimental and computational approach that allowed us to estimate the differential impact of the bcr-abl inhibitors nilotinib, dasatinib, Bosutinib and Bafetinib.	bafetinib	185-194	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
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.	Dasatinib	97-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-85
24091670-1	2013	Nilotinib is a second-generation tyrosine kinase inhibitor, designed to specifically inhibit break-point cluster region (BCR)-Abelson (ABL) and developed to treat chronic myeloid leukemia (CML) in patients showing a resistance to imatinib.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-138
24091670-7	2013	The inhibition of mTORC1 restored the response of BCR-ABL cell lines to nilotinib in the presence of SCF.	nilotinib	72-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
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 Mesylate	111-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-85
23892407-0	2013	Doxorubicin induces atypical NF-kappaB activation through c-Abl kinase activity in breast cancer cells.	Doxorubicin	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-63
23892407-6	2013	c-Abl was inhibited with Imatinib or by overexpressing a dominant negative form of c-Abl (K290R).	Imatinib Mesylate	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
23892407-14	2013	Overexpression of c-Abl K290R in T47D and MBCDF cells reduced basal and DOX-induced NF-kappaB activation as well as IkappaBalpha tyrosine phosphorylation.	Doxorubicin	72-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-23
23892407-14	2013	Overexpression of c-Abl K290R in T47D and MBCDF cells reduced basal and DOX-induced NF-kappaB activation as well as IkappaBalpha tyrosine phosphorylation.	Tyrosine	129-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-23
23383600-4	2013	Following approval of second-generation BCR-ABL inhibitors in the first-line setting (nilotinib, dasatinib), which have significantly faster and deeper response rates than imatinib, molecular-based surrogate markers at earlier time points of 3 and 6 months are also being explored, although longer follow-up is needed.	nilotinib	86-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
23383600-4	2013	Following approval of second-generation BCR-ABL inhibitors in the first-line setting (nilotinib, dasatinib), which have significantly faster and deeper response rates than imatinib, molecular-based surrogate markers at earlier time points of 3 and 6 months are also being explored, although longer follow-up is needed.	Dasatinib	97-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
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 Mesylate	148-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
23816609-0	2013	Through the open door: Preferential binding of dasatinib to the active form of BCR-ABL unveiled by in silico experiments.	Dasatinib	47-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
23892407-16	2013	CONCLUSIONS: Inhibition of c-Abl inactivated IkappaBalpha/NF-kappaB pathway is associated with IkappaBalpha tyrosine phosphorylation in breast cancer cells.	Tyrosine	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-32
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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
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 Mesylate	154-162	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
23816609-2	2013	The high affinity of dasatinib for the protein is currently assumed to result from its ability to bind both the active and inactive conformations of the BCR-ABL kinase.	Dasatinib	21-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
23816609-3	2013	In the present work, using state of the art molecular simulation techniques we prove that dasatinib exhibits a highly selective preference for the active (open) BCR-ABL conformation.	Dasatinib	90-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-168
23816609-4	2013	By using three different BCR-ABL conformations (active, inactive, and intermediate inactive) we show that, from a thermodynamic standpoint, the affinity of dasatinib for BCR-ABL drastically decreases in the order: active > alternative inactive > inactive, as a result of differential contributions from the single residues lining the kinase binding pocket and the concomitant stabilization/destabilization of the kinase hydrophobic spine.	Dasatinib	156-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
23816609-4	2013	By using three different BCR-ABL conformations (active, inactive, and intermediate inactive) we show that, from a thermodynamic standpoint, the affinity of dasatinib for BCR-ABL drastically decreases in the order: active > alternative inactive > inactive, as a result of differential contributions from the single residues lining the kinase binding pocket and the concomitant stabilization/destabilization of the kinase hydrophobic spine.	Dasatinib	156-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-177
23816609-5	2013	Molecule-pulling experiments also corroborate this trend as significantly lower forces and smaller times are required to extract dasatinib from its inactive BCR-ABL complexes with respect to the active complex counterparts.	Dasatinib	129-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-164
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 Mesylate	57-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-35
23707608-8	2013	Nilotinib, a second generation Bcr-Abl inhibitor, led to increased ROS generation, caspase activation, hERG block, and an arrhythmic beat pattern.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
24093059-9	2013	Our studies suggest that this piperazine derivative effectively (GI50 = 0.06-0.16 muM) inhibits cancer cell proliferation and induces caspase-dependent apoptosis via inhibiting multiple cancer signaling pathways including the PI3K/AKT, the Src family kinases and the BCR-ABL pathways.	Piperazine	30-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	267-274
24156423-3	2013	The results showed that triptolide could enhance the effect of imatinib on proliferation inhibition and apoptosis of K562/G01, arrested the cell cycle in G1 phase, down-regulated the expression of BCR/ABL gene and P-gp protein.	triptolide	24-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	197-204
24156423-4	2013	It is concluded that triptolide induces K562/G01 cell proliferation inhibition and apoptosis, the mechanism may be related to cell cycle arrest, decrease of P-gp protein expression, inhibition of BCR/ABL gene expression.	triptolide	21-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	196-203
24007855-0	2013	Impressive thrombocytosis evolving in a patient with a BCR-ABL positive CML in major molecular response during dasatinib treatment unmasks an additional JAK2V617F.	Dasatinib	111-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
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 Mesylate	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 Mesylate	131-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-108
23932071-0	2013	Exploration of N-(2-aminoethyl)piperidine-4-carboxamide as a potential scaffold for development of VEGFR-2, ERK-2 and Abl-1 multikinase inhibitor.	SCHEMBL2262712	15-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-121
23932071-3	2013	Herein, N-(4-((2-(2-(naphthaen-1-yl)acetamido)ethyl)carbamoyl)piperidin-4-yl)-6-(trifluoromethyl)nicotinamide (NEPT, 6a) was discovered as an active scaffold against VEGFR-2, ERK-2 and Abl-1 kinases through the combination of support vector machine, similarity searching and molecular docking.	N-(4-((2-(2-(naphthaen-1-yl)acetamido)ethyl)carbamoyl)piperidin-4-yl)-6-(trifluoromethyl)nicotinamide	111-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	185-190
23747655-3	2013	Bafetinib, a specific Abl/Lyn tyrosine kinase inhibitor has shown a potent antiproliferative activity in leukemic cells, but its effects on eosinophils have not been reported.	bafetinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-25
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 Mesylate	233-241	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
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.	alantolactone	100-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
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 Mesylate	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-178
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 Mesylate	126-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
23613107-6	2013	Bcr/Abl knockdown enhanced the apoptosis driven by alantolactone.	alantolactone	51-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
23613107-11	2013	Collectively, these findings suggest that alantolactone is a promising potent agent to fight against CML cells via the inhibition of the NF-kappaB signaling pathway and depletion of the Bcr/Abl protein.	alantolactone	42-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-193
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
23791922-0	2013	Hydroquinone-induced miR-122 down-regulation elicits ADAM17 up-regulation, leading to increased soluble TNF-alpha production in human leukemia cells with expressed Bcr/Abl.	hydroquinone	0-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	164-171
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 Mesylate	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
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%.	nilotinib	126-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
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%.	Dasatinib	140-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
23818519-5	2013	The observed up-regulation of ERK1/2 (downstream of NMDA receptor signaling) together with the fact that c-Abl integrates cytoplasmic and nuclear functions introduces a potential mechanism through which rapid signaling initiated at the plasma membrane may eventually determine the long term integrated response to corticosterone by impacting on the transcriptional machinery that is regulated by classical, nuclear mineralocorticoid, and glucocorticoid receptors.	Corticosterone	314-328	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-110
23965958-7	2013	Because BCR/ABL may induce reactive oxygen species and unfaithful DNA repair, it may affect the stability of mitochondrial DNA, influencing mitochondrial apoptotic signaling and in this way change the sensitivity of CML cells to TKIs.	Reactive Oxygen Species	27-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-15
23965958-8	2013	Moreover, cancer cells, including BCR/ABL-positive cells, show an increased level of glucose metabolism, resulting from the shift from oxidative phosphorylation to glycolysis to supply ATP for extensive proliferation.	Glucose	85-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-41
23965958-8	2013	Moreover, cancer cells, including BCR/ABL-positive cells, show an increased level of glucose metabolism, resulting from the shift from oxidative phosphorylation to glycolysis to supply ATP for extensive proliferation.	Adenosine Triphosphate	185-188	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-41
23551499-9	2013	The results indicate that BpirLAAO-I induces apoptosis and potentiates IM effect on BCR-ABL(+) cells.	bpirlaao-i	26-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
23986642-5	2013	Ponatinib (Iclusig ), an orally available, pan-tyrosine kinase inhibitor has a unique binding mechanism allowing inhibition of BCR-ABL kinases, including those with the T315I point mutation.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
23986642-5	2013	Ponatinib (Iclusig ), an orally available, pan-tyrosine kinase inhibitor has a unique binding mechanism allowing inhibition of BCR-ABL kinases, including those with the T315I point mutation.	ponatinib	11-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
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 Mesylate	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 Mesylate	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 Mesylate	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-41
23433665-10	2013	Nine out of the 15 patients with ABL mutation responded to a treatment switch to nilotinib (n=4), dasatinib (n=2), interferon (n=1) or hematopoietic stem cell transplantation (n=2).	nilotinib	81-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-36
23433665-10	2013	Nine out of the 15 patients with ABL mutation responded to a treatment switch to nilotinib (n=4), dasatinib (n=2), interferon (n=1) or hematopoietic stem cell transplantation (n=2).	Dasatinib	98-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-36
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 Mesylate	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-32
23790540-0	2013	Structure-based design of flavone-based inhibitors of wild-type and T315I mutant of ABL.	flavone	26-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-87
23790540-2	2013	Here, we report a series of flavone-based common inhibitors equipotent for the wild type and the most drug-resistant T315I mutant of BCR-ABL.	flavone	28-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
23790540-4	2013	Structural features relevant to the stabilization of the newly identified inhibitors in the ATP-binding site of ABL are discussed in detail.	Adenosine Triphosphate	92-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-115
23813855-5	2013	First, an in-house library of pyrazolo[3,4-d]pyrimidine derivatives, which were previously shown to be dual Abl and c-Src inhibitors, was analyzed by docking studies within the ATP binding site of Hck to select the best candidates to be tested in a cell-free assay.	pyrazolo(3,4-d)pyrimidine	30-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-111
23813855-5	2013	First, an in-house library of pyrazolo[3,4-d]pyrimidine derivatives, which were previously shown to be dual Abl and c-Src inhibitors, was analyzed by docking studies within the ATP binding site of Hck to select the best candidates to be tested in a cell-free assay.	Adenosine Triphosphate	177-180	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-111
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 Mesylate	42-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
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 Mesylate	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-93
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 Mesylate	154-162	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
23630094-5	2013	The ABL1 gene at 9q34 was targeted by these rearrangements leading to its overexpression in L-1236 cells, correlating with pharmacological resistance to treatment with the kinase inhibitor dasatinib.	Dasatinib	189-198	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-8
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	134-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-39
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 Mesylate	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
23936456-10	2013	Both canertinib and the FDA-approved ErbB1/2-directed TKI lapatinib abrogated proliferation and increased sensitivity to BCR/ABL-directed TKIs at clinically relevant doses.	Canertinib	5-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
23936456-10	2013	Both canertinib and the FDA-approved ErbB1/2-directed TKI lapatinib abrogated proliferation and increased sensitivity to BCR/ABL-directed TKIs at clinically relevant doses.	Lapatinib	58-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
23787811-6	2013	Administration of the brain-penetrant tyrosine kinase inhibitor Nilotinib decreases Abl activity and facilitates autophagic clearance of SNCA in transgenic and lentiviral gene transfer models.	nilotinib	64-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-87
23723070-5	2013	A pharmacological activator of AMPK, 5-amino-4-imidazole carboxamide riboside (AICAR), inhibited oxidative stress-induced phosphorylation of both caveolin-1 and c-Abl, which is the major kinase of caveolin-1, and endocytosis of albumin in human umbilical vein endothelial cell.	5-amino-4-imidazole carboxamide riboside	37-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-166
23723070-5	2013	A pharmacological activator of AMPK, 5-amino-4-imidazole carboxamide riboside (AICAR), inhibited oxidative stress-induced phosphorylation of both caveolin-1 and c-Abl, which is the major kinase of caveolin-1, and endocytosis of albumin in human umbilical vein endothelial cell.	acadesine	79-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-166
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.	Hydrogen Peroxide	148-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-32
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.	Hydrogen Peroxide	148-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-86
23740246-11	2013	More importantly, Abi1 knockdown inhibited c-Abl phosphorylation at Tyr-412 and the interaction of c-Abl with CAS.	Tyrosine	68-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-48
23721517-3	2013	This QDs modified electrode has been utilized to serve as a transducer surface for covalent immobilization of chronic myelogenous leukemia (CML) specific probe oligonucleotide, designed from the BCR-ABL fusion gene.	Oligonucleotides	160-175	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	195-202
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.	Adenosine Triphosphate	24-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-71
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 Mesylate	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-71
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 Mesylate	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 Mesylate	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 Mesylate	156-164	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
23466625-3	2013	We and others have shown that the BCR-ABL/SRC kinase inhibitor dasatinib may enhance or suppress T cells in vitro.	Dasatinib	63-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
24516315-2	2013	Imanitib was the first BCR-ABL targeted agent approved for the treatment of CML patients and confers significant response in most patients; however, a substantial number of patients are initially refractory to the drug or may develop resistance during the course of treatment.	imanitib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
23826126-2	2013	Imatinib, a BCR-Abl tyrosine kinase inhibitor, is a successful front-line treatment for chronic myelogenous leukemia (CML).	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
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.	Dasatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
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 Mesylate	161-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
23826126-3	2013	However, resistance to imatinib may be acquired by BCR-Abl mutations or hyperactivation of Src family kinases such as Lyn.	Imatinib Mesylate	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
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 Mesylate	10-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
23787070-4	2013	Ponatinib (AP24534) an orally active Bcr-Abl Tyrosine Kinase Inhibitor and Bafetinib (INNO-406) have efficacy against various point mutations in the Bcr-Abl kinase.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
23787070-4	2013	Ponatinib (AP24534) an orally active Bcr-Abl Tyrosine Kinase Inhibitor and Bafetinib (INNO-406) have efficacy against various point mutations in the Bcr-Abl kinase.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
23787070-4	2013	Ponatinib (AP24534) an orally active Bcr-Abl Tyrosine Kinase Inhibitor and Bafetinib (INNO-406) have efficacy against various point mutations in the Bcr-Abl kinase.	ponatinib	11-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
23787070-4	2013	Ponatinib (AP24534) an orally active Bcr-Abl Tyrosine Kinase Inhibitor and Bafetinib (INNO-406) have efficacy against various point mutations in the Bcr-Abl kinase.	ponatinib	11-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
23787070-4	2013	Ponatinib (AP24534) an orally active Bcr-Abl Tyrosine Kinase Inhibitor and Bafetinib (INNO-406) have efficacy against various point mutations in the Bcr-Abl kinase.	bafetinib	75-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
23787070-4	2013	Ponatinib (AP24534) an orally active Bcr-Abl Tyrosine Kinase Inhibitor and Bafetinib (INNO-406) have efficacy against various point mutations in the Bcr-Abl kinase.	bafetinib	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
23787070-5	2013	1, 3, 4 thiadiazole derivatives has also displayed moderate inhibitory action on both Abl and Src kinase family.	1,3,4-thiadiazole	0-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-89
23787070-6	2013	However there are varieties of Bcr-Abl inhibitors but Nilotinib is still the frontline tyrosine kinase inhibitors.	nilotinib	54-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
23645696-4	2013	Tyrosine phosphorylation of KAP1 is induced by several tyrosine kinases, such as Src, Lyn, Abl, and Brk.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-94
23684619-0	2013	Efficacy of ponatinib against ABL tyrosine kinase inhibitor-resistant leukemia cells.	ponatinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-33
23684619-10	2013	This study demonstrates that ponatinib has an anti-leukemia effect by reducing ABL and Lyn kinase activity and this information may be of therapeutic relevance.	ponatinib	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-82
23602444-6	2013	C[RW]5 was a noncompetitive Src kinase inhibitor, showing approximately fourfold more selectivity towards Src than Abl.	c[rw]5	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-118
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 Mesylate	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 Mesylate	4-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-90
23576564-2	2013	However, clinical responses seen in patients treated with the ABL TKI dasatinib despite its much shorter plasma half-life and the apparent rapid restoration of BCR-ABL signaling activity following once-daily dosing suggested acute, potent inhibition of kinase activity may be sufficient to irrevocably commit CML cells to apoptosis.	Dasatinib	70-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-65
23576564-2	2013	However, clinical responses seen in patients treated with the ABL TKI dasatinib despite its much shorter plasma half-life and the apparent rapid restoration of BCR-ABL signaling activity following once-daily dosing suggested acute, potent inhibition of kinase activity may be sufficient to irrevocably commit CML cells to apoptosis.	Dasatinib	70-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-167
23576564-5	2013	Among TKIs tested, ponatinib showed the most robust capacity for apoptotic commitment showing sustained suppression of BCR-ABL signaling even at low intracellular levels following extensive washout, consistent with high-affinity binding and slow dissociation from ABL kinase.	ponatinib	19-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-126
23576564-5	2013	Among TKIs tested, ponatinib showed the most robust capacity for apoptotic commitment showing sustained suppression of BCR-ABL signaling even at low intracellular levels following extensive washout, consistent with high-affinity binding and slow dissociation from ABL kinase.	ponatinib	19-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-126
23462796-8	2013	RESULTS: Imatinib stimulated ERK(thr202/tyr204) phosphorylation in a c-Abl-dependent manner.	Imatinib Mesylate	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-74
23462796-13	2013	c-Abl co-immunoprecipitated with SHIP2 and its binding to SHIP2 was largely reduced by imatinib but not by sunitinib.	Imatinib Mesylate	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
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 Mesylate	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-56
23629659-1	2013	In BCR-ABL-expressing cells, sphingolipid metabolism is altered.	Sphingolipids	29-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	3-10
23629659-2	2013	Because the first step of sphingolipid biosynthesis occurs in the endoplasmic reticulum (ER), our objective was to identify ABL targets in the ER.	Sphingolipids	26-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-127
23629659-5	2013	We demonstrated that the ER-resident human protein serine palmitoyltransferase long chain-1 (SPTLC1), which is the first enzyme of sphingolipid biosynthesis, is phosphorylated at Tyr(164) by the tyrosine kinase ABL.	Sphingolipids	131-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	211-214
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 Mesylate	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
23679864-4	2013	Decomposition analysis of the binding free energy showed that a decrease in the desolvation cost for binding in the ATP-binding site could be as important as the strengthening of enzyme-inhibitor interaction to enhance the potency of an ABL inhibitor with structural modifications.	Adenosine Triphosphate	116-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	237-240
23679864-7	2013	The results of molecular dynamics simulations indicated that the dynamic stabilities of the hydrogen bonds between the inhibitors and Met318 should also be considered in designing the potent common inhibitors of the wild-type and T315I mutant of ABL.	Hydrogen	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	246-249
23708966-5	2013	We also establish that chromatin alterations can themselves enhance KAT5 tyrosine phosphorylation and ATM-dependent signalling, and identify the proto-oncogene c-Abl as a mediator of this modification.	Tyrosine	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-165
23440701-0	2013	Induction of autophagy by Imatinib sequesters Bcr-Abl in autophagosomes and down-regulates Bcr-Abl protein.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
23440701-8	2013	Bcr-Abl protein expression was reduced with imatinib treatment.	Imatinib Mesylate	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 Mesylate	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 Mesylate	150-158	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
23157591-0	2013	Inhibition of PCAF by anacardic acid derivative leads to apoptosis and breaks resistance to DNA damage in BCR-ABL-expressing cells.	anacardic acid	22-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
23065516-3	2013	This study compares intracellular concentration of dasatinib and Bcr-Abl kinase inhibition in CML-CD34(+) progenitors and mononuclear cells induced by dasatinib.	Dasatinib	151-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
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 Mesylate	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-147
23536723-0	2013	Suppression of survivin induced by a BCR-ABL/JAK2/STAT3 pathway sensitizes imatinib-resistant CML cells to different cytotoxic drugs.	Imatinib Mesylate	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	192-197
23782379-4	2013	Fludarabine(Flu)/cyclophosphamide (CPA)/anti-thymocyte globulin were used for myeloablative conditioning, but the patient developed therapy-related leukemia harboring t(9;22)(q34;q11.2); minor BCR-ABL (t-leukemia with Ph) at the age of 32 months.	fludarabine	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	193-200
24385789-0	2013	Dasatinib May Override F317L BCR-ABL Kinase Domain Mutation in Patients with Chronic Myeloid Leukemia.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
23815902-0	2013	[Efficacy of dasatinib in treatment of imatinib-resistant BCR/ABL positive leukemia].	Dasatinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
23815902-0	2013	[Efficacy of dasatinib in treatment of imatinib-resistant BCR/ABL positive leukemia].	Imatinib Mesylate	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
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.	Dasatinib	60-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
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 Mesylate	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.	Dasatinib	47-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
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 Mesylate	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.	Dasatinib	21-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
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 Mesylate	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
24900720-4	2013	As expected, the uncleaved water-soluble prodrugs 7 and 8 showed no activity toward the enzymatic targets (c-Src and c-Abl) but revealed promising antiproliferative activity in myeloid cell lines, as a consequence of the in vitro hydrolysis of the selected solubilizing moiety, followed by the release of the active compounds (1 and 2).	Water	27-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-122
23536723-5	2013	However, cells insensitive to IM because of point mutations in the BCR-ABL kinase domain were highly responsive to hydroxyurea (HU) after survivin silencing.	Hydroxyurea	115-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
23502220-0	2013	Nilotinib is associated with a reduced incidence of BCR-ABL mutations vs imatinib in patients with newly diagnosed chronic myeloid leukemia in chronic phase.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
23691243-8	2013	Activity of the WAVE2 complex binding partner Abl kinase was also increased in WAVE2-KD cells, as assessed by tyrosine phosphorylation of the Abl substrate CrkL.	Tyrosine	110-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-49
23691243-8	2013	Activity of the WAVE2 complex binding partner Abl kinase was also increased in WAVE2-KD cells, as assessed by tyrosine phosphorylation of the Abl substrate CrkL.	Tyrosine	110-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-145
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 Mesylate	23-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-17
23502220-8	2013	Overall, nilotinib led to fewer treatment-emergent BCR-ABL mutations than imatinib and reduced rates of progression to AP/BC in patients with these mutations.	nilotinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
23538233-5	2013	It was suggested that the introduction of the tertiary amine moiety could improve Bcr-Abl inhibitory activity and antitumor effects.	Amines	55-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
23420553-0	2013	Apoptosis in chronic myeloid leukemia cells transiently treated with imatinib or dasatinib is caused by residual BCR-ABL kinase inhibition.	Imatinib Mesylate	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
23420553-0	2013	Apoptosis in chronic myeloid leukemia cells transiently treated with imatinib or dasatinib is caused by residual BCR-ABL kinase inhibition.	Dasatinib	81-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
23098068-6	2013	There was an up-regulation of antiapoptotic BCR/ABL, GCS and SK-1 genes and MRP1 transporter gene and down-regulation of apoptotic Bax and CerS1 genes in nilotinib-resistant cells.	nilotinib	154-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
23374223-4	2013	Imatinib (Glivec( )) is a tyrosine kinase inhibitor specific for PDGF-Rs, c-KappaIotaTau and BCR-ABL.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
23065514-0	2013	The quantitative level of T315I mutated BCR-ABL predicts for major molecular response to second-line nilotinib or dasatinib treatment in patients with chronic myeloid leukemia.	nilotinib	101-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
23065514-0	2013	The quantitative level of T315I mutated BCR-ABL predicts for major molecular response to second-line nilotinib or dasatinib treatment in patients with chronic myeloid leukemia.	Dasatinib	114-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
23299860-0	2013	Molecular subtype and response to dasatinib, an Src/Abl small molecule kinase inhibitor, in hepatocellular carcinoma cell lines in vitro.	Dasatinib	34-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-55
23380277-0	2013	A neuropharmacokinetic assessment of bafetinib, a second generation dual BCR-Abl/Lyn tyrosine kinase inhibitor, in patients with recurrent high-grade gliomas.	bafetinib	37-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
23320983-3	2013	The activity of BCR-ABL is known to be associated with the increased production of intracellular reactive oxygen species and spontaneous DNA damage, which when effected by impaired/inaccurate DNA repair systems result in increased susceptibility to CML progression.	Reactive Oxygen Species	97-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
23441067-0	2013	Alantolactone inhibits growth of K562/adriamycin cells by downregulating Bcr/Abl and P-glycoprotein expression.	alantolactone	0-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
23441067-0	2013	Alantolactone inhibits growth of K562/adriamycin cells by downregulating Bcr/Abl and P-glycoprotein expression.	Doxorubicin	38-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
23441067-3	2013	The purpose of this study was to assess the effects of alantolactone in the adriamycin (ADR)-resistant human erythroleukemia cell line K562/ADR, and provide evidence that it might function as a potent therapeutic agent in chronic myelogenous leukemia (CML) patients with Bcr/Abl and the multidrug-resistance phenotype.	alantolactone	55-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	271-278
23441067-4	2013	Our results showed that alantolactone significantly inhibited K562/ADR cell growth by downregulating Bcr/Abl and P-glycoprotein expression.	alantolactone	24-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
23441067-7	2013	Together, these results demonstrate that alantolactone may be a potent therapeutic agent against CML, and a potential Bcr/Abl inhibitor.	alantolactone	41-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
23299860-9	2013	Next, we evaluated whether molecular subgroup would have predictive value for response to the Src/Abl inhibitor dasatinib.	Dasatinib	112-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-101
23613955-0	2013	Inhibition of BCR/ABL protein expression by miR-203 sensitizes for imatinib mesylate.	Imatinib Mesylate	67-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
23546518-0	2013	Haematological cancer: Nilotinib reduces emergence of BCR-ABL mutations in CML.	nilotinib	23-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
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 Mesylate	90-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
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 Mesylate	123-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
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 Mesylate	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 Mesylate	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 Mesylate	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
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 Mesylate	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 Mesylate	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 Mesylate	142-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
23495751-12	2013	Our data confirmed Aurora A, B, and BCR-ABL as the main targets of tozasertib and identified TNK1, STK2, RPS6KA1, and RPS6KA3 as submicromolar off targets.	VX680	67-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
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 Mesylate	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 Mesylate	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
23556431-4	2013	RESULTS: We found the HDAC inhibitors vorinostat and/or pracinostat (SB939) induced apoptosis in BCR-ABL-expressing cells.	Vorinostat	38-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
23556431-4	2013	RESULTS: We found the HDAC inhibitors vorinostat and/or pracinostat (SB939) induced apoptosis in BCR-ABL-expressing cells.	SB939 compound	56-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
23556431-4	2013	RESULTS: We found the HDAC inhibitors vorinostat and/or pracinostat (SB939) induced apoptosis in BCR-ABL-expressing cells.	SB939 compound	69-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
23556431-6	2013	An Aurora kinase inhibitor, tozasertib (VX-680), inhibited growth, promoted pro-apoptotic activity, reduced the phosphorylation of BCR-ABL and Crk-L, and activated caspase-3 and poly (ADP-ribose) polymerase (PARP) in BCR-ABL-positive cells.	VX680	28-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
23556431-6	2013	An Aurora kinase inhibitor, tozasertib (VX-680), inhibited growth, promoted pro-apoptotic activity, reduced the phosphorylation of BCR-ABL and Crk-L, and activated caspase-3 and poly (ADP-ribose) polymerase (PARP) in BCR-ABL-positive cells.	VX680	28-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	217-224
23556431-6	2013	An Aurora kinase inhibitor, tozasertib (VX-680), inhibited growth, promoted pro-apoptotic activity, reduced the phosphorylation of BCR-ABL and Crk-L, and activated caspase-3 and poly (ADP-ribose) polymerase (PARP) in BCR-ABL-positive cells.	VX680	40-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
23556431-6	2013	An Aurora kinase inhibitor, tozasertib (VX-680), inhibited growth, promoted pro-apoptotic activity, reduced the phosphorylation of BCR-ABL and Crk-L, and activated caspase-3 and poly (ADP-ribose) polymerase (PARP) in BCR-ABL-positive cells.	VX680	40-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	217-224
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.	iodoacetamidobenzofuran	8-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-158
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 Mesylate	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 Mesylate	206-214	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
23370613-2	2013	Recently, we synthesized a new class of substituted 2-(3,4,5-trimethoxybenzoyl)-2-N,N-dimethylamino-benzo[b]furans, and among these 3-iodoacetylamino-6-methoxybenzofuran-2-yl(3,5-trimethoxyphenyl)methanone (TR120) showed marked cytotoxic activity in BCR-ABL-expressing cells.	2-(3,4,5-trimethoxybenzoyl)-2-n,n-dimethylamino-benzo[b]furans	52-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	250-257
23370613-2	2013	Recently, we synthesized a new class of substituted 2-(3,4,5-trimethoxybenzoyl)-2-N,N-dimethylamino-benzo[b]furans, and among these 3-iodoacetylamino-6-methoxybenzofuran-2-yl(3,5-trimethoxyphenyl)methanone (TR120) showed marked cytotoxic activity in BCR-ABL-expressing cells.	3-iodoacetylamino-6-methoxybenzofuran-2-yl(3,5-trimethoxyphenyl)methanone	132-205	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	250-257
23370613-3	2013	Interestingly, TR120 was more potent than imatinib in cell growth inhibition and apoptosis induction in both BCR-ABL-expressing K562 and KCL22 cells.	3-iodoacetylamino-6-methoxybenzofuran-2-yl(3,5-trimethoxyphenyl)methanone	15-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
23770790-0	2013	Profile of BCR-ABL transcript levels based on Sokal prognostic score in chronic myeloid leukemia patients treated with imatinib.	Imatinib Mesylate	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-18
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 Mesylate	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 Mesylate	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
23616953-1	2013	Ponatinib is a novel, next-generation, small-molecule tyrosine kinase inhibitor with potent activity against the BCR-ABL fusion oncogene as well as all other ABL kinase domain mutations that confer resistance to earlier generation tyrosine kinase inhibitors.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
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 Mesylate	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 Mesylate	19-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
23325923-7	2013	The C-terminal SH3-SH2-SH3 domain and proline-rich region of Vav1 are required for its interaction with c-Abl kinase, and c-Abl kinase probably regulates the activity of Vav1 by direct phosphorylation at Tyr-267 in the DH domain.	Proline	38-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-109
23325923-7	2013	The C-terminal SH3-SH2-SH3 domain and proline-rich region of Vav1 are required for its interaction with c-Abl kinase, and c-Abl kinase probably regulates the activity of Vav1 by direct phosphorylation at Tyr-267 in the DH domain.	Tyrosine	204-207	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-109
23325923-7	2013	The C-terminal SH3-SH2-SH3 domain and proline-rich region of Vav1 are required for its interaction with c-Abl kinase, and c-Abl kinase probably regulates the activity of Vav1 by direct phosphorylation at Tyr-267 in the DH domain.	Tyrosine	204-207	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-127
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 Mesylate	291-299	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
23337400-1	2013	Imatinib is a highly effective drug for the treatment of chronic myeloid leukemia (CML) that targets the BCR-ABL kinase.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-112
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 Mesylate	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	188-192
23247657-0	2013	The synthesis of Bcr-Abl inhibiting anticancer pharmaceutical agents imatinib, nilotinib and dasatinib.	Imatinib Mesylate	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
23247657-0	2013	The synthesis of Bcr-Abl inhibiting anticancer pharmaceutical agents imatinib, nilotinib and dasatinib.	nilotinib	79-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
23247657-0	2013	The synthesis of Bcr-Abl inhibiting anticancer pharmaceutical agents imatinib, nilotinib and dasatinib.	Dasatinib	93-102	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
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).	nilotinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
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).	Dasatinib	32-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
23201011-0	2013	Dihydroartemisinin inhibits the Bcr/Abl oncogene at the mRNA level in chronic myeloid leukemia sensitive or resistant to imatinib.	artenimol	0-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
24765523-5	2013	c-Abl also causes release of reactive oxygen species (ROS) from the mitochondria of the activated neutrophils.	Reactive Oxygen Species	29-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
24765523-5	2013	c-Abl also causes release of reactive oxygen species (ROS) from the mitochondria of the activated neutrophils.	Reactive Oxygen Species	54-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
23201011-0	2013	Dihydroartemisinin inhibits the Bcr/Abl oncogene at the mRNA level in chronic myeloid leukemia sensitive or resistant to imatinib.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
23201011-4	2013	In present research, we demonstrated that dihydroartemisinin (DHA), a safe and effective antimalarial analog of artemisinin, could significantly inhibit the Bcr/Abl fusion gene at the mRNA level in CML cells sensitive or resistant to imatinib (including the primary CML cells with T315I mutation) and induce cell death.	artenimol	42-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-164
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 Mesylate	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
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 Mesylate	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 Mesylate	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 Mesylate	221-238	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
23552567-1	2013	IMPORTANCE: Nilotinib, a recently approved multitargeted tyrosine kinase inhibitor targeting the BCR-Abl translocation involved in chronic myelogenous leukemia, reportedly produces alopecia according to the package insert, but clinical and histologic descriptions of the alopecia are lacking.	nilotinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
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 Mesylate	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.	nilotinib	121-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
22976128-0	2013	Imatinib-dependent tyrosine phosphorylation profiling of Bcr-Abl-positive chronic myeloid leukemia cells.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
22976128-0	2013	Imatinib-dependent tyrosine phosphorylation profiling of Bcr-Abl-positive chronic myeloid leukemia cells.	Tyrosine	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-45
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 Mesylate	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
23301703-7	2013	GZD824 represents a promising lead candidate for development of Bcr-Abl inhibitors to overcome acquired imatinib resistance.	Imatinib Mesylate	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
23301703-0	2013	Identification of GZD824 as an orally bioavailable inhibitor that targets phosphorylated and nonphosphorylated breakpoint cluster region-Abelson (Bcr-Abl) kinase and overcomes clinically acquired mutation-induced resistance against imatinib.	olverembatinib	18-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-144
23301703-0	2013	Identification of GZD824 as an orally bioavailable inhibitor that targets phosphorylated and nonphosphorylated breakpoint cluster region-Abelson (Bcr-Abl) kinase and overcomes clinically acquired mutation-induced resistance against imatinib.	olverembatinib	18-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	146-153
23301703-1	2013	Bcr-Abl(T315I) mutation-induced imatinib resistance remains a major challenge for clinical management of chronic myelogenous leukemia (CML).	Imatinib Mesylate	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
23301703-2	2013	Herein, we report GZD824 (10a) as a novel orally bioavailable inhibitor against a broad spectrum of Bcr-Abl mutants including T315I.	olverembatinib	18-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
23301703-7	2013	GZD824 represents a promising lead candidate for development of Bcr-Abl inhibitors to overcome acquired imatinib resistance.	olverembatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
23201011-4	2013	In present research, we demonstrated that dihydroartemisinin (DHA), a safe and effective antimalarial analog of artemisinin, could significantly inhibit the Bcr/Abl fusion gene at the mRNA level in CML cells sensitive or resistant to imatinib (including the primary CML cells with T315I mutation) and induce cell death.	artenimol	62-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-164
23201011-4	2013	In present research, we demonstrated that dihydroartemisinin (DHA), a safe and effective antimalarial analog of artemisinin, could significantly inhibit the Bcr/Abl fusion gene at the mRNA level in CML cells sensitive or resistant to imatinib (including the primary CML cells with T315I mutation) and induce cell death.	artemisinin	49-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-164
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.	artenimol	10-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
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.	artenimol	10-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185
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 Mesylate	364-372	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185
23273517-0	2013	Synthesis and biological evaluation of analogues of the kinase inhibitor nilotinib as Abl and Kit inhibitors.	nilotinib	73-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-89
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 Mesylate	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
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 Mesylate	107-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
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.	Dasatinib	169-178	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
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.	Dasatinib	169-178	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
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.	nilotinib	183-192	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
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.	nilotinib	183-192	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
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.	bosutinib	199-208	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
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.	ponatinib	213-222	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
23212614-0	2013	Oleylamine-carbonyl-valinol inhibits auto-phosphorylation activity of native and T315I mutated Bcr-Abl, and exhibits selectivity towards oncogenic Bcr-Abl in SupB15 ALL cell lines.	oleylamine-carbonyl-valinol	0-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
23212614-0	2013	Oleylamine-carbonyl-valinol inhibits auto-phosphorylation activity of native and T315I mutated Bcr-Abl, and exhibits selectivity towards oncogenic Bcr-Abl in SupB15 ALL cell lines.	oleylamine-carbonyl-valinol	0-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-154
23212614-4	2013	Previously, we have identified oleic acid as the active component in the mushroom Daedalea gibbosa that inhibited the kinase activity of Bcr-Abl.	Oleic Acid	31-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-144
23273517-4	2013	Docking of nilotinib and of analogues 2a-c to the binding pocket of Abl and of Kit showed that the lack of shape complementarity in Kit is compensated by the stabilizing effect from its juxtamembrane region.	nilotinib	11-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-71
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 Mesylate	237-245	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
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.	Dasatinib	249-258	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
23233201-4	2013	In the present study, we demonstrate that PECAM-1             is tyrosine phospho-rylated in its ITIM motifs in various BCR/ABL-expressing cells             including primary leukemia cells.	Tyrosine	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
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 Mesylate	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.	Dasatinib	27-36	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 Mesylate	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 Mesylate	207-215	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	391-398
23233201-6	2013	We also demonstrate by             using a substrate trapping mutant of SHP2 that tyrosine phosphorylated PECAM-1             binds SHP2 and is a major substrate for this tyrosine phosphatase in BCR/ABL-expressing             cells.	Tyrosine	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	199-202
22392508-1	2013	PURPOSE: Dasatinib is an oral tyrosine kinase inhibitor (TKI) of BCR-ABL and SRC family and ixabepilone is an epothilone B analog.	Dasatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
23218026-0	2013	Imatinib and Nilotinib inhibit Bcr-Abl-induced ROS through targeted degradation of the NADPH oxidase subunit p22phox.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
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 Mesylate	165-173	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-117
23218026-0	2013	Imatinib and Nilotinib inhibit Bcr-Abl-induced ROS through targeted degradation of the NADPH oxidase subunit p22phox.	nilotinib	13-22	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.	Reactive Oxygen Species	47-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
23218026-1	2013	Constitutive expression of the Bcr-Abl kinase in Chronic Myelogenous Leukaemia (CML) is known to produce elevated levels of Reactive Oxygen Species (ROS) which can enhance cell survival as well as generate genomic instability.	Reactive Oxygen Species	124-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
23218026-1	2013	Constitutive expression of the Bcr-Abl kinase in Chronic Myelogenous Leukaemia (CML) is known to produce elevated levels of Reactive Oxygen Species (ROS) which can enhance cell survival as well as generate genomic instability.	Reactive Oxygen Species	149-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
23218026-2	2013	Our laboratory has previously demonstrated that NADPH oxidase (Nox) activity contributes to intracellular-ROS levels in Bcr-Abl-positive cells, while inducing increased pro-survival signalling through the PI3K/Akt pathway.	Reactive Oxygen Species	106-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
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 Mesylate	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.	nilotinib	115-124	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.	Reactive Oxygen Species	160-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
22391570-1	2013	In chronic myelogenous leukemia, the constitutive activation of the BCR-ABL kinase transforms cells to an addicted state that requires glucose metabolism for survival.	Glucose	135-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
23218026-6	2013	Taken together we believe our results provide a possible link between Bcr-Abl signalling and ROS production through Nox activity and demonstrate a novel mechanism of action associated with Imatinib and Nilotinib treatment in CML.	Reactive Oxygen Species	93-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
23218026-6	2013	Taken together we believe our results provide a possible link between Bcr-Abl signalling and ROS production through Nox activity and demonstrate a novel mechanism of action associated with Imatinib and Nilotinib treatment in CML.	nilotinib	202-211	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
22410779-2	2013	The tyrosine kinase inhibitor imatinib effectively treats CML, but acquired resistance can develop because of BCR-ABL mutations.	Imatinib Mesylate	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
22391570-2	2013	We investigated S6K1, a protein kinase that drives glycolysis in leukemia cells, as a target for counteracting glucose-dependent survival induced by BCR-ABL.	Glucose	111-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
23319661-2	2013	Gleevec, a well-known therapeutic agent against chronic myelogenous leukemia, is an effective inhibitor of Abl tyrosine kinase.	Imatinib Mesylate	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-110
23319661-5	2013	Some have attributed the difference in binding specificity of Gleevec to subtle variations in ligand-protein interactions (binding affinity control), whereas others have proposed that it is the conformation of the DFG motif, in which ligand binding is only accessible to Abl and not to c-Src (conformational selection control).	1,3-Diphenylguanidine	214-217	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	271-274
24900659-3	2013	Docking studies show that Abl is able to allow the in situ click chemistry between specific azide and alkyne fragments by binding to Abl-active sites.	Azides	92-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-29
24900659-3	2013	Docking studies show that Abl is able to allow the in situ click chemistry between specific azide and alkyne fragments by binding to Abl-active sites.	Azides	92-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-136
24900659-3	2013	Docking studies show that Abl is able to allow the in situ click chemistry between specific azide and alkyne fragments by binding to Abl-active sites.	Alkynes	102-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-29
24900659-3	2013	Docking studies show that Abl is able to allow the in situ click chemistry between specific azide and alkyne fragments by binding to Abl-active sites.	Alkynes	102-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-136
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 Mesylate	71-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
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.	BI 2536	26-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
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.	Vorinostat	37-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
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 Mesylate	98-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
23204129-6	2013	BI2536/vorinostat cotreatment triggered pronounced mitochondrial dysfunction, inhibition of p-BCR/ABL, caspase activation, PARP cleavage, reactive oxygen species (ROS) generation, and DNA damage (manifest by increased expression of gammaH2A.X, p-ATM, p-ATR), events attenuated by the antioxidant TBAP.	Vorinostat	7-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
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 Mesylate	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
23053188-0	2013	Impact of BCR-ABL mutations on response to dasatinib after imatinib failure in elderly patients with chronic-phase chronic myeloid leukemia.	Dasatinib	43-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
23053188-4	2013	Our data suggest that, in elderly patients, detection of BCR-ABL mutations negatively affects response to dasatinib.	Dasatinib	106-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
23223358-1	2013	BCR-ABL1 compound mutations can confer high-level resistance to imatinib and other ABL1 tyrosine kinase inhibitors (TKIs).	Imatinib Mesylate	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-8
23223358-2	2013	The third-generation ABL1 TKI ponatinib is effective against BCR-ABL1 point mutants individually, but remains vulnerable to certain BCR-ABL1 compound mutants.	ponatinib	30-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-25
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 Mesylate	96-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	251-258
23117882-0	2013	ABL regulation by AXL promotes cisplatin resistance in esophageal cancer.	Cisplatin	31-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
23117882-8	2013	Mechanistic investigations revealed that AXL blocked CDDP-induced activation of endogenous p73beta (TP73), reducing its protein half-life, and inhibited CDDP-induced levels of p-c-ABL(Y412) and p-p73beta(Y99).	Cisplatin	53-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-183
23117882-8	2013	Mechanistic investigations revealed that AXL blocked CDDP-induced activation of endogenous p73beta (TP73), reducing its protein half-life, and inhibited CDDP-induced levels of p-c-ABL(Y412) and p-p73beta(Y99).	Cisplatin	153-157	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-183
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 Mesylate	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 Mesylate	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-99
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 Mesylate	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
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 Mesylate	134-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-13
22920907-1	2013	Heat shock protein (Hsp) 90 is an ATP-dependent molecular chaperone which stabilizes various oncogenic kinases, including HER2, EGFR, BCR-ABL, B-Raf and EML4-ALK, which are essential for tumor growth.	Adenosine Triphosphate	34-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
23151973-3	2013	To overcome this problem             a series of phenyl amino pyrimidine derivatives have been designed, prepared and             evaluated for anti-proliferative activity against the BCR-ABL-positive leukemia             cell line K562.	phenyl amino pyrimidine	49-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	184-191
24240798-3	2013	Dasatinib was administered to inhibit Bcr-Abl and Lyn kinase.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
24240798-5	2013	To our knowledge, this is the first report to describe the occurrence of a gradual increase in the Bcr-Abl transcript level prior to the diagnosis of Ph-positive CML in an individual with CLL who was successfully treated with dasatinib as the first-line therapy.	Dasatinib	226-235	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
22772060-1	2013	MK-0457, an Aurora kinase and BCR-ABL inhibitor, was studied on a Phase I/II study in 77 patients with refractory hematologic malignancies.	VX680	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
23674887-2	2013	Bosutinib effectively overcomes the majority of imatinib-resistance-conferring BCR-ABL mutations except V299L and T315I.	bosutinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
23674887-2	2013	Bosutinib effectively overcomes the majority of imatinib-resistance-conferring BCR-ABL mutations except V299L and T315I.	Imatinib Mesylate	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
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 Mesylate	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-16
22772060-0	2013	MK-0457, an Aurora kinase and BCR-ABL inhibitor, is active in patients with BCR-ABL T315I leukemia.	VX680	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
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 Mesylate	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 Mesylate	134-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-216
23493838-2	2013	Bosutinib effectively inhibits wild-type BCR-ABL and most imatinib-resistant BCR-ABL mutations except for V299L and T315I.	bosutinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
23493838-2	2013	Bosutinib effectively inhibits wild-type BCR-ABL and most imatinib-resistant BCR-ABL mutations except for V299L and T315I.	bosutinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
23569389-1	2013	Dasatinib is a dual tyrosine kinase inhibitor active against ABL and Src family kinases, and is approved for the treatment of chronic myeloid leukemia (CML) patients in chronic, accelerated, or blast phase with resistance or intolerance to imatinib therapy, for newly diagnosed chronic phase patients, and for adults with Philadelphia chromosome-positive acute lymphoblastic leukemia who have become resistant to or intolerant of other treatments.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-64
23493838-2	2013	Bosutinib effectively inhibits wild-type BCR-ABL and most imatinib-resistant BCR-ABL mutations except for V299L and T315I.	Imatinib Mesylate	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
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 Mesylate	169-177	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
24072218-2	2013	METHODS: Dasatinib is an oral multitarget tyrosine kinase inhibitor that targets BCR-ABL, c-Src, c-KIT, platelet-derived growth factor receptor beta, and EphA2.	Dasatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
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 Mesylate	215-223	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
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 Mesylate	228-236	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
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 Mesylate	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 Mesylate	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 Mesylate	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.	Dasatinib	40-49	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.	Dasatinib	40-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	236-243
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.	bosutinib	51-60	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.	bosutinib	51-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	236-243
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.	ponatinib	65-74	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.	ponatinib	65-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	236-243
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 Mesylate	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 Mesylate	128-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	236-243
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 Mesylate	171-179	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
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 Mesylate	148-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
22772060-6	2013	MK-0457 has important activity in patients with leukemias expressing the highly resistant T315I BCR-ABL mutation.	VX680	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
22781593-3	2013	Ponatinib (AP24534), which potently inhibits native and mutant BCR-ABL, also targets the FGFR family.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
22781593-3	2013	Ponatinib (AP24534), which potently inhibits native and mutant BCR-ABL, also targets the FGFR family.	ponatinib	11-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
22868969-4	2013	We found that NA10HD greatly increases outputs of both normal and Ph(+)/BCR-ABL(+) LTC-ICs, and this effect is particularly pronounced in cultures containing growth factor-producing feeders.	na10hd	14-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
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.	Arginine	46-49	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.	Arginine	46-49	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 Mesylate	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 Mesylate	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 Mesylate	71-88	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 Mesylate	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 Mesylate	90-96	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 Mesylate	90-96	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.	Anthracyclines	158-171	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.	Doxorubicin	173-184	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.	Arginine	285-288	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-45
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 Mesylate	6-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	189-194
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 Mesylate	163-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
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.	Dasatinib	188-197	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
23534290-5	2013	Thus, in ATC cells the ionizing radiation and Ptx exhibited competitive effects upon phosphorylation of cell cycle controllers: p53, pRb, CHK2, cAbl and expression of Bax.	Paclitaxel	46-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-148
22705319-0	2012	BCR/ABL modulates protein phosphorylation associated with the etoposide-induced DNA damage response.	Etoposide	62-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
22705319-7	2012	BCR/ABL was shown to significantly alter the response to etoposide in many cases.	Etoposide	57-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
22705319-12	2012	Furthermore we found that multiple protein phosphorylation changes mediated by BCR/ABL were connected to the increased activation of NFkappaB, a key survival transcription factor, after etoposide exposure.	Etoposide	186-195	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
23190395-8	2012	Using 1 as a competitive probe, we determined the extent to which ponatinib, a clinical Bcr-Abl inhibitor, targets Src-family kinases.	ponatinib	66-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
23074277-3	2012	Here we describe the unknown activity of the natural product berbamine that efficiently eradicates LSCs and T315I mutant Bcr-Abl clones.	berbamine	61-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
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 Mesylate	158-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
23138519-1	2012	Dasatinib is a multi-kinase inhibitor that potently inhibits Bcr-Abl, Src family and platelet-derived growth factor receptor kinases.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
23138519-3	2012	Clinical trials utilizing a combination of dasatinib and methotrexate in patients with Philadelphia chromosome positive and/or Bcr-Abl positive acute lymphoblastic leukemia are currently ongoing.	Dasatinib	43-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
23138519-3	2012	Clinical trials utilizing a combination of dasatinib and methotrexate in patients with Philadelphia chromosome positive and/or Bcr-Abl positive acute lymphoblastic leukemia are currently ongoing.	Methotrexate	57-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
23209150-4	2012	Accordingly, direct targeting of BCR-ABL through agents such as imatinib have profound antitumor effects.	Imatinib Mesylate	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
25998099-0	2012	K356dup--an in-frame insertion in the BCR-ABL gene in an imatinib-resistant chronic myeloid leukemia.	Imatinib Mesylate	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 Mesylate	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
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 Mesylate	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
22415796-8	2012	We show that upon the compounds tested, DHSI-15 and deoxyspergualin exert strongest antiproliferative effects on BCR-ABL cells including Imatinib resistant mutants.	dhsi-15	40-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
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.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-84
22415796-8	2012	We show that upon the compounds tested, DHSI-15 and deoxyspergualin exert strongest antiproliferative effects on BCR-ABL cells including Imatinib resistant mutants.	gusperimus	52-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
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.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
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 Mesylate	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 Mesylate	237-245	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
23238683-2	2012	Indeed, inhibition of BCR-ABL by imatinib, dasatinib or nilotinib triggers durable responses in most patients suffering from this disease.	Imatinib Mesylate	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
23238683-2	2012	Indeed, inhibition of BCR-ABL by imatinib, dasatinib or nilotinib triggers durable responses in most patients suffering from this disease.	Dasatinib	43-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
23238683-2	2012	Indeed, inhibition of BCR-ABL by imatinib, dasatinib or nilotinib triggers durable responses in most patients suffering from this disease.	nilotinib	56-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
23238683-4	2012	In this line, ponatinib (AP24534) has emerged as a promising therapeutic option in patients with all kinds of BCR-ABL mutations, especially the T315I one.	ponatinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
23238683-7	2012	Our results show that ponatinib is highly effective on both sensitive and resistant CML cell lines, whatever the mode of resistance and also on BaF3 murine B cells carrying native BCR-ABL or T315I mutation.	ponatinib	22-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	180-187
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 Mesylate	156-164	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	219-226
23190221-2	2012	Ponatinib (AP24534) is a potent oral tyrosine kinase inhibitor that blocks native and mutated BCR-ABL, including the gatekeeper mutant T315I, which is uniformly resistant to tyrosine kinase inhibitors.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
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 Mesylate	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
23190221-2	2012	Ponatinib (AP24534) is a potent oral tyrosine kinase inhibitor that blocks native and mutated BCR-ABL, including the gatekeeper mutant T315I, which is uniformly resistant to tyrosine kinase inhibitors.	ponatinib	11-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
22895079-2	2012	The BCR-ABL tyrosine kinase inhibitor imatinib is the standard treatment for Ph+ leukemia and plays efficacious role in CML.	Imatinib Mesylate	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
23190221-14	2012	CONCLUSIONS: Ponatinib was highly active in heavily pretreated patients with Ph-positive leukemias with resistance to tyrosine kinase inhibitors, including patients with the BCR-ABL T315I mutation, other mutations, or no mutations.	ponatinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-181
23088644-0	2012	Design, synthesis, and biological evaluation of 3-(1H-1,2,3-triazol-1-yl)benzamide derivatives as Potent Pan Bcr-Abl inhibitors including the threonine(315) isoleucine(315) mutant.	3-(1h-1,2,3-triazol-1-yl)benzamide	48-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
23088644-1	2012	A series of 3-(1H-1,2,3-triazol-1-yl)benzamide derivatives were designed and synthesized as new Bcr-Abl inhibitors by using combinational strategies of bioisosteric replacement, scaffold hopping, and conformational constraint.	3-(1h-1,2,3-triazol-1-yl)benzamide	12-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
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 Mesylate	153-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
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 Mesylate	247-255	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-49
22517301-1	2012	BACKGROUND: Compared with imatinib, nilotinib is a potent breakpoint cluster region/v-abl Abelson murine leukemia viral oncogene (bcr-abl) kinase inhibitor, and it induces higher rate and rapid complete cytogenetic response (CCyR), yet no clinical data are available regarding its efficacy against chronic myeloid leukemia (CML) stem cells.	nilotinib	36-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
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 Mesylate	112-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
23355941-0	2012	Contribution of BCR-ABL kinase domain mutations to imatinib mesylate resistance in Philadelphia chromosome positive Malaysian chronic myeloid leukemia patients.	Imatinib Mesylate	51-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
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 Mesylate	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 Mesylate	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 Mesylate	122-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
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 Mesylate	122-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
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 Mesylate	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
23044928-5	2012	Furthermore, the activity profile of ponatinib and DCC-2036 against a panel of 24 clinically relevant BCR/ABL mutants is presented and compared to the other TKIs.	ponatinib	37-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
23044928-5	2012	Furthermore, the activity profile of ponatinib and DCC-2036 against a panel of 24 clinically relevant BCR/ABL mutants is presented and compared to the other TKIs.	Dicyclohexylcarbodiimide	51-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
22895079-8	2012	Our results showed that oridonin inhibiting activations of LYN (one of SRC family kinases) and ABL and their downstream Akt/mTOR, Raf/MEK/ERK and STAT5 pathways, downregulated Bcl-2 but upregulated Bax protein and then induced apoptosis in Ph+ ALL cells.	oridonin	24-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-98
22992064-1	2012	INTRODUCTION: Dasatinib is a dual Abl/Src tyrosine kinase inhibitor (TKI), which was developed to treat patients with chronic myelogenous leukemia (CML), who had failed or were intolerant to therapy with imatinib.	Dasatinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-37
23125079-0	2012	Tetrandrine citrate eliminates imatinib-resistant chronic myeloid leukemia cells in vitro and in vivo by inhibiting Bcr-Abl/beta-catenin axis.	tetrandrine citrate	0-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
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 Mesylate	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
23125079-10	2012	Western blot results revealed that treatment of IM-resistant K562 cells with tetrandrine citrate resulted in a significant decrease of both p210(Bcr-Abl) and beta-catenin proteins, but IM did not affect the Bcr-Abl protein levels.	tetrandrine citrate	77-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-152
23125079-10	2012	Western blot results revealed that treatment of IM-resistant K562 cells with tetrandrine citrate resulted in a significant decrease of both p210(Bcr-Abl) and beta-catenin proteins, but IM did not affect the Bcr-Abl protein levels.	tetrandrine citrate	77-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	207-214
23125079-12	2012	RT-PCR results showed that tetrandrine treatment caused a decrease of Bcr-Abl mRNA.	tetrandrine	27-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
22874537-3	2012	Here we show that the BCR-ABL/Src kinase inhibitor dasatinib decreases PRH phosphorylation and increases PRH-dependent repression of Vegf and Vegfr-1.	Dasatinib	51-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
23125079-15	2012	Tetrandrine citrate-induced growth inhibition of leukemia cells may be involved in the depletion of p210(Bcr-Abl) mRNA and beta-catenin protein.	tetrandrine citrate	0-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-112
22642671-0	2012	Effects of the hedgehog inhibitor GDC-0449, alone or in combination with dasatinib, on BCR-ABL-positive leukemia cells.	HhAntag691	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
23010482-11	2012	Dasatinib suppressed phosphorylation of c-Src in both cell lines, but decreased repair of radiation-induced DNA damage in HN-5 cells only as evidenced by suppression of c-Abl and Nbs-1 activity, inhibition of the association between c-Src and EGFR or Her-2, prolongation of nuclear gamma-H2AX and 53BP1 foci and inhibition of EGFR nuclear localization and its association with DNA-PKcs.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	169-174
22642671-2	2012	In this study, we investigated the effects of the potent Hh antagonist GDC-0449 on the BCR-ABL-positive cell line OM9;22 and primary samples when leukemia cells were protected by a feeder cell line (S9 cells).	HhAntag691	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
22642671-11	2012	Data from this study suggest that administration of the Hh inhibitor GDC-0449 inhibits BCR-ABL-positive cell growth and enhances the cytotoxic effects of dasatinib in the presence of feeder cells.	HhAntag691	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
23363745-1	2012	OBJECTIVE: To establish a bcr-abl(+) cell line resistance to nilotinib, and to investigate the possible mechanisms of resistance.	nilotinib	61-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
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 Mesylate	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 Mesylate	38-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-161
22554713-2	2012	Nilotinib and dasatinib strongly reduced telomerase activity in BCR-ABL-positive (K562) and BCR-ABL-negative (HL60) cells, demonstrating that their effect on telomerase activity is uncoupled from their effect on BCR-ABL.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
22554713-2	2012	Nilotinib and dasatinib strongly reduced telomerase activity in BCR-ABL-positive (K562) and BCR-ABL-negative (HL60) cells, demonstrating that their effect on telomerase activity is uncoupled from their effect on BCR-ABL.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
22554713-2	2012	Nilotinib and dasatinib strongly reduced telomerase activity in BCR-ABL-positive (K562) and BCR-ABL-negative (HL60) cells, demonstrating that their effect on telomerase activity is uncoupled from their effect on BCR-ABL.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
22554713-2	2012	Nilotinib and dasatinib strongly reduced telomerase activity in BCR-ABL-positive (K562) and BCR-ABL-negative (HL60) cells, demonstrating that their effect on telomerase activity is uncoupled from their effect on BCR-ABL.	Dasatinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
22554713-2	2012	Nilotinib and dasatinib strongly reduced telomerase activity in BCR-ABL-positive (K562) and BCR-ABL-negative (HL60) cells, demonstrating that their effect on telomerase activity is uncoupled from their effect on BCR-ABL.	Dasatinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
22554713-2	2012	Nilotinib and dasatinib strongly reduced telomerase activity in BCR-ABL-positive (K562) and BCR-ABL-negative (HL60) cells, demonstrating that their effect on telomerase activity is uncoupled from their effect on BCR-ABL.	Dasatinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
23090888-9	2012	Although both are potent and specific BCR-ABL TKIs, dasatinib and nilotinib exhibit unique pharmacological profiles and response patterns relative to different patient characteristics, such as disease stage and BCR-ABL mutational status.	Dasatinib	52-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	211-218
23090888-9	2012	Although both are potent and specific BCR-ABL TKIs, dasatinib and nilotinib exhibit unique pharmacological profiles and response patterns relative to different patient characteristics, such as disease stage and BCR-ABL mutational status.	nilotinib	66-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
23090888-9	2012	Although both are potent and specific BCR-ABL TKIs, dasatinib and nilotinib exhibit unique pharmacological profiles and response patterns relative to different patient characteristics, such as disease stage and BCR-ABL mutational status.	nilotinib	66-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	211-218
23100300-2	2012	They show that the therapeutic drug arsenic trioxide (AS(2)O(3)) targets BCR-ABL for autophagic degradation via a p62/SQSTM1-dependent mechanism that is critical for the antileukemic effect of the drug.	Arsenic Trioxide	36-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
23100300-2	2012	They show that the therapeutic drug arsenic trioxide (AS(2)O(3)) targets BCR-ABL for autophagic degradation via a p62/SQSTM1-dependent mechanism that is critical for the antileukemic effect of the drug.	Arsenic Trioxide	54-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
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 Mesylate	128-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
22898604-0	2012	Autophagic degradation of the BCR-ABL oncoprotein and generation of antileukemic responses by arsenic trioxide.	Arsenic Trioxide	94-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
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 Mesylate	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 Mesylate	115-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
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 Mesylate	222-230	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
22988110-4	2012	Three different IP-MS experiments central to cell signaling pathways were sufficient to discover a BCR-ABL fusion in H929 cells: phosphotyrosine (pY) peptide IP, p85 regulatory subunit of phosphoinositide-3-kinase (PI3K) IP, and the GRB2 adaptor IP.	phosphotyrosine (py) peptide	129-157	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
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 Mesylate	81-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
22765290-3	2012	In this review, we focus on highlighting several representative plant natural compounds such as curcumin, resveratrol, paclitaxel, oridonin, quercetin and plant lectin - that may lead to cancer cell death - for regulation of some core autophagic pathways, involved in Ras-Raf signalling, Beclin-1 interactome, BCR-ABL, PI3KCI/Akt/mTOR, FOXO1 signalling and p53.	Quercetin	141-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	310-317
22647531-3	2012	This novel composite platform has been explored to fabricate an electrochemical DNA biosensor for detection of chronic myelogenous leukemia (CML) by immobilizing amine terminated oligonucleotide probe sequence containing 22 base pairs, identified from BCR-ABL fusion gene.	Amines	162-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	252-259
22647531-3	2012	This novel composite platform has been explored to fabricate an electrochemical DNA biosensor for detection of chronic myelogenous leukemia (CML) by immobilizing amine terminated oligonucleotide probe sequence containing 22 base pairs, identified from BCR-ABL fusion gene.	Oligonucleotides	179-194	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	252-259
22765290-3	2012	In this review, we focus on highlighting several representative plant natural compounds such as curcumin, resveratrol, paclitaxel, oridonin, quercetin and plant lectin - that may lead to cancer cell death - for regulation of some core autophagic pathways, involved in Ras-Raf signalling, Beclin-1 interactome, BCR-ABL, PI3KCI/Akt/mTOR, FOXO1 signalling and p53.	Curcumin	96-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	310-317
22765290-3	2012	In this review, we focus on highlighting several representative plant natural compounds such as curcumin, resveratrol, paclitaxel, oridonin, quercetin and plant lectin - that may lead to cancer cell death - for regulation of some core autophagic pathways, involved in Ras-Raf signalling, Beclin-1 interactome, BCR-ABL, PI3KCI/Akt/mTOR, FOXO1 signalling and p53.	Resveratrol	106-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	310-317
22765290-3	2012	In this review, we focus on highlighting several representative plant natural compounds such as curcumin, resveratrol, paclitaxel, oridonin, quercetin and plant lectin - that may lead to cancer cell death - for regulation of some core autophagic pathways, involved in Ras-Raf signalling, Beclin-1 interactome, BCR-ABL, PI3KCI/Akt/mTOR, FOXO1 signalling and p53.	Paclitaxel	119-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	310-317
22765290-3	2012	In this review, we focus on highlighting several representative plant natural compounds such as curcumin, resveratrol, paclitaxel, oridonin, quercetin and plant lectin - that may lead to cancer cell death - for regulation of some core autophagic pathways, involved in Ras-Raf signalling, Beclin-1 interactome, BCR-ABL, PI3KCI/Akt/mTOR, FOXO1 signalling and p53.	oridonin	131-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	310-317
23002203-0	2012	The growing arsenal of ATP-competitive and allosteric inhibitors of BCR-ABL.	Adenosine Triphosphate	23-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
23002203-2	2012	Recent advances in elucidating the structure, regulation, and signaling of BCR-ABL have led to the identification of allosteric sites that are distant from the ATP-binding pocket and are critical for BCR-ABL-dependent oncogenic transformation.	Adenosine Triphosphate	160-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
23002203-2	2012	Recent advances in elucidating the structure, regulation, and signaling of BCR-ABL have led to the identification of allosteric sites that are distant from the ATP-binding pocket and are critical for BCR-ABL-dependent oncogenic transformation.	Adenosine Triphosphate	160-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	200-207
23002203-3	2012	Here, we review the available data regarding the molecular mechanism of action and the specificity of ATP-competitive tyrosine kinase inhibitors targeting BCR-ABL.	Adenosine Triphosphate	102-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-162
23002203-4	2012	In addition, we discuss how targeting of allosteric sites could provide new opportunities to inhibit resistant BCR-ABL mutants, either alone or in combination with conventional ATP-competitive inhibitors.	Adenosine Triphosphate	177-180	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
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 Mesylate	100-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	5-12
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.	bosutinib	167-176	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	5-12
23187745-7	2012	The third-generation TKI ponatinib is a BCR-ABL inhibitor that has demonstrated significant activity, including in patients with the TKI resistance mutation T315I.	ponatinib	25-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
23187745-8	2012	The homoharringtonine derivative omacetaxine mepesuccinate, which inhibits protein synthesis, has also demonstrated clinical activity in CML, including in patients with TKI resistance due to T315I and in patients who have TKI resistance despite no evidence of ABL mutations.	Homoharringtonine	4-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	260-263
23187745-8	2012	The homoharringtonine derivative omacetaxine mepesuccinate, which inhibits protein synthesis, has also demonstrated clinical activity in CML, including in patients with TKI resistance due to T315I and in patients who have TKI resistance despite no evidence of ABL mutations.	Homoharringtonine	33-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	260-263
22633167-5	2012	Nilotinib is a highly selective inhibitor of the inactive conformation of ABL1 kinase.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-78
22633167-6	2012	An improved topologic fit to the ABL1 protein-binding surface contributes to its increased potency over imatinib.	Imatinib Mesylate	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 Mesylate	138-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
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 Mesylate	138-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-111
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 Mesylate	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
22985168-3	2012	The ABL-kinase inhibitors (AKIs) Imatinib, Nilotinib or Dasatinib, which target the ATP-binding site, are effective in Ph + leukemia.	Imatinib Mesylate	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
22985168-3	2012	The ABL-kinase inhibitors (AKIs) Imatinib, Nilotinib or Dasatinib, which target the ATP-binding site, are effective in Ph + leukemia.	nilotinib	43-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
22985168-3	2012	The ABL-kinase inhibitors (AKIs) Imatinib, Nilotinib or Dasatinib, which target the ATP-binding site, are effective in Ph + leukemia.	Dasatinib	56-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
22985168-3	2012	The ABL-kinase inhibitors (AKIs) Imatinib, Nilotinib or Dasatinib, which target the ATP-binding site, are effective in Ph + leukemia.	Adenosine Triphosphate	84-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
22985168-8	2012	Interestingly, the combination of Dasatinib and GNF-2 overcame resistance of BCR/ABL-T315I in all models used in a synergistic manner.	Dasatinib	34-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
22419518-2	2012	NK large granular lymphocyte expansions associated with improved survival have been described under monotherapy with the Bcr-Abl/Src inhibitor dasatinib, which inhibits NK cell functions in vitro.	Dasatinib	143-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
22696202-0	2012	Increased acetylation of lysine 317/320 of p53 caused by BCR-ABL protects from cytoplasmic translocation of p53 and mitochondria-dependent apoptosis in response to DNA damage.	Lysine	25-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
22696202-6	2012	In this study we have investigated whether the expression of BCR-ABL could influence the acetylation of p53, specifically at lysine 317/320 (K317/K320), which has been shown to regulate nuclear export and transcription-independent apoptotic activity of p53.	Lysine	125-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
22696202-7	2012	We found that BCR-ABL expression increases K317 acetylation of p53 and is able to prevent a drop in acetylation observed upon DNA damage, followed by translocation of p53 to the cytoplasm and by Bax activation.	1,2-cyclohexanedione	43-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
22570081-0	2012	Molecular interactions of c-ABL mutants in complex with imatinib/nilotinib: a computational study using linear interaction energy (LIE) calculations.	Imatinib Mesylate	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-31
22532521-0	2012	Platelet dysfunction associated with ponatinib, a new pan BCR-ABL inhibitor with efficacy for chronic myeloid leukemia resistant to multiple tyrosine kinase inhibitor therapy.	ponatinib	37-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
22570081-0	2012	Molecular interactions of c-ABL mutants in complex with imatinib/nilotinib: a computational study using linear interaction energy (LIE) calculations.	nilotinib	65-74	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 Mesylate	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 Mesylate	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-165
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.	nilotinib	131-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-165
22570081-5	2012	In addition, to understand the structural changes that are associated with resistance, we describe the behavior of water molecules that interact simultaneously with specific residues (Glu286, Lys271 and Asp381) of c-ABL (wild type or mutant) and their relationship with drug resistance.	Water	115-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	214-219
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 Mesylate	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 Mesylate	213-221	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	321-326
22570081-7	2012	Our results indicate that LIE was suitable to predict the superior inhibitory activity of nilotinib and the resistance to inhibition that was observed in c-ABL mutants.	nilotinib	90-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-159
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.	Water	56-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-23
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 Mesylate	185-193	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-23
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-138
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
22778153-6	2012	The ponatinib IC(50) values of BCR-ABL-expressing K562 cells transfected with ABCB1 and ABCG2 were approximately the same as and 2-fold higher than that of K562, respectively, consistent with ponatinib being a substrate of both proteins, but inhibiting its own transport, and resistance was also attenuated to a small degree by ponatinib-induced downregulation of ABCB1 and ABCG2 cell-surface expression on resistant K562 cells.	ponatinib	192-201	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
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.	Oligonucleotides	93-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-161
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.	Adenosine Triphosphate	166-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-161
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 Mesylate	284-292	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-161
22778153-0	2012	The novel BCR-ABL and FLT3 inhibitor ponatinib is a potent inhibitor of the MDR-associated ATP-binding cassette transporter ABCG2.	ponatinib	37-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
22778153-1	2012	Ponatinib is a novel tyrosine kinase inhibitor with potent activity against BCR-ABL with mutations, including T315I, and also against fms-like tyrosine kinase 3.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
22778153-6	2012	The ponatinib IC(50) values of BCR-ABL-expressing K562 cells transfected with ABCB1 and ABCG2 were approximately the same as and 2-fold higher than that of K562, respectively, consistent with ponatinib being a substrate of both proteins, but inhibiting its own transport, and resistance was also attenuated to a small degree by ponatinib-induced downregulation of ABCB1 and ABCG2 cell-surface expression on resistant K562 cells.	ponatinib	4-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
22448923-0	2012	Multifaceted actions of 8-amino-adenosine kill BCR-ABL positive cells.	8-aminoadenosine	24-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
22448923-1	2012	Survival of chronic myelogenous leukemia (CML) cells is dependent on BCR-ABL kinase, the activity of which is contingent on the level of BCR-ABL protein and the availability of adenosine triphosphate (ATP).	Adenosine Triphosphate	177-199	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
22448923-1	2012	Survival of chronic myelogenous leukemia (CML) cells is dependent on BCR-ABL kinase, the activity of which is contingent on the level of BCR-ABL protein and the availability of adenosine triphosphate (ATP).	Adenosine Triphosphate	201-204	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
22448923-2	2012	We hypothesized that 8-amino-adenosine (8-amino-Ado)-mediated reduction in cellular ATP level and inhibition of mRNA synthesis leading to a decrease in protein level would result in a multifaceted targeting of BCR-ABL.	8-aminoadenosine	21-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	210-217
22448923-2	2012	We hypothesized that 8-amino-adenosine (8-amino-Ado)-mediated reduction in cellular ATP level and inhibition of mRNA synthesis leading to a decrease in protein level would result in a multifaceted targeting of BCR-ABL.	8-aminoadenosine	40-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	210-217
22448923-2	2012	We hypothesized that 8-amino-adenosine (8-amino-Ado)-mediated reduction in cellular ATP level and inhibition of mRNA synthesis leading to a decrease in protein level would result in a multifaceted targeting of BCR-ABL.	Adenosine Triphosphate	84-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	210-217
22448923-4	2012	In parallel, 8-amino-Ado inhibited RNA synthesis and resulted in a depletion of BCR-ABL transcript.	8-aminoadenosine	13-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
22865631-0	2012	Gallic acid downregulates matrix metalloproteinase-2 (MMP-2) and MMP-9 in human leukemia cells with expressed Bcr/Abl.	Gallic Acid	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
22865631-3	2012	Gallic acid induced beta-TrCP upregulation evoked Bcr/Abl degradation in K562 cells, while overexpression of Bcr/Abl attenuated gallic acid induced MMP-2/MMP-9 downregulation.	Gallic Acid	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
22865631-3	2012	Gallic acid induced beta-TrCP upregulation evoked Bcr/Abl degradation in K562 cells, while overexpression of Bcr/Abl attenuated gallic acid induced MMP-2/MMP-9 downregulation.	Gallic Acid	128-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
22865631-4	2012	Overexpression of Bcr/Abl restored the levels of phospho-ERK and phospho-Akt but not JNK phosphorylation in gallic acid treated K562 cells.	Gallic Acid	108-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
22778153-6	2012	The ponatinib IC(50) values of BCR-ABL-expressing K562 cells transfected with ABCB1 and ABCG2 were approximately the same as and 2-fold higher than that of K562, respectively, consistent with ponatinib being a substrate of both proteins, but inhibiting its own transport, and resistance was also attenuated to a small degree by ponatinib-induced downregulation of ABCB1 and ABCG2 cell-surface expression on resistant K562 cells.	ponatinib	192-201	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
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 Mesylate	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
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 Mesylate	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-61
22641616-6	2012	The c-Abl inactive analogs induced cytotoxicity and ER stress, at similar or greater potencies and magnitudes as imatinib.	Imatinib Mesylate	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-9
22773836-12	2012	These studies establish a critical role for H(2)O(2) in angiotensin-II signaling to the endothelial cytoskeleton in a novel pathway that is critically dependent on MARCKS, Rac1, and c-Abl.	Hydrogen Peroxide	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-187
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 Mesylate	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
22467682-2	2012	Imatinib, an inhibitor of BCR-ABL, has emerged as the leading compound to treat CML patients.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
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 Mesylate	201-209	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	179-186
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 Mesylate	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
22402607-0	2012	SKLB1028, a novel oral multikinase inhibitor of EGFR, FLT3 and Abl, displays exceptional activity in models of FLT3-driven AML and considerable potency in models of CML harboring Abl mutants.	SKLB1028	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-66
22402607-0	2012	SKLB1028, a novel oral multikinase inhibitor of EGFR, FLT3 and Abl, displays exceptional activity in models of FLT3-driven AML and considerable potency in models of CML harboring Abl mutants.	SKLB1028	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	179-182
22521726-0	2012	Gadd45a transcriptional induction elicited by the Aurora kinase inhibitor MK-0457 in Bcr-Abl-expressing cells is driven by Oct-1 transcription factor.	VX680	74-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
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 Mesylate	246-254	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	191-198
22689211-0	2012	Complete morphologic and molecular remission after introduction of dasatinib in the treatment of a pediatric patient with t-cell acute lymphoblastic leukemia and ABL1 amplification.	Dasatinib	67-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-166
22689211-3	2012	Dasatinib, a second-generation tyrosine kinase inhibitor, directly targets the BCR-ABL gene.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
22689211-4	2012	We describe a pediatric case of T-cell ALL with amplification of the ABL1 gene in which remission was achieved only after the addition of dasatinib to conventional chemotherapy.	Dasatinib	138-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-73
22549737-3	2012	Fusing c-Abl to a mitochondrial translocation signal (MTS) that is activated by reactive oxygen species (ROS) will selectively target the mitochondria of cancer cells exhibiting an elevated ROS phenotype.	Reactive Oxygen Species	80-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	7-12
22549737-3	2012	Fusing c-Abl to a mitochondrial translocation signal (MTS) that is activated by reactive oxygen species (ROS) will selectively target the mitochondria of cancer cells exhibiting an elevated ROS phenotype.	Reactive Oxygen Species	105-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	7-12
22549737-3	2012	Fusing c-Abl to a mitochondrial translocation signal (MTS) that is activated by reactive oxygen species (ROS) will selectively target the mitochondria of cancer cells exhibiting an elevated ROS phenotype.	Reactive Oxygen Species	190-193	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	7-12
22549737-5	2012	METHODS: Confocal microscopy was used to determine mitochondrial colocalization of ectopically expressed c-Abl-EGFP/cMTS fusion across three cell lines (K562, Cos-7, and 1471.1) with varying levels of basal (and pharmacologically modulated) ROS.	carbonyl sulfide	159-162	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-110
22549737-5	2012	METHODS: Confocal microscopy was used to determine mitochondrial colocalization of ectopically expressed c-Abl-EGFP/cMTS fusion across three cell lines (K562, Cos-7, and 1471.1) with varying levels of basal (and pharmacologically modulated) ROS.	Reactive Oxygen Species	241-244	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-110
22549737-8	2012	RESULTS: The cMTS and cMTS/c-Abl fusions colocalized to the mitochondria in leukemic (K562) and breast (1471.1) cancer phenotypes (but not Cos-7 fibroblasts) in a ROS and PKC dependent manner.	Reactive Oxygen Species	163-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-32
22810897-2	2012	Here, we uncovered a previously uncharacterized role for the Abl family tyrosine kinases Abl and Arg in the regulation of T cell-dependent inflammatory responses and showed that the Abl family kinases were required for chemokine-induced T cell polarization and migration.	Arginine	97-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-64
22810897-3	2012	Our data demonstrated that Abl and Arg were activated downstream of chemokine receptors and mediated the chemokine-induced tyrosine phosphorylation of human enhancer of filamentation 1 (HEF1), an adaptor protein that is required for the activity of the guanosine triphosphatase Rap1, which mediates cell adhesion and migration.	Tyrosine	123-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-30
22314840-4	2012	Multiple rational design cycles were utilized to develop a lead peptide with a phenylalanine and alanine replaced by an (N-methyl)phenylalanine and isoleucine, respectively, to attain cytosolic peptidase resistance while maintaining Abl substrate efficacy.	Phenylalanine	79-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	233-236
22314840-4	2012	Multiple rational design cycles were utilized to develop a lead peptide with a phenylalanine and alanine replaced by an (N-methyl)phenylalanine and isoleucine, respectively, to attain cytosolic peptidase resistance while maintaining Abl substrate efficacy.	(n-methyl)phenylalanine	120-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	233-236
22314840-4	2012	Multiple rational design cycles were utilized to develop a lead peptide with a phenylalanine and alanine replaced by an (N-methyl)phenylalanine and isoleucine, respectively, to attain cytosolic peptidase resistance while maintaining Abl substrate efficacy.	Isoleucine	148-158	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	233-236
22591714-9	2012	Finally, we showed that MKN74 cells with CRKL amplification were responsive to the dual Src/BCR-ABL kinase inhibitor BMS354825, likely via the inhibition of CRKL phosphorylation, and that the proliferation of MKN74 cells was suppressed by treatment with a CRKL-targeting peptide.	Dasatinib	117-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
22397755-2	2012	Imatinib (IM) effectively targets Bcr-Abl tyrosine kinase, but development of resistance to IM occurs with varying frequency.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
22397755-10	2012	Resveratrol, a known Bcr-Abl inhibitor, reduced Gli-1 activation and inhibited the viability of CML cells.	Resveratrol	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
22397755-12	2012	Novel compounds inhibiting both Shh signaling and Bcr-Abl expression, such as resveratrol, may have potential to be effective agents against CML independent of IM resistance.	Resveratrol	78-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
22139798-7	2012	HO-1 up-regulation in BCR-ABL1-expressing cells was suppressed by diphenyleneiodonium (DPI), a chemical inhibitor of the NADPH oxidase.	diphenyleneiodonium	66-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-30
22139798-7	2012	HO-1 up-regulation in BCR-ABL1-expressing cells was suppressed by diphenyleneiodonium (DPI), a chemical inhibitor of the NADPH oxidase.	diphenyleneiodonium	87-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-30
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	89-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
22538170-1	2012	Dasatinib, a multitargeted inhibitor of BCR-ABL and SRC kinases, exhibits antitumor activity and extends the survival of patients with chronic myeloid leukemia (CML) and Philadelphia chromosome-positive acute lymphoblastic leukemia (ALL).	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
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 Mesylate	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
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 Mesylate	135-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
22349810-0	2012	Phase I trial of the combination of flavopiridol and imatinib mesylate in patients with Bcr-Abl+ hematological malignancies.	alvocidib	36-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
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 Mesylate	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	165-172
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 Mesylate	62-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-162
22327338-5	2012	By analysis of the adaptor proteins NCK1 and GRB2 mutants we further show that the negative loop on p38 is mediated by c-ABL phosphorylation at tyrosine 105 of the adaptor protein NCK1, while the phosphorylation at tyrosine 209 of GRB2 down-modulates ERK1/2 and JNKs signaling.	Tyrosine	144-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-124
22327338-5	2012	By analysis of the adaptor proteins NCK1 and GRB2 mutants we further show that the negative loop on p38 is mediated by c-ABL phosphorylation at tyrosine 105 of the adaptor protein NCK1, while the phosphorylation at tyrosine 209 of GRB2 down-modulates ERK1/2 and JNKs signaling.	Tyrosine	215-223	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-124
22428569-5	2012	Using this platform we have revealed that dexamethasone induces HS5 fibroblast proliferation and contact with multiple myeloma cells via a process involving Src/c-Abl kinases.	Dexamethasone	42-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-166
22428569-7	2012	Myeloma resistance to dexamethasone mediated by HS5 cells and osteoclasts was reversed by treatment with the Src/c-Abl inhibitor dasatinib but not with bortezomib.	Dexamethasone	22-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-118
22428569-7	2012	Myeloma resistance to dexamethasone mediated by HS5 cells and osteoclasts was reversed by treatment with the Src/c-Abl inhibitor dasatinib but not with bortezomib.	Dasatinib	129-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-118
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 Mesylate	100-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-57
22829974-0	2012	Prognostic factors influencing clinical outcome of allogeneic hematopoietic stem cell transplantation following imatinib-based therapy in BCR-ABL-positive ALL.	Imatinib Mesylate	112-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
21840128-1	2012	Nilotinib is a rationally designed tyrosine kinase inhibitor with improved specificity and binding affinity for BCR-ABL compared with imatinib.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
21565522-1	2012	Results from several trials in patients with newly diagnosed chronic myeloid leukemia in chronic phase (CML-CP) of dasatinib and nilotinib, two BCR-ABL inhibitors with higher in vitro potency compared with imatinib, have recently been reported.	nilotinib	129-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
22519766-6	2012	Ponatinib, a pan BCR-ABL TKI, while still under investigation, is very hopeful with its ability to overcome T315I mutations in resistant CML and Ph + ALL patients.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
23226579-4	2012	Thus, c-Abl/Arg may serve as molecular switches that suppress proliferation and invasion in response to some stimuli (e.g., ephrins) or when inactive/regulated, or as promote invasion and proliferation in response to other signals (e.g., activated growth factor receptors, loss of inhibitor expression), which induce sustained activation.	Arginine	12-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-11
23226579-7	2012	Targeted trials are critical for determining whether c-Abl/Arg inhibitors can be effective treatment options for patients whose tumors are driven by c-Abl/Arg.	Arginine	59-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-154
23226579-7	2012	Targeted trials are critical for determining whether c-Abl/Arg inhibitors can be effective treatment options for patients whose tumors are driven by c-Abl/Arg.	Arginine	155-158	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-58
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.	Adenosine Triphosphate	92-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
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.	Adenosine Triphosphate	116-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
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 Mesylate	160-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
23226581-7	2012	Furthermore, past and ongoing efforts to target Abl oncoproteins using ATP-competitive and allosteric inhibitors, as well as future possibilities using combination therapy, will be discussed.	Adenosine Triphosphate	71-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-51
25031941-3	2012	The tyrosine kinase inhibitors imatinib, nilotinib, and dasatinib block the BCR-ABL protein and prevent activation of the transformation pathways.	Imatinib Mesylate	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
25031941-3	2012	The tyrosine kinase inhibitors imatinib, nilotinib, and dasatinib block the BCR-ABL protein and prevent activation of the transformation pathways.	nilotinib	41-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
25031941-3	2012	The tyrosine kinase inhibitors imatinib, nilotinib, and dasatinib block the BCR-ABL protein and prevent activation of the transformation pathways.	Dasatinib	56-65	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.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
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 Mesylate	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
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 Mesylate	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 Mesylate	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 Mesylate	4-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
22330069-6	2012	Finally, we found that ATO also could downregulate protein level of bcr-abl in K562 and KCL-22.	Arsenic Trioxide	23-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
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 Mesylate	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	196-203
22076466-1	2012	Nilotinib (Tasigna) is a potent and selective BCR-ABL inhibitor approved for use in patients with newly diagnosed chronic myeloid leukemia (CML) in chronic phase (CML-CP) and in patients with CML-CP and accelerated phase (CML-AP) who are resistant to or intolerant of imatinib.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
22076466-1	2012	Nilotinib (Tasigna) is a potent and selective BCR-ABL inhibitor approved for use in patients with newly diagnosed chronic myeloid leukemia (CML) in chronic phase (CML-CP) and in patients with CML-CP and accelerated phase (CML-AP) who are resistant to or intolerant of imatinib.	nilotinib	11-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
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 Mesylate	160-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
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 Mesylate	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
22608253-13	2012	The PDGF/Abl tyrosine kinase inhibitor nilotinib, suppressed proliferation in LTED cells in the presence or absence of E. Nilotinib also suppressed ER-mediated transcription by destabilizing the ER and reducing recruitment of amplified in breast cancer-1 (AIB1) and the CREB binding protein (CBP) to the promoter of the E-responsive gene GREB1.	nilotinib	39-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-12
22608253-13	2012	The PDGF/Abl tyrosine kinase inhibitor nilotinib, suppressed proliferation in LTED cells in the presence or absence of E. Nilotinib also suppressed ER-mediated transcription by destabilizing the ER and reducing recruitment of amplified in breast cancer-1 (AIB1) and the CREB binding protein (CBP) to the promoter of the E-responsive gene GREB1.	nilotinib	122-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-12
22538123-9	2012	The validated method was applied to the Abl 1 kinase kinetic study and the K(m) and V(max) constants obtained for Abltide were 34.78 muM and 5.563 mumol/mg/min and for adenosine triphosphate (ATP) were 43.61 muM and 5.906 mumol/mg/min.	Adenosine Triphosphate	168-190	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-45
22538123-9	2012	The validated method was applied to the Abl 1 kinase kinetic study and the K(m) and V(max) constants obtained for Abltide were 34.78 muM and 5.563 mumol/mg/min and for adenosine triphosphate (ATP) were 43.61 muM and 5.906 mumol/mg/min.	Adenosine Triphosphate	192-195	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-45
22587422-4	2012	Despite the potent inhibition of BCR-ABL kinase by dasatinib, little is known about the relationship between dasatinib pharmacokinetics and the emergence of kinase domain mutations in vivo.	Dasatinib	51-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
22587422-10	2012	Notably, these data also suggest that newly acquired BCR-ABL mutations may be inhibited by an increased exposure of dasatinib.	Dasatinib	116-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
22349810-0	2012	Phase I trial of the combination of flavopiridol and imatinib mesylate in patients with Bcr-Abl+ hematological malignancies.	Imatinib Mesylate	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 Mesylate	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
22503441-3	2012	Here we review structure-based approaches underlying the development of several molecules that are currently in clinical trials, including the cMet inhibitor ARQ197 and the Bcr-Abl inhibitor ponatinib.	ponatinib	191-200	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	173-180
22388797-5	2012	Imatinib mesylate targets the oncogenic kinase activity of BCR-ABL.	Imatinib Mesylate	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 Mesylate	51-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
22276948-5	2012	Some NRTKs (e.g., Abl) phosphorylate p27 on Tyr 88, which facilitates a second modification on Tyr 74 by another NRTK (e.g., Src).	Tyrosine	44-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-21
22276948-5	2012	Some NRTKs (e.g., Abl) phosphorylate p27 on Tyr 88, which facilitates a second modification on Tyr 74 by another NRTK (e.g., Src).	Tyrosine	95-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-21
22285607-8	2012	These agents have demonstrated activity in patients harboring imatinib-resistant BCR-ABL mutations, except for the T315I substitution.	Imatinib Mesylate	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
22371878-1	2012	Bosutinib, a dual Src/Abl tyrosine kinase inhibitor (TKI), has shown potent activity against chronic myeloid leukemia (CML).	bosutinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-25
21892207-5	2012	Using siRNA and pharmacological approaches, we show that c-Abl/Arg activation is functionally relevant because it is requiredfor melanoma cell proliferation, survival and invasion.	Arginine	63-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-62
21892207-9	2012	Taken together, these data identify c-Abl and Arg as critical, novel, drug targets in metastatic melanoma, and indicate that nilotinib may be useful in preventing metastasis in patients with melanomas harboring active c-Abl and Arg.	nilotinib	125-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	218-223
22301057-3	2012	In this study, treatment with endothelin-1 (ET-1) and platelet-derived growth factor (PDGF) increased Abl phosphorylation at Tyr(412) (an indication of Abl activation) in vascular smooth muscle cells.	Tyrosine	125-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-105
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 Mesylate	78-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
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 Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-67
22344285-7	2012	Our results indicate that whilst both BCR-ABL and c-ABL shuttle from the cytoplasm to the nucleus following dasatinib treatment, the temporal dynamics are not synchronized.	Dasatinib	108-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
22344285-7	2012	Our results indicate that whilst both BCR-ABL and c-ABL shuttle from the cytoplasm to the nucleus following dasatinib treatment, the temporal dynamics are not synchronized.	Dasatinib	108-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-55
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 Mesylate	109-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
22462553-11	2012	Next, we found that STI571 could attenuate TRAIL-induced c-Abl, JNK and p38 activation in HCT116 cells.	Imatinib Mesylate	20-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-62
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 Mesylate	206-212	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-47
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 Mesylate	66-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-31
22334513-3	2012	Previous studies have established that ataxia telangiectasia mutated (ATM) activates nuclear Abl by phosphorylating serine 465 (S465) in the kinase domain in response to ionizing radiation (IR).	Serine	116-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-96
22291013-5	2012	Consistent with our previous overexpression studies, we found that H(2)O(2)-induced superoxide production by primary sperm cells was mediated by the non-receptor tyrosine kinase c-Abl.	Hydrogen Peroxide	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-183
22291013-5	2012	Consistent with our previous overexpression studies, we found that H(2)O(2)-induced superoxide production by primary sperm cells was mediated by the non-receptor tyrosine kinase c-Abl.	Superoxides	84-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-183
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 Mesylate	154-162	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-87
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 Mesylate	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.	Dasatinib	137-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	165-172
22262776-6	2012	SB216763, a specific GSK3 inhibitor, promoted an almost complete suppression of primary CML stem/progenitor cells when combined with IM, but not dasatinib, while sparing bcr-abl-negative cells.	SB 216763	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-177
21700731-0	2012	Phase II study of single-agent bosutinib, a Src/Abl tyrosine kinase inhibitor, in patients with locally advanced or metastatic breast cancer pretreated with chemotherapy.	bosutinib	31-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-51
22242557-5	2012	Interestingly, danusertib also inhibits several receptor tyrosine kinases such as Abl, Ret, FGFR-1 and TrkA.	danusertib	15-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-85
21544849-1	2012	The BCR-ABL inhibitor imatinib is a standard first-line therapy for patients with chronic myeloid leukemia.	Imatinib Mesylate	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
21933042-8	2012	The CBA technique detected all types of BCR-ABL proteins in leukemic cells with high specificity and sensitivity.	cba	4-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
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 Mesylate	146-154	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
21221851-0	2012	BCR-ABL isoforms associated with intrinsic or acquired resistance to imatinib: more heterogeneous than just ABL kinase domain point mutations?	Imatinib Mesylate	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
21221851-0	2012	BCR-ABL isoforms associated with intrinsic or acquired resistance to imatinib: more heterogeneous than just ABL kinase domain point mutations?	Imatinib Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-43
21221851-9	2012	We conclude that Abl KD point mutations represent a major mechanism of imatinib resistance.	Imatinib Mesylate	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-20
22238366-2	2012	Ponatinib (AP24534) is an oral multitargeted tyrosine kinase inhibitor being explored in a pivotal phase II trial in patients with chronic myelogenous leukemia due to its potent activity against BCR-ABL.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	195-202
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 Mesylate	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
22238366-2	2012	Ponatinib (AP24534) is an oral multitargeted tyrosine kinase inhibitor being explored in a pivotal phase II trial in patients with chronic myelogenous leukemia due to its potent activity against BCR-ABL.	ponatinib	11-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	195-202
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 Mesylate	236-244	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	283-290
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 Mesylate	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-144
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
22199356-0	2012	c-Abl tyrosine kinase regulates serum-induced nuclear export of diacylglycerol kinase alpha by phosphorylation at Tyr-218.	Tyrosine	114-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
22199356-3	2012	Here, we show that c-Abl directly phosphorylates diacylglycerol kinase alpha (DGKalpha), an important regulator of many cellular events through its conversion of diacylglycerol to phosphatidic acid.	Diglycerides	49-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-24
22199356-3	2012	Here, we show that c-Abl directly phosphorylates diacylglycerol kinase alpha (DGKalpha), an important regulator of many cellular events through its conversion of diacylglycerol to phosphatidic acid.	Phosphatidic Acids	180-197	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-24
22199356-7	2012	Moreover, an in vitro phosphorylation assay using purified mutants of DGKalpha identified Tyr-218 as a site of phosphorylation by c-Abl.	Tyrosine	90-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-135
22199356-9	2012	These results demonstrate that the nucleo-cytoplasmic shuttling of DGKalpha is orchestrated by tyrosine phosphorylation by the Src-activated tyrosine kinase c-Abl and that this phosphorylation is important for regulating the function of cytoplasmic and/or nuclear DGKalpha.	Tyrosine	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-162
22232548-4	2012	Recently, we showed that galectin-3 Tyr-107 is phosphorylated by c-Abl; concomitantly, it was also shown that galectin-3 can be cleaved at this site by prostate-specific antigen (PSA), a chymotrypsin-like serine protease, after Tyr-107, resulting in loss of galectin-3 multivalency while preserving its carbohydrate binding activity.	Tyrosine	36-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-70
22179664-0	2012	Phase I study of bosutinib, a src/abl tyrosine kinase inhibitor, administered to patients with advanced solid tumors.	bosutinib	17-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-37
22179664-1	2012	PURPOSE: Bosutinib, a potent ATP-competitive, quinolinecarbonitrile Src/Abl kinase inhibitor, was tested in this first-in-human phase I trial in patients with advanced solid tumor malignancies.	bosutinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-75
22340598-5	2012	SIRT1 effects were enhanced in combination with the BCR-ABL TKI imatinib.	Imatinib Mesylate	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
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.	1,3-Diphenylguanidine	71-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-130
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.	1,3-Diphenylguanidine	81-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-130
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.	1,3-Diphenylguanidine	81-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-130
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 Mesylate	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).	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
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 Mesylate	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%.	Dasatinib	42-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
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 Mesylate	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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
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 Mesylate	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.	Dasatinib	0-9	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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
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 Mesylate	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 Mesylate	137-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
22233429-12	2012	Dasatinib was generally equally effective in patients with or without BCR-ABL mutations at baseline.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
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 Mesylate	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
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.	Dasatinib	118-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
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.	nilotinib	133-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
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 Mesylate	304-312	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	283-290
21854543-11	2012	Imatinib induces remission in leukaemia patients that are positive for BCR-ABL or PDGFR fusions.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
22285209-2	2012	Second-generation BCR-ABL inhibitors have shorter onset times and higher rates of complete cytogenetic response (CCyR) than imatinib.	Imatinib Mesylate	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	193-200
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 Mesylate	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 Mesylate	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
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.	nilotinib	119-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
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.	Dasatinib	133-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
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 Mesylate	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
21724255-1	2012	The function of the natural modulators of BCR-ABL-induced signaling pathways could influence the results to imatinib treatment.	Imatinib Mesylate	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
22311485-0	2012	[Effect of dihydroartemisinin on the expression of BCR/ABL fusion gene in leukemia K562 cells].	artenimol	11-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
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 Mesylate	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 Mesylate	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-156
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.	nilotinib	41-50	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.	Dasatinib	167-176	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-156
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
21844872-5	2012	Recent randomized phase 3 trials have shown that first-line treatment with dasatinib or nilotinib-more potent BCR-ABL inhibitors-results in significantly higher rates and more rapid achievement of CCyR and MMR in comparison with standard-dose imatinib.	Dasatinib	75-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
21844872-5	2012	Recent randomized phase 3 trials have shown that first-line treatment with dasatinib or nilotinib-more potent BCR-ABL inhibitors-results in significantly higher rates and more rapid achievement of CCyR and MMR in comparison with standard-dose imatinib.	nilotinib	88-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
21844872-6	2012	These trials suggest that CML treatment can be improved with more potent BCR-ABL inhibition during initial therapy, but further follow-up is needed to confirm that the improved response rates with dasatinib and nilotinib are maintained long term.	nilotinib	211-220	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
22311485-1	2012	OBJECTIVE: To investigate the effect of dihydroartemisinin (DHA) on the BCR/ABL fusion gene in leukemia K562 cell.	artenimol	40-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
22311485-1	2012	OBJECTIVE: To investigate the effect of dihydroartemisinin (DHA) on the BCR/ABL fusion gene in leukemia K562 cell.	artenimol	60-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
22311485-4	2012	Expression of BCR/ABL fusion gene was analyzed by reverse transcription(RT-PCR) before and after DHA treatment.	artenimol	97-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
22311485-8	2012	The expression of BCR/ABL fusion gene, as detected by RT-PCR after incubating the K562 cells with 20 umol/L DHA, measured as DeltaCt = 4.45 +- 0.25 after 12 h and DeltaCt = 5.23 +- 0.21 after 24 h, which was significantly lower compared with that of the control ( DeltaCt = 4.23 +- 0.21, P < 0.05).	artenimol	108-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
22311485-9	2012	CONCLUSION: DHA can inhibit the proliferation of leukemia K562 cells and facilitate the induction of apoptosis by downregulating the expression of BCR/ABL fusion gene.	artenimol	12-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-154
22005133-5	2012	In 27 of 74 imatinib-resistant patients (36%), 15 different BCR-ABL TKD mutations were detected.	Imatinib Mesylate	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
21993902-2	2012	However, some patients with CML are less likely             to respond to imatinib, the inhibitor of Bcr-Abl kinase.	Imatinib Mesylate	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
22252550-6	2012	Furthermore, ABL1 directly phosphorylates NuMA, a binding partner of LGN, on tyrosine 1774.	Tyrosine	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-17
21717440-4	2012	Various strategies aimed at improving cytogenetic response have been explored, such as escalation of imatinib and switching to the newer breakpoint cluster region/v-abl Abelson murine leukemia viral oncogene (BCR-ABL) inhibitors dasatinib and nilotinib.	Dasatinib	229-238	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-216
21717440-4	2012	Various strategies aimed at improving cytogenetic response have been explored, such as escalation of imatinib and switching to the newer breakpoint cluster region/v-abl Abelson murine leukemia viral oncogene (BCR-ABL) inhibitors dasatinib and nilotinib.	nilotinib	243-252	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-216
22002881-0	2012	Nocodazole is a high-affinity ligand for the cancer-related kinases ABL, c-KIT, BRAF, and MEK.	Nocodazole	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-71
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 Mesylate	35-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
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 Mesylate	192-200	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 Mesylate	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 Mesylate	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 Mesylate	238-246	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	180-187
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	181-188
21691746-1	2012	PURPOSE: Bosutinib (SKI-606), a dual Src/Abl tyrosine kinase inhibitor, is in clinical development for the treatment of patients with chronic myelogenous leukemia (CML).	bosutinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-44
21732337-1	2012	BACKGROUND: Nilotinib is a selective, potent BCR-ABL inhibitor.	nilotinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
21751967-0	2012	Inhibition of cell growth and up-regulation of MAD2 in human oesophageal squamous cell carcinoma after treatment with the Src/Abl inhibitor dasatinib.	Dasatinib	140-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-129
23055606-0	2012	Nilotinib based pharmacophore models for BCRABL.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-47
23055606-2	2012	Imitanib, a small molecule ABL kinase inhibitor is a highly effective therapy for early phase chronic myeloid leukemia (CML), which has constitutively active ABL kinase activity owing to the over expression of the BCR-ABL fusion protein.	imitanib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	214-221
23055606-4	2012	Nilotinib, a second generation drug is more potent inhibitor of BCR-ABL than imatinib.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
23055606-9	2012	First kinase inhibitors were docked with the receptor (BCR-ABL) and nilotinib was selected as a pharmacophore due its high binding efficiency.	nilotinib	68-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
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 Mesylate	155-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
21943109-3	2012	Here, we report that HCH and its analogues induce killing of primary cells in CML patients and leukemic cell lines expressing wild type and mutated Bcr-Abl, including the T315I mutation, with minimal toxicity to normal human peripheral blood mononuclear cells.	2-hydroxychavicol	21-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	148-155
21943109-7	2012	One HCH analogue was also effective in vivo in SCID mice against grafts expressing the T315I mutation, although to a lesser extent than grafts expressing wild type Bcr-Abl, without showing significant bodyweight loss.	2-hydroxychavicol	4-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	164-171
22549445-0	2012	Morpholino Oligo Antisense efficiently suppresses BCR/ABL and cell proliferation in CML: specific inhibition of BCR-ABL gene expression by Morpholino Oligo Antisense in BCR-ABL(+) cells.	Morpholinos	0-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
22549445-0	2012	Morpholino Oligo Antisense efficiently suppresses BCR/ABL and cell proliferation in CML: specific inhibition of BCR-ABL gene expression by Morpholino Oligo Antisense in BCR-ABL(+) cells.	Morpholinos	0-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
22549445-0	2012	Morpholino Oligo Antisense efficiently suppresses BCR/ABL and cell proliferation in CML: specific inhibition of BCR-ABL gene expression by Morpholino Oligo Antisense in BCR-ABL(+) cells.	Morpholinos	0-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	169-176
22549445-0	2012	Morpholino Oligo Antisense efficiently suppresses BCR/ABL and cell proliferation in CML: specific inhibition of BCR-ABL gene expression by Morpholino Oligo Antisense in BCR-ABL(+) cells.	Morpholinos	139-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
22549445-0	2012	Morpholino Oligo Antisense efficiently suppresses BCR/ABL and cell proliferation in CML: specific inhibition of BCR-ABL gene expression by Morpholino Oligo Antisense in BCR-ABL(+) cells.	Morpholinos	139-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
22549445-0	2012	Morpholino Oligo Antisense efficiently suppresses BCR/ABL and cell proliferation in CML: specific inhibition of BCR-ABL gene expression by Morpholino Oligo Antisense in BCR-ABL(+) cells.	Morpholinos	139-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	169-176
22549445-4	2012	In the present study, the effect of  Morpholino Oligo Antisense in BCR/ABL oncogene silencing was evaluated.	Morpholinos	37-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
22549445-6	2012	The capacity of Morpholino Oligo Antisense in inhibiting the translation of p210(bcr-abl)  protein by a western blotting technique, inhibition of cell proliferation, and stimulation of apoptosis by flow cytometric analysis after 24 and 48 hours was studied.	Morpholinos	16-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
22549445-7	2012	Prolonged exposure of K562 cell line to Morpholino Oligo Antisense targeted against BCR-ABL showed proliferation inhibition  as the main feature.	Morpholinos	40-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
22549445-9	2012	The results indicate that Morpholino Oligo Antisense was able to inhibit p210(bcr-abl), but did not induce apoptosis  due to co-silencing of BCR.	Morpholinos	26-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
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 Mesylate	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
22675626-2	2012	Abl and its paralog, Arg, are unique among the tyrosine kinase family in that they contain an unusual extended C-terminal half consisting of multiple functional domains.	Arginine	21-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
22675626-4	2012	Indeed, a group of SH3-containing accessory proteins, or adaptor proteins, have been identified that bind to a proline-rich domain of the C-terminal portion of Abl and modulate its kinase activity, substrate recognition, and intracellular localization.	Proline	111-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-163
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 Mesylate	115-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-34
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.	nilotinib	260-269	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	233-240
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 Mesylate	18-26	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.	Dasatinib	271-280	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
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 Mesylate	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.	Dasatinib	271-280	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	233-240
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 Mesylate	6-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	233-240
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.	ponatinib	286-295	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
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.	nilotinib	260-269	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
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.	ponatinib	286-295	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	233-240
22846973-1	2012	BACKGROUND: With sorafenib displaying the highest affinities for Flt3, VEGFR (vascular endothelial growth factor receptor) and Raf and dasatinib for Abl and Src kinases, the profiles of kinases targeted by these inhibitors differ strongly.	Sorafenib	17-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-152
22846973-1	2012	BACKGROUND: With sorafenib displaying the highest affinities for Flt3, VEGFR (vascular endothelial growth factor receptor) and Raf and dasatinib for Abl and Src kinases, the profiles of kinases targeted by these inhibitors differ strongly.	Dasatinib	135-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-152
23049975-9	2012	CONCLUSIONS/SIGNIFICANCE: The present results suggest that c-Abl is a potential therapeutic target for ALS and that the c-Abl inhibitor dasatinib has neuroprotective properties in vitro and in vivo.	Dasatinib	136-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-64
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 Mesylate	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
23285088-3	2012	Nilotinib is 30 times more potent than imatinib towards BCR-ABL in vitro.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
23285088-3	2012	Nilotinib is 30 times more potent than imatinib towards BCR-ABL in vitro.	Imatinib Mesylate	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
23049975-9	2012	CONCLUSIONS/SIGNIFICANCE: The present results suggest that c-Abl is a potential therapeutic target for ALS and that the c-Abl inhibitor dasatinib has neuroprotective properties in vitro and in vivo.	Dasatinib	136-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-125
23028501-6	2012	We show that many translocation-prone pairs of regions genome-wide, including the cancer translocation partners BCR-ABL and MYC-IGH, display elevated Hi-C contact frequencies in normal human cells.	Histidine	150-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
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 Mesylate	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.	Cisplatin	191-200	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-167
22870341-0	2012	The proteolytic activity of separase in BCR-ABL-positive cells is increased by imatinib.	Imatinib Mesylate	79-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
22745749-6	2012	Nilotinib targets not only the BCR-ABL oncoprotein, but also platelet-derived growth factor (PDGF) receptor signalling.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
22879933-7	2012	Here we show that STI-571 (imatinib, inhibitor of c-Abl) inhibited RGDfV-induced ASM activity.	Imatinib Mesylate	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 Mesylate	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-55
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 Mesylate	102-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
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.	Dasatinib	112-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
22693568-3	2012	Inhibition of the oncogenic Abl kinase with imatinib reverses transformation, allowing progression to the next stage of B cell development.	Imatinib Mesylate	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-31
22253690-8	2012	Apoptin attributes such as SH2-like sequence similarity with CrkL SH2 domain, unique SH3 domain binding sequence, presence of proline-rich segments, and its nuclear affinity render the molecule capable of interaction with Bcr-Abl.	Proline	126-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	222-229
22558212-6	2012	YAP1 recruits c-Abl, a tyrosine kinase that binds and phosphorylates Nedd4.2 on tyrosine residues, thereby modifying its ubiquitin-ligase activity.	Tyrosine	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
22493660-0	2012	Structural and spectroscopic analysis of the kinase inhibitor bosutinib and an isomer of bosutinib binding to the Abl tyrosine kinase domain.	bosutinib	62-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-117
22493660-0	2012	Structural and spectroscopic analysis of the kinase inhibitor bosutinib and an isomer of bosutinib binding to the Abl tyrosine kinase domain.	bosutinib	89-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-117
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 Mesylate	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
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.	nilotinib	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
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.	Dasatinib	43-52	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.	bosutinib	34-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-77
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 Mesylate	135-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-77
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.	Nitriles	211-218	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-77
22493660-6	2012	We show that the fluorescence properties of these compounds allow inhibitor binding to be measured quantitatively, and that the infrared absorption of the nitrile group reveals a different electrostatic environment in the conserved ATP-binding sites of Abl and Src kinases.	Nitriles	155-162	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	253-256
22493660-6	2012	We show that the fluorescence properties of these compounds allow inhibitor binding to be measured quantitatively, and that the infrared absorption of the nitrile group reveals a different electrostatic environment in the conserved ATP-binding sites of Abl and Src kinases.	Adenosine Triphosphate	232-235	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	253-256
22238610-4	2012	We found that phosphorylation of PCNA at tyrosine 211 (Y211) enhanced its association with the non-receptor tyrosine kinase c-Abl.	Tyrosine	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-129
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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
21445688-5	2012	By using antibody which specifically recognizes phosphorylated serines (S807/811) in the c-Abl tyrosine kinase binding C-domain of human pRb, we provide evidence for the cell cycle-dependent changes in pRb-like proteins in root meristems cells of Vicia faba.	Serine	63-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-94
21890264-0	2011	Rapid automated detection of ABL kinase domain mutations in imatinib-resistant patients.	Imatinib Mesylate	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 Mesylate	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 Mesylate	37-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
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 Mesylate	147-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
22001646-0	2011	Nuclear c-Abl-mediated tyrosine phosphorylation induces chromatin structural changes through histone modifications that include H4K16 hypoacetylation.	Tyrosine	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-13
22021366-3	2011	We report that AMPK activators, such as metformin and 5-aminoimidazole-4-carboxamide ribonucleotide, suppress activation of the mTOR pathway in BCR-ABL-expressing cells.	Metformin	40-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
22021366-3	2011	We report that AMPK activators, such as metformin and 5-aminoimidazole-4-carboxamide ribonucleotide, suppress activation of the mTOR pathway in BCR-ABL-expressing cells.	AICA ribonucleotide	54-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
22001646-6	2011	Intriguingly, nuclear-targeted c-Abl induces heterochromatic profiles of histone methylation and acetylation, including hypoacetylation of histone H4 acetylated on lysine 16 (H4K16Ac).	Lysine	164-170	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-36
22001646-8	2011	Adriamycin-induced DNA damage stimulates translocation of c-Abl into the nucleus and induces chromatin structural changes together with H4K16 hypoacetylation.	Doxorubicin	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-63
22001646-10	2011	These results suggest that nuclear c-Abl plays an important role in chromatin dynamics through nuclear tyrosine phosphorylation-induced heterochromatic histone modifications.	Tyrosine	103-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-40
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 Mesylate	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 Mesylate	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 Mesylate	29-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
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 Mesylate	125-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
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 Mesylate	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-31
22033461-2	2011	And their potency as Abl kinase inhibitors have been screened by a robust virtual screening method developed based on the crystal structure (PDB code 2hyy) of Abl-imatinib complex using Surflex-Docking.	surflex	186-193	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-24
22033461-2	2011	And their potency as Abl kinase inhibitors have been screened by a robust virtual screening method developed based on the crystal structure (PDB code 2hyy) of Abl-imatinib complex using Surflex-Docking.	surflex	186-193	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-162
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 Mesylate	24-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-78
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.	Adenosine Triphosphate	175-178	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-78
22200699-6	2011	In K562/IR cell cultures, the expressions of p210(Bcr-Abl), IKKa and nuclear NF-kappaB p65 were all decreased following BBD9 and BBM treatments, but BBD9 produced more potent effect; cytoplasmic NF-kappaB p65 showed no obvious changes after the treatments.	Santowhite powder	129-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
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 Mesylate	35-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
22169319-2	2011	To date, a number of BCR/ABL transgenic animal models have been established using different promoter or tetracycline-controlling system.	Tetracycline	104-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
21900236-11	2011	Removal of zinc from Mt3 or pep1 with tetrakis(2-pyridylmethyl)ethylenediamine abrogated the effect of Mt3 on the association of c-Abl and F-actin, indicating that zinc binding is necessary for this action.	SCHEMBL231091	38-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-134
21602891-0	2011	Phosphorylation of Crk on tyrosine 251 in the RT loop of the SH3C domain promotes Abl kinase transactivation.	Tyrosine	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-85
21602891-5	2011	Using streptavidin-biotin pull downs and unbiased high-throughput Src Homology 2 (SH2) profiling approaches, we found that a pY251 phosphopeptide binds specifically to a subset of SH2 domains, including Abl and Arg SH2, and that binding of pY251 to Abl SH2 induces transactivation of Abl 1b.	Arginine	211-214	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	203-206
21602891-5	2011	Using streptavidin-biotin pull downs and unbiased high-throughput Src Homology 2 (SH2) profiling approaches, we found that a pY251 phosphopeptide binds specifically to a subset of SH2 domains, including Abl and Arg SH2, and that binding of pY251 to Abl SH2 induces transactivation of Abl 1b.	Arginine	211-214	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	249-252
21602891-5	2011	Using streptavidin-biotin pull downs and unbiased high-throughput Src Homology 2 (SH2) profiling approaches, we found that a pY251 phosphopeptide binds specifically to a subset of SH2 domains, including Abl and Arg SH2, and that binding of pY251 to Abl SH2 induces transactivation of Abl 1b.	Arginine	211-214	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	249-252
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 Mesylate	122-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
21763684-6	2011	Recent findings have implicated c-Abl in a cisplatin-induced signaling pathway eliciting death of immature oocytes.	Cisplatin	43-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-37
21763684-7	2011	Pharmacological inhibition of c-Abl by Imatinib (STI571) protects the ovarian reserve from the toxic effect of cisplatin.	Imatinib Mesylate	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 Mesylate	49-55	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.	Cisplatin	111-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-35
22024730-0	2011	Enhancement of specific cellular immune response induced by glycosyl-phosphatidylinositol-anchored BCR/ABL and mIL-12.	Glycosylphosphatidylinositols	60-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
21625221-0	2011	NF-kappaB suppresses ROS levels in BCR-ABL(+) cells to prevent activation of JNK and cell death.	Reactive Oxygen Species	21-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
21625221-2	2011	BCR-ABL, the oncoprotein associated with the majority of chronic myeloid leukemias (CMLs), induces accumulation of intracellular ROS, causing enhanced signaling downstream of PI3K.	Reactive Oxygen Species	129-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
21625221-5	2011	Here, we analyze the potential involvement of NF-kappaB in moderating BCR-ABL-induced ROS levels to protect from death.	Reactive Oxygen Species	86-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
21625221-6	2011	The data confirm that BCR-ABL promotes ROS and demonstrate that NF-kappaB prevents excessive levels.	Reactive Oxygen Species	39-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
21908430-2	2011	The additional approved ABL tyrosine kinase inhibitors (TKIs) nilotinib and dasatinib, along with investigational TKIs such as ponatinib (AP24534) and DCC-2036, support the possibility that mutation-mediated resistance in chronic myeloid leukemia can be fully controlled; however, the molecular events underlying resistance in patients lacking BCR-ABL point mutations are largely unknown.	nilotinib	62-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-27
21908430-2	2011	The additional approved ABL tyrosine kinase inhibitors (TKIs) nilotinib and dasatinib, along with investigational TKIs such as ponatinib (AP24534) and DCC-2036, support the possibility that mutation-mediated resistance in chronic myeloid leukemia can be fully controlled; however, the molecular events underlying resistance in patients lacking BCR-ABL point mutations are largely unknown.	Dasatinib	76-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	344-351
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 Mesylate	162-170	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-17
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.	nilotinib	255-264	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-17
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.	Dasatinib	272-281	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-17
21900237-0	2011	CDK1-mediated phosphorylation of Abi1 attenuates Bcr-Abl-induced F-actin assembly and tyrosine phosphorylation of WAVE complex during mitosis.	Tyrosine	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
21900237-5	2011	This mitotic inhibition of F-actin assembly is accompanied by an attenuation of Bcr-Abl-induced tyrosine phosphorylation of the WAVE complex.	Tyrosine	96-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
21900237-7	2011	The Abi1 phosphorylated on serine 216 displayed greatly reduced tyrosine phosphorylation in the hematopoietic cells transformed by Bcr-Abl.	Serine	27-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
21900237-7	2011	The Abi1 phosphorylated on serine 216 displayed greatly reduced tyrosine phosphorylation in the hematopoietic cells transformed by Bcr-Abl.	Tyrosine	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
21900237-8	2011	Moreover, a phosphomimetic mutation of serine 216 to aspartic acid in Abi1 was sufficient to attenuate Bcr-Abl-induced tyrosine phosphorylation of the WAVE complex and F-actin assembly.	Tyrosine	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
21745187-9	2011	Likewise, adaphostin functionally enhanced caffeine-induced Fas/FasL up-regulation in leukaemia cells that expressed Bcr/Abl.	Caffeine	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
21990039-0	2011	N-[2-Methyl-5-(triazol-1-yl)phenyl]pyrimidin-2-amine as a scaffold for the synthesis of inhibitors of Bcr-Abl.	n-[2-methyl-5-(triazol-1-yl)phenyl]pyrimidin-2-amine	0-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
21990039-1	2011	N-[2-Methyl-5-(triazol-1-yl)phenyl]pyrimidin-2-amine derivatives were synthesized and evaluated in vitro for their potential use as inhibitors of Bcr-Abl.	n-[2-methyl-5-(triazol-1-yl)phenyl]pyrimidin-2-amine	0-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	146-153
21745187-0	2011	Adaphostin promotes caffeine-evoked autocrine Fas-mediated death pathway activation in Bcr/Abl-positive leukaemia cells.	Caffeine	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
21769920-5	2011	Furthermore, Abl phosphorylates STH on its single tyrosine residue and STH increases tyrosine phosphorylation by Abl.	Tyrosine	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
21745187-0	2011	Adaphostin promotes caffeine-evoked autocrine Fas-mediated death pathway activation in Bcr/Abl-positive leukaemia cells.	ammonium ferrous sulfate	46-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
21745187-2	2011	Co-treatment with adaphostin (a Bcr/Abl inhibitor) was found to potentiate caffeine-induced Fas/FasL up-regulation.	Caffeine	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
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 Mesylate	68-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
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 Mesylate	159-176	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	259-266
21903771-0	2011	BCR-ABL transcript dynamics support the hypothesis that leukemic stem cells are reduced during imatinib treatment.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
21769920-5	2011	Furthermore, Abl phosphorylates STH on its single tyrosine residue and STH increases tyrosine phosphorylation by Abl.	Tyrosine	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-116
21769920-5	2011	Furthermore, Abl phosphorylates STH on its single tyrosine residue and STH increases tyrosine phosphorylation by Abl.	Tyrosine	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
21769920-5	2011	Furthermore, Abl phosphorylates STH on its single tyrosine residue and STH increases tyrosine phosphorylation by Abl.	Tyrosine	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-116
21718141-5	2011	Two imatinib-resistant K562 lines both had increased BCR-ABL expression as the apparent mode of resistance.	Imatinib Mesylate	4-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
21718141-6	2011	However, when a dasatinib-resistant K562 culture was generated we observed gradually increasing BCR-ABL expression which peaked prior to identification of the T315I mutation.	Dasatinib	16-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
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 Mesylate	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 Mesylate	16-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
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 Mesylate	30-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
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 Mesylate	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
21455220-4	2011	Met ensures cell survival through a new path in which c-Abl and p38-MAPK are employed to elicit p53 phosphorylation on Ser(392) and Mdm2 upregulation.	Serine	119-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-59
21705667-0	2011	Glucosylceramide synthase inhibitor PDMP sensitizes chronic myeloid leukemia T315I mutant to Bcr-Abl inhibitor and cooperatively induces glycogen synthase kinase-3-regulated apoptosis.	RV 538	36-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
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 Mesylate	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 Mesylate	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 Mesylate	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
21935931-7	2011	Our results also demonstrate that the AKT signaling pathway is involved in the regulation of Jab1 by Bcr-Abl because the AKT inhibitor LY294002 but not the ERK inhibitor PD98059 reduces Jab1 promoter activity and mRNA expression.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	135-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
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 Mesylate	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.	RV 538	13-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	159-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
20454833-0	2011	Ascorbate/menadione-induced oxidative stress kills cancer cells that express normal or mutated forms of the oncogenic protein Bcr-Abl.	Ascorbic Acid	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
20454833-0	2011	Ascorbate/menadione-induced oxidative stress kills cancer cells that express normal or mutated forms of the oncogenic protein Bcr-Abl.	Vitamin K 3	10-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
21570118-0	2011	AID expression is correlated with Bcr-Abl expression in CML-LBC and can be down-regulated by As2O3 and/or imatinib.	Arsenic Trioxide	93-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
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 Mesylate	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
21795709-5	2011	Inhibition of PTP1B elicits tyrosine phosphorylation of Bcr-Abl that triggers the degradation of Bcr-Abl through ubiquitination via the lysosomal pathway.	Tyrosine	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
21795709-5	2011	Inhibition of PTP1B elicits tyrosine phosphorylation of Bcr-Abl that triggers the degradation of Bcr-Abl through ubiquitination via the lysosomal pathway.	Tyrosine	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
21795709-6	2011	The degradation of Bcr-Abl consequently inhibits tyrosine phosphorylation of Bcr-Abl substrates and the downstream production of intracellular reactive oxygen species.	Tyrosine	49-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
21795709-6	2011	The degradation of Bcr-Abl consequently inhibits tyrosine phosphorylation of Bcr-Abl substrates and the downstream production of intracellular reactive oxygen species.	Tyrosine	49-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
21795709-6	2011	The degradation of Bcr-Abl consequently inhibits tyrosine phosphorylation of Bcr-Abl substrates and the downstream production of intracellular reactive oxygen species.	Reactive Oxygen Species	143-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
21795709-6	2011	The degradation of Bcr-Abl consequently inhibits tyrosine phosphorylation of Bcr-Abl substrates and the downstream production of intracellular reactive oxygen species.	Reactive Oxygen Species	143-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
21795709-7	2011	Furthermore, PTP1B inhibition reduces cell viability and the IC(50) of the Bcr-Abl inhibitor imatinib mesylate.	Imatinib Mesylate	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 Mesylate	218-226	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	270-277
21762985-0	2011	Low-level Bcr-Abl mutations are very rare in chronic myeloid leukemia patients who are in major molecular response on first-line nilotinib.	nilotinib	129-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
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.	nilotinib	134-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
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 Mesylate	193-201	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
21762985-5	2011	Our results suggest that a) Bcr-Abl mutations, even at low level, seem to be very rare in patients in MMR on first-line nilotinib; b) low-level mutations do not always predict for subsequent relapse.	nilotinib	120-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
21813412-8	2011	The siRNA knockdown of Src, Fyn, or Abl1 enhanced paclitaxel-mediated growth inhibition in ovarian cancer cells compared with a control siRNA.	Paclitaxel	50-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-40
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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
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 Mesylate	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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-159
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 Mesylate	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 Mesylate	55-72	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
21576001-0	2011	Reversal of Imatinib resistance in BCR-ABL-positive leukemia after inhibition of the Na+/H+ exchanger.	Imatinib Mesylate	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
21670084-2	2011	Among the most sensitive dasatinib targets are ABL, the SRC family kinases (SRC, LCK, HCK, FYN, YES, FGR, BLK, LYN, and FRK), and the receptor tyrosine kinases c-KIT, platelet-derived growth factor receptor (PDGFR) alpha and beta, discoidin domain receptor 1 (DDR1), c-FMS, and ephrin receptors.	Dasatinib	25-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
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 Mesylate	51-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
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.	Dasatinib	64-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
21902298-12	2011	Dasatinib was generally equally effective in patients with or without BCR-ABL mutations at baseline.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
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 Mesylate	120-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
21705667-12	2011	The synergistic efficacy was Bcr-Abl restricted and correlated to increased intracellular ceramide levels and acted through GSK-3-mediated apoptosis.	Ceramides	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
21863287-0	2011	RCSD1-ABL1-positive B lymphoblastic leukemia is sensitive to dexamethasone and tyrosine kinase inhibitors and rapidly evolves clonally by chromosomal translocations.	Dexamethasone	61-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-10
21637917-0	2011	BCR-ABL- and Ras-independent activation of Raf as a novel mechanism of Imatinib resistance in CML.	Imatinib Mesylate	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-16
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 Mesylate	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 Mesylate	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 Mesylate	247-255	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	213-220
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 Mesylate	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 Mesylate	285-293	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
21863287-7	2011	Tyrosine kinase inhibitors, imatinib and dasatinib, coadministered with dexamethasone achieved transient clinical effects in the present RCSD1-ABL1-positive ALL.	Imatinib Mesylate	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-147
21863287-7	2011	Tyrosine kinase inhibitors, imatinib and dasatinib, coadministered with dexamethasone achieved transient clinical effects in the present RCSD1-ABL1-positive ALL.	Dasatinib	41-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-147
21863287-7	2011	Tyrosine kinase inhibitors, imatinib and dasatinib, coadministered with dexamethasone achieved transient clinical effects in the present RCSD1-ABL1-positive ALL.	Dexamethasone	72-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-147
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 Mesylate	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
21663510-0	2011	Clinical outcome of chronic myeloid leukemia imatinib-resistant patients: do BCR-ABL kinase domain mutations affect patient survival?	Imatinib Mesylate	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 Mesylate	3-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
21665275-3	2011	AT9283 is a novel Aurora kinase inhibitor with secondary activity against FLT3 and ABL.	1-cyclopropyl-3-(3-(5-morpholin-4-ylmethyl-1H-benzoimidazol-2-yl)-1H-pyrazol-4-yl)urea	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-86
21251937-0	2011	Inhibition of PDGF, TGF-beta, and Abl signaling and reduction of liver fibrosis by the small molecule Bcr-Abl tyrosine kinase antagonist Nilotinib.	nilotinib	137-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-37
21251937-0	2011	Inhibition of PDGF, TGF-beta, and Abl signaling and reduction of liver fibrosis by the small molecule Bcr-Abl tyrosine kinase antagonist Nilotinib.	nilotinib	137-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
21251937-1	2011	BACKGROUND & AIMS: Nilotinib is a novel tyrosine kinase inhibitor of Bcr-Abl and other kinases.	Adenosine Monophosphate	12-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
21251937-1	2011	BACKGROUND & AIMS: Nilotinib is a novel tyrosine kinase inhibitor of Bcr-Abl and other kinases.	nilotinib	23-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
21251937-9	2011	Furthermore, PDGF- and TGFbeta-activated phosphorylated form(s) of Abl in human HSCs were inhibited by Nilotinib.	nilotinib	103-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-70
21251937-13	2011	We also observed reduced expression of phosphorylated ERK, Akt, and Abl in the Nilotinib-treated CCl(4) and BDL livers.	nilotinib	79-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-71
21251937-13	2011	We also observed reduced expression of phosphorylated ERK, Akt, and Abl in the Nilotinib-treated CCl(4) and BDL livers.	Cefaclor	97-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-71
21251937-15	2011	CONCLUSIONS: These studies uncover a novel role of Bcr-Abl activity in treatment of liver fibrosis through multiple mechanisms and indicate that Nilotinib represents a potentially effective antifibrotic agent.	nilotinib	145-154	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
21715330-5	2011	Incomplete binding-induced folding exposes tyrosine 88 of p27 for phosphorylation by the nonreceptor tyrosine kinase Abl.	Tyrosine	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-120
21621524-6	2011	PYR-41 also mediated cross-linking of specific protein kinases (Bcr-Abl, Jak2) to inhibit their signaling activity.	4(4-(5-nitro-furan-2-ylmethylene)-3,5-dioxo-pyrazolidin-1-yl)-benzoic acid ethyl ester	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
21861543-2	2011	It is an aminopyrimidine-based, high-affinity inhibitor of the tyrosine kinase activity of BCR-ABL.	2-aminopyrimidine	9-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
21600647-3	2011	In the present study, we document to explore an approach to simultaneously deliver two drugs at target sites (i.e. Bcr-Abl oncoprotein) using poly (lactide-co-glycolide) (PLGA) nanoparticles.	Polyglactin 910	142-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
21693657-0	2011	Imatinib sensitivity in BCR-ABL1-positive chronic myeloid leukemia cells is regulated by the remaining normal ABL1 allele.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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.	Tyrosine	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-8
21693657-6	2011	Furthermore, 12 genes associated with imatinib resistance were favorably deregulated in Abl1(-/-) leukemia.	Imatinib Mesylate	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-92
21440619-4	2011	Tyrosine phosphorylation of PKCdelta was required for PKCdelta binding to c-Abl in the cytoplasm, and inhibition of c-Abl by STI571 or knock-down of c-Abl by RNAi decreased the phosphorylation of PKCdelta.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-79
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 Mesylate	237-245	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-164
21440619-4	2011	Tyrosine phosphorylation of PKCdelta was required for PKCdelta binding to c-Abl in the cytoplasm, and inhibition of c-Abl by STI571 or knock-down of c-Abl by RNAi decreased the phosphorylation of PKCdelta.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-121
21440619-4	2011	Tyrosine phosphorylation of PKCdelta was required for PKCdelta binding to c-Abl in the cytoplasm, and inhibition of c-Abl by STI571 or knock-down of c-Abl by RNAi decreased the phosphorylation of PKCdelta.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-121
21440619-6	2011	Furthermore, we found that interaction of PKCdelta and c-Abl played a crucial role in p53 accumulation in the nucleus, which was linked to the apoptosis of NPCs in response to high glucose.	Glucose	181-188	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-60
21630681-0	2011	Synthesis and characterization of a BODIPY conjugate of the BCR-ABL kinase inhibitor Tasigna (nilotinib): evidence for transport of Tasigna and its fluorescent derivative by ABC drug transporters.	nilotinib	94-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
21756066-4	2011	For the first time, The results of this study showed for the first time that nilotinib induces apoptosis through upregulating ceramide synthase genes and downregulating SK-1 in CML cells in addition to inhibition of BCR/ABL.	nilotinib	77-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	216-223
21281966-2	2011	Specifically, inhibition of either c-abl, which modulates Rad51 directed homologous recombination or DNA-PK dependent nonhomologous end joining has been shown to sensitize primary CLL lymphocytes to chlorambucil.	Chlorambucil	199-211	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-40
21281966-3	2011	Here we report that inhibition of c-abl can result in a compensatory increase in DNA-PK and thus inhibition of both c-abl and DNA-PK optimally sensitizes CLL lymphocytes to chlorambucil.	Chlorambucil	173-185	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-39
21630681-1	2011	Tasigna (Nilotinib) is a BCR-ABL kinase inhibitor recently approved by the Food and Drug Administration, which is indicated for the treatment of drug-resistant chronic myelogenous leukemia (CML).	nilotinib	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
21630681-1	2011	Tasigna (Nilotinib) is a BCR-ABL kinase inhibitor recently approved by the Food and Drug Administration, which is indicated for the treatment of drug-resistant chronic myelogenous leukemia (CML).	nilotinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
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 Mesylate	70-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
21356308-2	2011	The induction of P-glycoprotein expression that occurred in response to adriamycin treatment was accompanied by increased phosphorylation of BCR-ABL and STAT5, as well as increased telomerase protein expression.	Doxorubicin	72-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-148
21781306-1	2011	BACKGROUND: The proto-oncogene, c-Abl encodes a ubiquitously expressed tyrosine kinase that critically governs the cell death response induced by genotoxic agents such as ionizing radiation and cisplatin.	Cisplatin	194-203	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-37
21781306-4	2011	RESULTS: We investigated the role of acetyl modification in regulating apoptotic activity of Abl and the results showed that DNA strand break-inducing agents, ionizing radiation and bleomycin induced Abl acetylation.	Bleomycin	182-191	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-96
21781306-4	2011	RESULTS: We investigated the role of acetyl modification in regulating apoptotic activity of Abl and the results showed that DNA strand break-inducing agents, ionizing radiation and bleomycin induced Abl acetylation.	Bleomycin	182-191	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	200-203
21781306-5	2011	Using mass spectrophotometry and site-specific acetyl antibody, we identified Abl K921, located in the DNA binding domain, and conforming to one of the lysine residue in the consensus acetylation motif (KXXK--X3-5--SGS) is acetylated following DNA damage.	Lysine	152-158	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-81
21700550-2	2011	In Philadelphia chromosome-positive (Ph(+)) ALL, the optimal treatment requires the addition of BCR-ABL tyrosine kinase inhibitors, as imatinib.	Imatinib Mesylate	135-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
21700550-6	2011	The first evaluations of AP24534 present this drug as a potent multi-targeted kinase inhibitor active against T315I and all other BCR-ABL mutants.	ponatinib	25-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
21633166-7	2011	M and MSL subtypes were enriched in GE for epithelial-mesenchymal transition, and growth factor pathways and cell models responded to NVP-BEZ235 (a PI3K/mTOR inhibitor) and dasatinib (an abl/src inhibitor).	Dasatinib	173-182	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	187-190
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
21483442-2	2011	Here, to enhance the BMS-214662 apoptotic effect, we further targeted the extracellular signal-regulated kinase (ERK) pathway, downstream of BCR-ABL, by treating CD34+ CML stem/progenitor cells with a highly selective adenosine triphosphate (ATP) non-competitive MEK inhibitor, PD184352.	Adenosine Triphosphate	218-240	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-148
21382639-1	2011	Chronic myeloid leukaemia has a specific therapy: BCR/ABL inhibitor imatinib.	Imatinib Mesylate	68-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
21654685-8	2011	Treatment with the Src/Abl inhibitor, dasatinib, reduced HOXC11-SRC-1 interaction and prevented recruitment of HOXC11 to the S100beta promoter.	Dasatinib	38-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-26
21489623-0	2011	NUP214-ABL1 positive T-cell acute lymphoblastic leukemia patient shows an initial favorable response to imatinib therapy post relapse.	Imatinib Mesylate	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 Mesylate	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
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 Mesylate	47-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
21715626-6	2011	Oxidative stress induces the c-Abl-dependent tyrosine phosphorylation of MST1 and increases the interaction between MST1 and FOXO3 (Forkhead box O3), thereby activating the MST1-FOXO signaling pathway, leading to cell death in both primary culture neurons and rat hippocampal neurons.	Tyrosine	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-34
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 Mesylate	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
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 Mesylate	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 Mesylate	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-46
27264123-4	2011	METHODS: We used the dHPLC based assay for the screening of ABL point mutations.	dhplc	21-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-63
21528941-1	2011	Dasatinib is an oral dual tyrosine kinase inhibitor active against ABL1 and SRC family kinases.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-71
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 Mesylate	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 Mesylate	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 Mesylate	128-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	259-266
21392556-6	2011	RESULTS: Expression of BCR-ABL increased both at RNA and protein levels in imatinib-resistant cell lines.	Imatinib Mesylate	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
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 Mesylate	62-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
21622134-0	2011	NPB001-05 inhibits Bcr-Abl kinase leading to apoptosis of imatinib-resistant cells.	Imatinib Mesylate	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
21677481-9	2011	In addition to being more potent than IM against wild-type BCR-ABL, nilotinib is significantly active against many IM-resistant BCR-ABL mutants.	nilotinib	68-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
21677481-9	2011	In addition to being more potent than IM against wild-type BCR-ABL, nilotinib is significantly active against many IM-resistant BCR-ABL mutants.	nilotinib	68-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
21292323-1	2011	Imatinib inhibits the ABL tyrosine kinase and is effective for the treatment of chronic myeloid leukemia (CML).	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-25
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 Mesylate	132-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	191-198
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 Mesylate	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
21482694-1	2011	Ponatinib (AP24534) is a novel multitargeted kinase inhibitor that potently inhibits native and mutant BCR-ABL at clinically achievable drug levels.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
21482694-1	2011	Ponatinib (AP24534) is a novel multitargeted kinase inhibitor that potently inhibits native and mutant BCR-ABL at clinically achievable drug levels.	ponatinib	11-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
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 Mesylate	155-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
21454413-6	2011	Similarly, the treatment of primary MALT lymphoma cells with the ABL inhibitors imatinib and dasatinib prevented tumor cell growth.	Imatinib Mesylate	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-68
21454413-6	2011	Similarly, the treatment of primary MALT lymphoma cells with the ABL inhibitors imatinib and dasatinib prevented tumor cell growth.	Dasatinib	93-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-68
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.	KW 2449	72-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
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.	KW 2449	72-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
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 Mesylate	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
21474579-1	2011	PURPOSE: The purpose of this study was to determine whether histone deacetylase (HDAC) inhibitors (HDACI) such as vorinostat or entinostat (SNDX-275) could increase the lethality of the dual Bcr/Abl-Aurora kinase inhibitor KW-2449 in various Bcr/Abl(+) human leukemia cells, including those resistant to imatinib mesylate (IM).	Vorinostat	114-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	191-198
21474579-1	2011	PURPOSE: The purpose of this study was to determine whether histone deacetylase (HDAC) inhibitors (HDACI) such as vorinostat or entinostat (SNDX-275) could increase the lethality of the dual Bcr/Abl-Aurora kinase inhibitor KW-2449 in various Bcr/Abl(+) human leukemia cells, including those resistant to imatinib mesylate (IM).	Vorinostat	114-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	242-249
21474579-1	2011	PURPOSE: The purpose of this study was to determine whether histone deacetylase (HDAC) inhibitors (HDACI) such as vorinostat or entinostat (SNDX-275) could increase the lethality of the dual Bcr/Abl-Aurora kinase inhibitor KW-2449 in various Bcr/Abl(+) human leukemia cells, including those resistant to imatinib mesylate (IM).	entinostat	128-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	191-198
21474579-1	2011	PURPOSE: The purpose of this study was to determine whether histone deacetylase (HDAC) inhibitors (HDACI) such as vorinostat or entinostat (SNDX-275) could increase the lethality of the dual Bcr/Abl-Aurora kinase inhibitor KW-2449 in various Bcr/Abl(+) human leukemia cells, including those resistant to imatinib mesylate (IM).	entinostat	128-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	242-249
21474579-1	2011	PURPOSE: The purpose of this study was to determine whether histone deacetylase (HDAC) inhibitors (HDACI) such as vorinostat or entinostat (SNDX-275) could increase the lethality of the dual Bcr/Abl-Aurora kinase inhibitor KW-2449 in various Bcr/Abl(+) human leukemia cells, including those resistant to imatinib mesylate (IM).	entinostat	140-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	191-198
21474579-1	2011	PURPOSE: The purpose of this study was to determine whether histone deacetylase (HDAC) inhibitors (HDACI) such as vorinostat or entinostat (SNDX-275) could increase the lethality of the dual Bcr/Abl-Aurora kinase inhibitor KW-2449 in various Bcr/Abl(+) human leukemia cells, including those resistant to imatinib mesylate (IM).	entinostat	140-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	242-249
21474579-2	2011	EXPERIMENTAL DESIGN: Bcr/Abl(+) chronic myelogenous leukemia (CML) and acute lymphoblastic leukemia (ALL) cells, including those resistant to IM (T315I, E255K), were exposed to KW-2449 in the presence or absence of vorinostat or SNDX-275, after which apoptosis and effects on signaling pathways were examined.	Vorinostat	215-225	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
21474579-2	2011	EXPERIMENTAL DESIGN: Bcr/Abl(+) chronic myelogenous leukemia (CML) and acute lymphoblastic leukemia (ALL) cells, including those resistant to IM (T315I, E255K), were exposed to KW-2449 in the presence or absence of vorinostat or SNDX-275, after which apoptosis and effects on signaling pathways were examined.	entinostat	229-237	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
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.	Adenosine Triphosphate	30-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
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 Mesylate	137-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
22035738-6	2011	Although both are potent and specific BCR-ABL TKIs, dasatinib and nilotinib exhibit unique pharmacological profiles and response patterns relative to different patient characteristics, such as disease stage and BCR-ABL mutational status.	Dasatinib	52-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	211-218
22035738-6	2011	Although both are potent and specific BCR-ABL TKIs, dasatinib and nilotinib exhibit unique pharmacological profiles and response patterns relative to different patient characteristics, such as disease stage and BCR-ABL mutational status.	nilotinib	66-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
22035738-6	2011	Although both are potent and specific BCR-ABL TKIs, dasatinib and nilotinib exhibit unique pharmacological profiles and response patterns relative to different patient characteristics, such as disease stage and BCR-ABL mutational status.	nilotinib	66-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	211-218
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 Mesylate	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-14
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 Mesylate	81-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	188-193
21505103-2	2011	The BCR-ABL(T315I) mutant is highly resistant to imatinib, nilotinib, and dasatinib, and is frequently detected in relapsed patients.	Imatinib Mesylate	49-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
21505103-2	2011	The BCR-ABL(T315I) mutant is highly resistant to imatinib, nilotinib, and dasatinib, and is frequently detected in relapsed patients.	nilotinib	59-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
21505103-2	2011	The BCR-ABL(T315I) mutant is highly resistant to imatinib, nilotinib, and dasatinib, and is frequently detected in relapsed patients.	Dasatinib	74-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
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 Mesylate	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
21277011-9	2011	In the paraffin-embedded specimens we tested, c-abl was expressed universally.	Paraffin	7-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-51
21480391-6	2011	Conversely, introducing kinase-activated c-ABL can rescue fulvestrant-induced ERalpha downregulation.	Fulvestrant	58-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-46
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 Mesylate	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-74
21443205-1	2011	A family of dual Src/Abl inhibitors characterized by a substituted pyrazolo[3,4-d]pyrimidine scaffold was previously reported by us and proved to be active against several tumor cell lines.	pyrazolo(3,4-d)pyrimidine	67-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-24
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 Mesylate	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 Mesylate	57-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
21463117-1	2011	Dasatinib is a kinase inhibitor that inhibits BCR-ABL, Src family kinases, c-Kit, and platelet-derived growth factor receptor kinase.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
21463117-3	2011	Potential targets for dasatinib in chronic lymphocytic leukemia (CLL) include Lyn (a Src family kinase), ABL, and the associated CD40 pathway.	Dasatinib	22-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-108
21443205-4	2011	A series of more soluble pyrazolo[3,4-d]pyrimidine derivatives were rationally designed and proved to maintain the dual Src/Abl activity of the lead.	pyrazolo(3,4-d)pyrimidine	25-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-127
21541334-0	2011	Abcg2 overexpression represents a novel mechanism for acquired resistance to the multi-kinase inhibitor Danusertib in BCR-ABL-positive cells in vitro.	danusertib	104-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
21541334-2	2011	Danusertib (formerly PHA-739358) is a potent pan-aurora and ABL kinase inhibitor with activity against known BCR-ABL mutations, including T315I.	danusertib	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
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 Mesylate	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
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 Mesylate	9-26	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 Mesylate	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-180
21575924-8	2011	Patients who relapse during treatment with dasatinib frequently carry the T315I mutation of BCR-ABL.	Dasatinib	43-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
21226671-1	2011	Dasatinib (BMS-354825, Sprycel ) is an oral, multitargeted inhibitor of receptor tyrosine kinases (RTKs), including BCR-ABL fusion protein, stem cell factor receptor (c-KIT), platelet-derived growth factor receptor (PDGFR), and Src family kinases (SFKs).	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
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 Mesylate	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 Mesylate	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-178
21295380-0	2011	Exploration of (S)-3-aminopyrrolidine as a potentially interesting scaffold for discovery of novel Abl and PI3K dual inhibitors.	(S)-3-Aminopyrrolidine	15-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-102
21295380-1	2011	Based on the literature-reported compensatory effect of PI3K on Abl inhibition and the improved preclinical effect of drug combination of Abl and PI3K inhibitors, a series of compounds bearing novel scaffold of (S)-3-aminopyrrolidine was identified as Abl and PI3K dual inhibitors through support vector machine screening tool, which were subsequently synthesized and tested.	(S)-3-Aminopyrrolidine	211-233	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-67
21295380-1	2011	Based on the literature-reported compensatory effect of PI3K on Abl inhibition and the improved preclinical effect of drug combination of Abl and PI3K inhibitors, a series of compounds bearing novel scaffold of (S)-3-aminopyrrolidine was identified as Abl and PI3K dual inhibitors through support vector machine screening tool, which were subsequently synthesized and tested.	(S)-3-Aminopyrrolidine	211-233	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-141
21295380-1	2011	Based on the literature-reported compensatory effect of PI3K on Abl inhibition and the improved preclinical effect of drug combination of Abl and PI3K inhibitors, a series of compounds bearing novel scaffold of (S)-3-aminopyrrolidine was identified as Abl and PI3K dual inhibitors through support vector machine screening tool, which were subsequently synthesized and tested.	(S)-3-Aminopyrrolidine	211-233	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-141
20942869-5	2011	Resistance of K562r due to duplication of autophosphorylation of wild-type Bcr-Abl was not overcome by dasatinib and nilotinib, but was sensitive to bortezomib.	Bortezomib	149-159	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
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 Mesylate	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
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.	Dasatinib	134-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
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.	nilotinib	148-157	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
21417343-1	2011	ABL2 (also known as ARG (ABL related gene)) is closely related to the well-studied Abelson kinase cABL.	Arginine	20-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-102
21417343-1	2011	ABL2 (also known as ARG (ABL related gene)) is closely related to the well-studied Abelson kinase cABL.	lauric acid	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-102
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).	Dasatinib	176-185	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
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 Mesylate	281-289	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
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 Mesylate	76-84	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.	Dasatinib	114-123	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.	nilotinib	125-134	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.	Bortezomib	150-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
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 Mesylate	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
21419932-1	2011	Nilotinib, a novel tyrosine kinase inhibitor (TKI) that inhibits BCR-ABL, the stem cell factor receptor (KIT), and platelet-derived growth factor receptor-alpha (PDGFRalpha), is approved for the treatment of patients with newly diagnosed Philadelphia chromosome-positive chronic myelogenous leukemia (CML) and those with CML that is imatinib-resistant or -intolerant.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
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 Mesylate	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
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.	nilotinib	0-9	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	152-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-178
21447799-2	2011	We performed global tyrosine phosphoprofiling by quantitative mass spectrometry of Bcr-Abl-transformed cells in which the activities of the SFKs were perturbed to build a detailed context-dependent network of cancer signaling.	Tyrosine	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
21320496-3	2011	The SH3 domain of Abi-1 and the proline-rich domain of c-Abl are involved in this interaction.	Proline	32-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-60
21233313-9	2011	Importantly, pimozide induces similar effects in the presence of the T315I BCR/ABL mutation that renders the kinase resistant to presently available inhibitors.	Pimozide	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
21248063-4	2011	Induction of apoptosis because of aggresomal compartmentalization of Bcr-Abl was observed in both imatinib-sensitive and -resistant cells.	Imatinib Mesylate	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
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 Mesylate	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
21498698-0	2011	Inhibition of c-ABL sensitizes breast cancer cells to the dual ErbB receptor tyrosine kinase inhibitor lapatinib (GW572016).	Lapatinib	103-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
21498698-0	2011	Inhibition of c-ABL sensitizes breast cancer cells to the dual ErbB receptor tyrosine kinase inhibitor lapatinib (GW572016).	Lapatinib	114-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
21498698-3	2011	In this study, we test whether the non-receptor tyrosine kinase c-Abl regulates the responsiveness of breast cancer cells to lapatinib and, if so, whether the combination treatment with lapatinib plus the c-ABL kinase inhibitor imatinib (STI571; Gleevec) can sensitize breast cancer cells to the treatment.	Lapatinib	125-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-69
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 Mesylate	100-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-43
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.	Lapatinib	177-186	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.	Lapatinib	34-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-94
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.	Lapatinib	137-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-94
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 Mesylate	152-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-94
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 Mesylate	42-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-27
20945321-9	2011	Although both are potent and specific BCR-ABL TKIs, dasatinib and nilotinib exhibit unique pharmacologic profiles and response patterns relative to different patient characteristics, such as disease stage and BCR-ABL mutation status.	Dasatinib	52-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-216
21166958-0	2011	Rakicidin A effectively induces apoptosis in hypoxia adapted Bcr-Abl positive leukemic cells.	rakicidin A	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
20945321-9	2011	Although both are potent and specific BCR-ABL TKIs, dasatinib and nilotinib exhibit unique pharmacologic profiles and response patterns relative to different patient characteristics, such as disease stage and BCR-ABL mutation status.	nilotinib	66-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
20945321-9	2011	Although both are potent and specific BCR-ABL TKIs, dasatinib and nilotinib exhibit unique pharmacologic profiles and response patterns relative to different patient characteristics, such as disease stage and BCR-ABL mutation status.	nilotinib	66-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-216
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 Mesylate	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 Mesylate	134-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
21198861-3	2011	The highest cytotoxic effect was seen when the TKI was followed by MEL; our results indicate that inhibition of BCR/ABL activity by IM increased the cytotoxicity of MEL by favoring the DNA damage induced by this drug and by shortening the time for DNA repair at the G2/M checkpoint.	Melphalan	67-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
21198861-5	2011	The drugs association was further tested in a type of BaF3 cells (TonB.210) where the BCR-ABL expression is inducible by doxycycline; in this model it was confirmed that a reduction of BCR/ABL activity resulted in an increased susceptibility to the cytotoxic effect of MEL.	Doxycycline	121-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-93
21198861-5	2011	The drugs association was further tested in a type of BaF3 cells (TonB.210) where the BCR-ABL expression is inducible by doxycycline; in this model it was confirmed that a reduction of BCR/ABL activity resulted in an increased susceptibility to the cytotoxic effect of MEL.	Doxycycline	121-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	185-192
21198861-5	2011	The drugs association was further tested in a type of BaF3 cells (TonB.210) where the BCR-ABL expression is inducible by doxycycline; in this model it was confirmed that a reduction of BCR/ABL activity resulted in an increased susceptibility to the cytotoxic effect of MEL.	Melphalan	269-272	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-93
21198861-5	2011	The drugs association was further tested in a type of BaF3 cells (TonB.210) where the BCR-ABL expression is inducible by doxycycline; in this model it was confirmed that a reduction of BCR/ABL activity resulted in an increased susceptibility to the cytotoxic effect of MEL.	Melphalan	269-272	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	185-192
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 Mesylate	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
21206969-6	2011	Data from the current study showed that 2 muM quercetin, a low concentration that represents less than 10% of its IC50 growth-inhibitory concentration as calculated from the average of eight distinct cancer cell lines, decreased the activity of 16 kinases by more than 80%, including ABL1, Aurora-A, -B, -C, CLK1, FLT3, JAK3, MET, NEK4, NEK9, PAK3, PIM1, RET, FGF-R2, PDGF-Ralpha and -Rss.	Quercetin	46-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	284-288
21263099-1	2011	UNLABELLED: PURPOSE Dasatinib is an orally available tyrosine kinase inhibitor with low nanomolar activity against SRC family kinases, BCR-ABL, c-KIT, EPHA2, and the PDGF-beta receptor.	Dasatinib	20-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
21183952-4	2011	Treatment of Bcr-Abl+ cells with Jak2 inhibitors for 4-6 h but not with IM also reduced Bcr-Abl protein and pTyr177 levels.	ptyr177	108-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
21183952-6	2011	Importantly, Jak2 inhibition decreased pTyr177 Bcr-Abl in immune complexes but did not reduce levels of Bcr-Abl, suggesting that the reduction of Bcr-Abl by Jak2 inhibition is a separate event from phosphorylation of Tyr177.	ptyr177	39-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
21209314-6	2011	We demonstrate that phosphorylation at serine 292 controls RIN1-mediated inhibition of cell migration by modulating the activation of Abl kinases.	Serine	39-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-137
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 Mesylate	68-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-94
21338916-0	2011	Discovery and characterization of a cell-permeable, small-molecule c-Abl kinase activator that binds to the myristoyl binding site.	myristoyl	108-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-72
21338916-2	2011	Here, we report a small-molecule c-Abl activator, DPH, that displays potent enzymatic and cellular activity in stimulating c-Abl activation.	Phenytoin	50-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-38
21338916-2	2011	Here, we report a small-molecule c-Abl activator, DPH, that displays potent enzymatic and cellular activity in stimulating c-Abl activation.	Phenytoin	50-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-128
21338916-3	2011	Structural analyses indicate that DPH binds to the myristoyl binding site and prevents the formation of the bent conformation of the alphaI helix through steric hindrance, a mode of action distinct from the previously identified allosteric c-Abl inhibitor, GNF-2, that also binds to the myristoyl binding site.	Phenytoin	34-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	240-245
21338916-4	2011	DPH represents the first cell-permeable, small-molecule tool compound for c-Abl activation.	Phenytoin	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-79
21148814-3	2011	The dual Src/Abl inhibitors BMS354825 and SKI-606 blocked Chk1-inhibitor-induced extracellular signal-regulated kinase 1/2 (ERK1/2) activation, markedly increasing apoptosis in association with BimEL up-regulation, p34(cdc2) activation, and DNA damage in MM cell lines and primary CD138(+) MM samples.	Dasatinib	28-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	386-393
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.	leptomycin B	137-149	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.	leptomycin B	137-149	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.	leptomycin B	137-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	386-393
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.	Tyrosine	234-243	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.	Tyrosine	234-243	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-91
21195056-0	2011	Bortezomib and sphingosine kinase inhibitor interact synergistically to induces apoptosis in BCR/ABl+ cells sensitive and resistant to STI571 through down-regulation Mcl-1.	Bortezomib	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
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 Mesylate	3-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
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.	Bortezomib	87-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
21195056-5	2011	Finally, the bortezomib/SKI regimen also potently induced the downregulation of BCR/ABL and Mcl-1 in human leukemia cells.	Bortezomib	13-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
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 Mesylate	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 Mesylate	43-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-177
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-130
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 Mesylate	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 Mesylate	177-185	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
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 Mesylate	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
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 Mesylate	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
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 Mesylate	24-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
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 Mesylate	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.	nilotinib	18-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
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 Mesylate	152-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
20717963-0	2011	Bcr-Abl-induced tyrosine phosphorylation of Emi1 to stabilize Skp2 protein via inhibition of ubiquitination in chronic myeloid leukemia cells.	Tyrosine	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
20717963-3	2011	Treatment of Bcr-Abl kinase inhibitor imatinib led to G1 growth arrest accompanied with reduced Skp2 expression.	Imatinib Mesylate	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
21072043-4	2011	The adapter protein growth factor receptor-binding protein-2 (Grb2) can bind phosphorylated BCR/ABL-Y177, induce Grb2-SoS complex formation and activate Ras signaling.	sulfur monoxide	118-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
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 Mesylate	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-22
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 Mesylate	19-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	265-272
21299455-3	2011	Imatinib, an inhibitor of BCR-ABL tyrosine kinase activity, has a dramatic effect on the natural history of the disease.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
21060940-5	2011	Systematic analysis of ATP-competitive inhibitors with varying linker lengths revealed that SRC and ABL have differential sensitivities to ligand presentation.	Adenosine Triphosphate	23-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-103
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 Mesylate	186-194	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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.	Dasatinib	199-208	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 Mesylate	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 Mesylate	107-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
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.	Dasatinib	130-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
21264552-6	2011	However, after the dasatinib treatment, wild-type BCR-ABL clone disappeared and T315I or F317L mutation was acquired in G250E and Y253H mutant clones on the same allele without the emergence of each sole mutant clone.	Dasatinib	19-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
21279819-0	2011	Successful treatment with nilotinib after imatinib failure in a CML patient with a four-way Ph chromosome translocation and point mutations in BCR/ABL gene.	nilotinib	26-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-150
21416861-0	2011	[Diagnosis and treatment of BCR/ABL-negative myeloproliferative diseases--principles and rationale of CZEMP recommendations].	czemp	102-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
21041018-0	2011	Carboxyamidotriazole inhibits cell growth of imatinib-resistant chronic myeloid leukaemia cells including T315I Bcr-Abl mutant by a redox-mediated mechanism.	carboxyamido-triazole	0-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
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 Mesylate	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
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 Mesylate	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 Mesylate	141-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
21041018-2	2011	Here, we show that treatment of cell lines harbouring wild type or mutant BCR-ABL with carboxyamidotriazole (CAI), a calcium influx and signal transduction inhibitor, inhibits cell growth, the expression of Bcr-Abl and its downstream signalling, and induces apoptosis.	carboxyamido-triazole	87-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
21041018-2	2011	Here, we show that treatment of cell lines harbouring wild type or mutant BCR-ABL with carboxyamidotriazole (CAI), a calcium influx and signal transduction inhibitor, inhibits cell growth, the expression of Bcr-Abl and its downstream signalling, and induces apoptosis.	carboxyamido-triazole	87-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	207-214
21041018-2	2011	Here, we show that treatment of cell lines harbouring wild type or mutant BCR-ABL with carboxyamidotriazole (CAI), a calcium influx and signal transduction inhibitor, inhibits cell growth, the expression of Bcr-Abl and its downstream signalling, and induces apoptosis.	carboxyamido-triazole	109-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
21041018-2	2011	Here, we show that treatment of cell lines harbouring wild type or mutant BCR-ABL with carboxyamidotriazole (CAI), a calcium influx and signal transduction inhibitor, inhibits cell growth, the expression of Bcr-Abl and its downstream signalling, and induces apoptosis.	carboxyamido-triazole	109-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	207-214
21041018-2	2011	Here, we show that treatment of cell lines harbouring wild type or mutant BCR-ABL with carboxyamidotriazole (CAI), a calcium influx and signal transduction inhibitor, inhibits cell growth, the expression of Bcr-Abl and its downstream signalling, and induces apoptosis.	Calcium	117-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
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 Mesylate	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 Mesylate	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
21098337-2	2011	The recognition that some patients experience relapse due to resistance-conferring point mutations within BCR-ABL sparked the development of the second-generation ABL kinase inhibitors nilotinib and dasatinib.	nilotinib	185-194	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
21098337-2	2011	The recognition that some patients experience relapse due to resistance-conferring point mutations within BCR-ABL sparked the development of the second-generation ABL kinase inhibitors nilotinib and dasatinib.	Dasatinib	199-208	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
21030238-1	2011	In this study, we used a biosensor chip featuring Abl tyrosine kinase-modified silicon nanowire field-effect transistors (SiNW-FETs) to detect adenosine triphosphate (ATP) liberated from HeLa cells that had been electrically stimulated.	Adenosine Triphosphate	143-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-53
21098337-5	2011	The leading third-generation clinical candidate for treatment-refractory CML, including patients with the T315I mutation, is ponatinib (AP24534), a pan-BCR-ABL inhibitor that has entered pivotal phase 2 testing.	ponatinib	125-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-159
21030238-1	2011	In this study, we used a biosensor chip featuring Abl tyrosine kinase-modified silicon nanowire field-effect transistors (SiNW-FETs) to detect adenosine triphosphate (ATP) liberated from HeLa cells that had been electrically stimulated.	Adenosine Triphosphate	167-170	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-53
21098337-6	2011	A second inhibitor with activity against the BCR-ABL(T315I) mutant, DCC-2036, is in phase 1 clinical evaluation.	Dicyclohexylcarbodiimide	68-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
21214929-10	2011	CONCLUSIONS: Data show that alpha-TEA in combination with DOXO or CDDP synergistically enhances apoptosis in TNBC via targeting p53-mediated genes in a p73-dependent manner, and that p73 responses are downstream of c-Abl, JNK and Yap.	2,5,7,8-tetramethyl-2R-(4R,8R,12-trimethyltridecyl)chroman-6-yloxy acetic acid	28-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	215-220
21224352-2	2011	In this study, we show that amiloride modulates the alternative splicing of various cancer genes, including Bcl-x, HIPK3, and BCR/ABL, and that this effect is not mainly related to pH alteration, which is a known effect of the drug.	Amiloride	28-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
21220945-1	2011	Therapies that target BCR-ABL in chronic myeloid leukemia, including imatinib, dasatinib and nilotinib, have dramatically improved patient outcome.	Imatinib Mesylate	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
21220945-1	2011	Therapies that target BCR-ABL in chronic myeloid leukemia, including imatinib, dasatinib and nilotinib, have dramatically improved patient outcome.	Dasatinib	79-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
21220945-1	2011	Therapies that target BCR-ABL in chronic myeloid leukemia, including imatinib, dasatinib and nilotinib, have dramatically improved patient outcome.	nilotinib	93-102	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 Mesylate	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.	Dasatinib	10-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
21220945-4	2011	In vitro, dasatinib and nilotinib inhibit most imatinib-resistant BCR-ABL mutations, except for T315I.	nilotinib	24-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
21220945-4	2011	In vitro, dasatinib and nilotinib inhibit most imatinib-resistant BCR-ABL mutations, except for T315I.	Imatinib Mesylate	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
20697894-0	2011	Characteristics of BCR-ABL kinase domain point mutations in Chinese imatinib-resistant chronic myeloid leukemia patients.	Imatinib Mesylate	68-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-26
20807497-5	2011	This dual detection technique was used to evaluate the inhibition of c-Abl kinase by imatinib and dasatinib.	Imatinib Mesylate	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-74
20807497-5	2011	This dual detection technique was used to evaluate the inhibition of c-Abl kinase by imatinib and dasatinib.	Dasatinib	98-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-74
20697894-11	2011	ABL mutations are common in Chinese imatinib-resistant CML patients and are associated with clinical resistance.	Imatinib Mesylate	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
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).	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
21209200-0	2011	Novel regulation of parkin function through c-Abl-mediated tyrosine phosphorylation: implications for Parkinson"s disease.	Tyrosine	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-49
21209200-2	2011	Here, we show that the stress-signaling non-receptor tyrosine kinase c-Abl links parkin to sporadic forms of PD via tyrosine phosphorylation.	Tyrosine	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-74
21209200-6	2011	Our results suggest that tyrosine phosphorylation of parkin by c-Abl is a major post-translational modification that leads to loss of parkin function and disease progression in sporadic PD.	Tyrosine	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-68
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 Mesylate	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
20974687-7	2011	Moreover, treatment with the BCR-ABL kinase inhibitor, Imatinib Mesylate, abolished CtIP accumulation.	Imatinib Mesylate	55-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
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 Mesylate	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 Mesylate	83-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
20952511-7	2011	Nilotinib and dasatinib (second-generation BCR-ABL inhibitors), at concentrations comparable to those used in therapy, increase the CKI but do not affect p27(Kip)1 level.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
20952511-7	2011	Nilotinib and dasatinib (second-generation BCR-ABL inhibitors), at concentrations comparable to those used in therapy, increase the CKI but do not affect p27(Kip)1 level.	Dasatinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-113
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 Mesylate	129-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
21643558-4	2011	GO-203 treatment resulted in the complete downregulation of Bcr-Abl expression and induced cell cycle arrest by a ROS-mediated mechanism that was blocked by the antioxidant N-acetylcysteine.	Acetylcysteine	173-189	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
22210962-1	2011	We report a Quantum mechanics/Molecular Mechanics-Poisson-Boltzmann/ Surface Area (QM/MM-PB/SA) method to calculate the binding free energy of c-Abl human tyrosine kinase by combining the QM and MM principles where the ligand is treated quantum mechanically and the rest of the receptor by classical molecular mechanics.	Lead	89-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-148
22210962-1	2011	We report a Quantum mechanics/Molecular Mechanics-Poisson-Boltzmann/ Surface Area (QM/MM-PB/SA) method to calculate the binding free energy of c-Abl human tyrosine kinase by combining the QM and MM principles where the ligand is treated quantum mechanically and the rest of the receptor by classical molecular mechanics.	2-chloro-10-(4'(N-beta-hydroxyethyl)piperazinyl-1')acetylphenothiazine	92-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-148
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 Mesylate	147-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-117
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
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 Mesylate	93-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	190-194
21792346-2	2011	The current second generation of FDA-approved ABL tyrosine kinase inhibitors, dasatinib and nilotinib, are more potent inhibitors of BCR-ABL1 kinase in vitro.	Dasatinib	78-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-49
21792346-2	2011	The current second generation of FDA-approved ABL tyrosine kinase inhibitors, dasatinib and nilotinib, are more potent inhibitors of BCR-ABL1 kinase in vitro.	Dasatinib	78-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-141
21792346-2	2011	The current second generation of FDA-approved ABL tyrosine kinase inhibitors, dasatinib and nilotinib, are more potent inhibitors of BCR-ABL1 kinase in vitro.	nilotinib	92-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-49
21792346-2	2011	The current second generation of FDA-approved ABL tyrosine kinase inhibitors, dasatinib and nilotinib, are more potent inhibitors of BCR-ABL1 kinase in vitro.	nilotinib	92-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-141
21294709-4	2011	The advent of resistance to imatinib and other TKIs in CML patients (often due to the presence of an ABL mutation at position 315) has led to a revived clinical interest in omacetaxine in CML patients who failed TKIs.	Homoharringtonine	173-184	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-104
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 Mesylate	140-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
21199784-4	2011	Abl kinases are activated to reorganize the host actin cytoskeleton and promote the direct tyrosine phosphorylation of viral surface proteins and injected bacterial type-III and type-IV effector molecules.	Tyrosine	91-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
20938045-2	2011	This assay employed a 2-step phosphorylation reaction: in the first step, purified recombinant c-Abl was activated by incubating with compound in the presence of adenosine triphosphate (ATP).	Adenosine Triphosphate	162-184	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-100
20938045-2	2011	This assay employed a 2-step phosphorylation reaction: in the first step, purified recombinant c-Abl was activated by incubating with compound in the presence of adenosine triphosphate (ATP).	Adenosine Triphosphate	186-189	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-100
20938045-4	2011	The assay was calibrated such that inactive c-Abl protein was activated by ATP alone to a degree that it not only demonstrated a measurable c-Abl activity but also maintained a robust assay window for screening.	Adenosine Triphosphate	75-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-49
20938045-4	2011	The assay was calibrated such that inactive c-Abl protein was activated by ATP alone to a degree that it not only demonstrated a measurable c-Abl activity but also maintained a robust assay window for screening.	Adenosine Triphosphate	75-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-145
21672337-2	2011	Treatment with molecular-targeted therapy is usually initiated with imatinib, an inhibitor of BCR-ABL tyrosine kinase.	Imatinib Mesylate	68-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
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 Mesylate	129-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	306-313
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.	nilotinib	139-148	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.	nilotinib	139-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	306-313
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.	Dasatinib	154-163	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.	Dasatinib	154-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	306-313
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.	cev	24-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-54
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.	cev	24-27	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 Mesylate	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 Mesylate	128-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-153
20962097-6	2011	While inhibitors of both Src and Abl family kinases, such as dasatinib (BMS-354825; Sprycel), are effective in limiting dissemination of VacV, VarV, and MPX in vitro, members of this class of drugs appear to have immunosuppressive effects in vivo that preclude their use as anti-infectives.	Dasatinib	61-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-36
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.	nilotinib	232-241	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	218-221
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 Mesylate	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
20673586-5	2011	In T315I and F317L mutated patients, CML-resistance appears to be promoted by SFKs kinase protein reactivation once the BCR-ABL mutated clone has decreased on Omacetaxine.	Homoharringtonine	159-170	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
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 Mesylate	125-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-189
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 Mesylate	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
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).	ttfx	258-262	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
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).	ttfx	258-262	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-160
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 Mesylate	286-294	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
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 Mesylate	34-51	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 Mesylate	286-294	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-160
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 Mesylate	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	181-188
21632458-4	2011	A number of such studies have been published, and now that two inhibitors-dasatinib and nilotinib-are available for the treatment of imatinib-resistant cases, it is tempting for clinicians to reason on the IC50 values to guess, case by case, which one will work best in patients harboring specific Bcr-Abl KD mutations.	Dasatinib	74-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	298-305
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).	ttfx	326-330	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
21632458-4	2011	A number of such studies have been published, and now that two inhibitors-dasatinib and nilotinib-are available for the treatment of imatinib-resistant cases, it is tempting for clinicians to reason on the IC50 values to guess, case by case, which one will work best in patients harboring specific Bcr-Abl KD mutations.	nilotinib	88-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	298-305
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 Mesylate	349-357	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
22110595-2	2011	In the present study, we have investigated the efficacy of microtubule stabilizing paclitaxel loaded magnetic nanoparticles (pac-MNPs) to ascertain its cytotoxic effect on Bcr-Abl positive K562 cells.	Paclitaxel	83-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-179
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 Mesylate	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
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.	Adenosine Triphosphate	99-102	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.	Adenosine Triphosphate	59-62	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.	Adenosine Triphosphate	59-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	218-221
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 Mesylate	125-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-189
21887305-12	2011	The mechanism of anti-leukemia for Icaritin is involved in the regulation of Bcr/Abl downstream signaling.	icaritin	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
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 Mesylate	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
21876762-2	2011	C3G is regulated by tyrosine phosphorylation on Y504, known to be mediated by c-Abl and Src family kinases.	Tyrosine	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-83
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 Mesylate	132-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
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 Mesylate	79-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
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 Mesylate	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 Mesylate	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-115
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 Mesylate	103-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
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 Mesylate	156-164	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
23284246-1	2011	Imatinib mesylate was the first BCR-ABL-target agent approved for the treatment of chronic myeloid leukemia.	Imatinib Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
20832390-0	2010	Involvement of ROS in chlorogenic acid-induced apoptosis of Bcr-Abl+ CML cells.	Reactive Oxygen Species	15-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
20832390-0	2010	Involvement of ROS in chlorogenic acid-induced apoptosis of Bcr-Abl+ CML cells.	Chlorogenic Acid	22-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
20832390-1	2010	Chlorogenic acid (Chl) has been reported to possess a wide range of biological and pharmacological properties including induction of apoptosis of Bcr-Abl(+) chronic myeloid leukemia (CML) cell lines and clinical leukemia samples via inhibition of Bcr-Abl phosphorylation.	Chlorogenic Acid	0-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	146-153
20832390-1	2010	Chlorogenic acid (Chl) has been reported to possess a wide range of biological and pharmacological properties including induction of apoptosis of Bcr-Abl(+) chronic myeloid leukemia (CML) cell lines and clinical leukemia samples via inhibition of Bcr-Abl phosphorylation.	Chlorogenic Acid	0-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	247-254
20832390-1	2010	Chlorogenic acid (Chl) has been reported to possess a wide range of biological and pharmacological properties including induction of apoptosis of Bcr-Abl(+) chronic myeloid leukemia (CML) cell lines and clinical leukemia samples via inhibition of Bcr-Abl phosphorylation.	Chlorogenic Acid	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	146-153
20832390-1	2010	Chlorogenic acid (Chl) has been reported to possess a wide range of biological and pharmacological properties including induction of apoptosis of Bcr-Abl(+) chronic myeloid leukemia (CML) cell lines and clinical leukemia samples via inhibition of Bcr-Abl phosphorylation.	Chlorogenic Acid	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	247-254
20832390-3	2010	Chl treatment induced an early accumulation of intracellular reactive oxygen species (ROS) in Bcr-Abl(+) cells leading to downregulation of Bcr-Abl phosphorylation and apoptosis.	Reactive Oxygen Species	61-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
20832390-3	2010	Chl treatment induced an early accumulation of intracellular reactive oxygen species (ROS) in Bcr-Abl(+) cells leading to downregulation of Bcr-Abl phosphorylation and apoptosis.	Reactive Oxygen Species	61-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
20832390-3	2010	Chl treatment induced an early accumulation of intracellular reactive oxygen species (ROS) in Bcr-Abl(+) cells leading to downregulation of Bcr-Abl phosphorylation and apoptosis.	Reactive Oxygen Species	86-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
20832390-3	2010	Chl treatment induced an early accumulation of intracellular reactive oxygen species (ROS) in Bcr-Abl(+) cells leading to downregulation of Bcr-Abl phosphorylation and apoptosis.	Reactive Oxygen Species	86-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
20832390-7	2010	Antioxidant NAC attenuated Chl-induced oxidative stress-mediated inhibition of Bcr-Abl phosphorylation, DR5 upregulation, caspase activation and CML cell death.	Chlorogenic Acid	27-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
20832390-10	2010	Collectively, our results establish the role of ROS for Chl-mediated preferential killing of Bcr-Abl(+) cells.	Reactive Oxygen Species	48-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
21154127-0	2010	Bafetinib, a dual Bcr-Abl/Lyn tyrosine kinase inhibitor for the potential treatment of leukemia.	bafetinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
21154127-1	2010	Bafetinib (NS-187, INNO-406) is a second-generation tyrosine kinase inhibitor in development by CytRx under license from Nippon Shinyaku for treating Bcr-Abl+ leukemia"s, including chronic myelogenous leukemia (CML) and Philadelphia+ acute lymphoblastic leukemia.	bafetinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
20970221-0	2010	2-Hydroxypropyl-beta-cyclodextrin strongly improves water solubility and anti-proliferative activity of pyrazolo[3,4-d]pyrimidines Src-Abl dual inhibitors.	2-Hydroxypropyl-beta-cyclodextrin	0-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-138
20970221-0	2010	2-Hydroxypropyl-beta-cyclodextrin strongly improves water solubility and anti-proliferative activity of pyrazolo[3,4-d]pyrimidines Src-Abl dual inhibitors.	Water	52-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-138
20970221-0	2010	2-Hydroxypropyl-beta-cyclodextrin strongly improves water solubility and anti-proliferative activity of pyrazolo[3,4-d]pyrimidines Src-Abl dual inhibitors.	pyrazolo(3,4-d)pyrimidine	104-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-138
20970221-1	2010	The main aim of this study was to enhance the solubility of pyrazolo[3,4-d]pyrimidines 1-8 able to strongly inhibit Src and Abl tyrosine kinase phosphorylation in cell-free assays and to significantly reduce leukemic and osteosarcoma cell lines growth, but characterized by very low solubility in aqueous media.	pyrazolo(3,4-d)pyrimidine	60-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-127
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 Mesylate	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
21073351-7	2010	In comparison with imatinib, nilotinib displays increased selectivity and potency at inhibiting proliferation of BCR-ABL expressing cells.	nilotinib	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
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 Mesylate	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 Mesylate	199-207	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	221-228
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 Mesylate	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
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 Mesylate	60-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
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 Mesylate	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 Mesylate	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
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 Mesylate	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
20937825-9	2010	Further, loss of Abl kinase signaling induces internalization of MT1-MMP from the cell surface, promotes its accumulation in the perinuclear compartment and inhibits MT1-MMP tyrosine phosphorylation.	Tyrosine	174-182	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-20
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
21056550-5	2010	Here we investigated the potential synergy between miR-15a/16-1 and ATO on Bcr-Abl positive leukemic K562 cells.	ato	68-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
21154127-1	2010	Bafetinib (NS-187, INNO-406) is a second-generation tyrosine kinase inhibitor in development by CytRx under license from Nippon Shinyaku for treating Bcr-Abl+ leukemia"s, including chronic myelogenous leukemia (CML) and Philadelphia+ acute lymphoblastic leukemia.	bafetinib	11-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
21154127-5	2010	Bafetinib inhibits 12 of the 13 most frequent imatinib-resistant Bcr-Abl point mutations, but not a Thr315Ile mutation.	bafetinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
21154127-5	2010	Bafetinib inhibits 12 of the 13 most frequent imatinib-resistant Bcr-Abl point mutations, but not a Thr315Ile mutation.	Imatinib Mesylate	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
21154127-6	2010	A small fraction of bafetinib crosses the blood-brain barrier, reaching brain concentrations adequate for suppression of Bcr-Abl+ cells.	bafetinib	20-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
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 Mesylate	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-49
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 Mesylate	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
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.	bafetinib	89-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
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 Mesylate	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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-143
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.	nilotinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
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.	nilotinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-143
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 Mesylate	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
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 Mesylate	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
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 Mesylate	144-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
20861316-4	2010	EC challenge with sphingosine 1-phosphate (S1P), a potent barrier-enhancing agonist, resulted in c-Abl and phosphorylated nmMLCK recruitment into caveolin-enriched microdomains, rapid increases in Abl kinase activity, and spatial targeting of c-Abl to barrier-promoting cortical actin structures.	sphingosine 1-phosphate	18-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-102
20861316-4	2010	EC challenge with sphingosine 1-phosphate (S1P), a potent barrier-enhancing agonist, resulted in c-Abl and phosphorylated nmMLCK recruitment into caveolin-enriched microdomains, rapid increases in Abl kinase activity, and spatial targeting of c-Abl to barrier-promoting cortical actin structures.	sphingosine 1-phosphate	18-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	243-248
20861316-4	2010	EC challenge with sphingosine 1-phosphate (S1P), a potent barrier-enhancing agonist, resulted in c-Abl and phosphorylated nmMLCK recruitment into caveolin-enriched microdomains, rapid increases in Abl kinase activity, and spatial targeting of c-Abl to barrier-promoting cortical actin structures.	sphingosine 1-phosphate	43-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-102
20861316-4	2010	EC challenge with sphingosine 1-phosphate (S1P), a potent barrier-enhancing agonist, resulted in c-Abl and phosphorylated nmMLCK recruitment into caveolin-enriched microdomains, rapid increases in Abl kinase activity, and spatial targeting of c-Abl to barrier-promoting cortical actin structures.	sphingosine 1-phosphate	43-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	243-248
20861316-5	2010	Conversely, reduced c-Abl expression in EC (siRNA) markedly attenuated S1P-mediated cortical actin formation, reduced the EC modulus of elasticity (assessed by atomic force microscopy), reduced nmMLCK and cortactin tyrosine phosphorylation, and attenuated S1P-mediated barrier enhancement.	Tyrosine	215-223	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-25
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 Mesylate	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
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 Mesylate	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-78
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 Mesylate	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-162
20563869-2	2010	In this study, we examined the intracellular signaling of Aurora kinases inhibitor, MK-0457 (VX-680), in BCR-ABL positive cell lines and in primary samples.	VX680	84-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-112
20563869-2	2010	In this study, we examined the intracellular signaling of Aurora kinases inhibitor, MK-0457 (VX-680), in BCR-ABL positive cell lines and in primary samples.	VX680	93-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-112
20563869-7	2010	BCR-ABL and Aurora A and B were reduced after vorinostat treatment.	Vorinostat	46-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
20629032-5	2010	Blockage of c-Abl using the tyrosine kinase inhibitor imatinib resulted in reduced cellular growth in both cell lines.	Imatinib Mesylate	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-17
20563869-9	2010	Our study increases insight into how MK-0457 may mediate its effects on BCR-ABL positive leukemia cells with T315I mutation, and information of potential therapeutic relevance.	VX680	37-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
20629079-1	2010	BACKGROUND: Dasatinib, an inhibitor of Src/Abl family kinases, can inhibit tumor growth of several solid tumors.	Dasatinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-46
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 Mesylate	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-17
20519627-0	2010	BCR-ABL SH3-SH2 domain mutations in chronic myeloid leukemia patients on imatinib.	Imatinib Mesylate	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
20404839-9	2010	Affinity-purified anti-ABL IgG contained an antibody fraction that recognizes the carbohydrate-binding site of ABL.	Carbohydrates	82-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-26
20404839-9	2010	Affinity-purified anti-ABL IgG contained an antibody fraction that recognizes the carbohydrate-binding site of ABL.	Carbohydrates	82-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-114
20143399-0	2010	The BCR/ABL-inhibitors imatinib, nilotinib and dasatinib differentially affect NK cell reactivity.	Imatinib Mesylate	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-11
20143399-0	2010	The BCR/ABL-inhibitors imatinib, nilotinib and dasatinib differentially affect NK cell reactivity.	nilotinib	33-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-11
20143399-0	2010	The BCR/ABL-inhibitors imatinib, nilotinib and dasatinib differentially affect NK cell reactivity.	Dasatinib	47-56	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 Mesylate	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 Mesylate	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-104
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.	nilotinib	126-135	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.	nilotinib	126-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-104
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.	Dasatinib	140-149	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.	Dasatinib	140-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-104
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 Mesylate	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 Mesylate	186-194	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-47
20860375-2	2010	Abltide, a model substrate for the Abl protein tyrosine kinase model, was coupled onto amine-terminated beads, incubated with ATP and recombinant c-Abl kinase, and released and further detected to determine phosphorylation.	Amines	87-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
20860375-2	2010	Abltide, a model substrate for the Abl protein tyrosine kinase model, was coupled onto amine-terminated beads, incubated with ATP and recombinant c-Abl kinase, and released and further detected to determine phosphorylation.	Adenosine Triphosphate	126-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
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 Mesylate	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-158
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.	Dasatinib	90-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-158
20699667-3	2010	We have recently shown that dual targeting of mTORC1 and mTORC2 complexes using a catalytic mTOR inhibitor, OSI-027, results in generation of potent antileukemic effects against BCR-ABL transformed cells.	OSI 027	108-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185
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 Mesylate	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	236-243
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 Mesylate	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 Mesylate	57-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
21091142-1	2010	Nilotinib (Tasigna( )) is a more potent BCR-ABL inhibitor than imatinib and was designed to overcome imatinib"s deficiencies.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
21091142-1	2010	Nilotinib (Tasigna( )) is a more potent BCR-ABL inhibitor than imatinib and was designed to overcome imatinib"s deficiencies.	nilotinib	11-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
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 Mesylate	143-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-78
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 Mesylate	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
20828158-2	2010	We recently reported the discovery of GNF-2 (1) and GNF-5 (2) as selective non-ATP competitive inhibitors of cellular Bcr-Abl kinase activity that target the myristate binding site.	Adenosine Triphosphate	79-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
20600357-7	2010	Our results demonstrate that tyrosines at positions 79, 107 and 118 can be phosphorylated in vitro and in vivo by c-Abl kinase.	Tyrosine	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-119
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 Mesylate	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 Mesylate	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 Mesylate	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-169
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 Mesylate	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
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 Mesylate	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 Mesylate	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
21030353-0	2010	The durable clearance of the T315I BCR-ABL mutated clone in chronic phase chronic myelogenous leukemia patients on omacetaxine allows tyrosine kinase inhibitor rechallenge.	Homoharringtonine	115-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
21030353-2	2010	PATIENTS AND METHODS: We have investigated the affect of subcutaneous omacetaxine (OMA, or homo-harringtonine) cycles on unmutated and T315I-mutated BCR-ABL transcripts in a series of 8 TKI-resistant chronic-phase CML patients and we have addressed the question of whether the administration of OMA could resensitize patients to TKIs.	Homoharringtonine	70-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
20600357-8	2010	Tyrosine 107 is the main target of c-Abl.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-40
20737438-4	2010	Loss of Abl function reduces FA, F-actin, and phosphorylated myosin light chain (pMLC) staining at the cell periphery, shifting the distribution of these elements more to the center of the cell than in wild-type (WT) and arg(-/-) cells.	Arginine	221-224	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-11
20737438-6	2010	Abl/Arg-dependent phosphorylation of p190RhoGAP (p190) promotes its binding to p120RasGAP (p120) to form a functional RhoA GTPase inhibitory complex, which attenuates RhoA activity and downstream pMLC and FA formation.	Arginine	4-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
20737438-2	2010	In spreading fibroblasts, the Abl family kinases, Abl and Arg, primarily localize to the nucleus and cell periphery, respectively.	Arginine	58-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-33
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 Mesylate	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
20597967-3	2010	The BCR/ABL1 kinase blocker imatinib shows major antileukaemic effects in most patients and is considered standard frontline therapy.	Imatinib Mesylate	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-12
20703259-0	2010	HH-GV-678, a novel selective inhibitor of Bcr-Abl, outperforms imatinib and effectively overrides imatinib resistance.	HH-GV-678	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
20597967-8	2010	For such patients, novel multikinase inhibitors such as nilotinib, dasatinib, bosutinib or bafetinib, which block the kinase activity of various BCR/ABL1 mutants, have been developed and reportedly exert antileukaemic effects in drug-resistant cells.	nilotinib	56-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-153
20597967-8	2010	For such patients, novel multikinase inhibitors such as nilotinib, dasatinib, bosutinib or bafetinib, which block the kinase activity of various BCR/ABL1 mutants, have been developed and reportedly exert antileukaemic effects in drug-resistant cells.	Dasatinib	67-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-153
20597967-8	2010	For such patients, novel multikinase inhibitors such as nilotinib, dasatinib, bosutinib or bafetinib, which block the kinase activity of various BCR/ABL1 mutants, have been developed and reportedly exert antileukaemic effects in drug-resistant cells.	bosutinib	78-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-153
20597967-8	2010	For such patients, novel multikinase inhibitors such as nilotinib, dasatinib, bosutinib or bafetinib, which block the kinase activity of various BCR/ABL1 mutants, have been developed and reportedly exert antileukaemic effects in drug-resistant cells.	bafetinib	91-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-153
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 Mesylate	63-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
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.	nilotinib	35-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
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.	nilotinib	35-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	224-231
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.	Dasatinib	59-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
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.	Dasatinib	59-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	224-231
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 Mesylate	166-174	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
20823226-2	2010	Here we show that the nonreceptor tyrosine kinase c-Abl phosphorylates tyrosine 143 of parkin, inhibiting parkin"s ubiquitin E3 ligase activity and protective function.	Tyrosine	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-55
20875551-2	2010	The introduction of imatinib, a tyrosine kinase inhibitor (TKI) specific for BCR-ABL, was a major breakthrough in CML therapy.	Imatinib Mesylate	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
20875551-8	2010	Although both are potent and specific BCR-ABL TKIs, dasatinib and nilotinib exhibit unique pharmacological profiles and response patterns relative to different patient characteristics, such as disease stage and BCR-ABL mutational status.	Dasatinib	52-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	211-218
20875551-8	2010	Although both are potent and specific BCR-ABL TKIs, dasatinib and nilotinib exhibit unique pharmacological profiles and response patterns relative to different patient characteristics, such as disease stage and BCR-ABL mutational status.	nilotinib	66-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
20875551-8	2010	Although both are potent and specific BCR-ABL TKIs, dasatinib and nilotinib exhibit unique pharmacological profiles and response patterns relative to different patient characteristics, such as disease stage and BCR-ABL mutational status.	nilotinib	66-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	211-218
20875554-6	2010	Third-generation TKIs and non-adenosine triphosphate (non-ATP) mimetic compounds with activity against ABL1 mutations associated with failure to approved TKIs are under development for patients who either have failed sequential therapy with at least two TKIs or carry the highly resistant T315I mutation.	Adenosine Triphosphate	30-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-107
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 Mesylate	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-16
20823226-6	2010	Conditional knockout of c-Abl in the nervous system also prevents the phosphorylation of parkin, the accumulation of its substrates, and subsequent neurotoxicity in response to MPTP intoxication.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	177-181	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-29
20823226-8	2010	Thus, tyrosine phosphorylation of parkin by c-Abl is a major posttranslational modification that inhibits parkin function, possibly contributing to pathogenesis of sporadic PD.	Tyrosine	6-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-49
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 Mesylate	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
20510935-5	2010	As a demonstration, a candidate peptide, TOP1, that weakly binds to the target protein, the Src homology 3 (SH3) domain of human Abelson tyrosine kinase (Abl), was fused to green fluorescent protein (GFP) and l-DOPA was site-specifically incorporated into the peptide region (TOP1-DOPA-GFP).	Levodopa	209-215	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-157
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 Mesylate	20-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
20510935-6	2010	TOP1-DOPA-GFP produced from Escherichia coli was used in a Western blot-type experiment to show that the Abl SH3 domain can be detected in one step by observing the fluorescence.	Dihydroxyphenylalanine	5-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-108
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 Mesylate	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 Mesylate	300-308	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	284-291
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 Mesylate	100-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
20930519-8	2010	We focus on recent efforts directed towards BCR-ABL, for which, significant progress has been made to develop allosteric inhibitors with promising therapeutic activity, especially in the context of overcoming clinically acquired resistance mutations to the first generation of ATP-competitive kinase inhibitors.	Adenosine Triphosphate	277-280	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
20350535-3	2010	With the success of targeting other oncogenic kinases such as BCR-ABL, KIT or members of the epidermal-growth factor receptor (EGFR) family in other cancers, the expectations were high when the first RAF kinase-targeting drug (sorafenib) reached clinical trials.	Sorafenib	227-236	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
20592495-3	2010	The present studies demonstrate that treatment of KU812 and K562 CML cells with GO-201, a cell-penetrating peptide inhibitor of MUC1-C oligomerization, downregulates Bcr-Abl expression and inhibits cell growth.	GO 201	80-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-173
20640942-2	2010	By directly targeting the Bcr-Abl kinase, imatinib leads to durable cytogenetic remissions and in turn improved survival.	Imatinib Mesylate	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
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 Mesylate	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
20471447-3	2010	MATERIALS AND METHODS: We established a new human BCR-ABL-positive acute lymphoblastic leukemia (ALL) cell line, SK-9 with the T315I mutation, from the peripheral blood of a 36-year-old female patient.	sk-9	113-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
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 Mesylate	81-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
20922699-12	2010	Inhibitors of the BCR-Abl tyrosine kinase domain on the Philadelphia chromosome (imatinib, nilotinib and dasatinib) may cause acute renal failure.	nilotinib	91-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
20922699-12	2010	Inhibitors of the BCR-Abl tyrosine kinase domain on the Philadelphia chromosome (imatinib, nilotinib and dasatinib) may cause acute renal failure.	Dasatinib	105-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
20808434-3	2010	To understand this, comprehensive analysis of hydrophobic interactions, hydrogen bonding and binding affinity have been analyzed at the interface of c-Src and c-Abl kinases and 4-amino substituted 1H-pyrazolo [3, 4-d] pyrimidine compounds.	Hydrogen	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-164
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 Mesylate	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
20447687-0	2010	A T315I mutation in e19a2 BCR/ABL1 chronic myeloid leukemia responding to dasatinib.	Dasatinib	74-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-34
20584982-2	2010	In the c-Abl tyrosine kinase, myristate binds within a hydrophobic pocket at the base of the kinase domain and latches the protein into an autoinhibitory conformation.	Myristic Acid	30-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	7-12
20548094-0	2010	Activity of the multitargeted kinase inhibitor, AT9283, in imatinib-resistant BCR-ABL-positive leukemic cells.	1-cyclopropyl-3-(3-(5-morpholin-4-ylmethyl-1H-benzoimidazol-2-yl)-1H-pyrazol-4-yl)urea	48-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
20548094-0	2010	Activity of the multitargeted kinase inhibitor, AT9283, in imatinib-resistant BCR-ABL-positive leukemic cells.	Imatinib Mesylate	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
20548094-2	2010	We describe the in vitro and in vivo effects of AT9283 (1-cyclopropyl-3[5-morpholin-4yl methyl-1H-benzomidazol-2-yl]-urea), a potent inhibitor of several protein kinases, including Aurora A, Aurora B, Janus kinase 2 (JAK2), JAK3, and ABL on diverse imatinib-resistant BCR-ABL(+) cells.	1-cyclopropyl-3-(3-(5-morpholin-4-ylmethyl-1H-benzoimidazol-2-yl)-1H-pyrazol-4-yl)urea	48-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	234-237
20548094-2	2010	We describe the in vitro and in vivo effects of AT9283 (1-cyclopropyl-3[5-morpholin-4yl methyl-1H-benzomidazol-2-yl]-urea), a potent inhibitor of several protein kinases, including Aurora A, Aurora B, Janus kinase 2 (JAK2), JAK3, and ABL on diverse imatinib-resistant BCR-ABL(+) cells.	1-cyclopropyl-3-(3-(5-morpholin-4-ylmethyl-1H-benzoimidazol-2-yl)-1H-pyrazol-4-yl)urea	48-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	268-275
20548094-2	2010	We describe the in vitro and in vivo effects of AT9283 (1-cyclopropyl-3[5-morpholin-4yl methyl-1H-benzomidazol-2-yl]-urea), a potent inhibitor of several protein kinases, including Aurora A, Aurora B, Janus kinase 2 (JAK2), JAK3, and ABL on diverse imatinib-resistant BCR-ABL(+) cells.	1-cyclopropyl-3[5-morpholin-4yl methyl-1h-benzomidazol-2-yl]-urea	56-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	234-237
20548094-2	2010	We describe the in vitro and in vivo effects of AT9283 (1-cyclopropyl-3[5-morpholin-4yl methyl-1H-benzomidazol-2-yl]-urea), a potent inhibitor of several protein kinases, including Aurora A, Aurora B, Janus kinase 2 (JAK2), JAK3, and ABL on diverse imatinib-resistant BCR-ABL(+) cells.	1-cyclopropyl-3[5-morpholin-4yl methyl-1h-benzomidazol-2-yl]-urea	56-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	268-275
20548094-4	2010	AT9283 inhibited proliferation in a panel of BaF3 and human BCR-ABL(+) cell lines both sensitive and resistant to imatinib because of a variety of mechanisms.	1-cyclopropyl-3-(3-(5-morpholin-4-ylmethyl-1H-benzoimidazol-2-yl)-1H-pyrazol-4-yl)urea	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
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 Mesylate	202-210	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-151
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 Mesylate	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-81
20718683-4	2010	Imatinib inhibits tyrosine kinase activity of Bcr-ABL and PDGF.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
20718683-5	2010	We hypothesize that patients with ATC that over-expresses PDGF receptors or cABL will respond to imatinib.	Imatinib Mesylate	97-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-80
20598684-2	2010	We previously demonstrated that Abl kinase activity is, itself, regulated by Abi1 subsequent to Abl kinase phosphorylation of Abi1 tyrosine 213 (pY213) [1].	Tyrosine	131-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-35
20581864-4	2010	Ectopic expression of c-Abl in mammalian cell lines, known to induce apoptosis, resulted in phosphorylation of endogenous C3G on Y504 coincident with cell detachment and chromatin condensation.	y504	129-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-27
20581864-8	2010	Activation of endogenous c-Abl by oxidative stress was associated with phosphorylation of cellular C3G on Y504.	y504	106-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-30
20598684-2	2010	We previously demonstrated that Abl kinase activity is, itself, regulated by Abi1 subsequent to Abl kinase phosphorylation of Abi1 tyrosine 213 (pY213) [1].	Tyrosine	131-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-99
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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
20563669-4	2010	Overexpression of c-Abl induces tyrosine phosphorylation of Pitx1, either directly or indirectly.	Tyrosine	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-23
20403398-7	2010	In addition, silencing of the BCR-ABL oncoprotein by both shRNA and siRNA delivered by Tat-LK15 is more efficient and longer lasting than that achieved using Lipofectamine and more importantly without considerable cytotoxicity.	Lipofectamine	158-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
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 Mesylate	163-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
20150913-2	2010	This study shows that c-Abl and Abl-related gene (Arg) associate with and phosphorylate Gal3.	Arginine	50-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-27
20150913-2	2010	This study shows that c-Abl and Abl-related gene (Arg) associate with and phosphorylate Gal3.	Arginine	50-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-27
20150913-3	2010	The SH (Src homology)3 domains of c-Abl/Arg bind to a P(80)GPPSGP motif of Gal3, and Tyr79 and Tyr118 are the major tyrosine phosphorylation sites.	Arginine	40-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-39
20150913-3	2010	The SH (Src homology)3 domains of c-Abl/Arg bind to a P(80)GPPSGP motif of Gal3, and Tyr79 and Tyr118 are the major tyrosine phosphorylation sites.	Tyrosine	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-39
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 Mesylate	63-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-48
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 Mesylate	189-197	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
20225261-2	2010	While designed to inhibit Abl and Src kinases, dasatinib shows multitarget effects, including inhibition of the macrophage colony-stimulating factor (M-CSF) receptor c-fms.	Dasatinib	47-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-29
20658954-1	2010	The introduction of BCR-ABL tyrosine kinase inhibitors such as imatinib has changed the treatment of chronic myelogenous leukemia (CML).	Imatinib Mesylate	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
20561787-3	2010	Kinase profiling showed that the imidazo[1,2-a]pyrazines could inhibit other kinases, including CHK2 and ABL, with equivalent or better potency depending on the pendant substitution.	imidazo(1,2-a)pyrazine	33-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-108
20621496-3	2010	Here, we present a structural comparison of the important and similar interactions necessary for Gleevec(R), Nexavar, and BIRB-796 to bind to their respective DFG-out allosteric binding pockets and the selectivity of each with respect to c-Abl, B-Raf, and p38alpha.	Sorafenib	109-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	238-243
20621496-3	2010	Here, we present a structural comparison of the important and similar interactions necessary for Gleevec(R), Nexavar, and BIRB-796 to bind to their respective DFG-out allosteric binding pockets and the selectivity of each with respect to c-Abl, B-Raf, and p38alpha.	birb	122-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	238-243
20557276-4	2010	AREAS COVERED IN THIS REVIEW: ATP-competitive compounds originally developed as Src inhibitors, showed to be also potent Abl inhibitors.	Adenosine Triphosphate	30-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-124
20557276-5	2010	Dasatinib, the first dual Src/Abl inhibitor approved by the US FDA in 2006 for the treatment of imatinib-resistant CML, is currently being tested in several clinical trials for the treatment of different solid tumors.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-33
20557276-6	2010	SKI-606 and AZD0530 are two other important dual Src/Abl inhibitors extensively tested in animal models and in clinical trials, but not entered into therapy yet.	bosutinib	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
20557276-6	2010	SKI-606 and AZD0530 are two other important dual Src/Abl inhibitors extensively tested in animal models and in clinical trials, but not entered into therapy yet.	saracatinib	12-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
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 Mesylate	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	204-211
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 Mesylate	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-49
20739730-4	2010	Blood gas analysis in the emergency department using an ABL 725 Radiometer analyser showed a severe metabolic acidosis with massive lactate elevation.	Lactic Acid	132-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-59
20541934-1	2010	A series of alkyne-containing type II inhibitors with potent inhibitory activity of T315I Bcr-Abl has been identified.	Alkynes	12-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
20616057-4	2010	Our studies establish that a unique dual mTORC2/mTORC1 inhibitor, OSI-027, induces potent suppressive effects on primitive leukemic progenitors from CML patients and generates antileukemic responses in cells expressing the T315I-BCR-ABL mutation, which is refractory to all BCR-ABL kinase inhibitors currently in clinical use.	OSI 027	66-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	229-236
20616057-4	2010	Our studies establish that a unique dual mTORC2/mTORC1 inhibitor, OSI-027, induces potent suppressive effects on primitive leukemic progenitors from CML patients and generates antileukemic responses in cells expressing the T315I-BCR-ABL mutation, which is refractory to all BCR-ABL kinase inhibitors currently in clinical use.	OSI 027	66-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	274-281
20616057-5	2010	Induction of apoptosis by OSI-027 appears to negatively correlate with induction of autophagy in some types of BCR-ABL transformed cells, as shown by the induction of autophagy during OSI-027-treatment and the potentiation of apoptosis by concomitant inhibition of such autophagy.	OSI 027	26-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
20179930-10	2010	TTFx was longer in patients who achieved greater than 50% reduction in BCR-ABL/ABL within 6 months (early molecular responder (EMR)) compared with those who did not (non-EMR; p < 0.001).	ttfx	0-4	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
20179930-10	2010	TTFx was longer in patients who achieved greater than 50% reduction in BCR-ABL/ABL within 6 months (early molecular responder (EMR)) compared with those who did not (non-EMR; p < 0.001).	ttfx	0-4	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-78
19862526-0	2010	Synergistic activity of nilotinib and established chemotherapeutic drugs in imatinib-sensitive and -resistant BCR-ABL-positive cells.	nilotinib	24-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
19862526-1	2010	We investigated various combination treatment regimens employing nilotinib with established chemotherapeutic agents (daunorubicin, mitoxantrone, etoposide and cytarabine) in imatinib-sensitive and -resistant BCR-ABL-positive cells.	nilotinib	65-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	208-215
20139893-1	2010	Abl tyrosine kinase inhibitors (TKIs) such as imatinib and dasatinib are ineffective against Bcr-Abl(+) leukemic stem cells.	Imatinib Mesylate	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
20139893-1	2010	Abl tyrosine kinase inhibitors (TKIs) such as imatinib and dasatinib are ineffective against Bcr-Abl(+) leukemic stem cells.	Dasatinib	59-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
20375898-1	2010	PURPOSE OF REVIEW: Dasatinib is a novel tyrosine-kinase inhibitor approved for treatment of BCR-ABL positive chronic myeloid leukemia (CML) and Philadelphia chromosome positive acute lymphoblastic leukemia (ALL) after imatinib failure.	Dasatinib	19-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
20362353-8	2010	Additionally, the arylstibonic acid compound was cytostatic in clear cell sarcoma cells, which express a chimera between the B-ZIP domain of ATF-1 and N-terminal activation domain of EWS but not in K562 cells that express a non-B-ZIP containing chimeric protein BCR-ABL.	arylstibonic acid	18-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	262-269
20409618-2	2010	Among the novel derivatives, 2-amino-6-{[2-(4-chlorophenyl)-2-oxoethyl]sulfanyl}-4-(3-thienyl)pyridine-3,5-dicarbonitrile (13 g) was identified as a submicromolar RET inhibitor, displaying 3- and 100-fold selectivity versus ALK and ABL kinases, respectively.	CHEMBL1172147	29-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	232-235
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 Mesylate	141-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
20508029-4	2010	Using a PCR-based method, this analysis revealed that i) BCR intron 14 brought a potential lariat branch point and the polypyrimidine tract, ii) the BCR-ABL breakpoint created a chimeric acceptor site, and iii) the inserted sequence of ABL intron Ib carried at its 3" end a well-conserved donor splice site.	polypyrimidine	119-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-156
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 Mesylate	164-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
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 Mesylate	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
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 Mesylate	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 Mesylate	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
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 Mesylate	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 Mesylate	81-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-164
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.	Dasatinib	141-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-96
20525993-1	2010	BACKGROUND: Nilotinib has been shown to be a more potent inhibitor of BCR-ABL than imatinib.	nilotinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
20305692-0	2010	Bortezomib decreases Rb phosphorylation and induces caspase-dependent apoptosis in Imatinib-sensitive and -resistant Bcr-Abl1-expressing cells.	Bortezomib	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-125
20222756-3	2010	Imatinib and dasatinib both target the tyrosine kinase activity of the BCR/ABL oncogenic fusion protein.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
20222756-3	2010	Imatinib and dasatinib both target the tyrosine kinase activity of the BCR/ABL oncogenic fusion protein.	Dasatinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
20222756-10	2010	Data suggest dasatinib 100 mg once daily achieves oncogenic shock and chronic inhibition of BCR/ABL activity, suggesting that in the future, pulse therapy with TKIs may be an option in some specific patients with CML.	Dasatinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	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 Mesylate	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 Mesylate	131-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-49
20042273-1	2010	Imatinib is a Bcr-Abl inhibitor used as first-line therapy of chronic myeloid leukemia (CML).	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
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 Mesylate	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
20310049-0	2010	Phase 1 study of INNO-406, a dual Abl/Lyn kinase inhibitor, in Philadelphia chromosome-positive leukemias after imatinib resistance or intolerance.	bafetinib	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-37
20529808-3	2010	The introduction of imatinib, a TK inhibitor (TKI) specific for BCR-ABL, was a major breakthrough in CML therapy.	Imatinib Mesylate	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
20529808-9	2010	Although both are potent and specific BCR-ABL TKIs, dasatinib and nilotinib exhibit unique pharmacologic profiles and response patterns relative to different patient characteristics, such as disease stage and BCR-ABL mutational status.	Dasatinib	52-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-216
20529808-9	2010	Although both are potent and specific BCR-ABL TKIs, dasatinib and nilotinib exhibit unique pharmacologic profiles and response patterns relative to different patient characteristics, such as disease stage and BCR-ABL mutational status.	nilotinib	66-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
20529808-9	2010	Although both are potent and specific BCR-ABL TKIs, dasatinib and nilotinib exhibit unique pharmacologic profiles and response patterns relative to different patient characteristics, such as disease stage and BCR-ABL mutational status.	nilotinib	66-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-216
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 Mesylate	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-73
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.	Dasatinib	122-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-73
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.	nilotinib	135-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-73
20445575-0	2010	Synergistic activity of the Src/Abl inhibitor bosutinib in combination with imatinib.	bosutinib	46-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-35
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 Mesylate	21-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
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.	dsbs	149-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
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 Mesylate	237-245	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	219-226
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.	pristimerin	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-165
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 Mesylate	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 Mesylate	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
20482842-4	2010	RESULTS: In this report, we discovered that pristimerin, a quinonemethide triterpenoid isolated from Celastraceae and Hippocrateaceae, inhibited growth and induced apoptosis in CML cells, including the cells harboring Bcr-Abl-T315I mutation.	pristimerin	44-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	218-225
20482842-5	2010	Additionally, pristimerin inhibited the growth of imatinib-resistant Bcr-Abl-T315I xenografts in nude mice.	pristimerin	14-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
20482842-5	2010	Additionally, pristimerin inhibited the growth of imatinib-resistant Bcr-Abl-T315I xenografts in nude mice.	Imatinib Mesylate	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
20482842-8	2010	Pristimerin potently inhibited two pairs of CML cell lines (KBM5 versus KBM5-T315I, 32D-Bcr-Abl versus 32D-Bcr-Abl-T315I) and primary cells from a CML patient with acquired resistance to imatinib.	pristimerin	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
20482842-8	2010	Pristimerin potently inhibited two pairs of CML cell lines (KBM5 versus KBM5-T315I, 32D-Bcr-Abl versus 32D-Bcr-Abl-T315I) and primary cells from a CML patient with acquired resistance to imatinib.	pristimerin	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
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 Mesylate	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 Mesylate	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 Mesylate	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
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 Mesylate	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-133
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 Mesylate	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
20407438-4	2010	METHODS: In this report, we analyse the effects of representative members of the novel pro-apoptotic microtubule depolymerising pyrrolo-1,5-benzoxazepines or PBOX compounds on chemotherapy-refractory CML cells using a series of Bcr-Abl mutant cell lines, clinical ex vivo patient samples and an in vivo mouse model.	-1,5-benzoxazepines	135-154	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	228-235
20520639-1	2010	Nilotinib is a highly selective Bcr-Abl inhibitor approved for imatinib-resistant chronic myeloid leukemia (CML).	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
20520639-1	2010	Nilotinib is a highly selective Bcr-Abl inhibitor approved for imatinib-resistant chronic myeloid leukemia (CML).	Imatinib Mesylate	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
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 Mesylate	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
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 Mesylate	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-11
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 Mesylate	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-16
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).	Dasatinib	62-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-16
20305692-4	2010	Our results show that cells that express Bcr-Abl1 are more sensitive to the inhibition of the proteasome with Bortezomib (Btz) than control cells.	Bortezomib	110-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-49
20305692-4	2010	Our results show that cells that express Bcr-Abl1 are more sensitive to the inhibition of the proteasome with Bortezomib (Btz) than control cells.	Bortezomib	122-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-49
20305692-6	2010	Furthermore, we show that Btz also induces cell-cycle arrest and apoptosis in cells expressing Bcr-Abl1 mutants that are resistant to IM.	Bortezomib	26-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-103
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 Mesylate	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
20094798-0	2010	Enhancement of imatinib-induced apoptosis of BCR/ABL-expressing cells by nutlin-3 through synergistic activation of the mitochondrial apoptotic pathway.	nutlin 3	73-81	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 Mesylate	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 Mesylate	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
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 Mesylate	70-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	212-219
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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.	Tyrosine	48-56	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.	Tyrosine	48-56	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.	Tyrosine	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
20020482-1	2010	Imatinib is an important anticancer drug, which binds specifically to the Abl kinase and blocks its signalling activity.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-98
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.	Everolimus	23-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-138
20228846-0	2010	Imatinib resistance associated with BCR-ABL upregulation is dependent on HIF-1alpha-induced metabolic reprograming.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
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 Mesylate	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 Mesylate	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-162
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 Mesylate	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 Mesylate	31-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-69
19643477-4	2010	Those effects are at least partly conditional upon the enhanced nuclear accumulation of p145 c-ABL through events encompassing post-translational modifications of p145 c-ABL (Thr(735) phosphorylation) precluding its nuclear export and of 14-3-3 sigma (Ser(186) phosphorylation by c-Jun N-terminal kinase [JNK]) promoting p145 c-ABL nuclear re-import.	Serine	252-255	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	168-173
19643477-3	2010	Here we show that IM and the mammalian target of rapamycin (mTOR) inhibitor RAD001 (Everolimus) have additive effects on BCR-ABL-expressing cells.	Everolimus	84-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
19643477-4	2010	Those effects are at least partly conditional upon the enhanced nuclear accumulation of p145 c-ABL through events encompassing post-translational modifications of p145 c-ABL (Thr(735) phosphorylation) precluding its nuclear export and of 14-3-3 sigma (Ser(186) phosphorylation by c-Jun N-terminal kinase [JNK]) promoting p145 c-ABL nuclear re-import.	Threonine	175-178	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-98
19643477-4	2010	Those effects are at least partly conditional upon the enhanced nuclear accumulation of p145 c-ABL through events encompassing post-translational modifications of p145 c-ABL (Thr(735) phosphorylation) precluding its nuclear export and of 14-3-3 sigma (Ser(186) phosphorylation by c-Jun N-terminal kinase [JNK]) promoting p145 c-ABL nuclear re-import.	Threonine	175-178	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	168-173
19643477-4	2010	Those effects are at least partly conditional upon the enhanced nuclear accumulation of p145 c-ABL through events encompassing post-translational modifications of p145 c-ABL (Thr(735) phosphorylation) precluding its nuclear export and of 14-3-3 sigma (Ser(186) phosphorylation by c-Jun N-terminal kinase [JNK]) promoting p145 c-ABL nuclear re-import.	Threonine	175-178	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	168-173
19643477-4	2010	Those effects are at least partly conditional upon the enhanced nuclear accumulation of p145 c-ABL through events encompassing post-translational modifications of p145 c-ABL (Thr(735) phosphorylation) precluding its nuclear export and of 14-3-3 sigma (Ser(186) phosphorylation by c-Jun N-terminal kinase [JNK]) promoting p145 c-ABL nuclear re-import.	Serine	252-255	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-98
19643477-4	2010	Those effects are at least partly conditional upon the enhanced nuclear accumulation of p145 c-ABL through events encompassing post-translational modifications of p145 c-ABL (Thr(735) phosphorylation) precluding its nuclear export and of 14-3-3 sigma (Ser(186) phosphorylation by c-Jun N-terminal kinase [JNK]) promoting p145 c-ABL nuclear re-import.	Serine	252-255	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	168-173
20406945-1	2010	Dasatinib is an orally administered multitargeted kinase inhibitor that targets Src family tyrosine kinases, Abl, c-Kit, and PDGFR.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-112
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 Mesylate	123-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
20388735-0	2010	Activity of the Aurora kinase inhibitor VX-680 against Bcr/Abl-positive acute lymphoblastic leukemias.	VX680	40-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-62
20388735-2	2010	VX-680 is a pan-Aurora kinase inhibitor active against all Bcr/Abl proteins but has not been extensively examined in preclinical models of Ph-positive ALL.	VX680	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-66
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 Mesylate	123-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
20442314-5	2010	Bcr-Abl leads to decreased expression of genes involved in the mitotic checkpoint activation--Mad2, Bub1, Bub3, and BubR1, resulting in mitosis perturbances, weakened mitotic checkpoint function, and mitotic slippage after nocodazole treatment.	Nocodazole	223-233	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
20442314-8	2010	Additionally, Bcr-Abl-expressing cells showed resistance to death activated by spindle defects, reversed by imatinib.	Imatinib Mesylate	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
20096388-2	2010	We recently encountered two cases of ethylene glycol poisoning with very high blood lactate concentrations on ABL blood gas analyzers.	Ethylene Glycol	37-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-113
20200154-2	2010	The cancer drug imatinib binds tightly to several homologous kinases, including Abl, but weakly to others, including Src.	Imatinib Mesylate	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
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.	1,3-Diphenylguanidine	55-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
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.	1,3-Diphenylguanidine	120-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
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.	DFG peptide	182-193	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
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.	1,3-Diphenylguanidine	120-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
20200154-11	2010	Thus, conformational selection, easy in Abl, difficult in Src, underpins imatinib specificity.	Imatinib Mesylate	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-43
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 Mesylate	191-199	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
20329739-3	2010	All isolated sesquiterpenes were assayed for cytotoxicity against two tyrosine kinase inhibitor-resistant cell lines, K562R and DA1-3b/M2(BCR-ABL).	Sesquiterpenes	13-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
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 Mesylate	143-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
20183853-3	2010	Four kinase systems (Src family, Abl/c-Kit, Syk/ZAP-70, and CDK2/4) were investigated, and differences in predicted water molecule locations and energetics were able to explain the experimentally observed binding selectivity profiles.	Water	116-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-36
20096388-6	2010	RESULTS: In case 1, all the chemistry instruments produced similar lactate results compared to that by ABL analyzer whereas in case 2, the lactate on the ABL was dramatically elevated compared to that from all the chemistry analyzers.	Lactic Acid	139-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-157
20096388-8	2010	Increased concentrations of glycolic acid resulted in a significant positive interference on lactate measurements on the ABL analyzer but none on other instruments.	glycolic acid	28-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-124
20096388-8	2010	Increased concentrations of glycolic acid resulted in a significant positive interference on lactate measurements on the ABL analyzer but none on other instruments.	Lactic Acid	93-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-124
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 Mesylate	93-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
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 Mesylate	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-87
20124512-10	2010	Thus, endogenous c-Abl mediates endothelial apoptosis induced by inhibition of integrins alphavbeta3/alphavbeta5 or by LatB-induced disruption of F-actin.	latrunculin B	119-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-22
20717479-0	2010	A Non-ATP-Competitive Dual Inhibitor of JAK2 and BCR-ABL Kinases: Elucidation of a Novel Therapeutic Spectrum Based on Substrate Competitive Inhibition.	Adenosine Triphosphate	6-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
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.	1,3-Diphenylguanidine	176-179	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-74
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 Mesylate	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.	Sorafenib	84-93	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.	Sorafenib	95-102	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.	doramapimod	123-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
20717479-1	2010	Here we report the discovery of ON044580, an alpha-benzoyl styryl benzyl sulfide that possesses potent inhibitory activity against two unrelated kinases, JAK2 and BCR-ABL, and exhibits cytotoxicity to human tumor cells derived from chronic myelogenous leukemia (CML) and myelodysplasia (MDS) patients or cells harboring a mutant JAK2 kinase.	alpha-benzoyl styryl benzyl sulfide	45-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
20425400-3	2010	The known molecular basis of CML has enabled the development of Abl-specific tyrosine kinase inhibitors, such as imatinib mesylate.	Imatinib Mesylate	113-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-67
20717479-2	2010	This novel spectrum of activity is explained by the non-ATP-competitive inhibition of JAK2 and BCR-ABL kinases.	Adenosine Triphosphate	56-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
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 Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-82
20111071-0	2010	Development of resistance to dasatinib in Bcr/Abl-positive acute lymphoblastic leukemia.	Dasatinib	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-49
20146241-9	2010	The spheroids of the four cell lines underwent apoptosis after treatment with the Src/Abl/Kit inhibitor PP1 or Src/Abl inhibitor bosutinib.	bosutinib	129-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-118
20111071-1	2010	Dasatinib is a potent dual Abl/Src inhibitor approved for treatment of Philadelphia chromosome-positive (Ph-positive) leukemias.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-30
20111071-4	2010	Here, the effect of dasatinib on treatment of Bcr/Abl-positive acute lymphoblastic leukemia (ALL) cells was evaluated in the presence of stromal support.	Dasatinib	20-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-53
20111071-5	2010	Dasatinib eradicated Bcr/Abl ALL cells, caused significant apoptosis and eliminated tyrosine phosphorylation on Bcr/Abl, Src, Crkl and Stat-5.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-28
20111071-5	2010	Dasatinib eradicated Bcr/Abl ALL cells, caused significant apoptosis and eliminated tyrosine phosphorylation on Bcr/Abl, Src, Crkl and Stat-5.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-119
20111071-5	2010	Dasatinib eradicated Bcr/Abl ALL cells, caused significant apoptosis and eliminated tyrosine phosphorylation on Bcr/Abl, Src, Crkl and Stat-5.	Tyrosine	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-119
20394535-0	2010	Imatinib-loaded polyelectrolyte microcapsules for sustained targeting of BCR-ABL+ leukemia stem cells.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
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 Mesylate	64-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
20043988-7	2010	In conclusion, H(2)O(2) stimulates NOX2-mediated superoxide generation in neutrophils and K562/NOX2 cells via a signaling pathway involving Ca(2+) influx and c-Abl tyrosine kinase acting upstream of PKCdelta.	Hydrogen Peroxide	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-163
20068223-7	2010	Bortezomib causes proteasome but not BCR-ABL inhibition and is also effective in inhibiting proteasome activity and inducing apoptosis in cell lines expressing BCR-ABL mutations, including T315I.	Bortezomib	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-167
20068223-8	2010	By targeting both TKI-insensitive stem and progenitor cells and TKI-resistant BCR-ABL mutations, we believe that bortezomib offers a potential therapeutic option in CML.	Bortezomib	113-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
20043988-0	2010	Regulation of phagocyte NADPH oxidase by hydrogen peroxide through a Ca(2+)/c-Abl signaling pathway.	Hydrogen Peroxide	41-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-81
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
20188579-0	2010	Design, synthesis and evaluation of (E)-alpha-benzylthio chalcones as novel inhibitors of BCR-ABL kinase.	(E)-alpha-benzylthio chalcone	36-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
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.	(E)-alpha-benzylthio chalcone	6-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	196-203
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.	(E)-alpha-benzylthio chalcone	6-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	276-283
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 Mesylate	159-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	196-203
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 Mesylate	24-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
20197479-4	2010	These strategies include upfront treatment with next-generation tyrosine kinase inhibitors, such as dasatinib, nilotinib, or bosutinib, which also target BCR-ABL but with increased in vitro potency compared with imatinib, and possibly a reduced potential for resistance.	Dasatinib	100-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-161
20197479-4	2010	These strategies include upfront treatment with next-generation tyrosine kinase inhibitors, such as dasatinib, nilotinib, or bosutinib, which also target BCR-ABL but with increased in vitro potency compared with imatinib, and possibly a reduced potential for resistance.	nilotinib	111-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-161
20197479-4	2010	These strategies include upfront treatment with next-generation tyrosine kinase inhibitors, such as dasatinib, nilotinib, or bosutinib, which also target BCR-ABL but with increased in vitro potency compared with imatinib, and possibly a reduced potential for resistance.	bosutinib	125-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-161
19922818-1	2010	As a drug used to treat imatinib-resistant and -intolerant, chronic and advanced phase chronic myelogenous leukaemia, nilotinib is well characterised as a potent inhibitor of the Abl tyrosine kinase activity of wild-type and imatinib-resistant mutant forms of BCR-Abl.	nilotinib	118-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	179-182
19922818-1	2010	As a drug used to treat imatinib-resistant and -intolerant, chronic and advanced phase chronic myelogenous leukaemia, nilotinib is well characterised as a potent inhibitor of the Abl tyrosine kinase activity of wild-type and imatinib-resistant mutant forms of BCR-Abl.	nilotinib	118-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	260-267
19922818-3	2010	Although an ATP-competitive inhibitor of Abl, nilotinib binds to a catalytically inactive conformation (DFG-out) of the activation loop.	nilotinib	46-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-44
19922818-4	2010	As a consequence of this, nilotinib exhibits time-dependent inhibition of Abl kinase in enzymatic assays, which can be extrapolated to other targets to explain differences between biochemical activity and cellular assays.	nilotinib	26-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-77
19922818-5	2010	Although these differences confound assessment of kinase selectivity, as assessed using a combination of protein binding and transphosphorylation assays, together with cellular autophosporylation and proliferation assays, well established kinase targets of nilotinib in rank order of inhibitory potency are DDR-1>DDR-2>BCR-Abl (Abl)>PDGFRalpha/beta>KIT>CSF-1R.	nilotinib	257-266	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	325-332
19922818-5	2010	Although these differences confound assessment of kinase selectivity, as assessed using a combination of protein binding and transphosphorylation assays, together with cellular autophosporylation and proliferation assays, well established kinase targets of nilotinib in rank order of inhibitory potency are DDR-1>DDR-2>BCR-Abl (Abl)>PDGFRalpha/beta>KIT>CSF-1R.	nilotinib	257-266	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	329-332
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 Mesylate	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 Mesylate	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 Mesylate	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-201
20207846-0	2010	Small interfering RNA against BCR-ABL transcripts sensitize mutated T315I cells to nilotinib.	nilotinib	83-92	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 Mesylate	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 Mesylate	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 Mesylate	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.	nilotinib	77-86	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.	nilotinib	77-86	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.	nilotinib	77-86	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 Mesylate	181-189	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
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).	nilotinib	193-202	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 Mesylate	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.	nilotinib	79-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
20207846-9	2010	In T315I cells BCR-ABL small interfering RNA with nilotinib had powerful effects on cell cycle distribution.	nilotinib	50-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
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 Mesylate	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 Mesylate	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.	nilotinib	104-113	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.	nilotinib	104-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	229-236
20038231-1	2010	The BCR-ABL inhibitor imatinib revolutionized the treatment of chronic myeloid leukemia (CML).	Imatinib Mesylate	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 Mesylate	112-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
20038231-5	2010	Dasatinib is a dual BCR-ABL/Src-family kinase (SFK) inhibitor approved for patients with imatinib-resistant and -intolerant CML in any phase and Ph+ ALL.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
20234815-0	2010	Enhanced resistance to tamoxifen by the c-ABL proto-oncogene in breast cancer.	Tamoxifen	23-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-45
20234815-4	2010	More importantly, inhibition of c-ABL resulted in sensitization to treatment by tamoxifen (TAM) in estrogen receptor-positive breast cancer cells, as manifested by inhibition of cell survival and suppression of anchorage-independent growth.	Tamoxifen	80-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-37
20234815-4	2010	More importantly, inhibition of c-ABL resulted in sensitization to treatment by tamoxifen (TAM) in estrogen receptor-positive breast cancer cells, as manifested by inhibition of cell survival and suppression of anchorage-independent growth.	Tamoxifen	91-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-37
20234815-7	2010	This study shows that c-ABL regulates the cellular response to TAM through functional interaction with the estrogen receptor, which suggests c-ABL as a therapeutic target and a prognostic tumor marker for breast cancer.	Tamoxifen	63-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-27
20234815-7	2010	This study shows that c-ABL regulates the cellular response to TAM through functional interaction with the estrogen receptor, which suggests c-ABL as a therapeutic target and a prognostic tumor marker for breast cancer.	Tamoxifen	63-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-146
20049867-6	2010	Functional analysis suggested that genistein-regulated protein tyrosine phosphorylation mainly by inhibiting the activity of tyrosine kinase EGFR, PDGFR, insulin receptor, Abl, Fgr, Itk, Fyn and Src.	Tyrosine	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-175
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 Mesylate	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 Mesylate	105-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	210-217
20126732-1	2010	Two different strategies, namely a dialdehyde-based cross-linking and photo-affinity labeling, have been developed to generate small molecule activity-based probes (ABPs) for the Abelson (Abl) tyrosine kinase, of which probe 13, derived from the photo-affinity approach, showed specific labeling of Abl kinase present in a crude mammalian proteome.	Dialdehyde	35-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	179-186
20126732-1	2010	Two different strategies, namely a dialdehyde-based cross-linking and photo-affinity labeling, have been developed to generate small molecule activity-based probes (ABPs) for the Abelson (Abl) tyrosine kinase, of which probe 13, derived from the photo-affinity approach, showed specific labeling of Abl kinase present in a crude mammalian proteome.	Dialdehyde	35-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	188-191
20145167-1	2010	PURPOSE: Dasatinib is a dual Src/Abl inhibitor recently approved for Bcr-Abl+ leukemias with resistance or intolerance to prior therapy.	Dasatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-36
20145167-1	2010	PURPOSE: Dasatinib is a dual Src/Abl inhibitor recently approved for Bcr-Abl+ leukemias with resistance or intolerance to prior therapy.	Dasatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
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 Mesylate	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
19881535-8	2010	In Bcr-Abl-expressing cells, we detected strong PLC-gamma1 activation, which was suppressed by imatinib.	Imatinib Mesylate	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	3-10
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 Mesylate	150-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-127
19631450-3	2010	We found that both proteins modulated their reciprocal tyrosine phosphorylation catalyzed by the non-receptor tyrosine kinase c-Abl.	Tyrosine	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-131
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.	Dasatinib	45-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
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 Mesylate	267-275	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
20139391-1	2010	BACKGROUND: Dasatinib 100 mg once daily achieves intermittent BCR-ABL kinase inhibition and is approved for chronic-phase chronic myeloid leukemia patients resistant or intolerant to imatinib.	Dasatinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
20108303-1	2010	BACKGROUND: The recently developed the Src and Abelson (Abl) kinase inhibitor dasatinib has antitumor effects in epithelial and mesenchymal tumors.	Dasatinib	78-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
20108303-1	2010	BACKGROUND: The recently developed the Src and Abelson (Abl) kinase inhibitor dasatinib has antitumor effects in epithelial and mesenchymal tumors.	Dasatinib	78-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-59
19714331-0	2010	Response to Imatinib mesylate in chronic myeloid leukemia patients with variant BCR-ABL fusion transcripts.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	106-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
19874801-1	2010	MK-0457 inhibits aurora, BCR-ABL and other kinases and may be clinically active in imatinib resistant leukemia.	VX680	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
19874801-3	2010	Aurora and BCR-ABL kinase inhibition were consistently measured at 20-100 nM and 2-10 microM MK-0457, respectively, but expression of T315I-BCR-ABL and overexpression of Lyn kinase reduced MK-0457 sensitivity.	VX680	93-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-18
19874801-6	2010	MK-0457 suppressed aurora kinase activity and induced apoptosis in imatinib resistant clinical specimens expressing T315I and other BCR-ABL mutations without effecting BCR-ABL kinase activity.	VX680	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
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.	Water	54-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-181
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.	triptolide	68-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-181
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 Mesylate	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 Mesylate	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
20149665-3	2010	We recently reported that triptolide (compound 1) could effectively kill CML cells including those harboring T315I mutant Bcr-Abl.	triptolide	26-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
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 Mesylate	88-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
20113198-1	2010	IMPORTANCE OF THE FIELD: Dasatinib is an oral, potent adenosine triphosphate-competitive inhibitor of multiple tyrosine kinases including BCR-ABL, c-KIT, platelet-derived growth factor receptor, and Src family kinases (SFKs).	Dasatinib	25-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
20113198-1	2010	IMPORTANCE OF THE FIELD: Dasatinib is an oral, potent adenosine triphosphate-competitive inhibitor of multiple tyrosine kinases including BCR-ABL, c-KIT, platelet-derived growth factor receptor, and Src family kinases (SFKs).	Adenosine Triphosphate	54-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
20181241-3	2010	Here, we present an Au-nanoparticles based approach for the molecular recognition and quantification of the BCR-ABL fusion transcript (mRNA), which is responsible for chronic myeloid leukemia (CML), and to the best of our knowledge it is the first time quantification of a specific mRNA directly in cancer cells is reported.	Gold	20-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
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 Mesylate	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 Mesylate	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 Mesylate	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.	nilotinib	37-46	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.	nilotinib	37-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
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 Mesylate	173-181	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-162
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 Mesylate	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 Mesylate	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 Mesylate	143-151	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 Mesylate	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 Mesylate	257-263	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 Mesylate	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
19818398-3	2010	Recently, biochemical evidence indicated that the c-Abl and Csk kinases were able to phosphorylate the tyrosine 170 (Y170) residue of c-Jun - which lies within the recognition motif of the Itch ubiquitin ligase - and also regulate its stability independent of the JNK phosphorylation sites.	Tyrosine	103-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-55
20132660-0	2010	Nilotinib significantly induces apoptosis in imatinib-resistant K562 cells with wild-type BCR-ABL, as effectively as in parental sensitive counterparts.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
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 Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
20132660-3	2010	Imatinib and nilotinib are chemotherapeutic drugs which specifically bind to the BCR-ABL and inhibit cancer cells.	nilotinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
20043988-7	2010	In conclusion, H(2)O(2) stimulates NOX2-mediated superoxide generation in neutrophils and K562/NOX2 cells via a signaling pathway involving Ca(2+) influx and c-Abl tyrosine kinase acting upstream of PKCdelta.	Superoxides	49-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-163
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 Mesylate	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.	Dasatinib	46-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
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 Mesylate	120-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
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 Mesylate	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 Mesylate	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-159
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 Mesylate	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-118
19783301-4	2010	Nilotinib, formerly known as AMN107, is a second-generation tyrosine kinase inhibitor 30-fold more potent than imatinib, with high affinity and selectivity on BCR/ABL, and also active against a wide range of mutant clones, except T315I mutation.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-166
19783301-4	2010	Nilotinib, formerly known as AMN107, is a second-generation tyrosine kinase inhibitor 30-fold more potent than imatinib, with high affinity and selectivity on BCR/ABL, and also active against a wide range of mutant clones, except T315I mutation.	nilotinib	29-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-166
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 Mesylate	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 Mesylate	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.	nilotinib	50-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-118
19906645-0	2010	Role of interfacial water molecules in proline-rich ligand recognition by the Src homology 3 domain of Abl.	Water	20-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-106
20072125-0	2010	Targeting Bcr-Abl by combining allosteric with ATP-binding-site inhibitors.	Adenosine Triphosphate	47-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
20072125-1	2010	In an effort to find new pharmacological modalities to overcome resistance to ATP-binding-site inhibitors of Bcr-Abl, we recently reported the discovery of GNF-2, a selective allosteric Bcr-Abl inhibitor.	Adenosine Triphosphate	78-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
20072125-2	2010	Here, using solution NMR, X-ray crystallography, mutagenesis and hydrogen exchange mass spectrometry, we show that GNF-2 binds to the myristate-binding site of Abl, leading to changes in the structural dynamics of the ATP-binding site.	Hydrogen	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-163
20072125-2	2010	Here, using solution NMR, X-ray crystallography, mutagenesis and hydrogen exchange mass spectrometry, we show that GNF-2 binds to the myristate-binding site of Abl, leading to changes in the structural dynamics of the ATP-binding site.	Adenosine Triphosphate	218-221	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-163
20072125-4	2010	These results show that therapeutically relevant inhibition of Bcr-Abl activity can be achieved with inhibitors that bind to the myristate-binding site and that combining allosteric and ATP-competitive inhibitors can overcome resistance to either agent alone.	Adenosine Triphosphate	186-189	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
19906645-0	2010	Role of interfacial water molecules in proline-rich ligand recognition by the Src homology 3 domain of Abl.	Proline	39-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-106
19906645-5	2010	In the light of these results, a new dual binding mechanism is proposed that provides a better description of proline-rich ligand recognition by Abl-SH3 and that has important implications for rational design.	Proline	110-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-148
20090934-15	2010	CONCLUSION/SIGNIFICANCE: Thus our study comprehensively illustrates that Resveratrol acts downstream of Bcr-Abl and inhibits Akt activity but stimulates ERK1/2 activity.	Resveratrol	73-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
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 Mesylate	122-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
19924787-1	2010	BACKGROUND: Dasatinib, a highly potent BCR-ABL inhibitor, is an effective treatment for patients with chronic myeloid leukemia in chronic phase (CML CP) after resistance, suboptimal response, or intolerance to prior imatinib.	Dasatinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
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.	Dasatinib	135-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
20460883-4	2010	The patient started taking nilotinib due to a persistent BCR/ABL value and residual mass in her ovaries after a second allo-HSCT.	nilotinib	27-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
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 Mesylate	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
19914245-6	2010	A phosphotyrosine-specific antibody indicated that MAVS was phosphorylated by c-Abl.	Phosphotyrosine	2-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-83
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 Mesylate	41-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-20
21364617-3	2010	Phopshorylation by c-Abl results in greater protein stability of both ectopically expressed and endogenous DeltaNp63alpha.	deltanp63alpha	107-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-24
19843070-0	2010	Contribution of BCR-ABL-independent activation of ERK1/2 to acquired imatinib resistance in K562 chronic myeloid leukemia cells.	Imatinib Mesylate	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
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 Mesylate	24-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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 Mesylate	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 Mesylate	204-212	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
19798105-8	2010	Interestingly, TSA induced UbB-dependent proteasomal degradation of BCR-ABL fusion protein in K562 leukemic cells.	trichostatin A	15-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
19950162-0	2010	Novel imatinib derivatives with altered specificity between Bcr-Abl and FMS, KIT, and PDGF receptors.	Imatinib Mesylate	6-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
21364617-5	2010	We further show that cisplatin induces c-Abl phosphorylation of DeltaNp63alpha and its binding to YAP.	Cisplatin	21-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-44
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-122
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 Mesylate	202-210	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
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.	Adenosine Triphosphate	35-38	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 Mesylate	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 Mesylate	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-160
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	11-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
20110615-0	2010	Tau phosphorylated at tyrosine 394 is found in Alzheimer"s disease tangles and can be a product of the Abl-related kinase, Arg.	Tyrosine	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-106
20110615-0	2010	Tau phosphorylated at tyrosine 394 is found in Alzheimer"s disease tangles and can be a product of the Abl-related kinase, Arg.	Arginine	123-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-106
20110615-4	2010	Recent reports state that tau can be phosphorylated at tyrosine residues by kinases including Fyn, Syk, and c-abl (Abl).	Tyrosine	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-113
20110615-4	2010	Recent reports state that tau can be phosphorylated at tyrosine residues by kinases including Fyn, Syk, and c-abl (Abl).	Tyrosine	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-118
20110615-8	2010	We report, for the first time, that Arg, the other member of the Abl family of tyrosine kinases, also phosphorylates tau at Y394 in a manner independent of Abl activity.	Arginine	36-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-68
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 Mesylate	202-210	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-167
20047099-0	2010	Successful prior treatment with dasatinib followed by stem cell transplantation in a patient with CML in blastic crisis with a BCR-ABL mutation.	Dasatinib	32-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
20047099-2	2010	Before dasatinib therapy, the patient was found to have a F359V BCR-ABL mutation.	Dasatinib	7-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
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 Mesylate	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	216-223
20048131-0	2010	(124)I-iodopyridopyrimidinone for PET of Abl kinase-expressing tumors in vivo.	iodopyridopyrimidinone	7-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-44
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.	nilotinib	128-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	216-223
19890374-0	2010	A comprehensive target selectivity survey of the BCR-ABL kinase inhibitor INNO-406 by kinase profiling and chemical proteomics in chronic myeloid leukemia cells.	bafetinib	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
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.	nilotinib	19-28	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 Mesylate	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
19798095-4	2010	Only a few BCR-ABL mutations seem to be less responsive to either nilotinib or dasatinib and it is recommended to choose the second-line TKI that has shown clinical activity against the specific mutation in these cases.	nilotinib	66-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-18
19798095-4	2010	Only a few BCR-ABL mutations seem to be less responsive to either nilotinib or dasatinib and it is recommended to choose the second-line TKI that has shown clinical activity against the specific mutation in these cases.	Dasatinib	79-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-18
19798095-7	2010	Here, we propose a treatment algorithm for imatinib-resistant patients based on BCR-ABL mutation status and patient history.	Imatinib Mesylate	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
19890374-1	2010	Resistance to the BCR-ABL tyrosine kinase inhibitor imatinib poses a pressing challenge in treating chronic myeloid leukemia (CML).	Imatinib Mesylate	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 Mesylate	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-161
19890374-3	2010	The second-generation BCR-ABL inhibitor INNO-406 is known to inhibit most BCR-ABL mutants and LYN efficiently.	bafetinib	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
19890374-3	2010	The second-generation BCR-ABL inhibitor INNO-406 is known to inhibit most BCR-ABL mutants and LYN efficiently.	bafetinib	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
19663771-8	2010	Pyrrolo[1,2-b][1,2,5]benzothiadiazepine 5,5-dioxides (PBTDs) induced apoptosis in human BCR-ABL expressing leukemia cells.	pyrrolo[1,2-b][1,2,5]benzothiadiazepine 5,5-dioxides	0-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
19924144-0	2010	Cathepsin B release after imatinib-mediated lysosomal membrane permeabilization triggers BCR-ABL cleavage and elimination of chronic myelogenous leukemia cells.	Imatinib Mesylate	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
19924144-2	2010	Through inhibition of BCR-ABL, Imatinib blocks several downstream pathways and induces apoptosis of BCR-ABL positive cells.	Imatinib Mesylate	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 Mesylate	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
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 Mesylate	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
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 Mesylate	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
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 Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-142
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	287-294
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 Mesylate	213-221	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
20072833-2	2010	It potently inhibits BCR-ABL and SRC-family kinases (SRC, LCK, YES, FYN), but also c-KIT, PDGFR-alpha and beta, and ephrin receptor kinase.Dasatinib is about 300 times more potent than imatinib in cells expressing unmutated BCR-ABL in vitro.	Dasatinib	139-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
20072833-2	2010	It potently inhibits BCR-ABL and SRC-family kinases (SRC, LCK, YES, FYN), but also c-KIT, PDGFR-alpha and beta, and ephrin receptor kinase.Dasatinib is about 300 times more potent than imatinib in cells expressing unmutated BCR-ABL in vitro.	Dasatinib	139-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	224-231
20072833-3	2010	The drug has demonstrated activity against clinically relevant mutations, including those associated with poor prognosis during ongoing imatinib therapy.Dasatinib is approved for the treatment of patients with BCR-ABL-positive chronic myeloid leukemia (CML), resistant or intolerant to imatinib in chronic, accelerated, and blast phase.	Dasatinib	153-162	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	210-217
20072834-3	2010	Nilotinib is a rationally designed second-generation tyrosine kinase inhibitor (TKI) with improved affinity and specificity against the BCR-ABL kinase, when compared with imatinib.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-143
20072835-1	2010	Bosutinib (SKI-606) is a 7-alkoxy-3-quinolinecarbonitrile, which functions as a dual inhibitor of Src and Abl kinases.	bosutinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-109
20072835-1	2010	Bosutinib (SKI-606) is a 7-alkoxy-3-quinolinecarbonitrile, which functions as a dual inhibitor of Src and Abl kinases.	bosutinib	11-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-109
20072835-1	2010	Bosutinib (SKI-606) is a 7-alkoxy-3-quinolinecarbonitrile, which functions as a dual inhibitor of Src and Abl kinases.	7-alkoxy-3-quinolinecarbonitrile	25-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-109
20072835-3	2010	The bcr-abl fusion gene product, a consecutively activated tyrosine kinase, which is crucial for the development of chronic myeloid leukaemia (CML), is highly sensitive to bosutinib.	bosutinib	172-181	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
20072835-6	2010	Remarkably, bosutinib has been found to be capable of overcoming the majority of IM-resistant bcr-abl mutations.	bosutinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
19663771-8	2010	Pyrrolo[1,2-b][1,2,5]benzothiadiazepine 5,5-dioxides (PBTDs) induced apoptosis in human BCR-ABL expressing leukemia cells.	pbtds	54-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
20072840-0	2010	Danusertib (formerly PHA-739358)--a novel combined pan-Aurora kinases and third generation Bcr-Abl tyrosine kinase inhibitor.	danusertib	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
20113282-2	2010	It has a 325 times stronger in vitro activity against to native BCR-ABL when comparing with imatinib.	Imatinib Mesylate	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
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 Mesylate	128-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-193
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.	nilotinib	213-222	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-193
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.	Dasatinib	224-233	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-193
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.	bosutinib	239-248	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-193
20072840-9	2010	Therefore, combined Aurora and Bcr-Abl inhibition (the latter including high-grade resistance conferring mutations) with compounds such as Danusertib represents a promising new strategy for treatment of Bcr-Abl positive leukemias, especially those in second and third line of treatment.	danusertib	139-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	203-210
19880502-1	2009	Preclinical studies of BCR-ABL mutation sensitivity to nilotinib or dasatinib suggested that the majority would be sensitive.	nilotinib	55-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
19880502-1	2009	Preclinical studies of BCR-ABL mutation sensitivity to nilotinib or dasatinib suggested that the majority would be sensitive.	Dasatinib	68-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
20041122-0	2009	Steered molecular dynamics simulations reveal the likelier dissociation pathway of imatinib from its targeting kinases c-Kit and Abl.	Imatinib Mesylate	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 Mesylate	159-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	213-216
20024108-5	2009	In this article, we have, for the first time, developed an efficient method for the construction of small molecule-based bisubstrate inhibitors of Abl kinase using click chemistry.	bisubstrate	121-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-150
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 Mesylate	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	206-209
19889540-0	2009	Structure-activity relationships of 6-(2,6-dichlorophenyl)-8-methyl-2-(phenylamino)pyrido[2,3-d]pyrimidin-7-ones: toward selective Abl inhibitors.	6-(2,6-dichlorophenyl)-8-methyl-2-(phenylamino)pyrido[2,3-d]pyrimidin-7-ones	36-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-134
19889540-1	2009	We report the design, synthesis, and structure-activity relationship (SAR) of a series of novel pyrido[2,3-d]pyrimidin-7-one compounds as potent Abl kinase inhibitors.	Pyrido[2,3-d]pyrimidin-7(8H)-one	96-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-148
19833721-0	2009	Dynamin 2 and c-Abl are novel regulators of hyperoxia-mediated NADPH oxidase activation and reactive oxygen species production in caveolin-enriched microdomains of the endothelium.	Reactive Oxygen Species	92-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
19833721-3	2009	Silencing caveolin-1 (which blocks CEM formation) and/or c-Abl expression with small interference RNA inhibited hyperoxia-mediated tyrosine phosphorylation and association of dynamin 2 with p47(phox) and ROS production.	Tyrosine	131-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-62
19833721-3	2009	Silencing caveolin-1 (which blocks CEM formation) and/or c-Abl expression with small interference RNA inhibited hyperoxia-mediated tyrosine phosphorylation and association of dynamin 2 with p47(phox) and ROS production.	Reactive Oxygen Species	204-207	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-62
19833721-5	2009	Using purified recombinant proteins, we observed that c-Abl tyrosine-phosphorylated dynamin 2, and this phosphorylation increased p47(phox)/dynamin 2 association (change in the dissociation constant (K(d)) from 85.8 to 6.9 nm).	Tyrosine	60-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-59
19833721-7	2009	These results suggest that hyperoxia induces c-Abl-mediated dynamin 2 phosphorylation required for recruitment of p47(phox) to CEMs and subsequent ROS production in lung endothelium.	Reactive Oxygen Species	147-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-50
19779040-0	2009	Dasatinib treatment of chronic-phase chronic myeloid leukemia: analysis of responses according to preexisting BCR-ABL mutations.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
19779040-1	2009	Dasatinib is a BCR-ABL inhibitor with 325-fold higher potency than imatinib against unmutated BCR-ABL in vitro.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
19779040-1	2009	Dasatinib is a BCR-ABL inhibitor with 325-fold higher potency than imatinib against unmutated BCR-ABL in vitro.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
19779040-1	2009	Dasatinib is a BCR-ABL inhibitor with 325-fold higher potency than imatinib against unmutated BCR-ABL in vitro.	Imatinib Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
19779040-3	2009	Here, dasatinib efficacy was analyzed in patients recruited to phase 2/3 trials with chronic-phase chronic myeloid leukemia with or without BCR-ABL mutations after prior imatinib.	Dasatinib	6-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
19779040-9	2009	Overall, dasatinib has durable efficacy in patients with or without BCR-ABL mutations.	Dasatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
19822896-1	2009	Nilotinib has a higher binding affinity and selectivity for BCR-ABL with respect to imatinib and is an effective treatment of chronic myeloid leukemia (CML) after imatinib failure.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
19672773-1	2009	Dasatinib, a dual Src/Abl tyrosine kinase inhibitor, has significant antileukemic effects against various imatinib mesylate-resistant BCR/ABL mutants.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-25
19672773-1	2009	Dasatinib, a dual Src/Abl tyrosine kinase inhibitor, has significant antileukemic effects against various imatinib mesylate-resistant BCR/ABL mutants.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
19672773-1	2009	Dasatinib, a dual Src/Abl tyrosine kinase inhibitor, has significant antileukemic effects against various imatinib mesylate-resistant BCR/ABL mutants.	Imatinib Mesylate	106-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
19672773-2	2009	Despite well-documented inhibitory effects of dasatinib on BCR/ABL kinase, the exact downstream cellular events leading to generation of its potent antileukemic effects remain to be defined.	Dasatinib	46-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-66
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.	Dasatinib	205-214	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-182
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 Mesylate	251-259	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-182
19672773-6	2009	Altogether, our findings suggest a critical role for p38 MAPK pathway in the generation of antileukemic effects of dasatinib, and raise the possibility that development of novel means to enhance p38 MAPK activation in BCR/ABL expressing cells may be an approach to promote antileukemic responses and, possibly, reverse T315I mutation-mediated resistance.	Dasatinib	115-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	218-225
20017607-5	2009	Dasatinib is a dual Abl/Src kinase TKI that is structurally unrelated to imatinib and is approved for therapy of all phases of CML in patients who are resistant or intolerant to imatinib.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-23
19651622-8	2009	In contrast to MAPK inhibitors, dasatinib, a clinical drug directed against BCR-ABL, which is the cause of chronic myelogenous leukemia, affected nearly 1,000 phosphopeptides.	Dasatinib	32-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
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 Mesylate	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 Mesylate	143-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
19844167-5	2009	We found such genetic lesions to predict activity of geldanamycin-derived Hsp90 inhibitors as well as of the clinically approved SRC/ABL-inhibitor dasatinib.	Dasatinib	147-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-136
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 Mesylate	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
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.	nilotinib	230-239	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
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.	Dasatinib	243-252	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
19878872-3	2009	We report design and preclinical evaluation of AP24534, a potent, orally available multitargeted kinase inhibitor active against T315I and other BCR-ABL mutants.	ponatinib	47-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-152
19878872-5	2009	Our work supports clinical evaluation of AP24534 as a pan-BCR-ABL inhibitor for treatment of CML.	ponatinib	41-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
19838099-1	2009	Dasatanib, which has been approved for rescue therapy for patients with imatinib-resistant chronic myelogenous leukemia and Philadelphia chromosome positive acute lymphoblastic leukemia, is a novel, orally available multitargeted kinase inhibitor of BCR-ABL and SRC family kinases (Quintas-Cardama et al, J Clin Oncol 2007;25:3908-14).	dasatanib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	250-257
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 Mesylate	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-145
19766113-0	2009	MMR/c-Abl-dependent activation of ING2/p73alpha signaling regulates the cell death response to N-methyl-N"-nitro-N-nitrosoguanidine.	Methylnitronitrosoguanidine	95-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-9
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 Mesylate	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 Mesylate	142-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
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 Mesylate	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-78
19748671-0	2010	Response to imatinib in a patient with chronic myeloid leukemia simultaneously expressing p190(BCR-ABL) oncoprotein and JAK2V617F mutation.	Imatinib Mesylate	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
19590902-8	2009	Significant decrease in the incidence of CRB was observed when prophylactic TPA/tobra ABL was used in the high-risk group (P = 0.0201).	Tetradecanoylphorbol Acetate	76-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-89
19329185-2	2009	Treatment of Imatinib or LY294002 reduced Skp2 mRNA in BCR-ABL-positive K562 cells.	Imatinib Mesylate	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
19329185-2	2009	Treatment of Imatinib or LY294002 reduced Skp2 mRNA in BCR-ABL-positive K562 cells.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	25-33	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 Mesylate	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 Mesylate	230-238	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
19590902-11	2009	However, both the overall and infection-free survival of the catheters in the high-risk group significantly improved while the patients were receiving TPA/tobra ABL prophylaxis, becoming similar to the outcomes of the catheters in the average-risk group and exhibiting statistically non-significant differences (P = 0.5571 and P = 0.9711, respectively).	Tetradecanoylphorbol Acetate	151-154	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-164
19706883-0	2009	Acute dasatinib exposure commits Bcr-Abl-dependent cells to apoptosis.	Dasatinib	6-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
19679652-6	2009	We also demonstrate that GNF-2 can inhibit enzymatic and cellular kinase activity of Arg, a kinase highly homologous to c-Abl, which is also likely to be regulated through intramolecular binding of an NH(2)-terminal myristate lipid.	Arginine	85-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-125
19679652-6	2009	We also demonstrate that GNF-2 can inhibit enzymatic and cellular kinase activity of Arg, a kinase highly homologous to c-Abl, which is also likely to be regulated through intramolecular binding of an NH(2)-terminal myristate lipid.	myristate lipid	216-231	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-125
19679652-7	2009	These results suggest that non-ATP-competitive inhibitors, such as GNF-2, can serve as chemical tools that can discriminate between c-Abl isoform-specific behaviors.	Adenosine Triphosphate	31-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-137
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 Mesylate	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 Mesylate	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
19789182-0	2009	Tyrosine phosphorylation of nuclear-membrane protein emerin by Src, Abl and other kinases.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-71
19706883-2	2009	Surprisingly, the second-generation Bcr-Abl inhibitor, dasatinib, was reported to be clinically effective with once-daily dosing, despite a short (3- to 5-hour) plasma half-life.	Dasatinib	55-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
19706883-4	2009	Such acute treatments with clinically achievable dasatinib concentrations also irreversibly committed Bcr-Abl+ CML cell lines to apoptotic cell death.	Dasatinib	49-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
19706883-5	2009	Potent transient Bcr-Abl inhibition using the alternative inhibitor, nilotinib, also resulted in cell death.	nilotinib	69-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
19793709-1	2009	The introduction of the BCR-ABL inhibitor imatinib revolutionized the treatment of patients with chronic myeloid leukemia (CML).	Imatinib Mesylate	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
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 Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
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).	Adenosine Triphosphate	59-62	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).	Adenosine Triphosphate	59-62	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 Mesylate	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 Mesylate	137-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-167
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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.	Dasatinib	84-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
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.	Dasatinib	84-93	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 Mesylate	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 Mesylate	102-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
21083014-0	2009	Bosutinib: a dual SRC/ABL kinase inhibitor for the treatment of chronic myeloid leukemia.	bosutinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-25
21083014-3	2009	Bosutinib (SKI-606), a 7-alkoxy-3-quinolinecarbonitrile, functions as a dual inhibitor of SRC and ABL kinases, and preclinical studies demonstrated a high antiproliferative activity in human and murine CML cell lines.	bosutinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-101
21083014-3	2009	Bosutinib (SKI-606), a 7-alkoxy-3-quinolinecarbonitrile, functions as a dual inhibitor of SRC and ABL kinases, and preclinical studies demonstrated a high antiproliferative activity in human and murine CML cell lines.	bosutinib	11-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-101
19794096-0	2009	A novel dasatinib-sensitive RCSD1-ABL1 fusion transcript in chemotherapy-refractory adult pre-B lymphoblastic leukemia with t(1;9)(q24;q34).	Dasatinib	8-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-38
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 Mesylate	118-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
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 Mesylate	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 Mesylate	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 Mesylate	244-252	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
19702336-6	2009	Translation assays with isolated ribosomes that were phosphorylated in vitro by kinases PKA, PKCdelta, or Abl Tyr showed up to 30% inhibition due to phosphorylation.	Tyrosine	110-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-109
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 Mesylate	161-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
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 Mesylate	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
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 Mesylate	168-176	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-55
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.	DFG peptide	87-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
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 Mesylate	231-239	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
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 Mesylate	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 Mesylate	3-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
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 Mesylate	22-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
19920925-5	2009	The development of novel agents designed to overcome IM resistance, while still primarily targeted on BCR-ABL, led to the creation of the high affinity aminopyrimidine inhibitor, nilotinib.	2-aminopyrimidine	152-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
19920925-5	2009	The development of novel agents designed to overcome IM resistance, while still primarily targeted on BCR-ABL, led to the creation of the high affinity aminopyrimidine inhibitor, nilotinib.	nilotinib	179-188	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
19920925-6	2009	Nilotinib is much more potent as a BCR-ABL inhibitor than IM and inhibits both wild type and IM-resistant BCR-ABL with significant clinical activity across the entire spectrum of BCR-ABL mutants with the exception of T315I.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
19920925-6	2009	Nilotinib is much more potent as a BCR-ABL inhibitor than IM and inhibits both wild type and IM-resistant BCR-ABL with significant clinical activity across the entire spectrum of BCR-ABL mutants with the exception of T315I.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
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 Mesylate	92-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-150
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 Mesylate	164-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-57
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 Mesylate	42-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
19920925-6	2009	Nilotinib is much more potent as a BCR-ABL inhibitor than IM and inhibits both wild type and IM-resistant BCR-ABL with significant clinical activity across the entire spectrum of BCR-ABL mutants with the exception of T315I.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
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 Mesylate	120-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-154
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	138-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-119
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	157-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
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.	Dasatinib	149-158	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
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.	nilotinib	162-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
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 Mesylate	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 Mesylate	155-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
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 Mesylate	35-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
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 Mesylate	191-199	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
19369965-7	2009	Here, we show that T315I (i) requires autophosphorylation at tyrosine 177 in the BCR-portion to mediate resistance against the inhibition of oligomerization; (ii) restores the capacity to mediate factor-independent growth of loss-of-function mutants due to an increase in or activation of ABL-kinase; (iii) leads to phosphorylation of endogenous BCR, suggesting aberrant substrate activation by BCR/ABL harboring the T315I mutation.	Tyrosine	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	289-292
19369965-7	2009	Here, we show that T315I (i) requires autophosphorylation at tyrosine 177 in the BCR-portion to mediate resistance against the inhibition of oligomerization; (ii) restores the capacity to mediate factor-independent growth of loss-of-function mutants due to an increase in or activation of ABL-kinase; (iii) leads to phosphorylation of endogenous BCR, suggesting aberrant substrate activation by BCR/ABL harboring the T315I mutation.	Tyrosine	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	395-402
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 Mesylate	80-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	146-153
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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
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 Mesylate	209-217	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
19723894-4	2009	We found that triptolide, a diterpenoid, at nanomolar concentrations, promoted equally significant death of KBM5 cells, a cell line derived from a Bcr-Abl-bearing blast crisis CML patient and KBM5STI571 cells, an imatinib-resistant KBM5 subline bearing the T315I mutation.	triptolide	14-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-154
19723894-5	2009	Similarly, Ba/F3 cells harboring mutated BCR-ABL were as sensitive as Ba/F3Bcr-Abl(p210wt) cells to triptolide.	triptolide	100-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
19723894-6	2009	Importantly, triptolide induced apoptosis in primary samples from blast crisis CML patients, who showed resistance to Bcr-Abl TKIs in vivo, with less toxicity to normal cells.	triptolide	13-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
19723894-7	2009	Triptolide decreased X-linked inhibitor of apoptosis protein, Mcl-1, and Bcr-Abl protein levels in K562, KBM5, and KBM5STI571 cells and in cells from blast crisis CML patients.	triptolide	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
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.	Adenosine Triphosphate	28-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
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.	Adenosine Triphosphate	52-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
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 Mesylate	225-233	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
19541823-0	2009	KW-2449, a novel multikinase inhibitor, suppresses the growth of leukemia cells with FLT3 mutations or T315I-mutated BCR/ABL translocation.	KW 2449	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-124
19541823-1	2009	KW-2449, a multikinase inhibitor of FLT3, ABL, ABL-T315I, and Aurora kinase, is under investigation to treat leukemia patients.	KW 2449	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-45
19541823-1	2009	KW-2449, a multikinase inhibitor of FLT3, ABL, ABL-T315I, and Aurora kinase, is under investigation to treat leukemia patients.	KW 2449	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
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 Mesylate	3-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
19654305-4	2009	As several downstream mediators of BCR-ABL are regulated by the proteasome degradation pathway, we also show that inhibition of this pathway, using bortezomib, causes regression of CML-like disease.	Bortezomib	148-158	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
19654305-5	2009	Bortezomib treatment led to inhibition of BCR-ABL-induced suppression of FoxO proteins and their proapoptotic targets, tumor necrosis factor-related apoptosis-inducing ligand and BIM, thereby providing novel insights into the molecular effects of proteasome inhibitor therapy.	Bortezomib	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
19654305-6	2009	We additionally show sensitivity of imatinib-resistant BCR-ABL T315I cells to bortezomib.	Imatinib Mesylate	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
19654305-6	2009	We additionally show sensitivity of imatinib-resistant BCR-ABL T315I cells to bortezomib.	Bortezomib	78-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
19654305-7	2009	Our data delineate the involvement of FoxO proteins in BCR-ABL-induced evasion of apoptosis and provide evidence that bortezomib is a candidate therapeutic in the treatment of BCR-ABL-induced leukemia.	Bortezomib	118-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
19654305-7	2009	Our data delineate the involvement of FoxO proteins in BCR-ABL-induced evasion of apoptosis and provide evidence that bortezomib is a candidate therapeutic in the treatment of BCR-ABL-induced leukemia.	Bortezomib	118-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	176-183
19442657-2	2009	Here we show that the interaction between hMSH5 and c-Abl confers ionizing radiation (IR)-induced apoptotic response by promoting c-Abl activation and p73 accumulation, and these effects are greatly enhanced in cells expressing hMSH5(P29S) (i.e. the hMSH5 variant possessing a proline to serine change within the N-terminal (Px)(5) dipeptide repeat).	Proline	277-284	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-57
19442657-2	2009	Here we show that the interaction between hMSH5 and c-Abl confers ionizing radiation (IR)-induced apoptotic response by promoting c-Abl activation and p73 accumulation, and these effects are greatly enhanced in cells expressing hMSH5(P29S) (i.e. the hMSH5 variant possessing a proline to serine change within the N-terminal (Px)(5) dipeptide repeat).	Serine	288-294	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-57
19442657-2	2009	Here we show that the interaction between hMSH5 and c-Abl confers ionizing radiation (IR)-induced apoptotic response by promoting c-Abl activation and p73 accumulation, and these effects are greatly enhanced in cells expressing hMSH5(P29S) (i.e. the hMSH5 variant possessing a proline to serine change within the N-terminal (Px)(5) dipeptide repeat).	Dipeptides	332-341	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-57
19442657-3	2009	Our current study provides the first evidence that the (Px)(5) dipeptide repeat plays an important role in modulating the interaction between hMSH5 and c-Abl and alteration of this dipeptide repeat in hMSH5(P29S) leads to increased IR sensitivity owing to enhanced caspase-3-mediated apoptosis.	Dipeptides	63-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-157
19261608-7	2009	The Abl kinase inhibitors and depletion of Bcr-Abl induced the expression of PHLPP1 and PHLPP2, which dephosphorylated Ser-473 on Akt1, -2, and -3, resulting in inhibited proliferation of CML cells.	Serine	119-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
19261608-10	2009	Thus, Bcr-Abl represses the expression of PHLPP1 and PHLPP2 and continuously activates Akt1, -2, and -3 via phosphorylation on Ser-473, resulting in the proliferation of CML cells.	Serine	127-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-13
19727206-1	2009	A 23-year old woman with acute biphenotypic leukemia (ABL) complained of chest pain with cough, high fever and hemoptysis during induction chemotherapy, although she had been treated with anti-biotics and micafungin.	Micafungin	205-215	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-57
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 Mesylate	46-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-27
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 Mesylate	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-105
19167064-0	2009	Is it possible to discontinue imatinib mesylate therapy in Chronic Myeloid Leukemia patients with undetectable BCR/ABL?	Imatinib Mesylate	30-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
19344757-6	2009	We show that pharmacologic inhibition or genetic deletion of cAbl causes a defect in tyrosine phosphorylation of the cytoskeletal adapter CrkII.	Tyrosine	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-65
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 Mesylate	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 Mesylate	178-186	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-149
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 Mesylate	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
19295545-1	2009	Dasatinib, a broad-spectrum tyrosine kinase inhibitor (TKI), predominantly targets BCR-ABL and SRC oncoproteins and also inhibits off-target kinases, which may result in unexpected drug responses.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
19295548-2	2009	In this study, inducible expression of Bcr-Abl in TonB.210 cells is associated with increased production of intracellular reactive oxygen species (ROS), which is thought to play a role in survival signaling when generated at specific levels.	Reactive Oxygen Species	122-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
19470755-5	2009	Abl binds a proline-rich motif in Cdo via its SH3 domain, and these regions of Abl and Cdo are required for their promyogenic effects.	Proline	12-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
19295548-2	2009	In this study, inducible expression of Bcr-Abl in TonB.210 cells is associated with increased production of intracellular reactive oxygen species (ROS), which is thought to play a role in survival signaling when generated at specific levels.	Reactive Oxygen Species	147-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
19295548-3	2009	Elevated ROS in Bcr-Abl-expressing cells were found to activate PI3k/Akt pathway members such as Akt and GSK3beta as well as downstream targets beta-catenin and Mcl-1.	Reactive Oxygen Species	9-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
19295548-6	2009	Knock-down experiments using siRNA suggest that Nox-4 is the main source of increased ROS following Bcr-Abl expression.	Reactive Oxygen Species	86-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
19295548-7	2009	We showed that Bcr-Abl-induced ROS could also increase survival pathway signaling through redox inhibition of PP1alpha, a serine threonine phosphatase that negatively regulates the PI3k/Akt pathway.	Reactive Oxygen Species	31-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
19295548-8	2009	Overall our results demonstrate that Bcr-Abl expression increases Nox-4-generated ROS, which in turn increases survival signaling through PI3k/Akt pathway by inhibition of PP1alpha, thus contributing to the high level of resistance to apoptosis seen in these Bcr-Abl-expressing cells.	Reactive Oxygen Species	82-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
19295548-8	2009	Overall our results demonstrate that Bcr-Abl expression increases Nox-4-generated ROS, which in turn increases survival signaling through PI3k/Akt pathway by inhibition of PP1alpha, thus contributing to the high level of resistance to apoptosis seen in these Bcr-Abl-expressing cells.	Reactive Oxygen Species	82-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	259-266
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 Mesylate	97-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	202-209
19394693-4	2009	After starting nilotinib 400mg orally twice daily, she achieved CCyR at 3, 6, and 11 months, suggesting that second-generation TKIs can result in favorable responses in patients with ETV6/ABL rearrangement who relapse after imatinib.	nilotinib	15-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	188-191
19470755-5	2009	Abl binds a proline-rich motif in Cdo via its SH3 domain, and these regions of Abl and Cdo are required for their promyogenic effects.	Proline	12-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-82
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.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-58
19423701-0	2009	Phosphorylation of RACK1 on tyrosine 52 by c-Abl is required for insulin-like growth factor I-mediated regulation of focal adhesion kinase.	Tyrosine	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-48
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 Mesylate	91-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-80
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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
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 Mesylate	146-154	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
19378338-0	2009	NF-kappaB inhibition triggers death of imatinib-sensitive and imatinib-resistant chronic myeloid leukemia cells including T315I Bcr-Abl mutants.	Imatinib Mesylate	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
19378338-0	2009	NF-kappaB inhibition triggers death of imatinib-sensitive and imatinib-resistant chronic myeloid leukemia cells including T315I Bcr-Abl mutants.	Imatinib Mesylate	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 Mesylate	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.	AS602868	60-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	180-187
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 Mesylate	145-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	180-187
19602287-3	2009	It creates a docking site for SH2-domain containing proteins, such as ShcA, ShcB, ShcC, Grb7, Grb2, as well as adapter proteins, such as Crk and Nck, that regulate important biological processes, cytosolic tyrosine kinases, such as Abl, Lyn and Src, which regulate signal transduction pathways, and enzymes that control phosphatidylinositols levels and signaling, such as PLC-gamma.	Phosphatidylinositols	320-341	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	232-235
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 Mesylate	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
19652056-0	2009	Impact of baseline BCR-ABL mutations on response to nilotinib in patients with chronic myeloid leukemia in chronic phase.	nilotinib	52-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
19548306-10	2009	The results also showed that berbamine was able to down-regulate BCR-ABL and phospho-BCR-ABL proteins by affecting bcr-abl mRNA expression and decrease expression of nuclear NF-kappaB, phospho-IkappaBalpha, IKKalpha, and Survivin.	berbamine	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
19548306-10	2009	The results also showed that berbamine was able to down-regulate BCR-ABL and phospho-BCR-ABL proteins by affecting bcr-abl mRNA expression and decrease expression of nuclear NF-kappaB, phospho-IkappaBalpha, IKKalpha, and Survivin.	berbamine	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
19548306-10	2009	The results also showed that berbamine was able to down-regulate BCR-ABL and phospho-BCR-ABL proteins by affecting bcr-abl mRNA expression and decrease expression of nuclear NF-kappaB, phospho-IkappaBalpha, IKKalpha, and Survivin.	berbamine	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
19402171-2	2009	Loss of response on imatinib is often because of BCR-ABL mutations.	Imatinib Mesylate	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
19402171-3	2009	Dasatinib is a 325-fold more potent inhibitor of Bcr-Abl than imatinib and has been associated with high rates of durable responses in patients with CML in chronic phase (CP) after imatinib failure.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
19275932-8	2009	c-Abl phosphorylates three tyrosine residues on PDGFR-beta (Y686, Y934, Y970), while Arg only phosphorylatesY686.	Tyrosine	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
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 Mesylate	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-161
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 Mesylate	131-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-25
19268463-6	2009	Treatment with apicidin resulted in down-regulation of Bcr-Abl and inhibition of its downstream target, PI3K/AKT-NF-kappaB pathway.	apicidin	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
19268463-8	2009	These results suggest that apicidin may sensitize K562 cells to TRAIL-induced apoptosis through caspase-dependent mitochondrial pathway by regulating expression of Bcr-Abl and its related anti-apoptotic proteins.	apicidin	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	164-171
19268463-9	2009	Therefore, the present study suggests that combination of apicidin and TRAIL may be an effective strategy for treating TRAIL-resistant Bcr-Abl expressing CML cells.	apicidin	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
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 Mesylate	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
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 Mesylate	61-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-77
19493708-1	2009	Nilotinib (AMN-107, Tasigna) is a small-molecule inhibitor of BCR/ABL, approved for chronic myelogenous leukemia.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
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.	Inositol	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-169
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.	Etoposide	196-205	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-169
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 Mesylate	211-219	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-169
19557636-2	2009	T315I (Treonine-->Isoleucine) is a mutation in the exon 6 of BCR-ABL gene that makes the protein resistant to kinase inhibitors currently used for treating CML.	treonine	7-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
19557636-2	2009	T315I (Treonine-->Isoleucine) is a mutation in the exon 6 of BCR-ABL gene that makes the protein resistant to kinase inhibitors currently used for treating CML.	Isoleucine	21-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
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 Mesylate	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
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.	PD 166326	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
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 Mesylate	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 Mesylate	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 Mesylate	170-178	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
19369231-1	2009	Dasatinib is the most potent BCR-ABL inhibitor, with 325-fold higher potency than imatinib against unmutated BCR-ABL in vitro.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
19369231-1	2009	Dasatinib is the most potent BCR-ABL inhibitor, with 325-fold higher potency than imatinib against unmutated BCR-ABL in vitro.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
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 Mesylate	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 Mesylate	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 Mesylate	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-29
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 Mesylate	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	148-151
19326384-2	2009	New compounds designed on the basis of the model were found to have very good affinity for the target, providing further validation of the model itself.The X-ray crystallographic coordinates of the Abl tyrosine kinase domain in its active, inactive, and Src-like inactive conformations were used as targets to simulate the binding mode of a large series of pyrazolo[3,4-d]pyrimidines (known Abl inhibitors) by means of GOLD software.	pyrazolo(3,4-d)pyrimidine	357-383	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	198-201
19268463-0	2009	Cotreatment with apicidin overcomes TRAIL resistance via inhibition of Bcr-Abl signaling pathway in K562 leukemia cells.	apicidin	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
19519355-0	2009	Nilotinib therapy in chronic myelogenous leukemia: the strength of high selectivity on BCR/ABL.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
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.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
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 Mesylate	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
19282395-1	2009	Dasatinib was approved in 2006 for the treatment of imatinib-resistant chronic myelogenous leukemia and functions primarily through the inhibition of BCR-ABL and Src kinase.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
19395585-1	2009	Dasatinib is a tyrosine kinase inhibitor (including BCR-ABL and the SRC family) that is effective in patients with chronic myeloid leukemia.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
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 Mesylate	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
19502190-3	2009	Dasatinib is the first and only dual BCR-ABL/SRC family kinase inhibitor approved by the U.S. Food and Drug Administration for the treatment of patients with CML in any phase or Philadelphia chromosome-positive acute lymphoblastic leukemia who are resistant to or intolerant of imatinib.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
19502192-1	2009	Dasatinib, an oral inhibitor of multiple tyrosine kinases, including BCR-ABL, Src, and platelet-derived growth factor receptor, was approved for patients with imatinib-resistant or -intolerant chronic myeloid leukemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL).	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
19262594-0	2009	Short-term intense Bcr-Abl kinase inhibition with nilotinib is adequate to trigger cell death in BCR-ABL(+) cells.	nilotinib	50-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
19449194-1	2009	Nilotinib is a second-generation BCR-ABL kinase inhibitor with improved potency and selectivity compared to imatinib.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
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 Mesylate	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
19091403-0	2009	Molecular response to imatinib in patient with Ph negative p190 BCR-ABL transcript positive chronic myeloid leukemia with cyclic leukocytosis.	Imatinib Mesylate	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 Mesylate	172-180	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
19509264-0	2009	Efficacy and pharmacodynamic effects of bosutinib (SKI-606), a Src/Abl inhibitor, in freshly generated human pancreas cancer xenografts.	bosutinib	40-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-70
19509264-2	2009	The purpose of the study was to investigate the in vivo efficacy and pharmacodynamic effects of bosutinib (SKI-606), a Src/Abl inhibitor, using a panel of human pancreatic tumor xenografts.	bosutinib	96-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-126
19519539-0	2009	Basis for resistance to imatinib in 16 BCR-ABL mutants as determined using molecular dynamics.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	228-236	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	312-319
19571508-0	2009	[Correlation of quantification of major bcr-abl mRNA between TMA (transcription mediated amplification) method and real-time quantitative PCR].	tma	61-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
19571508-6	2009	The results indicated that Amp-CML had a significant correlation with Fusion Quant M-BCR (R>0.971, P<0.01), a standard nucleic acid quantitative method used in Europe and RQ-PCR (R>0.974, P<0.01), especially in samples with more than 100 copies/microg RNA of major bcr-abl mRNA.	Adenosine Monophosphate	27-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	277-284
19571508-7	2009	These data suggest that Amp-CML is reliable for monitoring major bcr-abl mRNA in patients having achieved an MMR.	Adenosine Monophosphate	24-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
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 Mesylate	33-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-97
19220809-2	2009	In particular, constitutive tyrosine kinase (TK) activity of p210 BCR-ABL blocks c-Jun N-terminal kinase (JNK) phosphorylation leading to 14-3-3 sigma phosphorylation at a critical residue (Ser(186)) for c-ABL binding in response to DNA damage.	Serine	190-193	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
19220809-6	2009	Further investigation on CS profiles of c-ABL- and p210 BCR-ABL-containing complexes revealed the mechanism likely involved 14-3-3 precluded phosphorylation in CML cells.	Cesium	25-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-45
19220809-6	2009	Further investigation on CS profiles of c-ABL- and p210 BCR-ABL-containing complexes revealed the mechanism likely involved 14-3-3 precluded phosphorylation in CML cells.	Cesium	25-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
19262594-0	2009	Short-term intense Bcr-Abl kinase inhibition with nilotinib is adequate to trigger cell death in BCR-ABL(+) cells.	nilotinib	50-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
19363859-0	2009	Hair depigmentation during chemotherapy with dasatinib, a dual Bcr-Abl/Src family tyrosine kinase inhibitor.	Dasatinib	45-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
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.	Glucose	21-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
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 Mesylate	140-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
19380743-1	2009	The tyrosine kinase Bcr-Abl causes chronic myeloid leukemia and is the cognate target of tyrosine kinase inhibitors like imatinib.	Imatinib Mesylate	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
19380743-6	2009	Certain components still appear to interact with Bcr-Abl in a phosphotyrosine-independent manner.	Phosphotyrosine	62-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
19285032-3	2009	Here, we provide evidence that c-ABL, a tyrosine kinase activated by DNA damage which phosphorylates RAD51 on Tyr-315, works at a previously unrecognized, proximal step to initiate RAD51 assembly.	Tyrosine	110-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-36
19285032-6	2009	We show that phosphorylation on Tyr-315 by c-ABL is required for chromatin association of oligomerization-defective RAD51 mutants, but is insufficient to restore oligomerization.	Tyrosine	32-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-48
19167484-3	2009	Phosphotyrosine profiling array showed that PTP inhibition following Cr(VI) exposure increased tyrosine phosphorylation of specific proteins, such as FGR and ABL, which are upstream regulators of both Erk and Akt pathways.	Phosphotyrosine	0-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-161
19167484-3	2009	Phosphotyrosine profiling array showed that PTP inhibition following Cr(VI) exposure increased tyrosine phosphorylation of specific proteins, such as FGR and ABL, which are upstream regulators of both Erk and Akt pathways.	Tyrosine	7-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-161
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 Mesylate	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 Mesylate	19-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
19013641-2	2009	Dasatinib is a tyrosine kinase inhibitor with activity against BCR-ABL, platelet-derived growth factor receptors (PDGFRs), c- KIT, fibroblast growth factor receptors (FGFRs), SRC family kinases (SFKs), and EPHA receptors, all of which have been implicated in the pathogenesis of Ph- leukemias and myeloid disorders.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
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 Mesylate	129-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
19260709-8	2009	The newly discovered rescue agent 2-aminoimidazole is about as efficient as imidazole in rescuing R/A Src and Abl.	2-aminoimidazole	34-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-113
19260709-8	2009	The newly discovered rescue agent 2-aminoimidazole is about as efficient as imidazole in rescuing R/A Src and Abl.	imidazole	41-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-113
19171873-0	2009	ICSBP-mediated immune protection against BCR-ABL-induced leukemia requires the CCL6 and CCL9 chemokines.	ccl6	79-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
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 Mesylate	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
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 Mesylate	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 Mesylate	57-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-150
20641197-0	2004	[(111)In]-Ethylenedicysteine-murine anti-phosphotyrosine antibody The overexpression or constitutive activation of non-receptor tyrosine kinase (TK) such as Src- and Bcr-Abl is one of the several mechanisms known to initiate and participate in the progression and metastasis of cancer (1, 2).	ethylene dicysteine	10-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-173
18978822-0	2009	Dasatinib-induced restoration of donor chimerism in BCR-ABL1-positive ALL after failure of imatinib therapy and allo-SCT.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-60
19291100-7	2009	SB163 also induced a dose inhibition of Abl and PDGFR.	sb163	0-5	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-43
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 Mesylate	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
19549414-1	2009	Recent work indicates that an Aurora kinase inhibitor MK-0457 (VX-680), a small-molecule inhibitor of Aurora kinases A, B, C and BCR-ABL, FLT-3, JAK-2, can block the progression of cell growth cycle, causing apoptosis in a range of human tumors.	VX680	54-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-136
19549414-1	2009	Recent work indicates that an Aurora kinase inhibitor MK-0457 (VX-680), a small-molecule inhibitor of Aurora kinases A, B, C and BCR-ABL, FLT-3, JAK-2, can block the progression of cell growth cycle, causing apoptosis in a range of human tumors.	VX680	63-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-136
19401345-0	2009	Abnormalities in glucose uptake and metabolism in imatinib-resistant human BCR-ABL-positive cells.	Imatinib Mesylate	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.	Glucose	90-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
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.	Lactic Acid	116-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
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.	Trichloroacetic Acid	162-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
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 Mesylate	182-190	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
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 Mesylate	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 Mesylate	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 Mesylate	133-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	169-176
19366808-0	2009	Sorafenib induces apoptosis specifically in cells expressing BCR/ABL by inhibiting its kinase activity to activate the intrinsic mitochondrial pathway.	Sorafenib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-68
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	217-225	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	258-261
19366808-2	2009	Here, we show that the multikinase inhibitor sorafenib inhibits proliferation and induces apoptosis at much lower concentrations in Ton.B210 cells when driven by inducibly expressed BCR/ABL than when driven by interleukin-3.	Sorafenib	45-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-189
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.	Sorafenib	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
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 Mesylate	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
19366808-5	2009	It was further revealed that sorafenib activates Bax and caspase-3 and reduces mitochondrial membrane potential specifically in BCR/ABL-driven cells.	Sorafenib	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-135
19366808-6	2009	Sorafenib also inhibited BCR/ABL-induced tyrosine phosphorylation of its cellular substrates and its autophosphorylation in Ton.B210.	Sorafenib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-32
19366808-6	2009	Sorafenib also inhibited BCR/ABL-induced tyrosine phosphorylation of its cellular substrates and its autophosphorylation in Ton.B210.	Tyrosine	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-32
19366808-7	2009	It was finally shown that sorafenib inhibits the kinase activity of BCR/ABL as well as its E255K and T315I mutants in in vitro kinase assays.	Sorafenib	26-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
19366808-8	2009	These results indicate that sorafenib induces apoptosis of BCR/ABL-expressing cells, at least partly, by inhibiting BCR/ABL to activate the mitochondria-mediated apoptotic pathway.	Sorafenib	28-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-66
19366808-8	2009	These results indicate that sorafenib induces apoptosis of BCR/ABL-expressing cells, at least partly, by inhibiting BCR/ABL to activate the mitochondria-mediated apoptotic pathway.	Sorafenib	28-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
19366808-9	2009	Thus, sorafenib may provide an effective therapeutic measure to treat Ph+ leukemias, particularly those expressing the T315I mutant, which is totally resistant to imatinib and the second generation BCR/ABL inhibitors.	Sorafenib	6-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	202-205
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 Mesylate	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 Mesylate	125-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	173-180
19151780-0	2009	Nuclear entrapment of BCR-ABL by combining imatinib mesylate with leptomycin B does not eliminate CD34+ chronic myeloid leukaemia cells.	Imatinib Mesylate	43-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
19151780-0	2009	Nuclear entrapment of BCR-ABL by combining imatinib mesylate with leptomycin B does not eliminate CD34+ chronic myeloid leukaemia cells.	leptomycin B	66-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
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 Mesylate	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
19203346-1	2009	Resistance to imatinib is commonly associated with reactivation of Bcr-Abl signalling.	Imatinib Mesylate	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 Mesylate	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 Mesylate	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
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 Mesylate	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 Mesylate	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 Mesylate	270-278	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
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 Mesylate	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-154
19351832-7	2009	Knocking down the expression level of miR-221 and miR-222 with antagonist miRs in the LNCaP-Abl cell line restored the response to the DHT induction of PSA transcription and also increased the growth response of the LNCaP-Abl cells to the androgen treatment.	Dihydrotestosterone	135-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-95
19351832-7	2009	Knocking down the expression level of miR-221 and miR-222 with antagonist miRs in the LNCaP-Abl cell line restored the response to the DHT induction of PSA transcription and also increased the growth response of the LNCaP-Abl cells to the androgen treatment.	Dihydrotestosterone	135-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	222-225
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 Mesylate	123-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
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 Mesylate	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
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 Mesylate	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
19363859-2	2009	This article reports the case of a patient who experienced depigmentation of her eyelashes, eyebrows, and temporal scalp hair six-to-eight weeks after initiating treatment with dasatinib (BMS-354825 or Sprycel), a novel dual Bcr-Abl/Src family tyrosine kinase inhibitor for chronic myeloid leukemia (CML).	Dasatinib	177-186	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	225-232
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 Mesylate	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.	nilotinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
19158834-3	2009	Among these, nilotinib is more potent against BCR-ABL than imatinib, and is effective against many imatinib-resistant BCR-ABL mutants.	nilotinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
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 Mesylate	99-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
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 Mesylate	105-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	185-190
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 Mesylate	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 Mesylate	147-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	212-219
19536317-2	2009	Imatinib mesylate, a BCR-ABL TK inhibitor, is the frontline therapy for CML.	Imatinib Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
19536317-7	2009	Dasatinib is well tolerated and has broad efficacy, resulting in durable responses in patients with any BCR-ABL mutation except for T3151 and mutations in codon 317 - most commonly F317L - including mutations that were highly resistant to imatinib, such as L248, Y253, E255, F359, and H396.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
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 Mesylate	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 Mesylate	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
19240172-0	2009	Triptolide inhibits Bcr-Abl transcription and induces apoptosis in STI571-resistant chronic myelogenous leukemia cells harboring T315I mutation.	triptolide	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
19338751-0	2009	Mechanism of MK-0457 efficacy against BCR-ABL positive leukemia cells.	VX680	13-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
19338751-8	2009	These results indicate that MK-0457 is effective in CML cells by the down-regulation of HSPs which may relate to BCR-ABL stability, and offer new information regarding the molecular basis of strategy against to CML.	VX680	28-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
19208803-0	2009	A systems biology understanding of the synergistic effects of arsenic sulfide and Imatinib in BCR/ABL-associated leukemia.	arsenic trisulfide	62-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
19208803-0	2009	A systems biology understanding of the synergistic effects of arsenic sulfide and Imatinib in BCR/ABL-associated leukemia.	Imatinib Mesylate	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 Mesylate	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-148
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.	arsenic trisulfide	62-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-148
19208803-4	2009	In this CML model, AS targets BCR/ABL through the ubiquitination of key lysine residues, leading to its proteasomal degradation, whereas IM inhibits the PI3K/AKT/mTOR pathway.	Lysine	72-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
19153832-0	2009	N-acetyl cysteine enhances imatinib-induced apoptosis of Bcr-Abl+ cells by endothelial nitric oxide synthase-mediated production of nitric oxide.	Acetylcysteine	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
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 Mesylate	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
19153832-0	2009	N-acetyl cysteine enhances imatinib-induced apoptosis of Bcr-Abl+ cells by endothelial nitric oxide synthase-mediated production of nitric oxide.	Nitric Oxide	87-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
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 Mesylate	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
19153832-2	2009	Bcr-Abl kinase stimulates the production of H(2)O(2), which in turn activates Abl kinase.	Hydrogen Peroxide	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
19153832-4	2009	MATERIALS AND METHODS: Effects of imatinib and NAC either alone or in combination were assessed on Bcr-Abl(+) cells to measure apoptosis.	Acetylcysteine	47-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
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 Mesylate	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
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.	Acetylcysteine	196-199	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.	Nitroprusside	17-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
19153832-11	2009	Indeed, NO donor sodium nitroprusside (SNP) also enhanced imatinib-mediated apoptosis of Bcr-Abl(+) cells.	Imatinib Mesylate	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.	Acetylcysteine	12-15	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 Mesylate	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.	Nitric Oxide	87-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
19156526-5	2009	Moreover, deletion of a domain in c-Abl, the PIP box, disrupts its interaction with PCNA, abolishes the PCNA-induced degradation of nuclear c-Abl, and substantially increases the nuclear c-Abl apoptotic function.	piperidine	45-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-39
19156526-5	2009	Moreover, deletion of a domain in c-Abl, the PIP box, disrupts its interaction with PCNA, abolishes the PCNA-induced degradation of nuclear c-Abl, and substantially increases the nuclear c-Abl apoptotic function.	piperidine	45-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-145
19156526-5	2009	Moreover, deletion of a domain in c-Abl, the PIP box, disrupts its interaction with PCNA, abolishes the PCNA-induced degradation of nuclear c-Abl, and substantially increases the nuclear c-Abl apoptotic function.	piperidine	45-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-145
19240172-6	2009	RESULTS: Triptolide potently down-regulated the mRNA and protein levels of Bcr-Abl independently of the caspase or proteosome activation in CML cells.	triptolide	9-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
19240172-10	2009	CONCLUSIONS: These findings suggest that triptolide is a promising agent to overcome STI571-resistant CML cells, and warrant a clinical trial of triptolide derivatives for CML with Bcr-Abl-T315I mutation.	triptolide	41-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	181-188
19240172-10	2009	CONCLUSIONS: These findings suggest that triptolide is a promising agent to overcome STI571-resistant CML cells, and warrant a clinical trial of triptolide derivatives for CML with Bcr-Abl-T315I mutation.	triptolide	145-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	181-188
19275507-1	2009	Dasatinib, a tyrosine kinase inhibitor of BCR-ABL, was originally approved for the second-line treatment of any-phase chronic myelogenous leukemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leukemia at a dosage of 70 mg twice daily.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
19234221-6	2009	After activated, c-Abl kinase increases the tyrosine phosphorylation of Vav.	Tyrosine	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-22
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 Mesylate	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 Mesylate	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 Mesylate	120-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	225-232
19135772-2	2009	The purpose of this study was to develop an enzyme-linked immunosorbent (ELISA) method to measure total tyrosine phosphorylation (P-Tyr) in small samples of cells that express BCR-ABL and to compare to more established methods.	Tyrosine	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	176-183
19135772-5	2009	RESULTS: In vitro exposure to TKI resulted in decreases in the level of P-Tyr, in both BCR-ABL-positive cell lines and primary CD34(+) CML samples, which were comparable to the reduction in P-Tyr by flow cytometry and phosphorylation of CrkL by either Western blot or flow cytometry.	Tyrosine	74-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
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.	bzlllcocho	156-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
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 Mesylate	200-208	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
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.	bzlllcocho	221-231	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
19006173-8	2009	Endogenous c-Jun expression was analyzed to determine the effective concentration of STI571 for inhibiting Bcr-Abl signaling.	Imatinib Mesylate	85-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
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 Mesylate	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
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 Mesylate	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
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 Mesylate	171-179	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-68
19039322-2	2009	Here, we characterized the target profile of the dual SRC/ABL inhibitor bosutinib employing a two-tiered approach using chemical proteomics to identify natural binders in whole cell lysates of primary CML and K562 cells in parallel to in vitro kinase assays against a large recombinant kinase panel.	bosutinib	72-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-61
19347730-1	2009	FB2 is a novel Abl/Src dual tyrosine kinase inhibitor which is designed to overcome imatinib resistance.	Imatinib Mesylate	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-18
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 Mesylate	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	183-190
19304540-12	2009	Imatinib treatment and allo-HSCT can both improve the OSs of 2-yrs of the patients with BCR/ABL(+)-ALL.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
19304540-12	2009	Imatinib treatment and allo-HSCT can both improve the OSs of 2-yrs of the patients with BCR/ABL(+)-ALL.	OSS	54-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
19320153-3	2009	This is the first study to report vertical variations of PBDEs in the ABL and one of only a few studies to investigate vertical distributions of persistent organic pollutants.	Halogenated Diphenyl Ethers	57-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-73
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 Mesylate	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-63
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.	Dasatinib	107-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-63
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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
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 Mesylate	244-252	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
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 Mesylate	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	176-179
20616897-5	2009	Dasatinib is a multi-target kinase inhibitor which has increased potency and is able to inhibit most Bcr-Abl mutant cell lines.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
19164531-4	2009	Hydrogen exchange mass spectrometry (HX MS) was used to compare the conformations of wild-type Abl with a nonmyristoylated form and with 3 clinically relevant imatinib resistance mutants (T315I, Y253H and E255V).	Hydrogen	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-98
19920910-6	2009	Nilotinib (Tasigna, AMN107, Novartis) is a close analog of imatinib with approximately 20-fold higher potency for BCR-ABL kinase inhibition.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
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 Mesylate	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
19014912-9	2009	Both Hsp90 cleavage and Bcr-Abl degradation were observed by incubating K562 cells with another H(2)O(2)-generating system (glucose/glucose oxidase) and by incubating KU812 cells (another leukemia cell line) with ascorbate/menadione.	Ascorbic Acid	213-222	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
19216789-13	2009	CONCLUSION: Our results indicate that AZD0530 targets both Src and Bcr-Abl kinase activity and reduces the leukaemic maintenance by Bcr-Abl.	saracatinib	38-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
19216789-13	2009	CONCLUSION: Our results indicate that AZD0530 targets both Src and Bcr-Abl kinase activity and reduces the leukaemic maintenance by Bcr-Abl.	saracatinib	38-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
19014912-9	2009	Both Hsp90 cleavage and Bcr-Abl degradation were observed by incubating K562 cells with another H(2)O(2)-generating system (glucose/glucose oxidase) and by incubating KU812 cells (another leukemia cell line) with ascorbate/menadione.	Vitamin K 3	223-232	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
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 Mesylate	30-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
19014913-2	2009	In this report, we describe how a novel non-toxic G1-arresting compound, pyrrolo-1,5-benzoxazepine (PBOX)-21, potentiates the apoptotic ability of STI571 in Bcr-Abl-positive CML cells.	pyrrolo-1,5-benzoxazepine	73-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-164
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 Mesylate	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
19180499-3	2009	Immunohistochemical analyses of skin biopsy specimens demonstrated reductions of phosphorylated PDGFRbeta and Abl with imatinib therapy.	Imatinib Mesylate	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-113
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 Mesylate	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-142
19100678-0	2009	Combined BCR-ABL inhibition with lentiviral-delivered shRNA and dasatinib augments induction of apoptosis in Philadelphia-positive cells.	Dasatinib	64-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
19100678-1	2009	OBJECTIVE: This study investigated two approaches, short hairpin RNA (shRNA) and the potent ABL inhibitor, dasatinib, alone and together, to achieve complete inhibition of BCR-ABL activity in Philadelphia-positive (Ph(+)) cells.	Dasatinib	107-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-95
19100678-1	2009	OBJECTIVE: This study investigated two approaches, short hairpin RNA (shRNA) and the potent ABL inhibitor, dasatinib, alone and together, to achieve complete inhibition of BCR-ABL activity in Philadelphia-positive (Ph(+)) cells.	Dasatinib	107-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-179
19100678-11	2009	CONCLUSION: These results confirm that by lowering BCR-ABL levels with shRNA, complete inhibition of oncoprotein activity can be achieved with a lower concentration of dasatinib, thus providing a rationale for combining these approaches in the setting of high target expression, such as found in advanced phase disease and in the stem cell compartment.	Dasatinib	168-177	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-108
18835038-0	2009	Renal failure and recovery associated with second-generation Bcr-Abl kinase inhibitors in imatinib-resistant chronic myelogenous leukemia.	Imatinib Mesylate	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
19020542-3	2009	BCR/ABL-expressing cell lines show an increase in DNA breaks after treatment with etoposide as compared to control cells.	Etoposide	82-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
19190119-2	2009	BMS-354825 (dasatinib) is an ATP-competitive small-molecule inhibitor effective in treating drug-resistant tumors with mutant BCR-ABL, KIT, and epidermal growth factor receptor by blocking tyrosine phosphorylation sites that are critical in tumorigenesis.	Dasatinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
19190119-2	2009	BMS-354825 (dasatinib) is an ATP-competitive small-molecule inhibitor effective in treating drug-resistant tumors with mutant BCR-ABL, KIT, and epidermal growth factor receptor by blocking tyrosine phosphorylation sites that are critical in tumorigenesis.	Adenosine Triphosphate	29-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
19296866-10	2009	Imatinib (Glivec), the most successful of protein kinase inhibitors, targets the inactive conformation of ABL tyrosine kinase.	Imatinib Mesylate	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 Mesylate	10-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-109
19296866-11	2009	Newer compounds, such as dasatinib, which targets the ABL active state, have been developed to increase potency and have proved effective for some, but not all, drug-resistant mutations.	Dasatinib	25-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-57
19075254-0	2009	Activity of bosutinib, dasatinib, and nilotinib against 18 imatinib-resistant BCR/ABL mutants.	nilotinib	38-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
19075254-0	2009	Activity of bosutinib, dasatinib, and nilotinib against 18 imatinib-resistant BCR/ABL mutants.	Imatinib Mesylate	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
19109024-3	2009	In this article, we will report the design and synthesis of a novel 1,4-benzoxazin-3-one chemical library 4 and the inhibitory activities against KDR and ABL which are closely related to chronic diseases such as cancer.	2H-1,4-Benzoxazin-3(4H)-one	68-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-157
18809244-1	2009	INTRODUCTION: Imatinib mesylate is a tyrosine kinase receptor inhibitor targeted against PDGFR alpha and beta, c-kit and bcr-abl.	Imatinib Mesylate	14-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
18984583-4	2009	Here we report the crystal structure of the non-liganded form of Lyn kinase domain, as well as in complex with three different inhibitors: the ATP analogue AMP-PNP; the pan Src kinase inhibitor PP2; and the BCR-Abl/Src-family inhibitor Dasatinib.	Dasatinib	236-245	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	207-214
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 Mesylate	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 Mesylate	60-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
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 Mesylate	38-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-27
19188713-2	2009	Nilotinib is a novel tyrosine kinase inhibitor targeting KIT (CD117), PDGFR and BCR-ABL and inhibiting the proliferation of both imatinib-sensitive and imatinib-resistant cells in vitro.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
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 Mesylate	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
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 Mesylate	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 Mesylate	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
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 Mesylate	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
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 Mesylate	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-169
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 Mesylate	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
19936007-2	2009	The current frontline therapy in CML is the BCR-ABL tyrosine kinase inhibitor, Imatinib.	Imatinib Mesylate	79-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
17590240-0	2009	Epigallocatechin gallate (EGCG) suppresses beta-amyloid-induced neurotoxicity through inhibiting c-Abl/FE65 nuclear translocation and GSK3 beta activation.	epigallocatechin gallate	0-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-102
17590240-0	2009	Epigallocatechin gallate (EGCG) suppresses beta-amyloid-induced neurotoxicity through inhibiting c-Abl/FE65 nuclear translocation and GSK3 beta activation.	epigallocatechin gallate	26-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-102
17590240-6	2009	Furthermore, EGCG also decreased nuclear translocation of c-Abl and blocked APP-C99-dependent GSK3 beta activation, and these inhibitory effects occurred through the interruption of c-Abl/Fe65 interaction.	epigallocatechin gallate	13-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-63
17590240-6	2009	Furthermore, EGCG also decreased nuclear translocation of c-Abl and blocked APP-C99-dependent GSK3 beta activation, and these inhibitory effects occurred through the interruption of c-Abl/Fe65 interaction.	epigallocatechin gallate	13-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-187
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.	Hemin	0-5	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
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 Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
19806784-9	2009	These data clearly indicate that: (a) cellular heme resulted from de novo biosynthesis and hemin uptake alters the developmental stage of human Bcr-Abl(+) CML cells and their susceptibility to imatinib; (b) cellular heme counteracts the ability of imatinib to repress Bcl-2 and Nrf2 gene expression; and (c) inhibitors of de novo biosynthesis can be developed and combined with imatinib to enhance its antileukemic activity.	Heme	47-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
19806784-9	2009	These data clearly indicate that: (a) cellular heme resulted from de novo biosynthesis and hemin uptake alters the developmental stage of human Bcr-Abl(+) CML cells and their susceptibility to imatinib; (b) cellular heme counteracts the ability of imatinib to repress Bcl-2 and Nrf2 gene expression; and (c) inhibitors of de novo biosynthesis can be developed and combined with imatinib to enhance its antileukemic activity.	Hemin	91-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
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 Mesylate	198-206	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
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 Mesylate	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 Mesylate	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
19552835-0	2009	[Major molecular response to imatinib in a patient with acute mixed lineage leukemia expressing a novel BCR/ABL transcript].	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	150-158	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
18696070-0	2009	Flow cytometric assay of phosphotyrosine levels in Bcr-Abl-positive chronic myelogenous leukemias: a potential prognostic marker.	Phosphotyrosine	25-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
18696070-1	2009	Assay of phosphotyrosine levels using flow cytometry has been used to identify patients with chronic myelogenous leukemia positive for the Bcr-Abl fusion gene.	Phosphotyrosine	9-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-146
18696070-12	2009	Flow cytometric analysis of phosphotyrosine levels is a reliable and convenient adjuvant technique for diagnosis of Bcr-Abl-positive leukemias and shows promise for serial evaluation of patients undergoing treatment.	Phosphotyrosine	28-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
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 Mesylate	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
19067400-7	2009	Maternal cigarette smoking and aspirin use each increased the risk of AB-L, but not TLD; while decongestants and possibly antihypertensive medications increased the risk of TLD, but not AB-L.	Aspirin	31-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-74
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 Mesylate	96-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-85
19115309-7	2009	Moreover, it was also demonstrated that this ATP noncompetitive inhibitor differentiates between two conformers of c-Abl kinases: the phosphorylated active and dephosphorylated inactive forms (IC(50(active form))=1049 nM and IC(50(inactive form))=54 nM).	Adenosine Triphosphate	45-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-120
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 Mesylate	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
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 Mesylate	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
23480335-5	2009	Recently, the benzotriazine core was used to develop selective kinase inhibitors targeting SRC, VEGFr2, BCR-ABL and BCR-ABL-T315I.	Triazines	14-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
23480335-5	2009	Recently, the benzotriazine core was used to develop selective kinase inhibitors targeting SRC, VEGFr2, BCR-ABL and BCR-ABL-T315I.	Triazines	14-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
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.	Dasatinib	28-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
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.	nilotinib	42-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
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 Mesylate	155-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
19542604-6	2009	Src family kinases and spleen tyrosine kinase (Syk) have been shown to phosphorylate tyrosine 18 while c-Abl is capable of phosphorylating tyrosine 394.	Tyrosine	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-108
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 Mesylate	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 Mesylate	207-215	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-111
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 Mesylate	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-111
18835981-4	2009	Here we present evidence of distinct STI571-induced modulation of abl functions using high-resolution live-cell imaging approaches.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	65-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-108
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 Mesylate	18-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-68
19563028-0	2009	[Arsenic trioxide inhibits cell growth in imatinib-resistant bcr-abl mutant cell lines in vitro].	Arsenic Trioxide	1-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
19563028-0	2009	[Arsenic trioxide inhibits cell growth in imatinib-resistant bcr-abl mutant cell lines in vitro].	Imatinib Mesylate	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.	Arsenic Trioxide	36-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
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.	Arsenic Trioxide	54-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
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 Mesylate	89-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
19563028-5	2009	For the 5 bcr-abl mutants frequently happened in CML patients, As2O3 significantly inhibited the expression of bcr-abl fusion protein and phosphorylated CRKL and induced apoptosis in a dose-dependent manner as compared with that for 32Dp210.	Arsenic Trioxide	63-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
19563028-5	2009	For the 5 bcr-abl mutants frequently happened in CML patients, As2O3 significantly inhibited the expression of bcr-abl fusion protein and phosphorylated CRKL and induced apoptosis in a dose-dependent manner as compared with that for 32Dp210.	Arsenic Trioxide	63-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
19563028-7	2009	CONCLUSION: As2O3 remarkably inhibits cell growth and induces apoptosis of IM-resistant bcr-abl mutant cell lines in vitro, suggesting that it might be a potential therapeutic agent for IM-resistant CML patients.	Arsenic Trioxide	12-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	221-228
18945674-4	2008	Inhibition, depletion, or knockout of the Abl family kinases, Abl and Arg, resulted in a dramatic reduction in the intracellular activities of the lysosomal glycosidases alpha-galactosidase, alpha-mannosidase and neuraminidase.	Arginine	70-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-45
19006406-6	2008	Notably, separations of fluorescently labeled ABL substrate peptide from its phosphorylated counterpart were achieved using a high-salt physiological buffer with near-baseline resolution in 10 s. PC-coated devices were used to successfully separate enhanced green fluorescent protein (eGFP) from a fusion protein (eGFP-Crakl) with an efficiency of 358,000 and 278,000 plates/m respectively in less than 12 s. These SBM-based coatings may enable the separation of a broad range of analytes and may be ideal in biological applications for microfluidics.	Salts	131-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-49
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 Mesylate	171-179	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-159
19066472-2	2008	While Src and Bcr-Abl were shown to be responsible for tyrosine phosphorylation, no data are available on the dephosphorylation of p27(Kip1) and the phosphatase involved.	Tyrosine	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
19077273-6	2008	RESULTS: Intracellular applications of active Abl, but not heat-inactivated Abl, decreased NMDA-evoked currents in isolated hippocampal neurons.	N-Methylaspartate	91-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-49
19077273-8	2008	The Abl kinase inhibitor, STI571, blocked the inhibition of NMDA currents by Abl.	Imatinib Mesylate	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 Mesylate	26-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-80
19077273-8	2008	The Abl kinase inhibitor, STI571, blocked the inhibition of NMDA currents by Abl.	N-Methylaspartate	60-64	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.	N-Methylaspartate	60-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-80
19077273-12	2008	We show that the inhibition of NMDA receptor currents by Abl kinase is blocked by the inclusion of the Rho kinase inhibitor, Y-27632, and that activation of Abl correlates with an increase in ROCK tyrosine phosphorylation.	Y 27632	125-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-60
19077273-12	2008	We show that the inhibition of NMDA receptor currents by Abl kinase is blocked by the inclusion of the Rho kinase inhibitor, Y-27632, and that activation of Abl correlates with an increase in ROCK tyrosine phosphorylation.	Y 27632	125-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-160
19077273-12	2008	We show that the inhibition of NMDA receptor currents by Abl kinase is blocked by the inclusion of the Rho kinase inhibitor, Y-27632, and that activation of Abl correlates with an increase in ROCK tyrosine phosphorylation.	Tyrosine	197-205	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-60
19077273-12	2008	We show that the inhibition of NMDA receptor currents by Abl kinase is blocked by the inclusion of the Rho kinase inhibitor, Y-27632, and that activation of Abl correlates with an increase in ROCK tyrosine phosphorylation.	Tyrosine	197-205	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-160
19061839-1	2008	The BCR-ABL inhibitor dasatinib achieves clinical remissions in chronic myeloid leukemia (CML) patients using a dosing schedule that achieves potent but transient BCR-ABL inhibition.	Dasatinib	22-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
19061839-1	2008	The BCR-ABL inhibitor dasatinib achieves clinical remissions in chronic myeloid leukemia (CML) patients using a dosing schedule that achieves potent but transient BCR-ABL inhibition.	Dasatinib	22-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
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.	Dasatinib	58-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
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 Mesylate	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
19061839-5	2008	In CML patients receiving dasatinib once daily, response correlates with the magnitude of BCR-ABL kinase inhibition, thereby demonstrating the potential clinical utility of intermittent potent kinase inhibitor therapy.	Dasatinib	26-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-153
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-162
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.	nilotinib	10-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-153
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.	nilotinib	10-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-162
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.	Dasatinib	24-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-153
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.	Dasatinib	24-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-162
19062342-1	2008	The dual c-abl/Src kinase inhibitor, dasatinib, utilized to treat chronic myeloid leukaemia (CML) when used at clinically attainable sublethal concentrations, synergistically sensitized primary chronic lymphocytic leukaemia (CLL) lymphocytes to chlorambucil and fludarabine.	Dasatinib	37-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-14
19062342-1	2008	The dual c-abl/Src kinase inhibitor, dasatinib, utilized to treat chronic myeloid leukaemia (CML) when used at clinically attainable sublethal concentrations, synergistically sensitized primary chronic lymphocytic leukaemia (CLL) lymphocytes to chlorambucil and fludarabine.	Chlorambucil	245-257	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-14
19062342-1	2008	The dual c-abl/Src kinase inhibitor, dasatinib, utilized to treat chronic myeloid leukaemia (CML) when used at clinically attainable sublethal concentrations, synergistically sensitized primary chronic lymphocytic leukaemia (CLL) lymphocytes to chlorambucil and fludarabine.	fludarabine	262-273	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-14
19062342-3	2008	Dasatinib resistance and poorer dasatinib-mediated sensitization to chlorambucil and fludarabine was associated with higher expression of c-abl protein levels.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-143
19062342-3	2008	Dasatinib resistance and poorer dasatinib-mediated sensitization to chlorambucil and fludarabine was associated with higher expression of c-abl protein levels.	Dasatinib	32-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-143
19062342-3	2008	Dasatinib resistance and poorer dasatinib-mediated sensitization to chlorambucil and fludarabine was associated with higher expression of c-abl protein levels.	Chlorambucil	68-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-143
19062342-3	2008	Dasatinib resistance and poorer dasatinib-mediated sensitization to chlorambucil and fludarabine was associated with higher expression of c-abl protein levels.	fludarabine	85-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-143
19047139-4	2008	Dasatinib (BMS-354825) is a potent dual Abl/Src kinase inhibitor approved for clinical use in CML patients.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-43
19047139-7	2008	Dasatinib showed potent Src inhibitory activity in CML progenitors, inhibiting both Bcr-Abl-dependent and -independent Src activity.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-91
19047139-8	2008	In contrast, Imatinib inhibited only Bcr-Abl-dependent Src activity.	Imatinib Mesylate	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-44
19047139-12	2008	Our results indicate that Dasatinib, in addition to potent anti-Bcr-Abl kinase activity, effectively inhibits Src kinase activity and downstream signaling pathways in CML progenitors but does not induce a strong proapoptotic response.	Dasatinib	26-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-71
19047160-0	2008	Evidence that resistance to nilotinib may be due to BCR-ABL, Pgp, or Src kinase overexpression.	nilotinib	28-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
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 Mesylate	8-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
19047160-9	2008	In contrast, dasatinib, a dual Bcr-Abl and Src kinase inhibitor, inhibited the phosphorylation of both BCR-ABL and Lyn, and induced apoptosis of the Bcr-Abl cell line overexpressing p53/56 Lyn.	Dasatinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
19047160-9	2008	In contrast, dasatinib, a dual Bcr-Abl and Src kinase inhibitor, inhibited the phosphorylation of both BCR-ABL and Lyn, and induced apoptosis of the Bcr-Abl cell line overexpressing p53/56 Lyn.	Dasatinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
19047160-9	2008	In contrast, dasatinib, a dual Bcr-Abl and Src kinase inhibitor, inhibited the phosphorylation of both BCR-ABL and Lyn, and induced apoptosis of the Bcr-Abl cell line overexpressing p53/56 Lyn.	Dasatinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
19075636-4	2008	However, Bcr-Abl contains also additional functional domains, in particular a DBL homology (DH) domain with guanine-exchange function (GEF) which can activate small GTPases of Rho family and a Src-homology3 (SH3) domain which recruits other proteins with GEF activity.	Guanine	108-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
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 Mesylate	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
18342402-1	2008	The synthesis of new 4-amino substituted pyrazolo[3,4-d]pyrimidines along with their activity in cell-free enzymatic assays on Src and Abl tyrosine kinases is reported.	4-amino substituted pyrazolo[3,4-d]pyrimidines	21-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-138
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 Mesylate	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
19039626-0	2008	Retention but significant reduction of BCR-ABL transcript in hematopoietic stem cells in chronic myelogenous leukemia after imatinib therapy.	Imatinib Mesylate	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 Mesylate	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 Mesylate	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
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 Mesylate	97-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-18
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 Mesylate	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 Mesylate	99-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-132
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 Mesylate	97-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
18992904-2	2008	The cytotoxic activities of all compounds were investigated on K562R (imatinib-resistant) human chronic myeloid leukaemia and DA1-3b/M2(BCR-ABL) (dasatinib-resistant) mouse leukemia cell line.	Dasatinib	146-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-143
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).	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
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 Mesylate	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 Mesylate	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	7-11
19056677-0	2008	BCR-ABL alternative splicing as a common mechanism for imatinib resistance: evidence from molecular dynamics simulations.	Imatinib Mesylate	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 Mesylate	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	207-214
18775435-0	2008	Tyrosine phosphorylation in the SH3 domain disrupts negative regulatory interactions within the c-Abl kinase core.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-101
18794796-2	2008	Global inhibition of myeloid Src family kinase (SFK) activity with the broad-spectrum pyrrolo-pyrimidine inhibitor, A-419259, blocks proliferation and induces apoptosis in CML cell lines, suggesting that transformation by Bcr-Abl requires SFK activity.	pyrrolopyrimidine	86-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	222-229
18794796-2	2008	Global inhibition of myeloid Src family kinase (SFK) activity with the broad-spectrum pyrrolo-pyrimidine inhibitor, A-419259, blocks proliferation and induces apoptosis in CML cell lines, suggesting that transformation by Bcr-Abl requires SFK activity.	A 419259	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	222-229
19001122-4	2008	Abl-dependent down-regulation of Rap1-GTP causes cell rounding and detachment only when the Rho-ROCK1 pathway is also activated, for example, by lysophosphatidic acid (LPA).	lysophosphatidic acid	145-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
19001122-4	2008	Abl-dependent down-regulation of Rap1-GTP causes cell rounding and detachment only when the Rho-ROCK1 pathway is also activated, for example, by lysophosphatidic acid (LPA).	lysophosphatidic acid	168-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
19111001-2	2008	In the present study, treatment with IQDMA inhibited phosphorylation of epidermal growth factor receptor (EGFR), Src, Bcr-Abl, and Janus-activated kinase (JAK2) in a time-dependent manner.	N'-(11H-indolo(3,2-c)quinolin-6-yl)-N,N-dimethylethane-1,2-diamine	37-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
18816068-0	2008	Electrochemical biosensor for detection of BCR/ABL fusion gene using locked nucleic acids on 4-aminobenzenesulfonic acid-modified glassy carbon electrode.	4-sulfanilic acid	93-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
18816068-0	2008	Electrochemical biosensor for detection of BCR/ABL fusion gene using locked nucleic acids on 4-aminobenzenesulfonic acid-modified glassy carbon electrode.	Carbon	137-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
18948750-4	2008	The sphingolipid killed CML derived KBM5 cells and, to a lesser extent, imatinib-resistant KBM5-STI cells suggesting that BCR-ABL can not completely block C6-ceramide-induced apoptosis but the kinase may regulate the process.	Sphingolipids	4-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
18948750-4	2008	The sphingolipid killed CML derived KBM5 cells and, to a lesser extent, imatinib-resistant KBM5-STI cells suggesting that BCR-ABL can not completely block C6-ceramide-induced apoptosis but the kinase may regulate the process.	Ceramides	158-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
19111001-7	2008	Taken together, these results indicate that IQDMA causes significant induction of apoptosis in K562 cells via downregulation of EGFR, Src, Bcr-Abl, JAK2, and STAT5 signaling and modulation of p21, p27, cyclin D1, Mcl-1, Bcl-X(L), and VEGF proteins.	N'-(11H-indolo(3,2-c)quinolin-6-yl)-N,N-dimethylethane-1,2-diamine	44-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-146
19010823-3	2008	Dasatinib (BMS-354825) is a dual Src/Abl kinase inhibitor with potent antiproliferative activity against hematologic malignancies harboring activated BCR-ABL.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
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 Mesylate	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.	Glycogen	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
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 Mesylate	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 Mesylate	15-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-123
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 Mesylate	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-52
18956997-5	2008	Nilotinib is a new small-molecule inhibitor of tyrosine kinase rationally developed from the crystalline structure of the imatinib-ABL complex.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-134
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.	2-aminopyrimidine	17-32	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 Mesylate	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 Mesylate	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 Mesylate	114-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
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.	doxm	81-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
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 Mesylate	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 Mesylate	26-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
18679417-3	2008	We sought to investigate the Src-mediated oncogenic pathways and tumor biology using AZD0530, a novel Src family kinase/Abl dual-kinase inhibitor that is entering phase II clinical trials.	saracatinib	85-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-123
18940662-1	2008	The cancer drug, Imatinib, is a selective Abl kinase inhibitor that does not inhibit the closely related kinase c-Src.	Imatinib Mesylate	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 Mesylate	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.	1,3-Diphenylguanidine	141-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-73
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 Mesylate	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-74
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 Mesylate	127-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-153
18669873-8	2008	Compared with imatinib, dasatinib achieved superior intracellular levels and BCR-ABL suppression even in cells with low or blocked hOCT1.	Dasatinib	24-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
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 Mesylate	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	148-151
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).	Dasatinib	0-9	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 Mesylate	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-40
18827006-4	2008	Consistent with these data, SHP-2 is required for Abl-dependent PDGF-mediated proliferation since expression of an activated form of SHP-2 rescues the ability of Abl-Arg null fibroblasts to transit from G1 to S phase, whereas inhibition of SHP-2 signaling reduces the ability of Abl kinases to rescue the proliferation defect.	Arginine	166-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-53
18827006-4	2008	Consistent with these data, SHP-2 is required for Abl-dependent PDGF-mediated proliferation since expression of an activated form of SHP-2 rescues the ability of Abl-Arg null fibroblasts to transit from G1 to S phase, whereas inhibition of SHP-2 signaling reduces the ability of Abl kinases to rescue the proliferation defect.	Arginine	166-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-165
18827006-4	2008	Consistent with these data, SHP-2 is required for Abl-dependent PDGF-mediated proliferation since expression of an activated form of SHP-2 rescues the ability of Abl-Arg null fibroblasts to transit from G1 to S phase, whereas inhibition of SHP-2 signaling reduces the ability of Abl kinases to rescue the proliferation defect.	Arginine	166-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-165
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 Mesylate	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
18701449-8	2008	In response to DNA damage, Yap1 is phosphorylated by c-Abl at the position Tyr-357.	Tyrosine	75-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-58
18797457-3	2008	Dasatinib, which is a multi-targeted kinase inhibitor mainly developed for Bcr-Abl and Src family kinases, has recently been shown to have significant activity against EphA2.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
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 Mesylate	33-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
18829489-4	2008	Combined treatment with vorinostat and MK-0457 resulted in greater attenuation of Aurora and Bcr-Abl (in K562) kinase activity and levels as well as synergistically induced apoptosis of OCI-AML3, HL-60, and K562 cells.	Vorinostat	24-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
18829489-4	2008	Combined treatment with vorinostat and MK-0457 resulted in greater attenuation of Aurora and Bcr-Abl (in K562) kinase activity and levels as well as synergistically induced apoptosis of OCI-AML3, HL-60, and K562 cells.	VX680	39-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
18829489-5	2008	MK-0457 plus vorinostat also induced synergistic apoptosis of BaF3 cells with ectopic overexpression of wild-type or mutant Bcr-Abl.	VX680	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
18829489-5	2008	MK-0457 plus vorinostat also induced synergistic apoptosis of BaF3 cells with ectopic overexpression of wild-type or mutant Bcr-Abl.	Vorinostat	13-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
18829496-2	2008	EXPERIMENTAL DESIGN: We used TF-1 BCR/ABL cells, by introducing the BCR/ABL gene into a leukemia cell line, TF-1 and K562, and established dasatinib- (BMS-R) and imatinib-resistant (IM-R) cells.	Dasatinib	139-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
18829496-2	2008	EXPERIMENTAL DESIGN: We used TF-1 BCR/ABL cells, by introducing the BCR/ABL gene into a leukemia cell line, TF-1 and K562, and established dasatinib- (BMS-R) and imatinib-resistant (IM-R) cells.	Dasatinib	139-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
18829496-4	2008	RESULTS: The IC(50) of dasatinib was 0.75 nmol/L (TF-1 BCR/ABL), 1 nmol/L (K562), 7.5 nmol/L (TF-1 BCR/ABL IM-R), 10 nmol/L (K562 IM-R), 15 micromol/L (TF-1 BCR/ABL BMS-R), and 25 micromol/L (K562 BMS-R).	Dasatinib	23-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-62
18829496-4	2008	RESULTS: The IC(50) of dasatinib was 0.75 nmol/L (TF-1 BCR/ABL), 1 nmol/L (K562), 7.5 nmol/L (TF-1 BCR/ABL IM-R), 10 nmol/L (K562 IM-R), 15 micromol/L (TF-1 BCR/ABL BMS-R), and 25 micromol/L (K562 BMS-R).	Dasatinib	23-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
18829496-4	2008	RESULTS: The IC(50) of dasatinib was 0.75 nmol/L (TF-1 BCR/ABL), 1 nmol/L (K562), 7.5 nmol/L (TF-1 BCR/ABL IM-R), 10 nmol/L (K562 IM-R), 15 micromol/L (TF-1 BCR/ABL BMS-R), and 25 micromol/L (K562 BMS-R).	Dasatinib	23-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-106
18829496-7	2008	We found that protein levels of BCR/ABL were reduced in dasatinib-resistant cell lines.	Dasatinib	56-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
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 Mesylate	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 Mesylate	205-213	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-118
18922118-4	2008	Nilotinib is a tyrosine kinase inhibitor 30-fold more potent than imatinib against BCR-ABL kinase.	Imatinib Mesylate	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
18922118-5	2008	Nilotinib is active against a wide range of imatinib-resistant BCR-ABL mutant isoforms, except for T315I.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
18922118-5	2008	Nilotinib is active against a wide range of imatinib-resistant BCR-ABL mutant isoforms, except for T315I.	Imatinib Mesylate	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
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 Mesylate	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 Mesylate	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 Mesylate	153-170	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	238-245
18615681-0	2008	Chronic phase of ETV6-ABL1 positive CML responds to imatinib.	Imatinib Mesylate	52-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-26
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
18852120-1	2008	Imatinib mesylate is a potent, molecularly targeted therapy against the oncogenic tyrosine kinase BCR-ABL.	Imatinib Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
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 Mesylate	189-197	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
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 Mesylate	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
18759402-8	2008	The RDF design allows inclusion of extended binding determinants to maximize recognition by the cognate kinase, which has now permitted the construction of chemosensors for a variety of representative Ser/Thr (PKC alpha, PKC betaIota, PKC delta, Pim2, Akt1, MK2, and PKA) as well as receptor (IRK) and nonreceptor (Src, Abl) Tyr kinases with greatly enhanced selectivity.	Serine	201-204	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	320-323
18809728-5	2008	Moreover, we demonstrate that although Abl does not regulate the recruitment of CrkL-C3G into the membrane, it does affect the tyrosine phosphorylation of C3G, which is required for its guanine nucleotide exchange factor activity toward Rap1.	Tyrosine	127-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-42
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 Mesylate	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
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 Mesylate	68-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-99
18922118-0	2008	Nilotinib: a phenylamino-pyrimidine derivative with activity against BCR-ABL, KIT and PDGFR kinases.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
18922118-0	2008	Nilotinib: a phenylamino-pyrimidine derivative with activity against BCR-ABL, KIT and PDGFR kinases.	phenylamino-pyrimidine	13-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
18922118-1	2008	The BCR-ABL kinase inhibitor imatinib mesylate is currently the standard therapy for patients with chronic myeloid leukemia (CML).	Imatinib Mesylate	29-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
18922118-4	2008	Nilotinib is a tyrosine kinase inhibitor 30-fold more potent than imatinib against BCR-ABL kinase.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
19383348-1	2008	We have identified differentially regulated genes in chronic myeloid leukemia (CML) cells upon short treatment with the broad-spectrum Bcr-Abl inhibitor dasatinib.	Dasatinib	153-162	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
19383348-2	2008	The highly specific Bcr-Abl inhibitor nilotinib caused a very similar gene expression signature, validating the identified differentially regulated genes as a read-out of Bcr-Abl activity and implying that Bcr-Abl is the functionally central target of dasatinib in CML cells.	nilotinib	38-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
19383348-2	2008	The highly specific Bcr-Abl inhibitor nilotinib caused a very similar gene expression signature, validating the identified differentially regulated genes as a read-out of Bcr-Abl activity and implying that Bcr-Abl is the functionally central target of dasatinib in CML cells.	nilotinib	38-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-178
19383348-2	2008	The highly specific Bcr-Abl inhibitor nilotinib caused a very similar gene expression signature, validating the identified differentially regulated genes as a read-out of Bcr-Abl activity and implying that Bcr-Abl is the functionally central target of dasatinib in CML cells.	nilotinib	38-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-178
19383348-2	2008	The highly specific Bcr-Abl inhibitor nilotinib caused a very similar gene expression signature, validating the identified differentially regulated genes as a read-out of Bcr-Abl activity and implying that Bcr-Abl is the functionally central target of dasatinib in CML cells.	Dasatinib	252-261	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
19383348-2	2008	The highly specific Bcr-Abl inhibitor nilotinib caused a very similar gene expression signature, validating the identified differentially regulated genes as a read-out of Bcr-Abl activity and implying that Bcr-Abl is the functionally central target of dasatinib in CML cells.	Dasatinib	252-261	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-178
19383348-2	2008	The highly specific Bcr-Abl inhibitor nilotinib caused a very similar gene expression signature, validating the identified differentially regulated genes as a read-out of Bcr-Abl activity and implying that Bcr-Abl is the functionally central target of dasatinib in CML cells.	Dasatinib	252-261	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-178
19383348-4	2008	Expression of both proteins is upregulated upon Bcr-Abl expression and inhibited by dasatinib and nilotinib.	Dasatinib	84-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
19383348-4	2008	Expression of both proteins is upregulated upon Bcr-Abl expression and inhibited by dasatinib and nilotinib.	nilotinib	98-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
21127752-1	2008	The BCR-ABL kinase inhibitor imatinib mesylate is currently the standard therapy for patients with chronic myeloid leukemia (CML).	Imatinib Mesylate	29-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
18757400-5	2008	Imatinib-mediated inhibition of BCR/ABL abrogated this effect, implicating a kinase-dependent mechanism.	Imatinib Mesylate	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 Mesylate	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
18790751-5	2008	We show that xanthohumol strongly inhibited Bcr-Abl expression at both mRNA and protein levels and show that xanthohumol caused elevation of intracellular reactive oxygen species and that the antioxidant N-acetylcysteine blunted xanthohumol-induced events.	xanthohumol	13-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
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 Mesylate	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 Mesylate	163-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
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 Mesylate	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 Mesylate	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
18827790-8	2008	Dasatinib and nilotinib are the most extensively studied second-generation BCR-ABL tyrosine kinase inhibitors, and are currently approved for treating patients following imatinib failure.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
18827790-8	2008	Dasatinib and nilotinib are the most extensively studied second-generation BCR-ABL tyrosine kinase inhibitors, and are currently approved for treating patients following imatinib failure.	nilotinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
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 Mesylate	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 Mesylate	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 Mesylate	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-30
18759691-4	2008	In order to override this resistance, several second generation ATP-competitive Abl TKIs including dasatinib, nilotinib, bosutinib and INNO-406 have been developed.	Adenosine Triphosphate	64-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
18759691-4	2008	In order to override this resistance, several second generation ATP-competitive Abl TKIs including dasatinib, nilotinib, bosutinib and INNO-406 have been developed.	Dasatinib	99-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
18759691-4	2008	In order to override this resistance, several second generation ATP-competitive Abl TKIs including dasatinib, nilotinib, bosutinib and INNO-406 have been developed.	nilotinib	110-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
18759691-4	2008	In order to override this resistance, several second generation ATP-competitive Abl TKIs including dasatinib, nilotinib, bosutinib and INNO-406 have been developed.	bosutinib	121-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
18759691-4	2008	In order to override this resistance, several second generation ATP-competitive Abl TKIs including dasatinib, nilotinib, bosutinib and INNO-406 have been developed.	bafetinib	135-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
18691885-0	2008	Novel N9-arenethenyl purines as potent dual Src/Abl tyrosine kinase inhibitors.	n9-arenethenyl purines	6-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-51
18691885-1	2008	Novel N(9)-arenethenyl purines, optimized potent dual Src/Abl tyrosine kinase inhibitors, are described.	n(9)-arenethenyl purines	6-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-61
18790751-5	2008	We show that xanthohumol strongly inhibited Bcr-Abl expression at both mRNA and protein levels and show that xanthohumol caused elevation of intracellular reactive oxygen species and that the antioxidant N-acetylcysteine blunted xanthohumol-induced events.	Acetylcysteine	204-220	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
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 Mesylate	120-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
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 Mesylate	120-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-179
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 Mesylate	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
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 Mesylate	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
18477770-8	2008	In 3 additional patients, isolated CNS relapse occurred during dasatinib therapy; and in 2 of them, it was caused by expansion of a BCR-ABL-mutated dasatinib-resistant clone, implying selection pressure exerted by the compound in the CNS.	Dasatinib	148-157	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
18621522-0	2008	N-(thiazol-2-yl)-2-thiophene carboxamide derivatives as Abl inhibitors identified by a pharmacophore-based database screening of commercially available compounds.	n-(thiazol-2-yl)-2-thiophene carboxamide	0-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-59
18621522-1	2008	Suggestions derived from a previous ligand-based ligand design approach and docking calculations aimed at finding compound with affinity toward Abl and molecular scaffolds previously untested as Abl inhibitors, led to the identification of commercially available N-(thiazol-2-yl)-2-thiophene carboxamide derivatives with affinity in a cell-free assay up to low nanomolar concentrations, significantly enhanced with respect to that of their parent compounds previously reported.	n-(thiazol-2-yl)-2-thiophene carboxamide	263-303	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-147
18621522-1	2008	Suggestions derived from a previous ligand-based ligand design approach and docking calculations aimed at finding compound with affinity toward Abl and molecular scaffolds previously untested as Abl inhibitors, led to the identification of commercially available N-(thiazol-2-yl)-2-thiophene carboxamide derivatives with affinity in a cell-free assay up to low nanomolar concentrations, significantly enhanced with respect to that of their parent compounds previously reported.	n-(thiazol-2-yl)-2-thiophene carboxamide	263-303	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	195-198
18621522-2	2008	In particular, among compounds of the Asinex database, molecular docking simulations guided the choice of high-affinity ligands, predicting their binding mode and their interaction pattern with the Abl catalytic binding site.	asinex	38-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	198-201
18524993-1	2008	Expression of oncogenic BCR-ABL in chronic myeloid leukemia (CML) results in increased reactive oxygen species (ROS) that in turn cause increased DNA damage, including DNA double-strand breaks (DSBs).	Reactive Oxygen Species	87-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
18524993-1	2008	Expression of oncogenic BCR-ABL in chronic myeloid leukemia (CML) results in increased reactive oxygen species (ROS) that in turn cause increased DNA damage, including DNA double-strand breaks (DSBs).	Reactive Oxygen Species	112-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
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 Mesylate	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-33
18505786-8	2008	Together, these findings indicate that vorinostat strikingly increases MK-0457 activity against IM-sensitive and -resistant CML cells through inactivation of Bcr/Abl and aurora kinases, as well as by induction of Bim.	Vorinostat	39-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-184
18665830-0	2008	Different kinetic patterns of BCR-ABL transcript levels in imatinib-treated chronic myeloid leukemia patients after achieving complete cytogenetic response.	Imatinib Mesylate	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 Mesylate	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
18665830-6	2008	We concluded that the depth of BCR-ABL reduction after CCyR is more critical than when CCyR is first achieved.	ccyr	55-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
18830516-7	2008	Patients on imatinib who cease responding may have mutations on their ABL gene.	Imatinib Mesylate	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-73
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 Mesylate	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
18718056-8	2008	HDAC inhibitor FK228-induced BCR-ABL degradation did not enhanced by CHIP.	romidepsin	15-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
18519516-0	2008	Centrosome aberrations and G1 phase arrest after in vitro and in vivo treatment with the SRC/ABL inhibitor dasatinib.	Dasatinib	107-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-96
18519516-1	2008	BACKGROUND: Dasatinib is a multitargeted inhibitor of ABL, the SRC family, and other tyrosine kinases.	Dasatinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-57
18243808-12	2008	Val (6), Ala (7) and Trp (344) were found to be stabilizing residues in the native protein (1OPL) coded by ABL1 gene.	Valine	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-111
18243808-12	2008	Val (6), Ala (7) and Trp (344) were found to be stabilizing residues in the native protein (1OPL) coded by ABL1 gene.	Alanine	9-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-111
18243808-12	2008	Val (6), Ala (7) and Trp (344) were found to be stabilizing residues in the native protein (1OPL) coded by ABL1 gene.	Tryptophan	21-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-111
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 Mesylate	60-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-44
18632630-3	2008	Treatment of cells that express the mutated receptor variants with the Met inhibitor SU11274 leads, in a mutant-dependent manner, to a reduction of tyrosine phosphorylated levels of Abl and Rad51, impairs radiation-induced nuclear translocation of Rad51, and acts as a radiosensitizer together with the p53 inhibitor pifithrin-alpha by increasing cellular double-strand DNA break levels following exposure to ionizing radiation.	((3Z)-N-(3-chlorophenyl)-3-((3,5-dimethyl-4-((4-methylpiperazin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-N-methyl-2-oxo-2,3-dihydro-1H-indole-5-sulfonamide)	85-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-185
18632630-3	2008	Treatment of cells that express the mutated receptor variants with the Met inhibitor SU11274 leads, in a mutant-dependent manner, to a reduction of tyrosine phosphorylated levels of Abl and Rad51, impairs radiation-induced nuclear translocation of Rad51, and acts as a radiosensitizer together with the p53 inhibitor pifithrin-alpha by increasing cellular double-strand DNA break levels following exposure to ionizing radiation.	Tyrosine	148-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-185
18632630-4	2008	Finally, we propose that in order to overcome a mutation-dependent resistance to SU11274, this aberrant molecular axis may alternatively be targeted with the Abl inhibitor, nilotinib.	((3Z)-N-(3-chlorophenyl)-3-((3,5-dimethyl-4-((4-methylpiperazin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-N-methyl-2-oxo-2,3-dihydro-1H-indole-5-sulfonamide)	81-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-161
18632630-4	2008	Finally, we propose that in order to overcome a mutation-dependent resistance to SU11274, this aberrant molecular axis may alternatively be targeted with the Abl inhibitor, nilotinib.	nilotinib	173-182	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-161
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
18490454-8	2008	In addition, c-Abl modulates Cdk5 activity via phosphorylation of tyrosine 15 in cooperation with cleavage of p35 to p25.	Tyrosine	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-18
18490454-9	2008	Our results show that c-Abl and Cdk5 cooperatively regulate maximal activation of p53, resulting in neuronal death in response to oxidative stress by hydrogen peroxide.	Hydrogen Peroxide	150-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-27
18374481-0	2008	Galangin increases the cytotoxic activity of imatinib mesylate in imatinib-sensitive and imatinib-resistant Bcr-Abl expressing leukemia cells.	Imatinib Mesylate	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 Mesylate	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 Mesylate	14-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
18374481-3	2008	Galangin induced an arrest of cells in G0-G1phase of cell cycle and a decrease in pRb, cdk4, cdk1, cycline B levels; moreover, it was able to induce a monocytic differentiation of leukemic Bcr-Abl+ cells.	galangin	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	189-196
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 Mesylate	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
18528985-1	2008	Alternating short and long bond length (ABL) distortions observed within the ring structures of molecular metal oxide anions or polyoxometalates (POMs) are reminiscent of the cooperative linear ABL distortions in perovskite d(0) metal oxides.	metal oxide	106-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-43
18528985-1	2008	Alternating short and long bond length (ABL) distortions observed within the ring structures of molecular metal oxide anions or polyoxometalates (POMs) are reminiscent of the cooperative linear ABL distortions in perovskite d(0) metal oxides.	metal oxide	106-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	194-197
18528985-1	2008	Alternating short and long bond length (ABL) distortions observed within the ring structures of molecular metal oxide anions or polyoxometalates (POMs) are reminiscent of the cooperative linear ABL distortions in perovskite d(0) metal oxides.	metal oxides	229-241	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-43
18528985-1	2008	Alternating short and long bond length (ABL) distortions observed within the ring structures of molecular metal oxide anions or polyoxometalates (POMs) are reminiscent of the cooperative linear ABL distortions in perovskite d(0) metal oxides.	metal oxides	229-241	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	194-197
18577747-0	2008	Association between imatinib-resistant BCR-ABL mutation-negative leukemia and persistent activation of LYN kinase.	Imatinib Mesylate	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
18577747-2	2008	BCR-ABL mutations are associated with failure of imatinib treatment in many CML patients.	Imatinib Mesylate	49-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
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 Mesylate	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
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 Mesylate	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 Mesylate	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
18326784-0	2008	Dual inhibition of c-abl and PDGF receptor signaling by dasatinib and nilotinib for the treatment of dermal fibrosis.	Dasatinib	56-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-24
18326784-0	2008	Dual inhibition of c-abl and PDGF receptor signaling by dasatinib and nilotinib for the treatment of dermal fibrosis.	nilotinib	70-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-24
18326784-2	2008	The aim of the present study was to evaluate the antifibrotic potential of dasatinib and nilotinib, 2 novel inhibitors of c-abl and PDGF, which are well tolerated and have recently been approved.	Dasatinib	75-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-127
18326784-2	2008	The aim of the present study was to evaluate the antifibrotic potential of dasatinib and nilotinib, 2 novel inhibitors of c-abl and PDGF, which are well tolerated and have recently been approved.	nilotinib	89-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-127
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 Mesylate	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 Mesylate	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
18061664-1	2008	Imatinib mesylate is a selective inhibitor of the bcr/abl, c-kit and PDGF receptor tyrosine kinases.	Imatinib Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
18559612-2	2008	The tyrosine kinase (TK) inhibitor dasatinib is 325-fold more potent against Bcr-Abl TK than imatinib in vitro, significantly inhibiting wild-type KIT and platelet-derived growth factor receptor beta TKs, and is active against cells carrying the mutant KIT-D816V gene.	Dasatinib	35-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
18418407-0	2008	Disruption of the Bcr-Abl/Hsp90 protein complex: a possible mechanism to inhibit Bcr-Abl-positive human leukemic blasts by novobiocin.	Novobiocin	123-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
18418407-0	2008	Disruption of the Bcr-Abl/Hsp90 protein complex: a possible mechanism to inhibit Bcr-Abl-positive human leukemic blasts by novobiocin.	Novobiocin	123-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
18418407-6	2008	Co-treatment with the proteasome inhibitor N-acetyl leucyl-leucyl norlucinal increases NB-mediated accumulation of Bcr-Abl in the detergent-insoluble cellular fraction, which demonstrates that NB promotes proteasomal degradation of Bcr-Abl.	n-acetyl leucyl-leucyl norlucinal	43-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
18418407-6	2008	Co-treatment with the proteasome inhibitor N-acetyl leucyl-leucyl norlucinal increases NB-mediated accumulation of Bcr-Abl in the detergent-insoluble cellular fraction, which demonstrates that NB promotes proteasomal degradation of Bcr-Abl.	n-acetyl leucyl-leucyl norlucinal	43-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	232-239
18452076-2	2008	New challenges have emerged with respect to induction of resistance to imatinib via ABL mutations.	Imatinib Mesylate	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-87
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 Mesylate	147-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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 Mesylate	147-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
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 Mesylate	110-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
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 Mesylate	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 Mesylate	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	216-223
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.	nilotinib	94-103	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.	nilotinib	94-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	216-223
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.	Dasatinib	108-117	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.	Dasatinib	108-117	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	139-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
19707354-6	2008	Inhibition of autophagy is a particularly attractive strategy for the treatment of imatinib-refractory chronic myelogenous leukemia (CML) since a combination of CQ with the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) compromises the survival of even BCR-ABL-T315I+ imatinib-resistant CML.	Chloroquine	161-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	260-267
19707354-6	2008	Inhibition of autophagy is a particularly attractive strategy for the treatment of imatinib-refractory chronic myelogenous leukemia (CML) since a combination of CQ with the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) compromises the survival of even BCR-ABL-T315I+ imatinib-resistant CML.	Vorinostat	188-219	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	260-267
18395492-0	2008	The Src/ABL kinase inhibitor dasatinib (BMS-354825) inhibits function of normal human T-lymphocytes in vitro.	Dasatinib	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-11
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 Mesylate	36-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
18395492-0	2008	The Src/ABL kinase inhibitor dasatinib (BMS-354825) inhibits function of normal human T-lymphocytes in vitro.	Dasatinib	40-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-11
18395492-1	2008	Dasatinib (BMS-354825) is a Src/ABL tyrosine kinase inhibitor currently approved for the treatment of chronic myeloid leukemia.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-35
18395492-2	2008	Dasatinib has increased potency against ABL compared to the current therapy imatinib, and is effective in many cases where disease is resistant to imatinib.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-43
18245170-7	2008	Resveratrol action was independent of BCR-ABL expression and phosphorylation, and in agreement was additive to BCR-ABL silencing.	Resveratrol	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
18245170-7	2008	Resveratrol action was independent of BCR-ABL expression and phosphorylation, and in agreement was additive to BCR-ABL silencing.	Resveratrol	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
18245170-8	2008	Finally, phytoalexin inhibited the growth of BaF3 cells expressing mutant BCR-ABL proteins found in resistant patients, including the multiresistant T315I mutation.	phytoalexins	9-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
18533795-4	2008	Imatinib mesylate, an orally available tyrosine kinase inhibitor that targets Bcr-Abl, entered clinical evaluation in 1998.	Imatinib Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
18541900-1	2008	PURPOSE: Dasatinib is a BCR-ABL inhibitor, 325-fold more potent than imatinib against unmutated BCR-ABL in vitro.	Dasatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
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 Mesylate	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-64
18541900-1	2008	PURPOSE: Dasatinib is a BCR-ABL inhibitor, 325-fold more potent than imatinib against unmutated BCR-ABL in vitro.	Dasatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
18541900-1	2008	PURPOSE: Dasatinib is a BCR-ABL inhibitor, 325-fold more potent than imatinib against unmutated BCR-ABL in vitro.	Imatinib Mesylate	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
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 Mesylate	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 Mesylate	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
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 Mesylate	8-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-111
18338755-8	2008	The new Abl kinase inhibitor nilotinib was 10-fold more potent than IM in inhibiting the growth of K562 cells.	nilotinib	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-11
18338755-11	2008	The new dual Abl/Lyn inhibitor INNO-406 (formerly NS-187) was slightly more potent than nilotinib in inhibiting the growth of all 3 cell lines.	bafetinib	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
18338755-11	2008	The new dual Abl/Lyn inhibitor INNO-406 (formerly NS-187) was slightly more potent than nilotinib in inhibiting the growth of all 3 cell lines.	bafetinib	50-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
18497981-2	2008	Recently, a selective Abl kinase inhibitor, Imatinib mesylate, was introduced as a first line therapy for CML.	Imatinib Mesylate	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 Mesylate	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 Mesylate	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
18367522-9	2008	These results indicate that MA sequences within the Gag moiety of the v-Abl protein contribute to proper localization by playing a dominant role in trafficking of the v-Abl molecule.	Glycosaminoglycans	52-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-75
18367522-9	2008	These results indicate that MA sequences within the Gag moiety of the v-Abl protein contribute to proper localization by playing a dominant role in trafficking of the v-Abl molecule.	Glycosaminoglycans	52-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-172
18191450-2	2008	Dasatinib exhibited the strongest potency against BCR-ABL with little selectivity over SFKs.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
18191450-3	2008	Nilotinib exhibited a weaker affinity than the other inhibitors, but was highly specific for ABL and may be useful for the treatment of P-glycoprotein overexpressing leukemic cells.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-96
18191450-4	2008	INNO-406 had an intermediate affinity for BCR-ABL between that of dasatinib and nilotinib, and inhibited only SFKs LCK and LYN among SFKs.	bafetinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
18191450-5	2008	Both nilotinib and INNO-406 were potent inhibitors of the dasatinib-resistant T315A, F317L and F317V BCR-ABL mutations.	nilotinib	5-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
18191450-5	2008	Both nilotinib and INNO-406 were potent inhibitors of the dasatinib-resistant T315A, F317L and F317V BCR-ABL mutations.	Dasatinib	58-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
18354488-1	2008	The BCR-ABL oncogenic tyrosine kinase causes chronic myeloid leukemia and is the target for imatinib therapy.	Imatinib Mesylate	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
18354488-2	2008	During imatinib treatment, cells are selected in some patients with BCR-ABL kinase domain mutations that render decreased drug sensitivity.	Imatinib Mesylate	7-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
18385754-4	2008	Here, we showed that beta-phenylethyl isothiocyanate (PEITC), a natural compound found in vegetables, is effective in killing CML cells expressing T315I BCR-ABL.	phenethyl isothiocyanate	21-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
18385754-4	2008	Here, we showed that beta-phenylethyl isothiocyanate (PEITC), a natural compound found in vegetables, is effective in killing CML cells expressing T315I BCR-ABL.	phenethyl isothiocyanate	54-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
18385754-5	2008	Treatment of leukemia cell lines harboring wild-type or mutant Bcr-Abl with 10 microM PEITC resulted in an elevated ROS stress and a redox-mediated degradation of the BCR-ABL protein, leading to massive death of the leukemia cells.	phenethyl isothiocyanate	86-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
18385754-5	2008	Treatment of leukemia cell lines harboring wild-type or mutant Bcr-Abl with 10 microM PEITC resulted in an elevated ROS stress and a redox-mediated degradation of the BCR-ABL protein, leading to massive death of the leukemia cells.	phenethyl isothiocyanate	86-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-174
18385754-5	2008	Treatment of leukemia cell lines harboring wild-type or mutant Bcr-Abl with 10 microM PEITC resulted in an elevated ROS stress and a redox-mediated degradation of the BCR-ABL protein, leading to massive death of the leukemia cells.	ros	116-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
18385754-7	2008	We further showed that the ROS-induced degradation of BCR-ABL was mediated partially by caspase-3 and the proteasome pathway.	ros	27-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
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 Mesylate	144-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
18401417-9	2008	Moreover, dasatinib was active in a NUP214-ABL1-positive leukemia xenograft murine model and in marrow lymphoblasts from a patient with NUP214-ABL1-positive T-ALL.	Dasatinib	10-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-147
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 Mesylate	83-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	254-261
18452309-2	2008	The exact contributions that the NCap makes in stabilizing the various intramolecular interactions within c-Abl are less clear.	ncap	33-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-111
18452309-5	2008	Under physiological conditions, the Abl SH3 domain underwent partial unfolding and its unfolding half-life was slowed during binding to the SH2 kinase linker, providing a unique assay for testing NCap-induced stabilization of the SH3 domain in various constructs.	ncap	196-200	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-39
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 Mesylate	144-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
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).	Dasatinib	157-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
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 Mesylate	29-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
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.	Agar	108-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
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 Mesylate	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
18328268-1	2008	Here we report c-Abl kinase inhibition mediated by a phosphotyrosine located in trans in the c-Abl substrate, Abi1.	Phosphotyrosine	53-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-20
18328268-1	2008	Here we report c-Abl kinase inhibition mediated by a phosphotyrosine located in trans in the c-Abl substrate, Abi1.	Phosphotyrosine	53-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-98
18328268-2	2008	The mechanism, which is pertinent to the nonmyristoylated c-Abl kinase, involves high affinity concurrent binding of the phosphotyrosine pY213 to the Abl SH2 domain and binding of a proximal PXXP motif to the Abl SH3 domain.	phosphotyrosine py213	121-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-63
18328268-2	2008	The mechanism, which is pertinent to the nonmyristoylated c-Abl kinase, involves high affinity concurrent binding of the phosphotyrosine pY213 to the Abl SH2 domain and binding of a proximal PXXP motif to the Abl SH3 domain.	phosphotyrosine py213	121-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-63
18328268-2	2008	The mechanism, which is pertinent to the nonmyristoylated c-Abl kinase, involves high affinity concurrent binding of the phosphotyrosine pY213 to the Abl SH2 domain and binding of a proximal PXXP motif to the Abl SH3 domain.	phosphotyrosine py213	121-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-153
18328268-3	2008	Abi1 regulation of c-Abl in vivo appears to play a critical role, as demonstrated by inhibition of pY412 phosphorylation of the nonmyristoylated Abl by coexpression of Abi1.	py412	99-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-24
18328268-4	2008	Pervanadate-induced c-Abl kinase activity was also reduced upon expression of the wild type Abi1 but not by expression of the Y213 to F213 mutant Abi1 in LNCaP cells, which are naturally deficient in the regulatory pY213.	pervanadate	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-25
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 Mesylate	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
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 Mesylate	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-55
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 Mesylate	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-141
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 Mesylate	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-150
18491988-1	2008	Targeted therapy with the Abl kinase inhibitor imatinib has markedly improved the outlook for patients with chronic myeloid leukemia (CML).	Imatinib Mesylate	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-29
18491988-3	2008	This discovery prompted the development of new Abl kinase inhibitors, among which nilotinib and dasatinib have gained regulatory approval.	nilotinib	82-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
18491988-3	2008	This discovery prompted the development of new Abl kinase inhibitors, among which nilotinib and dasatinib have gained regulatory approval.	Dasatinib	96-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	65-73	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.	nilotinib	102-111	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.	nilotinib	102-111	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.	Dasatinib	115-124	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.	Dasatinib	115-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-185
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.	nilotinib	168-177	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 Mesylate	195-203	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	7-14
18367481-3	2008	A minimum dose (200 mg) required for effective BCR-ABL inhibition in imatinib resistant/intolerant leukemia was determined.	Imatinib Mesylate	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
18367481-4	2008	The pre-clinical activity profile of nilotinib against mutant BCR-ABL was largely confirmed.	nilotinib	37-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
18367481-6	2008	Finally, rapid BCR-ABL-reactivation shortly after starting nilotinib treatment was seen in acute lymphoblastic leukemia patients with progressive disease carrying the P-loop mutations Y253H, E255K, or mutation T315I.	nilotinib	59-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
18367481-7	2008	Monitoring the actual BCR-ABL inhibition in nilotinib treated patients using pCRKL as a surrogate is a means to establish effective dosing and to characterize resistance mechanisms against nilotinib.	nilotinib	44-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
18367481-7	2008	Monitoring the actual BCR-ABL inhibition in nilotinib treated patients using pCRKL as a surrogate is a means to establish effective dosing and to characterize resistance mechanisms against nilotinib.	nilotinib	189-198	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
18353972-3	2008	STI571, a c-Abl kinase inhibitor, only inhibited bFGF- but not VEGF-induced angiogenesis.	Imatinib Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-15
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 Mesylate	61-69	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 Mesylate	182-190	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-152
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 Mesylate	238-246	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-110
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 Mesylate	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
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.	PD 173955	132-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
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 Mesylate	172-180	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
18483293-1	2008	Blockade of Bcr-Abl by the inhibitor Imatinib has proven efficacious in the therapy of chronic myelogenous leukemia (CML).	Imatinib Mesylate	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 Mesylate	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
18367669-1	2008	Imatinib inhibits Bcr-Abl, the oncogenic tyrosine kinase that causes chronic myeloid leukemia.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
18367669-2	2008	The second-line inhibitors nilotinib and dasatinib are effective in patients with imatinib resistance resulting from Bcr-Abl kinase domain mutations.	nilotinib	27-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
18367669-2	2008	The second-line inhibitors nilotinib and dasatinib are effective in patients with imatinib resistance resulting from Bcr-Abl kinase domain mutations.	Dasatinib	41-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
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 Mesylate	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
18367669-6	2008	Combining SGX393 with nilotinib or dasatinib preempted emergence of resistant subclones, including Bcr-Abl(T315I).	nilotinib	22-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
18367669-6	2008	Combining SGX393 with nilotinib or dasatinib preempted emergence of resistant subclones, including Bcr-Abl(T315I).	Dasatinib	35-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
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 Mesylate	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
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 Mesylate	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
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.	nilotinib	86-95	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 Mesylate	178-186	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
18235045-5	2008	Lyn also negatively regulates c-Cbl stability, whereas c-Cbl tyrosine phosphorylation is mediated by BCR-ABL.	Tyrosine	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
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 Mesylate	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 Mesylate	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 Mesylate	159-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-182
18287094-7	2008	The inhibitory activities of BCR-ABL ultimately result in impaired IFNalpha-mediated protection against encephalomyocarditis virus infection and reversal of IFN-dependent growth suppression.	ifnalpha	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
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 Mesylate	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 Mesylate	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 Mesylate	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
18338744-0	2008	Molecular basis explanation for imatinib resistance of BCR-ABL due to T315I and P-loop mutations from molecular dynamics simulations.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	189-197	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	181-188
18413841-1	2008	PURPOSE: The dual BCR-ABL/SRC kinase inhibitor dasatinib entered the clinic for the treatment of chronic myeloid leukemia and Ph+ acute lymphoblastic leukemia.	Dasatinib	47-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
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 Mesylate	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
18331839-6	2008	Two example protein domains (Csk and Abl tyrosine kinase domain) with N-terminal Cys are demonstrated using this method.	Cysteine	81-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-40
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 Mesylate	125-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-36
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 Mesylate	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 Mesylate	3-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	188-195
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 Mesylate	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 Mesylate	10-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-127
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 Mesylate	160-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-149
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 Mesylate	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
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 Mesylate	99-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
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.	Dasatinib	164-173	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
18273048-2	2008	We investigated whether nilotinib, a more potent BCR-ABL kinase inhibitor could target CML primitive progenitors more effectively than imatinib.	nilotinib	24-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
18273048-4	2008	Nilotinib inhibited BCR-ABL kinase activity at lower concentrations than imatinib.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
18398719-3	2008	However, BCR/ABL also enhances DNA damage caused by endogenous reactive oxygen species and exogenous genotoxic treatment.	Reactive Oxygen Species	63-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
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 Mesylate	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-40
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.	Dasatinib	97-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-40
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.	nilotinib	111-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-40
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 Mesylate	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
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 Mesylate	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
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 Mesylate	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
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 Mesylate	125-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
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 Mesylate	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
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 Mesylate	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-193
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 Mesylate	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.	Dasatinib	0-9	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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
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 Mesylate	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 Mesylate	79-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
18428043-9	2008	Point mutations in the kinase domain of BCR-ABL are the most common cause of acquired resistance to imatinib treatment.	Imatinib Mesylate	100-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
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 Mesylate	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
18257513-0	2008	Structure-based optimization of pyrazolo[3,4-d]pyrimidines as Abl inhibitors and antiproliferative agents toward human leukemia cell lines.	pyrazolo(3,4-d)pyrimidine	32-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-65
18285444-3	2008	Tyrosine phosphorylation and kinase activity of PKCdelta are required for PKCdelta binding to Abl in the ER.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-97
18285444-5	2008	Furthermore, the inhibitor of PKCdelta kinase activity rottlerin blocks the translocation of the PKCdelta-Abl complex from the ER to the mitochondria and confers protection against apoptosis.	rottlerin	55-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-109
18257513-1	2008	Results from molecular docking calculations and Grid mapping laid the foundations for a structure-based optimization approach to improve the biological properties of pyrazolo-pyrimidine derivatives in terms of inhibition of Abl enzymatic activity and antiproliferative properties toward human leukemia cells.	1H-pyrazolo[4,3-d]pyrimidine	166-185	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	224-227
18257513-2	2008	Insertion of halogen substituents with various substitution patterns, suggested by simulations, led to a significant improvement of leukemia cell growth inhibition and to an increase up to 1 order of magnitude of the affinity toward Abl.	Halogens	13-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	233-236
18347292-0	2008	Bullous sweet syndrome in a patient with t(9;22)(q34;q11)-positive chronic myeloid leukemia treated with the tyrosine kinase inhibitor nilotinib: interphase cytogenetic detection of BCR-ABL- positive lesional cells.	nilotinib	135-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-189
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 Mesylate	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
18347292-7	2008	Fluorescence in situ hybridization analysis of paraffin-embedded tissue revealed a BCR-ABL fusion, indicating the presence of t(9;22)(q34;q11).	Paraffin	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
19254881-2	2008	However, point mutations in the kinase domain of Bcr-Abl can lead to imatinib resistance and reactivation of kinase activity.	Imatinib Mesylate	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-138
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 Mesylate	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-35
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 Mesylate	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 Mesylate	178-195	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-158
19254884-5	2008	Dasatinib is also an oral kinase inhibitor, but it has increased potency for Brc-Abl compared with imatinib.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-84
19254884-8	2008	Nilotinib, which has been recently approved, has increased potency for Brc-Abl compared with imatinib and has demonstrated activity in patients with imatinib-resistant and -intolerant chronic- and accelerated-phase CML.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-78
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 Mesylate	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 Mesylate	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
18160052-5	2008	Transfected kinase-active GFP-c-Abl colocalized with vesicular sites of superoxide production in a Ca(2+)-dependent manner.	Superoxides	72-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-35
18160052-8	2008	Furthermore, H(2)O(2)-induced NOX5 activity correlated with increased localization of c-Abl to the membrane fraction, and NOX5 proteins could be coimmunoprecipitated with GFP-Abl proteins.	Hydrogen Peroxide	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-91
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 Mesylate	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 Mesylate	212-220	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	176-183
18059481-9	2008	Imatinib promoted nuclear transport of p210(BCR-ABL)-positive foci.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
18079735-0	2008	Targeting 14-3-3 sensitizes native and mutant BCR-ABL to inhibition with U0126, rapamycin and Bcl-2 inhibitor GX15-070.	U 0126	73-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
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 Mesylate	8-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
18079735-1	2008	Small molecule tyrosine kinase inhibitors, such as imatinib, are effective therapies for BCR-ABL-mediated human leukemias.	Imatinib Mesylate	51-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
18079735-5	2008	Moreover, R18 sensitized BCR-ABL-transformed cells to inhibition with MEK1 inhibitor U0126, Bcl-2 inhibitor GX15-070, or mTOR inhibitor rapamycin.	U 0126	85-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
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 Mesylate	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 Mesylate	235-243	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	206-210
18024796-4	2008	Moreover, targeting Hsp32/HO-1 by either pegylated zinc protoporphyrine (PEG-ZnPP) or styrene maleic acid-micelle-encapsulated ZnPP (SMA-ZnPP) resulted in growth inhibition of BCR/ABL-transformed cells.	2-Butenedioic acid (2Z)-, polymer with ethenylbenzene	86-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	176-183
18024796-4	2008	Moreover, targeting Hsp32/HO-1 by either pegylated zinc protoporphyrine (PEG-ZnPP) or styrene maleic acid-micelle-encapsulated ZnPP (SMA-ZnPP) resulted in growth inhibition of BCR/ABL-transformed cells.	sma-znpp	133-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	176-183
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.	Polyethylene Glycols	15-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	213-220
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.	zinc protoporphyrin	32-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	213-220
17700528-2	2008	We recently demonstrated that endogenous Abl kinases (c-Abl, Arg) are activated by deregulated ErbB receptors and Src kinases, and drive invasion of aggressive breast cancer cells.	Arginine	61-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-44
17700528-2	2008	We recently demonstrated that endogenous Abl kinases (c-Abl, Arg) are activated by deregulated ErbB receptors and Src kinases, and drive invasion of aggressive breast cancer cells.	Arginine	61-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-59
18376233-3	2008	Imatinib, a potent inhibitor of BCR-ABL and c-kit, also inhibits the platelet-derived growth factor receptor tyrosine kinase.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
17570524-0	2008	A recurrent splicing variant without c-ABL Exon 7 in Imatinib-resistant patients.	Imatinib Mesylate	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-42
18079735-5	2008	Moreover, R18 sensitized BCR-ABL-transformed cells to inhibition with MEK1 inhibitor U0126, Bcl-2 inhibitor GX15-070, or mTOR inhibitor rapamycin.	obatoclax	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
18079735-5	2008	Moreover, R18 sensitized BCR-ABL-transformed cells to inhibition with MEK1 inhibitor U0126, Bcl-2 inhibitor GX15-070, or mTOR inhibitor rapamycin.	Sirolimus	136-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
18079735-7	2008	Furthermore, R18-induced apoptotic cell death in cells expressing diverse imatinib-resistant BCR-ABL mutants, including T315I.	Imatinib Mesylate	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-35
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-120
18223278-0	2008	Dynamics of BCR-ABL mutated clones prior to hematologic or cytogenetic resistance to imatinib.	Imatinib Mesylate	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
18078752-0	2008	Discovery and SAR of 1,3,4-thiadiazole derivatives as potent Abl tyrosine kinase inhibitors and cytodifferentiating agents.	1,3,4-thiadiazole	21-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-64
18078752-1	2008	A series of substituted benzoylamino-2-[(4-benzyl)thio]-1,3,4-thiadiazoles has been discovered as potent Abl tyrosine kinase inhibitors.	benzoylamino-2-[(4-benzyl)thio]-1,3,4-thiadiazoles	24-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-108
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 Mesylate	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 Mesylate	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 Mesylate	207-215	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-189
18245668-0	2008	IkappaB kinase beta inhibition induces cell death in Imatinib-resistant and T315I Dasatinib-resistant BCR-ABL+ cells.	Dasatinib	82-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
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 Mesylate	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.	Dasatinib	175-184	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
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 Mesylate	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
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 Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	339-346
18202781-3	2008	Dasatinib, an oral multi-targeted inhibitor of several kinases including BCR-ABL and SRC-family kinases, is also active against c-KIT and PDGFR.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
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 Mesylate	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 Mesylate	24-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-39
17962511-1	2008	Dasatinib is an oral small molecule inhibitor of Abl and Src family tyrosine kinases (SFK), including p56(Lck) (Lck).	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-52
18161990-2	2008	The interaction of c-Abl with the Abl interactor protein Abi2 is shown to be negatively regulated by phosphorylation of serines 637 and 638.	Serine	120-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-24
18161990-2	2008	The interaction of c-Abl with the Abl interactor protein Abi2 is shown to be negatively regulated by phosphorylation of serines 637 and 638.	Serine	120-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-24
18161990-5	2008	Mutation of serines 637-639 to alanine (3A) or aspartate (3D) results in an increased tyrosine kinase activity of c-Abl 3D, and a slight reduction of the activity of the 3A mutant, as compared to wild-type (WT) c-Abl.	Serine	12-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-119
18161990-5	2008	Mutation of serines 637-639 to alanine (3A) or aspartate (3D) results in an increased tyrosine kinase activity of c-Abl 3D, and a slight reduction of the activity of the 3A mutant, as compared to wild-type (WT) c-Abl.	Serine	12-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	211-216
18161990-5	2008	Mutation of serines 637-639 to alanine (3A) or aspartate (3D) results in an increased tyrosine kinase activity of c-Abl 3D, and a slight reduction of the activity of the 3A mutant, as compared to wild-type (WT) c-Abl.	Alanine	31-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-119
18161990-5	2008	Mutation of serines 637-639 to alanine (3A) or aspartate (3D) results in an increased tyrosine kinase activity of c-Abl 3D, and a slight reduction of the activity of the 3A mutant, as compared to wild-type (WT) c-Abl.	Alanine	31-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	211-216
18161990-5	2008	Mutation of serines 637-639 to alanine (3A) or aspartate (3D) results in an increased tyrosine kinase activity of c-Abl 3D, and a slight reduction of the activity of the 3A mutant, as compared to wild-type (WT) c-Abl.	Aspartic Acid	47-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-119
18161990-5	2008	Mutation of serines 637-639 to alanine (3A) or aspartate (3D) results in an increased tyrosine kinase activity of c-Abl 3D, and a slight reduction of the activity of the 3A mutant, as compared to wild-type (WT) c-Abl.	Aspartic Acid	47-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	211-216
17893873-0	2008	c-Abl activates p38 MAPK independently of its tyrosine kinase activity: Implications in cisplatin-based therapy.	Cisplatin	88-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
17893873-2	2008	In this sense, a growing body of evidences supports the role of c-Abl as a major determinant of p38 MAPK activation, especially in response to genotoxic stress when triggered by cisplatin.	Cisplatin	178-187	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-69
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 Mesylate	66-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-54
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
17918184-7	2008	Treatment with the dual specific Abl/c-Src kinase inhibitor AZD0530 significantly reduces the growth inhibitory effect of high EGF concentrations, signifying that EGFR induced IRF-1 is responsible for the observed growth inhibition.	saracatinib	60-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-36
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 Mesylate	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
18165572-8	2008	Blood glucose was measured by ABL 800FLEX immediately after sampling.	Blood Glucose	0-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-33
18215092-1	2008	Dasatinib is a small-molecule inhibitor of multiple tyrosine kinases, including BCR-ABL, SRC, c-KIT, ephrin A receptor and platelet-derived growth factor-beta receptor kinases, at nanomolar concentrations.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
19039205-0	2008	Imatinib mesylate resistance in a chronic myeloid leukemia patient with a novel e8a2 BCR-ABL transcript variant.	Imatinib Mesylate	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 Mesylate	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 Mesylate	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
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 Mesylate	202-219	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
18346528-6	2008	Imatinib resistance has, in part, been addressed with the introduction of the new BCR-ABL inhibitors, namely dasatinib and nilotinib.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
18346528-6	2008	Imatinib resistance has, in part, been addressed with the introduction of the new BCR-ABL inhibitors, namely dasatinib and nilotinib.	Dasatinib	109-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
18346528-6	2008	Imatinib resistance has, in part, been addressed with the introduction of the new BCR-ABL inhibitors, namely dasatinib and nilotinib.	nilotinib	123-132	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 Mesylate	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 Mesylate	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 Mesylate	158-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-193
18215092-2	2008	In vitro, dasatinib is 325-fold more potent than imatinib against cells expressing wild-type BCR-ABL.	Dasatinib	10-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
18215092-2	2008	In vitro, dasatinib is 325-fold more potent than imatinib against cells expressing wild-type BCR-ABL.	Imatinib Mesylate	49-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
18028486-1	2008	The effect of ABT-737, a BH3-mimicking inhibitor for anti-apoptotic Bcl-2 and Bcl-X(L), but not Mcl-1, against Bcr-Abl-positive (Bcr-Abl(+)) leukaemic cells was examined.	ABT-737	14-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
19850986-0	2008	Radicicol-mediated inhibition of Bcr-Abl in K562 cells induced p38-MAPK dependent erythroid differentiation and PU.1 down-regulation.	monorden	0-9	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 Mesylate	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 Mesylate	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-159
18028486-1	2008	The effect of ABT-737, a BH3-mimicking inhibitor for anti-apoptotic Bcl-2 and Bcl-X(L), but not Mcl-1, against Bcr-Abl-positive (Bcr-Abl(+)) leukaemic cells was examined.	ABT-737	14-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
18028486-2	2008	ABT-737 potently induced apoptosis in Bcr-Abl(+) chronic myeloid leukaemia (CML) cell lines and primary CML samples in vitro and prolonged the survival of mice xenografted with BV173 cells, a CML cell line.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
18028486-4	2008	Thus, the cell killing effect of ABT-737 must be determined not only by the expression patterns of Bcl-2 family proteins but also by other mechanisms, such as high expression of Bcr-Abl, or a drug-efflux pump, in CML cells.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	33-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185
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.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
18294126-2	2008	Imatinib inhibits the activity of chimeric kinase BCR-ABL, which is responsible for the development of CML.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
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 Mesylate	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
18028486-6	2008	The combination of homoharringtonine that reduces Mcl-1 enhanced the killing by ABT-737 strongly in Bcr-Abl(+) cells even with T315I mutation.	Homoharringtonine	19-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
18028486-6	2008	The combination of homoharringtonine that reduces Mcl-1 enhanced the killing by ABT-737 strongly in Bcr-Abl(+) cells even with T315I mutation.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	80-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
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 Mesylate	151-159	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	205-212
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 Mesylate	144-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
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 Mesylate	143-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
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 Mesylate	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 Mesylate	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 Mesylate	76-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
19075651-4	2008	The recognition of the BCR-ABL gene and corresponding protein led to the synthesis of small-molecule drugs, designed to interfere with BCR-ABL tyrosine kinase activation by competitive binding at the ATP-binding site.	Adenosine Triphosphate	200-203	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
19075651-4	2008	The recognition of the BCR-ABL gene and corresponding protein led to the synthesis of small-molecule drugs, designed to interfere with BCR-ABL tyrosine kinase activation by competitive binding at the ATP-binding site.	Adenosine Triphosphate	200-203	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
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 Mesylate	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 Mesylate	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
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 Mesylate	18-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	3-6
18673174-7	2008	A majority of these relapsed patients have several point mutations at and around the ATP binding pocket of the ABL kinase domain in BCR-ABL.	Adenosine Triphosphate	85-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-114
18673174-7	2008	A majority of these relapsed patients have several point mutations at and around the ATP binding pocket of the ABL kinase domain in BCR-ABL.	Adenosine Triphosphate	85-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
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 Mesylate	57-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
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.	Dasatinib	103-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
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.	nilotinib	118-127	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 Mesylate	102-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
18836918-2	2008	One such example is the new group of tyrosine kinase inhibitors, exemplified by the Bcr-Abl inhibitor imatinib (Glivec).	Imatinib Mesylate	112-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
18095887-4	2008	However, patients may develop imatinib resistance, which is often due to BCR-ABL mutations.	Imatinib Mesylate	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
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.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
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 Mesylate	111-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
18318563-4	2008	Major cytogenetic response rates did not differ between imatinib-resistant and -intolerant patients, and nilotinib was effective in patients with BCR-ABL mutations (except T315I).	nilotinib	105-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	146-153
19074121-7	2008	In this review, we will discuss the current status of the ATP-competitive and non-ATP-competitive Bcr-Abl tyrosine kinase inhibitors.	Adenosine Triphosphate	82-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
18401881-1	2008	Imatinib is a small-molecule inhibitor of BCR-ABL tyrosine kinase activity, with proven efficacy and tolerability.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	147-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-169
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 Mesylate	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
18436994-0	2008	Dasatinib treatment can overcome imatinib and nilotinib resistance in CML patient carrying F359I mutation of BCR-ABL oncogene.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
18436994-0	2008	Dasatinib treatment can overcome imatinib and nilotinib resistance in CML patient carrying F359I mutation of BCR-ABL oncogene.	nilotinib	46-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
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 Mesylate	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 Mesylate	52-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
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.	nilotinib	135-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
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.	Dasatinib	148-157	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
18436994-4	2008	The sequencing of BCR-ABL kinase domains was performed and revealed the presence of a F359I point mutation (TTC-to-ATC nucleotide change leading to Phe-to-Ile amino acid substitution).	Phenylalanine	148-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
17882283-7	2008	In 1996, Brian Druker discovered imatinib-a small molecule ABL inhibitor with exceptional therapeutic activity in CML.	Imatinib Mesylate	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 Mesylate	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.	Dasatinib	31-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
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.	Dasatinib	31-40	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.	Dasatinib	31-40	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 Mesylate	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 Mesylate	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
18974832-0	2008	Growth arrest of BCR-ABL positive cells with a sequence-specific polyamide-chlorambucil conjugate.	polyamide-chlorambucil	65-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
19166098-3	2008	NUP214-ABL1 and EML1-ABL1 display constitutive kinase activity and are sensitive to the kinase inhibitor imatinib.	Imatinib Mesylate	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 Mesylate	105-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-25
19116712-2	2008	The ABL kinase inhibitor imatinib is effective in most patients and considered standard first-line therapy.	Imatinib Mesylate	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
18056927-4	2007	Imatinib, a BCR-ABL inhibitor, has significantly decreased CML mortality by stopping disease progression in CP.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
18056927-14	2007	Dasatinib is the second BCR-ABL inhibitor to become available.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
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 Mesylate	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
18056927-16	2007	Dasatinib also inhibits SRC kinase, which may play a role in both maintaining BCR-ABL activity and in BCR-ABL independent signaling pathways.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
18056927-16	2007	Dasatinib also inhibits SRC kinase, which may play a role in both maintaining BCR-ABL activity and in BCR-ABL independent signaling pathways.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
18056932-7	2007	Imatinib, the first approved tyrosine kinase inhibitor, functions by blocking the ATP binding site on the BCR-ABL kinase.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
18056932-7	2007	Imatinib, the first approved tyrosine kinase inhibitor, functions by blocking the ATP binding site on the BCR-ABL kinase.	Adenosine Triphosphate	82-85	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 Mesylate	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 Mesylate	92-100	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.	Adenosine Triphosphate	131-153	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.	Adenosine Triphosphate	155-158	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-130
18056932-16	2007	The second generation BCR-ABL inhibitor, dasatinib, can block the activity of many of these mutations; however, the T315I mutation, at present, is resistant to all available kinase inhibitors.	Dasatinib	41-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
17846156-3	2007	Here we describe data demonstrating that chronic cocaine exposure causes long-lasting changes in encoding properties in the ABL and the OFC during learning and reversal in an odor-guided task.	Cocaine	49-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-127
17846156-4	2007	In particular, these data suggest that inflexible encoding in ABL neurons may be the proximal cause of cocaine-induced behavioral inflexibility, and that a loss of outcome-expectant encoding in OFC neurons could be a more distal contributor to this impairment.	Cocaine	103-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-65
17720881-0	2007	Chemical proteomic profiles of the BCR-ABL inhibitors imatinib, nilotinib, and dasatinib reveal novel kinase and nonkinase targets.	Imatinib Mesylate	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
17720881-0	2007	Chemical proteomic profiles of the BCR-ABL inhibitors imatinib, nilotinib, and dasatinib reveal novel kinase and nonkinase targets.	nilotinib	64-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
17720881-0	2007	Chemical proteomic profiles of the BCR-ABL inhibitors imatinib, nilotinib, and dasatinib reveal novel kinase and nonkinase targets.	Dasatinib	79-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
17720881-1	2007	The BCR-ABL tyrosine kinase inhibitor imatinib represents the current frontline therapy in chronic myeloid leukemia.	Imatinib Mesylate	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
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 Mesylate	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
17720881-2	2007	Because many patients develop imatinib resistance, 2 second-generation drugs, nilotinib and dasatinib, displaying increased potency against BCR-ABL were developed.	nilotinib	78-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
17720881-2	2007	Because many patients develop imatinib resistance, 2 second-generation drugs, nilotinib and dasatinib, displaying increased potency against BCR-ABL were developed.	Dasatinib	92-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
17785585-1	2007	Dasatinib and nilotinib are potent tyrosine kinase inhibitors (TKIs) with activity against many imatinib-resistant chronic myeloid leukemia (CML) clones with BCR-ABL kinase domain (KD) mutations, except T315I.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-165
17785585-1	2007	Dasatinib and nilotinib are potent tyrosine kinase inhibitors (TKIs) with activity against many imatinib-resistant chronic myeloid leukemia (CML) clones with BCR-ABL kinase domain (KD) mutations, except T315I.	nilotinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-165
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 Mesylate	71-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-150
17715389-0	2007	Nilotinib (formerly AMN107), a highly selective BCR-ABL tyrosine kinase inhibitor, is effective in patients with Philadelphia chromosome-positive chronic myelogenous leukemia in chronic phase following imatinib resistance and intolerance.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
17715389-0	2007	Nilotinib (formerly AMN107), a highly selective BCR-ABL tyrosine kinase inhibitor, is effective in patients with Philadelphia chromosome-positive chronic myelogenous leukemia in chronic phase following imatinib resistance and intolerance.	nilotinib	20-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
17715389-1	2007	Nilotinib, an orally bioavailable, selective Bcr-Abl tyrosine kinase inhibitor, is 30-fold more potent than imatinib in pre-clinical models, and overcomes most imatinib resistant BCR-ABL mutations.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
17715389-1	2007	Nilotinib, an orally bioavailable, selective Bcr-Abl tyrosine kinase inhibitor, is 30-fold more potent than imatinib in pre-clinical models, and overcomes most imatinib resistant BCR-ABL mutations.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	179-186
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.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
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.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	180-187
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 Mesylate	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
19662183-0	2007	NS-187 (INNO-406), a Bcr-Abl/Lyn dual tyrosine kinase inhibitor.	bafetinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
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 Mesylate	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 Mesylate	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 Mesylate	7-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
19662183-6	2007	We set out to develop a novel drug whose affinity for Abl is higher than that of imatinib and whose specificity in inhibiting Lyn is higher than that of SFK/Abl inhibitors such as dasatinib (Sprycel) or bosutinib (SKI-606).	Dasatinib	180-189	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-160
19662183-6	2007	We set out to develop a novel drug whose affinity for Abl is higher than that of imatinib and whose specificity in inhibiting Lyn is higher than that of SFK/Abl inhibitors such as dasatinib (Sprycel) or bosutinib (SKI-606).	bosutinib	203-212	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-57
19662183-7	2007	Our work has led to the development of NS-187 (INNO-406), a novel Abl/Lyn dual tyrosine kinase inhibitor with clinical prospects.	bafetinib	39-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-69
19662183-7	2007	Our work has led to the development of NS-187 (INNO-406), a novel Abl/Lyn dual tyrosine kinase inhibitor with clinical prospects.	inno	47-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-69
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-124
19248584-9	2008	Dasatinib, dual Bcr-Abl/Src kinase inhibitor, is of high activity and induces hematologic and cytogenetic responses in patients with chronic myelogenous leukaemia in blast crisis.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
18771174-2	2008	c-Abl is a tyrosine-kinase that takes part in protein phosphorylation on tyrosine.	Tyrosine	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
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 Mesylate	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 Mesylate	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 Mesylate	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
18035968-2	2007	In an in vitro study, dasatinib had 325-fold greater potency than imatinib for inhibiting unmutated BCR-ABL.	Dasatinib	22-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
18035968-2	2007	In an in vitro study, dasatinib had 325-fold greater potency than imatinib for inhibiting unmutated BCR-ABL.	Imatinib Mesylate	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
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 Mesylate	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 Mesylate	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
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 Mesylate	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-40
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 Mesylate	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-144
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 Mesylate	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
17728783-0	2007	Deregulation of the Wilms" tumour gene 1 protein (WT1) by BCR/ABL1 mediates resistance to imatinib in human leukaemia cells.	Imatinib Mesylate	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-66
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
18067005-3	2007	The investigation of therapeutic options post-imatinib failure resulted in the development and regulatory approval of dasatinib, a BCR-ABL and SRC-family kinase inhibitor.	Dasatinib	118-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
18067005-6	2007	Nilotinib is an analog of imatinib with similar multiple kinase targets, but without inhibition of SRC, and reduced in vitro activity against BCR-ABL P-loop mutations compared with dasatinib.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
17604596-0	2007	Docosahexaenoic acid enhances the toxic effect of imatinib on Bcr-Abl expressing HL-60 cells.	Docosahexaenoic Acids	0-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
17604596-0	2007	Docosahexaenoic acid enhances the toxic effect of imatinib on Bcr-Abl expressing HL-60 cells.	Imatinib Mesylate	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 Mesylate	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.	Docosahexaenoic Acids	57-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
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 Mesylate	127-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
17827012-0	2007	The design and preliminary structure-activity relationship studies of benzotriazines as potent inhibitors of Abl and Abl-T315I enzymes.	Triazines	70-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-112
17827012-0	2007	The design and preliminary structure-activity relationship studies of benzotriazines as potent inhibitors of Abl and Abl-T315I enzymes.	Triazines	70-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-120
17827012-1	2007	We describe the design, synthesis and structure-activity relationship studies in optimizing a series of benzotriazine compounds as potent inhibitors of both Abl and Abl-T315I enzymes.	Triazines	104-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-160
17827012-1	2007	We describe the design, synthesis and structure-activity relationship studies in optimizing a series of benzotriazine compounds as potent inhibitors of both Abl and Abl-T315I enzymes.	Triazines	104-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	165-168
18974832-2	2008	Imatinib, a selective inhibitor of the Bcr-Abl tyrosine kinase, has significantly improved the clinical outcome of patients with CML.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
18974832-6	2008	Here we report that a DNA sequence-specific pyrrole-imidazole polyamide-chlorambucil conjugate, 1R-Chl, causes growth arrest of cells harboring both unmutated BCR-ABL and three imatinib resistant strains.	pyrrole-imidazole polyamide-chlorambucil	44-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-166
17268817-0	2007	Dasatinib, an orally active small molecule inhibitor of both the src and abl kinases, selectively inhibits growth of basal-type/"triple-negative" breast cancer cell lines growing in vitro.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-76
17268817-1	2007	Dasatinib is an orally active small molecule kinase inhibitor of both the src and abl proteins.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-85
18158072-17	2007	CONCLUSIONS: Dasatinib has a wider spectrum of activity against a broader range of BCR-ABL forms than existing TK inhibitors.	Dasatinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
17587335-0	2007	Anaplasma phagocytophilum AnkA secreted by type IV secretion system is tyrosine phosphorylated by Abl-1 to facilitate infection.	Tyrosine	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-103
17587335-7	2007	Yeast two-hybrid and coimmunoprecipitation analyses demonstrated that AnkA could bind to Abl-interactor 1 (Abi-1), an adaptor protein that interacts with Abl-1 tyrosine kinase, thus mediating AnkA phosphorylation.	lauric acid	89-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-159
17804414-2	2007	Critical for the regulation of PKD1 activity in response to oxidative stress are Src- and Abl-mediated tyrosine phosphorylations that eventually lead to protein kinase Cdelta (PKCdelta)-mediated activation of PKD1.	Tyrosine	103-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-93
17804421-0	2007	MLH1- and ATM-dependent MAPK signaling is activated through c-Abl in response to the alkylator N-methyl-N"-nitro-N"-nitrosoguanidine.	Methylnitronitrosoguanidine	95-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-65
18020922-0	2007	Management of Bcr-Abl-positive leukemias with dasatinib.	Dasatinib	46-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
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 Mesylate	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 Mesylate	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 Mesylate	54-61	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 Mesylate	54-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	284-291
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 Mesylate	166-174	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	295-302
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 Mesylate	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
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 Mesylate	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 Mesylate	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
17637811-11	2007	BCR-ABL peptide vaccination may improve control of CML, especially in patients responding well to imatinib.	Imatinib Mesylate	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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 Mesylate	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
17704648-2	2007	We here demonstrate that three newly developed dual selective Src/Abl kinase inhibitors (SrcK-I) (AZM559756, AZD0530 and AZD0424) are able to induce apoptosis and cell cycle arrest in BCR-ABL, c-KIT and platelet-derived growth factor-negative lymphoma cell lines.	azm559756	98-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	184-191
18158072-9	2007	Dasatinib has shown in vitro and in vivo activity against BCR-ABL, including mutations that are resistant to other available TK inhibitors.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
17704648-2	2007	We here demonstrate that three newly developed dual selective Src/Abl kinase inhibitors (SrcK-I) (AZM559756, AZD0530 and AZD0424) are able to induce apoptosis and cell cycle arrest in BCR-ABL, c-KIT and platelet-derived growth factor-negative lymphoma cell lines.	saracatinib	109-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	184-191
17704648-2	2007	We here demonstrate that three newly developed dual selective Src/Abl kinase inhibitors (SrcK-I) (AZM559756, AZD0530 and AZD0424) are able to induce apoptosis and cell cycle arrest in BCR-ABL, c-KIT and platelet-derived growth factor-negative lymphoma cell lines.	AZD-0424	121-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	184-191
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 Mesylate	80-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-152
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 Mesylate	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
17881650-0	2007	Interferon-alpha or homoharringtonine as salvage treatment for chronic myeloid leukemia patients who acquire the T315I BCR-ABL mutation.	Homoharringtonine	20-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-126
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.	Dasatinib	68-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
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.	nilotinib	82-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
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 Mesylate	123-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
17496201-2	2007	Dasatinib, a novel, oral, multitargeted kinase inhibitor of BCR-ABL and SRC family kinases, has previously induced responses in patients with imatinib-resistant or -intolerant Ph-positive ALL.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
17496201-7	2007	The presence of BCR-ABL mutations conferring imatinib resistance did not preclude a response to dasatinib.	Imatinib Mesylate	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
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 Mesylate	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 Mesylate	228-236	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.	dastinib	333-341	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.	nilotinib	343-352	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 Mesylate	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 Mesylate	53-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
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.	Dasatinib	230-239	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
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.	nilotinib	244-253	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
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 Mesylate	96-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
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 Mesylate	139-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-56
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 Mesylate	139-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
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 Mesylate	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
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 Mesylate	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 Mesylate	19-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
17987222-4	2007	Nilotinib (Tasigna; Novartis) is a second-generation tyrosine kinase inhibitor with 30-fold higher potency against BCR-ABL kinase than imatinib.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
17727673-13	2007	For systemic treatment and prophylaxis, BCR/ABL kinase inhibitors crossing the blood-brain barrier such as dasatinib should be considered in patients with CNS relapse.	Dasatinib	107-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
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 Mesylate	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
17929114-0	2007	The Bcr-Abl tyrosine kinase inhibitor imatinib and promising new agents against Philadelphia chromosome-positive leukemias.	Imatinib Mesylate	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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-141
17929114-6	2007	Inhibitors of Abl TK are divided into two main groups, namely, ATP-competitive and ATP noncompetitive inhibitors.	Adenosine Triphosphate	63-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-17
17929114-6	2007	Inhibitors of Abl TK are divided into two main groups, namely, ATP-competitive and ATP noncompetitive inhibitors.	Adenosine Triphosphate	83-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-17
17929114-7	2007	The ATP-competitive inhibitors fall into two subclasses, the Src/Abl inhibitors, and the 2-phenylaminopyrimidine-based compounds.	Adenosine Triphosphate	4-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-68
17929114-8	2007	Dasatinib (formerly BMS-354825), AP23464, SKI-606, and PD166326 are classified as Src/Abl inhibitors, while nilotinib (AMN107) and INNO-406 (NS-187) belong to the latter subclass of inhibitors.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-89
17929114-8	2007	Dasatinib (formerly BMS-354825), AP23464, SKI-606, and PD166326 are classified as Src/Abl inhibitors, while nilotinib (AMN107) and INNO-406 (NS-187) belong to the latter subclass of inhibitors.	PD 166326	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-89
17929114-12	2007	However, an ATP-competitive inhibitor that can inhibit the phosphorylation of T315I Bcr-Abl has not yet been developed.	Adenosine Triphosphate	12-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
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 Mesylate	60-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
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 Mesylate	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
17970609-20	2007	Imatinib functions by competing with adenosine triphosphate (ATP) for binding to the BCr-ABL tyrosine kinase.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
17970609-20	2007	Imatinib functions by competing with adenosine triphosphate (ATP) for binding to the BCr-ABL tyrosine kinase.	Adenosine Triphosphate	37-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
17970609-20	2007	Imatinib functions by competing with adenosine triphosphate (ATP) for binding to the BCr-ABL tyrosine kinase.	Adenosine Triphosphate	61-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
17970609-31	2007	resistance is usually caused by mutations within BCr-ABL, decreasing the affinity of imatinib binding.	Imatinib Mesylate	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 Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
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.	Adenosine Triphosphate	72-94	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.	Adenosine Triphosphate	72-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
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.	Adenosine Triphosphate	96-99	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.	Adenosine Triphosphate	96-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
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.	Adenosine Triphosphate	166-169	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.	Adenosine Triphosphate	166-169	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 Mesylate	185-193	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
17970610-16	2007	dasatinib is a next-generation kinase inhibitor that binds to both SrC and to multiple conformations of BCR-ABL.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
17970610-17	2007	It is capable of blocking several BCR-ABL mutants that are resistant to imatinib.	Imatinib Mesylate	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
17588140-0	2007	The functional role of cysteine residues for c-Abl kinase activity.	Cysteine	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-50
17588140-3	2007	In this study, we show that the kinase activity of the non-receptor tyrosine kinase c-Abl is inhibited by in vitro thiol modification; specifically, the cysteine residues of c-Abl are modified by S-glutathionylation and by thiol alkylating agents such as 4-acetamido-4"-maleimidylstilbene-2,2"-disulfonic acid and N-ethylmaleimide.	Sulfhydryl Compounds	115-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-89
17588140-3	2007	In this study, we show that the kinase activity of the non-receptor tyrosine kinase c-Abl is inhibited by in vitro thiol modification; specifically, the cysteine residues of c-Abl are modified by S-glutathionylation and by thiol alkylating agents such as 4-acetamido-4"-maleimidylstilbene-2,2"-disulfonic acid and N-ethylmaleimide.	Sulfhydryl Compounds	115-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-179
17588140-3	2007	In this study, we show that the kinase activity of the non-receptor tyrosine kinase c-Abl is inhibited by in vitro thiol modification; specifically, the cysteine residues of c-Abl are modified by S-glutathionylation and by thiol alkylating agents such as 4-acetamido-4"-maleimidylstilbene-2,2"-disulfonic acid and N-ethylmaleimide.	Cysteine	153-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-89
17588140-3	2007	In this study, we show that the kinase activity of the non-receptor tyrosine kinase c-Abl is inhibited by in vitro thiol modification; specifically, the cysteine residues of c-Abl are modified by S-glutathionylation and by thiol alkylating agents such as 4-acetamido-4"-maleimidylstilbene-2,2"-disulfonic acid and N-ethylmaleimide.	Cysteine	153-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-179
17588140-3	2007	In this study, we show that the kinase activity of the non-receptor tyrosine kinase c-Abl is inhibited by in vitro thiol modification; specifically, the cysteine residues of c-Abl are modified by S-glutathionylation and by thiol alkylating agents such as 4-acetamido-4"-maleimidylstilbene-2,2"-disulfonic acid and N-ethylmaleimide.	Sulfhydryl Compounds	223-228	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-89
17588140-3	2007	In this study, we show that the kinase activity of the non-receptor tyrosine kinase c-Abl is inhibited by in vitro thiol modification; specifically, the cysteine residues of c-Abl are modified by S-glutathionylation and by thiol alkylating agents such as 4-acetamido-4"-maleimidylstilbene-2,2"-disulfonic acid and N-ethylmaleimide.	Sulfhydryl Compounds	223-228	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-179
17588140-3	2007	In this study, we show that the kinase activity of the non-receptor tyrosine kinase c-Abl is inhibited by in vitro thiol modification; specifically, the cysteine residues of c-Abl are modified by S-glutathionylation and by thiol alkylating agents such as 4-acetamido-4"-maleimidylstilbene-2,2"-disulfonic acid and N-ethylmaleimide.	4-acetamido-4'-maleimidylstilbene-2,2'-disulfonic acid	255-309	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-89
17588140-3	2007	In this study, we show that the kinase activity of the non-receptor tyrosine kinase c-Abl is inhibited by in vitro thiol modification; specifically, the cysteine residues of c-Abl are modified by S-glutathionylation and by thiol alkylating agents such as 4-acetamido-4"-maleimidylstilbene-2,2"-disulfonic acid and N-ethylmaleimide.	4-acetamido-4'-maleimidylstilbene-2,2'-disulfonic acid	255-309	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-179
17588140-3	2007	In this study, we show that the kinase activity of the non-receptor tyrosine kinase c-Abl is inhibited by in vitro thiol modification; specifically, the cysteine residues of c-Abl are modified by S-glutathionylation and by thiol alkylating agents such as 4-acetamido-4"-maleimidylstilbene-2,2"-disulfonic acid and N-ethylmaleimide.	Ethylmaleimide	314-330	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-89
17588140-3	2007	In this study, we show that the kinase activity of the non-receptor tyrosine kinase c-Abl is inhibited by in vitro thiol modification; specifically, the cysteine residues of c-Abl are modified by S-glutathionylation and by thiol alkylating agents such as 4-acetamido-4"-maleimidylstilbene-2,2"-disulfonic acid and N-ethylmaleimide.	Ethylmaleimide	314-330	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-179
17588140-4	2007	Modification of cysteine residues of c-Abl tyrosine kinase using glutathione disulfide and thiol alkylating agents corresponds to a concomitant loss of kinase activity.	Cysteine	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-42
17588140-4	2007	Modification of cysteine residues of c-Abl tyrosine kinase using glutathione disulfide and thiol alkylating agents corresponds to a concomitant loss of kinase activity.	Glutathione Disulfide	65-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-42
17588140-4	2007	Modification of cysteine residues of c-Abl tyrosine kinase using glutathione disulfide and thiol alkylating agents corresponds to a concomitant loss of kinase activity.	Sulfhydryl Compounds	91-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-42
17686996-4	2007	The Abl kinase inhibitor, imatinib, also stimulates cell spreading and its effect is overridden by the imatinib-resistant AblT315I.	Imatinib Mesylate	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
17686996-4	2007	The Abl kinase inhibitor, imatinib, also stimulates cell spreading and its effect is overridden by the imatinib-resistant AblT315I.	Imatinib Mesylate	103-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
17686996-5	2007	Expression of Abl but not AbkKD in Abl/Arg-deficient cells again inhibits spreading.	Arginine	39-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-17
17686996-7	2007	Ectopic expression of CrkII, a Rac activator that is inactivated by Abl-mediated tyrosine phosphorylation, antagonizes Abl-mediated dorsal membrane localization of RacV12.	Tyrosine	81-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-71
17686996-7	2007	Ectopic expression of CrkII, a Rac activator that is inactivated by Abl-mediated tyrosine phosphorylation, antagonizes Abl-mediated dorsal membrane localization of RacV12.	Tyrosine	81-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-122
17686996-9	2007	These results suggest that Abl tyrosine kinase, through CrkII phosphorylation and in collaboration with dynamin-2 can regulate the partitioning of Rac-GTP to favor dorsal ruffles during cell spreading.	rac-gtp	147-154	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-30
17853901-1	2007	The introduction of the BCR-ABL kinase inhibitor imatinib mesylate (Gleevec; Novartis) revolutionized the treatment of chronic myeloid leukaemia (CML).	Imatinib Mesylate	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 Mesylate	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.	nilotinib	41-50	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.	nilotinib	41-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	289-296
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.	Dasatinib	75-84	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.	Dasatinib	75-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	289-296
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	159-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
17671436-5	2007	We recently showed that inhibition of heat shock protein 90 (Hsp90) by a novel Hsp90 inhibitor, IPI- 504, causes BCR-ABL protein degradation, decreased numbers of leukemia stem cells, and prolonged survival of mice with CML induced by BCR-ABL-T315I.	tanespimycin	96-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
17671436-5	2007	We recently showed that inhibition of heat shock protein 90 (Hsp90) by a novel Hsp90 inhibitor, IPI- 504, causes BCR-ABL protein degradation, decreased numbers of leukemia stem cells, and prolonged survival of mice with CML induced by BCR-ABL-T315I.	tanespimycin	96-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	235-242
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 Mesylate	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 Mesylate	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-137
17701954-9	2007	Dasatinib is a multitargeted kinase inhibitor of BCR-ABL, SRC, C-KIT, PDGFRs, and ephrin A receptor kinases.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
17701954-12	2007	Nilotinib is another BCR-ABL targeted agent that is similar in structure to imatinib but has significantly greater binding affinity.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
17701954-12	2007	Nilotinib is another BCR-ABL targeted agent that is similar in structure to imatinib but has significantly greater binding affinity.	Imatinib Mesylate	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
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 Mesylate	39-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
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.	Glycogen	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
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 Mesylate	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 Mesylate	15-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-123
17620332-7	2007	First, anti-phosphotyrosine blots indicate that c-Abl tyrosine kinase activation is concomitant with FAK dephosphorylation in response to insulin, whereas c-Abl inhibition is accompanied by FAK phosphorylation in response to insulin, a response similar to that observed with IGF-I.	Phosphotyrosine	12-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-53
17623672-6	2007	Our results show that the activation of WAVE3 to promote actin remodeling is enhanced by the c-Abl-mediated tyrosine phosphorylation of WAVE3.	Tyrosine	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-98
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
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 Mesylate	27-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
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 Mesylate	103-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-178
17510658-0	2007	Apoptosis-based dual molecular targeting by INNO-406, a second-generation Bcr-Abl inhibitor, and ABT-737, an inhibitor of antiapoptotic Bcl-2 proteins, against Bcr-Abl-positive leukemia.	ABT-737	97-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-167
17892306-3	2007	This technique required the engineering of Abl/Arg to utilize an unnatural ATP analogue as a phospho-donor.	Arginine	47-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-46
17892306-3	2007	This technique required the engineering of Abl/Arg to utilize an unnatural ATP analogue as a phospho-donor.	Adenosine Triphosphate	75-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-46
17892306-4	2007	Mutation of T334A and T361A in Abl and Arg, respectively, altered their nucleotide specificity and allowed them to utilize N6-benzyl-ATP as a phospho-donor.	Arginine	39-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-34
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 Mesylate	159-176	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
17510658-4	2007	ABT-737, an inhibitor of antiapoptotic Bcl-2 and Bcl-X(L), greatly enhanced the apoptosis by INNO-406, even in INNO-406-less sensitive cells with Bcr-Abl point mutations except T315I mutation.	ABT-737	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	146-153
17892306-4	2007	Mutation of T334A and T361A in Abl and Arg, respectively, altered their nucleotide specificity and allowed them to utilize N6-benzyl-ATP as a phospho-donor.	N6-Benzyl-ATP	123-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-34
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 Mesylate	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 Mesylate	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
17804707-6	2007	The cocrystal structure of T315I Abl kinase domain provides the structural basis for this activity: the inhibitor associates with an active conformation of the kinase domain in the ATP-binding pocket and lacks the steric hindrance imposed by the substitution of threonine by isoleucine.	Adenosine Triphosphate	181-184	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-36
17804707-6	2007	The cocrystal structure of T315I Abl kinase domain provides the structural basis for this activity: the inhibitor associates with an active conformation of the kinase domain in the ATP-binding pocket and lacks the steric hindrance imposed by the substitution of threonine by isoleucine.	Threonine	262-271	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-36
17804707-6	2007	The cocrystal structure of T315I Abl kinase domain provides the structural basis for this activity: the inhibitor associates with an active conformation of the kinase domain in the ATP-binding pocket and lacks the steric hindrance imposed by the substitution of threonine by isoleucine.	Isoleucine	275-285	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-36
17768119-0	2007	Clinical outcome of 27 imatinib mesylate-resistant chronic myelogenous leukemia patients harboring a T315I BCR-ABL mutation.	Imatinib Mesylate	23-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
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 Mesylate	110-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
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.	Dasatinib	123-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
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 Mesylate	152-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
17710227-8	2007	Our findings demonstrate the potential hazards of sequential kinase inhibitor therapy and suggest a role for a combination of ABL kinase inhibitors, perhaps including VX-680, to prevent the outgrowth of cells harboring drug-resistant BCR-ABL mutations.	VX680	167-173	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	234-241
17569822-0	2007	Bcr-Abl-independent imatinib-resistant K562 cells show aberrant protein acetylation and increased sensitivity to histone deacetylase inhibitors.	Imatinib Mesylate	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
17530620-0	2007	First and second line imatinib treatment in chronic myelogenous leukemia patients expressing rare e1a2 or e19a2 BCR-ABL transcripts.	Imatinib Mesylate	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
17530620-8	2007	We conclude that in patients with rare BCR-ABL variants, the effectiveness of imatininb treatment may be influenced by the CML stage besides the actual molecular type of the rare transcript.	imatininb	78-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	127-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	221-228
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 Mesylate	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 Mesylate	157-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	274-281
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 Mesylate	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-126
17596313-0	2007	Gag influences transformation by Abelson murine leukemia virus and suppresses nuclear localization of the v-Abl protein.	Glycosaminoglycans	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-111
17596313-2	2007	Although the Gag-derived myristoylation signal targets the v-Abl protein to the plasma membrane, the protein contains the entire MA and p12 sequences and a small number of CA-derived residues.	Glycosaminoglycans	13-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-64
17596313-6	2007	Although all of the mutant proteins retained kinase activity, those defective in transformation were reduced in their ability to activate Erk, suggesting a role for Gag sequences in v-Abl signaling.	Glycosaminoglycans	165-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-187
17596313-7	2007	Immunofluorescence analysis revealed that a v-Abl protein retaining only the first 34 amino acids of Gag localized to the nucleus.	Glycosaminoglycans	101-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-49
17596313-8	2007	These data indicate that Gag sequences are important for normal v-Abl signaling and that they suppress nuclear localization of the molecule.	Glycosaminoglycans	25-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-69
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.	Sorafenib	26-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
17595328-8	2007	Together, these findings suggest that sorafenib effectively induces apoptosis in highly imatinib-resistant chronic myelogenous leukemia cells, most likely by inhibiting or down-regulating targets (i.e., STAT5 and Mcl-1) downstream or independent of Bcr/Abl.	Sorafenib	38-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	249-256
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 Mesylate	64-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
17595328-1	2007	The effects of the multikinase inhibitor sorafenib (BAY 43-9006), an agent shown previously to induce apoptosis in human leukemia cells through inhibition of myeloid cell leukemia-1 (Mcl-1) translation, have been examined in Bcr/Abl(+) leukemia cells resistant to imatinib mesylate (IM).	Sorafenib	41-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	225-232
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.	Sorafenib	79-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	179-186
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 Mesylate	119-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	179-186
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 Mesylate	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-140
17595328-4	2007	Induction of apoptosis by sorafenib was associated with rapid and pronounced down-regulation of Mcl-1 and diminished signal transducer and activator of transcription (STAT) 5 phosphorylation and reporter activity but only very modest and delayed inactivation of the Bcr/Abl downstream target Crkl.	Sorafenib	26-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	266-273
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.	Dasatinib	56-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-140
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 Mesylate	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	255-262
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.	bosutinib	80-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-140
17684099-0	2007	The Btk tyrosine kinase is a major target of the Bcr-Abl inhibitor dasatinib.	Dasatinib	67-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
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 Mesylate	49-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-47
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.	2-Methoxyestradiol	88-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-47
17697368-11	2007	CONCLUSION: It is concluded that Shb promotes 2-ME-induced PC3 cell apoptosis by increased pro-apoptotic signaling via the c-Abl pathway and that this causes reduced tumor growth in vivo.	2-Methoxyestradiol	46-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-128
17475908-3	2007	In fact, high levels of p210-BCR/ABL are required for enhanced hnRNP-E2 expression, which depends on phosphorylation of hnRNP-E2 serines 173, 189, and 272 and threonine 213 by the BCR/ABL-activated MAPK(ERK1/2).	Serine	129-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-36
17446106-1	2007	Molecular modeling by 3D-QSAR comparative molecular field analysis (CoMFA) and comparative molecular similarity indices analysis (CoMSIA) were employed on a series of phenylaminopyrimidine-based (PAP) Bcr-Abl inhibitors.	phenylaminopyrimidine	167-188	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	201-208
17446106-5	2007	Based on the contour interpretation, the attachment of hydrophobic and bulky groups to the phenyl and pyrrolidine (D- and E-ring of NS-187, respectively) along with highly electronegative groups around the D-ring are important structural features for the design of second-generation Bcr-Abl inhibitors.	3-azido-2,7-naphthalene disulfonate	67-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	283-290
17475908-3	2007	In fact, high levels of p210-BCR/ABL are required for enhanced hnRNP-E2 expression, which depends on phosphorylation of hnRNP-E2 serines 173, 189, and 272 and threonine 213 by the BCR/ABL-activated MAPK(ERK1/2).	Serine	129-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-36
17475908-3	2007	In fact, high levels of p210-BCR/ABL are required for enhanced hnRNP-E2 expression, which depends on phosphorylation of hnRNP-E2 serines 173, 189, and 272 and threonine 213 by the BCR/ABL-activated MAPK(ERK1/2).	Threonine	159-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-36
17671155-2	2007	Imatinib mesylate is one such agent inhibiting the tyrosine kinase that results from the Bcr-Abl translocation.	Imatinib Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
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 Mesylate	58-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-33
17683977-2	2007	Blocking BCR-ABL by the ABL tyrosine kinase inhibitor imatinib mesylate (IM, Gleevec) is clinically highly efficient.	Imatinib Mesylate	54-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
17267032-0	2007	Pivanex, a histone deacetylase inhibitor, induces changes in BCR-ABL expression and when combined with STI571, acts synergistically in a chronic myelocytic leukemia cell line.	pivalyloxymethyl butyrate	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
17671641-2	2007	This in turn led to the development of imatinib mesylate, a clinically successful inhibitor of the BCR-ABL kinase.	Imatinib Mesylate	39-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
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 Mesylate	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 Mesylate	192-200	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
17475908-3	2007	In fact, high levels of p210-BCR/ABL are required for enhanced hnRNP-E2 expression, which depends on phosphorylation of hnRNP-E2 serines 173, 189, and 272 and threonine 213 by the BCR/ABL-activated MAPK(ERK1/2).	Threonine	159-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-36
17475908-4	2007	Serine/threonine to alanine substitution abolishes hnRNP-E2 phosphorylation and markedly decreases its stability in BCR/ABL-expressing myeloid precursors.	Serine	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
17475908-4	2007	Serine/threonine to alanine substitution abolishes hnRNP-E2 phosphorylation and markedly decreases its stability in BCR/ABL-expressing myeloid precursors.	Threonine	7-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
17475908-4	2007	Serine/threonine to alanine substitution abolishes hnRNP-E2 phosphorylation and markedly decreases its stability in BCR/ABL-expressing myeloid precursors.	Alanine	20-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
17267032-4	2007	We demonstrated that in K562, the CML cell line, pivaloyloxymethyl butyrate (Pivanex)-induced apoptosis, differentiation and reduced BCR-ABL protein levels and that the combination of Pivanex with STI571 acted synergistically.	pivalyloxymethyl butyrate	49-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
17267032-4	2007	We demonstrated that in K562, the CML cell line, pivaloyloxymethyl butyrate (Pivanex)-induced apoptosis, differentiation and reduced BCR-ABL protein levels and that the combination of Pivanex with STI571 acted synergistically.	pivalyloxymethyl butyrate	77-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
17554384-8	2007	In contrast to AML cell lines, BCR-ABL transformed human cells showed resistance to ABT-737, which might be due to the induction of MCL1 by BCR-ABL.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	84-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
17554384-8	2007	In contrast to AML cell lines, BCR-ABL transformed human cells showed resistance to ABT-737, which might be due to the induction of MCL1 by BCR-ABL.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	84-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
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 Mesylate	142-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-112
17618275-4	2007	Complex formation results in Abl-mediated phosphorylation of beta-catenin on tyrosine 489, leading to a decrease in its affinity for N-cadherin, loss of N-cadherin function, and targeting of phospho-Y489-beta-catenin to the nucleus.	Tyrosine	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-32
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 Mesylate	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
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 Mesylate	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 Mesylate	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
17431132-4	2007	Enhanced ATM kinase-dependent phosphorylation of Nbs1 on serine 343 (S343) in response to genotoxic treatment was detected in leukemia cells expressing BCR/ABL and other FTKs in comparison to normal counterparts stimulated with IL-3, GM-CSF, and SCF.	Serine	57-63	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 Mesylate	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 Mesylate	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 Mesylate	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	197-204
17223257-0	2007	Camptothecin acts synergistically with imatinib and overcomes imatinib resistance through Bcr-Abl independence in human K562 cells.	Camptothecin	0-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
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 Mesylate	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-159
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 Mesylate	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 Mesylate	4-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	227-234
17627925-5	2007	No interference of glyoxylic acid could be observed with Vitros 950, but a positive interference could be observed with ABL 725 and 825, OMNI S, CCX4 and Architect ci8200 A linear relationship between apparent lactate concentration found with ABL 725 and 825, OMNI S, CCX 4, and glyoxylic acid could be observed (0,94 < r < 0,99), a weaker interference being observed with Rapid Lab 1265 and Architect ci 8200.	Lactic Acid	210-217	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	243-246
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 Mesylate	145-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-77
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 Mesylate	110-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
17591830-2	2007	Imatinib, an inhibitor of the BCR-ABL tyrosine kinase, significantly improves the outcome of patients with CML.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
17475248-7	2007	Coexpression of N-Wasp-Crib inhibited C3G induced as well as c-Abl-induced filopodia and wiskostatin, a pharmacological inhibitor of N-Wasp attenuates C3G-induced filopodia.	wiskostatin	89-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-66
17642017-0	2007	Drug evaluation: Nilotinib - a novel Bcr-Abl tyrosine kinase inhibitor for the treatment of chronic myelocytic leukemia and beyond.	nilotinib	17-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
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 Mesylate	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 Mesylate	171-179	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
17642017-5	2007	Attempts to circumvent resistance to imatinib led to the discovery of nilotinib (Tasigna; Novartis AG), a novel, potent and selective oral Bcr-Abl kinase inhibitor.	nilotinib	70-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-146
17549412-1	2007	Approximately 30% of chronic myeloid leukemia patients show initially no response to Imatinib, a potent inhibitor of BCR-ABL.	Imatinib Mesylate	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
17495969-3	2007	Here, we investigated the potential synergy of bortezomib and ATO on Bcr-Abl(+) leukemic K562 cells.	Bortezomib	47-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
17495969-3	2007	Here, we investigated the potential synergy of bortezomib and ATO on Bcr-Abl(+) leukemic K562 cells.	Arsenic Trioxide	62-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
17495969-4	2007	The results showed that cotreatment of bortezomib at 32 nM, a half concentration for growth arrest, and ATO at 1 microM, a dose with no significant cytotoxic effect, synergistically induced apoptosis in the cell line, followed by enhanced mitochondrial dysfunction, release of cytochrome c and apoptosis-inducing factor, caspase-3 cleavage and degradation of poly-adenosine diphosphate-ribose polymerase together with the decreased Bcr-Abl protein.	Bortezomib	39-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	432-439
17495969-4	2007	The results showed that cotreatment of bortezomib at 32 nM, a half concentration for growth arrest, and ATO at 1 microM, a dose with no significant cytotoxic effect, synergistically induced apoptosis in the cell line, followed by enhanced mitochondrial dysfunction, release of cytochrome c and apoptosis-inducing factor, caspase-3 cleavage and degradation of poly-adenosine diphosphate-ribose polymerase together with the decreased Bcr-Abl protein.	Arsenic Trioxide	104-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	432-439
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-46
17613767-1	2007	The aminopyrimidine inhibitor AMN107 (Nilotinib) was rationally designed to antagonize the aberrant tyrosine kinase activity of Bcr-Abl-positive cells.	2-aminopyrimidine	4-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
17613767-1	2007	The aminopyrimidine inhibitor AMN107 (Nilotinib) was rationally designed to antagonize the aberrant tyrosine kinase activity of Bcr-Abl-positive cells.	nilotinib	30-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
17613767-1	2007	The aminopyrimidine inhibitor AMN107 (Nilotinib) was rationally designed to antagonize the aberrant tyrosine kinase activity of Bcr-Abl-positive cells.	nilotinib	38-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
17213809-1	2007	Dasatinib is an ATP-competitive, multi-targeted SRC and ABL kinase inhibitor that can bind BCR-ABL in both the active and inactive conformations.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
17213809-1	2007	Dasatinib is an ATP-competitive, multi-targeted SRC and ABL kinase inhibitor that can bind BCR-ABL in both the active and inactive conformations.	Adenosine Triphosphate	16-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
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 Mesylate	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
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.	Dasatinib	49-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
17187856-0	2007	N-Benzyladriamycin-14-valerate (AD 198) cytotoxicty circumvents Bcr-Abl anti-apoptotic signaling in human leukemia cells and also potentiates imatinib cytotoxicity.	N-benzyladriamycin-14-valerate	0-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
17187856-2	2007	Currently, the most effective treatment of CML is the inhibition of Bcr-Abl activity by imatinib mesylate (Gleevec).	Imatinib Mesylate	88-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
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 Mesylate	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 Mesylate	114-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
17187856-7	2007	At sub-cytotoxic doses, AD 198 and its cellular metabolite, N-benzyladriamycin (AD 288) sensitize CML cells to imatinib through a supra-additive reduction in the level of Bcr-Abl protein expression.	N-benzyladriamycin	60-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-178
17317857-3	2007	Dasatinib, a significantly more potent inhibitor of BCR-ABL, is safe and effective in this population.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
17347407-0	2007	Role of BCR/ABL gene-expression levels in determining the phenotype and imatinib sensitivity of transformed human hematopoietic cells.	Imatinib Mesylate	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-15
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 Mesylate	127-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
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 Mesylate	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
17303698-0	2007	Identification of BCR-ABL point mutations conferring resistance to the Abl kinase inhibitor AMN107 (nilotinib) by a random mutagenesis study.	nilotinib	92-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
17303698-0	2007	Identification of BCR-ABL point mutations conferring resistance to the Abl kinase inhibitor AMN107 (nilotinib) by a random mutagenesis study.	nilotinib	100-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
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 Mesylate	79-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-150
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 Mesylate	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
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 Mesylate	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
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 Mesylate	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-139
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 Mesylate	38-46	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 Mesylate	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 Mesylate	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 Mesylate	145-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-170
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.	nilotinib	38-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
19707323-0	2007	Imatinib and tyrosine kinase inhibition, in the management of BCR-ABL negative myeloproliferative disorders.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
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.	Zoledronic Acid	0-15	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.	Zoledronic Acid	0-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	176-183
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 Mesylate	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 Mesylate	164-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	176-183
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 Mesylate	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 Mesylate	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
17431887-6	2007	Novel agents include dasatinib, a potent TKI that inhibits several critical oncogenic proteins and which has recently been approved for patients with CML who are resistant or intolerant to imatinib; and nilotinib, a potent selective Bcr-Abl kinase inhibitor currently in clinical development.	nilotinib	203-212	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	233-240
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.	Dasatinib	124-133	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 Mesylate	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 Mesylate	211-219	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
17291840-0	2007	High-performance liquid chromatography method with ultraviolet detection for the quantification of the BCR-ABL inhibitor nilotinib (AMN107) in plasma, urine, culture medium and cell preparations.	nilotinib	121-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
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 Mesylate	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 Mesylate	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
17609876-0	2007	Therapeutic application of small interfering RNA directed against bcr-abl transcripts to a patient with imatinib-resistant chronic myeloid leukaemia.	Imatinib Mesylate	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 Mesylate	231-239	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
17538248-3	2007	Apoptosis induced by imatinib and nilotinib was determined in BCR-ABL expressing cell lines and primary CML CD34+ cells.	Imatinib Mesylate	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.	nilotinib	34-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
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 Mesylate	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.	nilotinib	82-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
17550858-0	2007	Enhanced Bcr-Abl-specific antileukemic activity of arsenic trioxide (Trisenox) through glutathione-depletion in imatinib-resistant cells.	Arsenic Trioxide	51-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
17550858-0	2007	Enhanced Bcr-Abl-specific antileukemic activity of arsenic trioxide (Trisenox) through glutathione-depletion in imatinib-resistant cells.	Arsenic Trioxide	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
17550858-0	2007	Enhanced Bcr-Abl-specific antileukemic activity of arsenic trioxide (Trisenox) through glutathione-depletion in imatinib-resistant cells.	Glutathione	87-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
17550858-0	2007	Enhanced Bcr-Abl-specific antileukemic activity of arsenic trioxide (Trisenox) through glutathione-depletion in imatinib-resistant cells.	Imatinib Mesylate	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 Mesylate	33-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
17550858-2	2007	Arsenic trioxide (ATO) has Bcr-Abl suppressing activity in vitro.	Arsenic Trioxide	0-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
17550858-2	2007	Arsenic trioxide (ATO) has Bcr-Abl suppressing activity in vitro.	Arsenic Trioxide	18-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
17550858-5	2007	GSH-depletion promotes enhanced Bcr-Abl specific activity of ATO through avid repression of Bcr-Abl protein levels and total cellular Bcr-Abl activity.	Glutathione	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
17550858-5	2007	GSH-depletion promotes enhanced Bcr-Abl specific activity of ATO through avid repression of Bcr-Abl protein levels and total cellular Bcr-Abl activity.	Glutathione	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
17550858-5	2007	GSH-depletion promotes enhanced Bcr-Abl specific activity of ATO through avid repression of Bcr-Abl protein levels and total cellular Bcr-Abl activity.	Glutathione	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
17291840-0	2007	High-performance liquid chromatography method with ultraviolet detection for the quantification of the BCR-ABL inhibitor nilotinib (AMN107) in plasma, urine, culture medium and cell preparations.	nilotinib	132-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
17513418-0	2007	c-Abl tyrosine kinase and inhibition by the cancer drug imatinib (Gleevec/STI-571).	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-34
17513418-5	2007	Notably, this phosphotyrosine residue is lacking in c-Abl, where instead autoinhibition is mediated by an interaction between the kinase domain and the N-terminal myristoyl modification.	Phosphotyrosine	14-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-57
17513418-7	2007	These differences help explain the ability of imatinib to preferentially inhibit Abl over Src.	Imatinib Mesylate	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-84
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-46
17208297-0	2007	BCR-ABL mutant kinetics in CML patients treated with dasatinib.	Dasatinib	53-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
17208297-2	2007	Here, we monitored the mutated BCR-ABL transcripts during the follow-up of 12 CML patients treated with dasatinib.	Dasatinib	104-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
17208297-4	2007	Clinical responses were correlated to the in vitro sensitivity of BCR-ABL mutants to dasatinib, however, some discrepancies were observed in a subfraction of CML patients, suggesting subtle differences between in vitro observations and clinical entities and/or the onset of other mechanisms responsible for dasatinib resistance.	Dasatinib	85-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
17610380-2	2007	In this study, we report mechanisms of action of histone deacetylase (HDAC) inhibitor, depsipeptide (FK228) in BCR/ABL-expressing cell lines and its effectiveness in imatinib-resistant cells from patients with blast crisis of CML.	Depsipeptides	87-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
17610380-2	2007	In this study, we report mechanisms of action of histone deacetylase (HDAC) inhibitor, depsipeptide (FK228) in BCR/ABL-expressing cell lines and its effectiveness in imatinib-resistant cells from patients with blast crisis of CML.	romidepsin	101-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
17610380-3	2007	FK228 potently induced apoptosis of TF-1 BCR/ABL, K562, and H7 BCR/ABL cells.	romidepsin	0-5	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-48
17610380-3	2007	FK228 potently induced apoptosis of TF-1 BCR/ABL, K562, and H7 BCR/ABL cells.	romidepsin	0-5	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
17376680-0	2007	Structural factors contributing to the Abl/Lyn dual inhibitory activity of 3-substituted benzamide derivatives.	3-substituted benzamide	75-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-42
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 Mesylate	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.	Oligonucleotides	3-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	173-180
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 Mesylate	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 Mesylate	78-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	173-180
17160016-5	2007	Restoration of CCL9 expression in 32D-BCR/ABL cells had no effect on the in vitro proliferation of these cells, but reduced their leukemogenic potential in vivo, possibly by recruitment of CD3-positive immune cells.	ccl9	15-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
17376680-1	2007	To investigate why 3-substituted benzamide derivatives show dual inhibition of Abl and Lyn protein tyrosine kinases, we determined their inhibitory activities against Abl and Lyn, carried out molecular modeling, and conducted a structure-activity relationship study with the aid of a newly determined X-ray structure of the Abl/Lyn dual inhibitor INNO-406 (formerly known as NS-187) bound to human Abl.	3-substituted benzamide	19-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-82
17376680-1	2007	To investigate why 3-substituted benzamide derivatives show dual inhibition of Abl and Lyn protein tyrosine kinases, we determined their inhibitory activities against Abl and Lyn, carried out molecular modeling, and conducted a structure-activity relationship study with the aid of a newly determined X-ray structure of the Abl/Lyn dual inhibitor INNO-406 (formerly known as NS-187) bound to human Abl.	3-substituted benzamide	19-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-170
17376680-1	2007	To investigate why 3-substituted benzamide derivatives show dual inhibition of Abl and Lyn protein tyrosine kinases, we determined their inhibitory activities against Abl and Lyn, carried out molecular modeling, and conducted a structure-activity relationship study with the aid of a newly determined X-ray structure of the Abl/Lyn dual inhibitor INNO-406 (formerly known as NS-187) bound to human Abl.	3-substituted benzamide	19-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-170
17376680-1	2007	To investigate why 3-substituted benzamide derivatives show dual inhibition of Abl and Lyn protein tyrosine kinases, we determined their inhibitory activities against Abl and Lyn, carried out molecular modeling, and conducted a structure-activity relationship study with the aid of a newly determined X-ray structure of the Abl/Lyn dual inhibitor INNO-406 (formerly known as NS-187) bound to human Abl.	3-substituted benzamide	19-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-170
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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
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 Mesylate	165-173	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
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 Mesylate	128-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-167
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 Mesylate	160-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	5-12
17374613-8	2007	In fact, three cytosolic glycoproteins, in the range 45-66 kDa, showed a 50-70% decrease of their sialic acid content upon Neu2 expression, supporting their possible role as modulators of the Bcr-Abl complex.	N-Acetylneuraminic Acid	98-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	192-199
17610380-10	2007	In conclusion, FK228 potently induces apoptosis of CML cells by acetylation and degradation of BCR/ABL protein.	romidepsin	15-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
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.	2,4-Dinitrophenol	55-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
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 Mesylate	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.	rottlerin	0-9	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 Mesylate	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 Mesylate	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.	rottlerin	33-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	279-286
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 Mesylate	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 Mesylate	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-112
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 Mesylate	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 Mesylate	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
17218385-8	2007	Notably, the dasatinib/PD184352 regimen was active against leukemic cells exhibiting various forms of imatinib mesylate resistance, including Bcr/Abl overexpression, Lyn activation, and several Bcr/Abl kinase domain mutations (eg, E255K, M351T), but not T315I.	Dasatinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
17218385-8	2007	Notably, the dasatinib/PD184352 regimen was active against leukemic cells exhibiting various forms of imatinib mesylate resistance, including Bcr/Abl overexpression, Lyn activation, and several Bcr/Abl kinase domain mutations (eg, E255K, M351T), but not T315I.	Dasatinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	194-201
17218385-8	2007	Notably, the dasatinib/PD184352 regimen was active against leukemic cells exhibiting various forms of imatinib mesylate resistance, including Bcr/Abl overexpression, Lyn activation, and several Bcr/Abl kinase domain mutations (eg, E255K, M351T), but not T315I.	2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
17218385-8	2007	Notably, the dasatinib/PD184352 regimen was active against leukemic cells exhibiting various forms of imatinib mesylate resistance, including Bcr/Abl overexpression, Lyn activation, and several Bcr/Abl kinase domain mutations (eg, E255K, M351T), but not T315I.	2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	194-201
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.	dasatanib	59-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
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.	rottlerin	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	219-227	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
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.	rottlerin	26-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-167
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).	phenylaminopyrimidine	4-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-124
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 Mesylate	35-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-124
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 Mesylate	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 Mesylate	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 Mesylate	105-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	224-231
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
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 Mesylate	102-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-130
20425353-4	2007	BCR/ABL may also stimulate generation of reactive oxygen species and enhance spontaneous DNA damage in tumor cells.	Reactive Oxygen Species	41-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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 Mesylate	201-209	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-22
17446929-7	2007	Thus, in response to treatment with cisplatin, but not other chemotherapeutic agents, TAp73 underwent c-Abl-dependent phosphorylation, which promoted dissociation of the DeltaNp63alpha/TAp73 protein complex, TAp73-dependent transcription of proapoptotic Bcl-2 family members, and apoptosis.	Cisplatin	36-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-107
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 Mesylate	183-191	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	146-153
17457302-0	2007	Second generation inhibitors of BCR-ABL for the treatment of imatinib-resistant chronic myeloid leukaemia.	Imatinib Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	211-218
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 Mesylate	19-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
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 Mesylate	38-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
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 Mesylate	19-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
17389688-4	2007	Expression of Bcr-Abl induces tyrosine phosphorylation of Abi1.	Tyrosine	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
17185463-3	2007	Dasatinib is a novel, oral, multitargeted kinase inhibitor of BCR-ABL and SRC family kinases.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
17185463-8	2007	Response rates were similar in patients with and without BCR-ABL mutations known to confer resistance to imatinib.	Imatinib Mesylate	105-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
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 Mesylate	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 Mesylate	138-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
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 Mesylate	120-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
17389688-8	2007	More importantly, disruption of the interaction between Bcr-Abl and Abi1 by mutations either in Bcr-Abl or Abi1 not only abolished tyrosine phosphorylation of Abi1 and membrane translocation of Abi1/WAVE2, but also inhibited Bcr-Abl-stimulated actin cytoskeleton remodeling, integrin clustering and cell adhesion to fibronectin.	Tyrosine	131-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
17389688-8	2007	More importantly, disruption of the interaction between Bcr-Abl and Abi1 by mutations either in Bcr-Abl or Abi1 not only abolished tyrosine phosphorylation of Abi1 and membrane translocation of Abi1/WAVE2, but also inhibited Bcr-Abl-stimulated actin cytoskeleton remodeling, integrin clustering and cell adhesion to fibronectin.	Tyrosine	131-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
17389688-8	2007	More importantly, disruption of the interaction between Bcr-Abl and Abi1 by mutations either in Bcr-Abl or Abi1 not only abolished tyrosine phosphorylation of Abi1 and membrane translocation of Abi1/WAVE2, but also inhibited Bcr-Abl-stimulated actin cytoskeleton remodeling, integrin clustering and cell adhesion to fibronectin.	Tyrosine	131-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
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 Mesylate	49-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-30
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 Mesylate	192-200	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
17043649-1	2007	Imatinib targets the Bcr-Abl oncogene that causes chronic myelogenous leukemia (CML) in humans.	Imatinib Mesylate	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 Mesylate	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 Mesylate	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
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.	PD 166326	26-34	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.	PD 166326	26-34	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 Mesylate	194-202	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	177-184
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.	PD 166326	206-214	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	177-184
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.	4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide	228-236	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 Mesylate	291-299	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
17407569-10	2007	We suggest that the experimental differences in binding energetics can be at least partially ascribed to the absence in the R21A Spc-SH3:P41 complex of several buried water molecules, which have been proposed previously to contribute largely to the highly negative enthalpy and entropy of binding in the Abl-SH3:P41 complex.	Water	167-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	304-307
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
17488685-0	2007	Characterization of ABL1 expression in adult T-cell acute lymphoblastic leukemia by oligonucleotide array analysis.	Oligonucleotides	84-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-24
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 Mesylate	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-177
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 Mesylate	9-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-177
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.	PBOX-6	63-90	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 Mesylate	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 Mesylate	59-76	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.	PBOX-6	152-159	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).	PBOX-6	15-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
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 Mesylate	27-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
17202400-5	2007	Potentiation of PBOX-6-induced apoptosis by STI-571 was specific to Bcr-Abl-positive leukemia cells with no cytoxic effects observed on normal peripheral blood cells.	PBOX-6	16-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
16916543-0	2007	Long-term remission in BCR/ABL-positive AML-M6 patient treated with Imatinib Mesylate.	Imatinib Mesylate	68-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-30
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 Mesylate	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 Mesylate	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
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 Mesylate	56-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-84
17431118-1	2007	Dasatinib (BMS-354825) is a novel, oral, potent, multi-targeted kinase inhibitor of Bcr-Abl and Src family kinases (SFK) and is a promising cancer therapeutic agent.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
17431118-2	2007	Preclinical data indicate that dasatinib is 325-fold more potent than imatinib against cells expressing wild-type Bcr-Abl, and that dasatinib is active against 18 of 19 Bcr-Abl mutations known to cause imatinib resistance.	Dasatinib	31-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
17431118-2	2007	Preclinical data indicate that dasatinib is 325-fold more potent than imatinib against cells expressing wild-type Bcr-Abl, and that dasatinib is active against 18 of 19 Bcr-Abl mutations known to cause imatinib resistance.	Dasatinib	132-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	169-176
17431118-10	2007	Our findings indicate that inhibition of Stat5 signaling downstream of Bcr-Abl/SFKs contributes to the action of dasatinib, and, conversely, that increasing cell density up-regulates Stat5 activation and confers resistance to dasatinib.	Dasatinib	113-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
17431118-11	2007	Moreover, the level of phosphorylated Stat5 in CML cells represents a mechanistically relevant biomarker for monitoring inhibition of Bcr-Abl signaling by dasatinib in CML patients using convenient immunocytochemical assays.	Dasatinib	155-164	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
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 Mesylate	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 Mesylate	145-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	241-248
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 Mesylate	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 Mesylate	116-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	168-173
17211892-4	2007	We report that the ARG core domain is homologous to the corresponding ABL region, therefore suggesting that ARG catalytic activity is likely regulated by the same SH3-SH2 clamp described for ABL.	Arginine	19-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-73
17211892-4	2007	We report that the ARG core domain is homologous to the corresponding ABL region, therefore suggesting that ARG catalytic activity is likely regulated by the same SH3-SH2 clamp described for ABL.	Arginine	19-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	191-194
17211892-4	2007	We report that the ARG core domain is homologous to the corresponding ABL region, therefore suggesting that ARG catalytic activity is likely regulated by the same SH3-SH2 clamp described for ABL.	Arginine	108-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-73
17211892-4	2007	We report that the ARG core domain is homologous to the corresponding ABL region, therefore suggesting that ARG catalytic activity is likely regulated by the same SH3-SH2 clamp described for ABL.	Arginine	108-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	191-194
17211892-9	2007	Finally, our analyses show that the C-terminal actin-binding domain of ARG displays a four-helix bundle structure similar to the one reported for the corresponding ABL region.	Arginine	71-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	164-167
17493320-0	2007	[Construction of 293pT2-P210 cell line enables expression of bcr/abl to be regulated by Tet-off inducing-expression-system].	tetramethylenedisulfotetramine	88-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
17493320-4	2007	The purpose of this study was to construct a cell line model that bcr/abl expression can be regulated by Tet-off inducing-expression-system.	tetramethylenedisulfotetramine	105-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
17493320-8	2007	The results showed that individual subclones expressing bcr/abl after withdrawing doxycycline were 293pT2-P210 cell line.	Doxycycline	82-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
17493320-9	2007	In conclusion, selected 293pT2-P210 cells are cells that bcr/abl expression can be regulated by Tet-off inducing-expression-system.	tetramethylenedisulfotetramine	96-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
17138817-2	2007	Dasatinib, a novel, highly potent, oral, multitargeted kinase inhibitor of BCR-ABL and SRC family kinases, induced cytogenetic responses in a phase 1 study in imatinib-resistant or -intolerant CML and was well tolerated.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
17138817-6	2007	Importantly, comparable responses were achieved by patients carrying BCR-ABL mutations conferring imatinib resistance.	Imatinib Mesylate	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
17138817-7	2007	Dasatinib also induced molecular responses, reducing BCR-ABL/ABL transcript ratios from 66% at baseline to 2.6% at 9 months.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
17138817-7	2007	Dasatinib also induced molecular responses, reducing BCR-ABL/ABL transcript ratios from 66% at baseline to 2.6% at 9 months.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-60
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 Mesylate	39-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	169-176
17360569-1	2007	The kinase inhibitor imatinib mesylate targeting the oncoprotein Bcr-Abl has revolutionized the treatment of chronic myeloid leukemia (CML).	Imatinib Mesylate	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 Mesylate	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 Mesylate	177-185	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
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 Mesylate	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-146
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 Mesylate	49-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	200-203
17318191-0	2007	Bcr-Abl stabilizes beta-catenin in chronic myeloid leukemia through its tyrosine phosphorylation.	Tyrosine	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
17318191-1	2007	Self-renewal of Bcr-Abl(+) chronic myeloid leukemia (CML) cells is sustained by a nuclear activated serine/threonine-(S/T) unphosphorylated beta-catenin.	Serine	100-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
17318191-1	2007	Self-renewal of Bcr-Abl(+) chronic myeloid leukemia (CML) cells is sustained by a nuclear activated serine/threonine-(S/T) unphosphorylated beta-catenin.	Threonine	107-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
17306540-5	2007	Even though cortactin can be tyrosine phosphorylated by Src-family kinases in vitro [8], we show that Abl and Arg are more adept at binding and phosphorylating cortactin.	Tyrosine	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-105
17306540-8	2007	We provide evidence that Abl/Arg-mediated phosphorylation of cortactin is required for this PDGF-induced dorsal-wave response.	Arginine	29-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-28
17167796-4	2007	While Imatinib binding is highly sensitive to the activation state of the enzyme, the computed binding profile of Dasatinib is remarkably tolerant to the conformational state of ABL.	Dasatinib	114-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-181
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 Mesylate	130-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
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 Mesylate	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.	nilotinib	23-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
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.	nilotinib	23-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
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.	nilotinib	23-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
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.	nilotinib	34-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
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.	nilotinib	34-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
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.	nilotinib	34-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
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 Mesylate	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 Mesylate	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 Mesylate	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	194-201
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.	nilotinib	80-89	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.	nilotinib	80-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	194-201
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 Mesylate	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 Mesylate	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	220-227
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.	nilotinib	119-128	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.	nilotinib	102-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
17341836-5	2007	GK03225 possesses an Iressa-like quinazoline ring structure, and its chemical analog, 11N-078, suppresses c-Abl human tyrosine kinase activity.	gk03225	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-111
17341836-5	2007	GK03225 possesses an Iressa-like quinazoline ring structure, and its chemical analog, 11N-078, suppresses c-Abl human tyrosine kinase activity.	N-(2,4-dichlorophenyl)-6,7-dimethoxyquinazolin-4-amine	86-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-111
17295370-0	2007	Inhibition of Bcr-Abl phosphorylation and induction of apoptosis by pyrazolo[3,4-d]pyrimidines in human leukemia cells.	pyrazolo(3,4-d)pyrimidine	68-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
17295370-1	2007	A series of pyrazolo[3,4-d]pyrimidines, previously found to be Src inhibitors, was tested for their ability to inhibit proliferation of three Bcr-Abl-positive human leukemia cell lines (K-562, KU-812, and MEG-01), on the basis of the experimental evidence that various Src inhibitors are also active against Bcr-Abl kinase (the so called dual Src/Abl inhibitors).	pyrazolo(3,4-d)pyrimidine	12-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
17295370-1	2007	A series of pyrazolo[3,4-d]pyrimidines, previously found to be Src inhibitors, was tested for their ability to inhibit proliferation of three Bcr-Abl-positive human leukemia cell lines (K-562, KU-812, and MEG-01), on the basis of the experimental evidence that various Src inhibitors are also active against Bcr-Abl kinase (the so called dual Src/Abl inhibitors).	pyrazolo(3,4-d)pyrimidine	12-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	308-315
17295370-1	2007	A series of pyrazolo[3,4-d]pyrimidines, previously found to be Src inhibitors, was tested for their ability to inhibit proliferation of three Bcr-Abl-positive human leukemia cell lines (K-562, KU-812, and MEG-01), on the basis of the experimental evidence that various Src inhibitors are also active against Bcr-Abl kinase (the so called dual Src/Abl inhibitors).	pyrazolo(3,4-d)pyrimidine	12-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	146-149
17295370-2	2007	They reduce Bcr-Abl tyrosine phosphorylation and promote apoptosis of the Bcr-Abl-expressing cells.	Tyrosine	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
17382013-4	2007	The Bcr-Abl tyrosine kinase inhibitor imatinib represented a major advance over conventional CML therapy.	Imatinib Mesylate	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
17382017-4	2007	One of the more common mutations results from the substitution of isoleucine for threonine at Abl amino acid position 351, known as the T315I mutation.	Isoleucine	66-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-97
17382017-4	2007	One of the more common mutations results from the substitution of isoleucine for threonine at Abl amino acid position 351, known as the T315I mutation.	Threonine	81-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-97
17382019-1	2007	Imatinib and other Abl tyrosine kinase inhibitors (TKIs), such as dasatinib and nilotinib, have significantly improved the outcome of patients with chronic myeloid leukemia.	Dasatinib	66-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-22
17382019-1	2007	Imatinib and other Abl tyrosine kinase inhibitors (TKIs), such as dasatinib and nilotinib, have significantly improved the outcome of patients with chronic myeloid leukemia.	nilotinib	80-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-22
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
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.	Dasatinib	156-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
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.	nilotinib	169-178	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
17338645-0	2007	Imatinib mesylate, a selective inhibitor of BCR-ABL, in chronic myeloid leukemia.	Imatinib Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
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 Mesylate	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
17355221-5	2007	Initial data on the second-generation BCR-ABL inhibitors, dasatinib and nilotinib, indicate a potentially greater efficacy than imatinib, but the improvement is likely to be modest.	Dasatinib	58-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
17355221-5	2007	Initial data on the second-generation BCR-ABL inhibitors, dasatinib and nilotinib, indicate a potentially greater efficacy than imatinib, but the improvement is likely to be modest.	nilotinib	72-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
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 Mesylate	53-70	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 Mesylate	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 Mesylate	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 Mesylate	53-61	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).	Dasatinib	275-284	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
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 Mesylate	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	168-175
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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
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 Mesylate	151-159	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
17252009-0	2007	Mutations of the BCR-ABL-kinase domain occur in a minority of patients with stable complete cytogenetic response to imatinib.	Imatinib Mesylate	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 Mesylate	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
17329198-0	2007	Second-line treatment with dasatinib in patients resistant to imatinib can select novel inhibitor-specific BCR-ABL mutants in Ph+ ALL.	Dasatinib	27-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
17252018-5	2007	We compared two such compounds with different modes of action, adaphostin and 17-allylamino-17-demethoxygeldanamycin (17-AAG), for their cytotoxic effect and ability to induce the downregulation of cellular proteins in a murine haemopoietic cell line transformed with human p210(Bcr-Abl), and two subclones resistant to imatinib owing to an Abl-kinase domain mutation (E255K) or amplification of the BCR-ABL gene, respectively.	tanespimycin	78-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	279-286
17252018-5	2007	We compared two such compounds with different modes of action, adaphostin and 17-allylamino-17-demethoxygeldanamycin (17-AAG), for their cytotoxic effect and ability to induce the downregulation of cellular proteins in a murine haemopoietic cell line transformed with human p210(Bcr-Abl), and two subclones resistant to imatinib owing to an Abl-kinase domain mutation (E255K) or amplification of the BCR-ABL gene, respectively.	tanespimycin	78-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	283-286
17252018-5	2007	We compared two such compounds with different modes of action, adaphostin and 17-allylamino-17-demethoxygeldanamycin (17-AAG), for their cytotoxic effect and ability to induce the downregulation of cellular proteins in a murine haemopoietic cell line transformed with human p210(Bcr-Abl), and two subclones resistant to imatinib owing to an Abl-kinase domain mutation (E255K) or amplification of the BCR-ABL gene, respectively.	tanespimycin	78-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	400-407
17252018-5	2007	We compared two such compounds with different modes of action, adaphostin and 17-allylamino-17-demethoxygeldanamycin (17-AAG), for their cytotoxic effect and ability to induce the downregulation of cellular proteins in a murine haemopoietic cell line transformed with human p210(Bcr-Abl), and two subclones resistant to imatinib owing to an Abl-kinase domain mutation (E255K) or amplification of the BCR-ABL gene, respectively.	tanespimycin	118-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	279-286
17252018-5	2007	We compared two such compounds with different modes of action, adaphostin and 17-allylamino-17-demethoxygeldanamycin (17-AAG), for their cytotoxic effect and ability to induce the downregulation of cellular proteins in a murine haemopoietic cell line transformed with human p210(Bcr-Abl), and two subclones resistant to imatinib owing to an Abl-kinase domain mutation (E255K) or amplification of the BCR-ABL gene, respectively.	tanespimycin	118-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	283-286
17252018-5	2007	We compared two such compounds with different modes of action, adaphostin and 17-allylamino-17-demethoxygeldanamycin (17-AAG), for their cytotoxic effect and ability to induce the downregulation of cellular proteins in a murine haemopoietic cell line transformed with human p210(Bcr-Abl), and two subclones resistant to imatinib owing to an Abl-kinase domain mutation (E255K) or amplification of the BCR-ABL gene, respectively.	tanespimycin	118-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	400-407
17252018-6	2007	We found that, whereas 17-AAG selectively killed Bcr-Abl-positive cells and inhibited proteins dependent on heat-shock protein 90 for their stability (p210(Bcr-Abl) and Akt), adaphostin induced the downregulation of multiple cell-signalling proteins (p210(Bcr-Abl), Akt, Bcr, Abl and STAT5a) and was cytotoxic to both Bcr-Abl-positive and -negative cells.	tanespimycin	23-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
17252018-6	2007	We found that, whereas 17-AAG selectively killed Bcr-Abl-positive cells and inhibited proteins dependent on heat-shock protein 90 for their stability (p210(Bcr-Abl) and Akt), adaphostin induced the downregulation of multiple cell-signalling proteins (p210(Bcr-Abl), Akt, Bcr, Abl and STAT5a) and was cytotoxic to both Bcr-Abl-positive and -negative cells.	tanespimycin	23-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
17252018-6	2007	We found that, whereas 17-AAG selectively killed Bcr-Abl-positive cells and inhibited proteins dependent on heat-shock protein 90 for their stability (p210(Bcr-Abl) and Akt), adaphostin induced the downregulation of multiple cell-signalling proteins (p210(Bcr-Abl), Akt, Bcr, Abl and STAT5a) and was cytotoxic to both Bcr-Abl-positive and -negative cells.	tanespimycin	23-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
17252018-6	2007	We found that, whereas 17-AAG selectively killed Bcr-Abl-positive cells and inhibited proteins dependent on heat-shock protein 90 for their stability (p210(Bcr-Abl) and Akt), adaphostin induced the downregulation of multiple cell-signalling proteins (p210(Bcr-Abl), Akt, Bcr, Abl and STAT5a) and was cytotoxic to both Bcr-Abl-positive and -negative cells.	tanespimycin	23-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-163
17252018-6	2007	We found that, whereas 17-AAG selectively killed Bcr-Abl-positive cells and inhibited proteins dependent on heat-shock protein 90 for their stability (p210(Bcr-Abl) and Akt), adaphostin induced the downregulation of multiple cell-signalling proteins (p210(Bcr-Abl), Akt, Bcr, Abl and STAT5a) and was cytotoxic to both Bcr-Abl-positive and -negative cells.	tanespimycin	23-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-163
17355866-0	2007	c-Src binds to the cancer drug imatinib with an inactive Abl/c-Kit conformation and a distributed thermodynamic penalty.	Imatinib Mesylate	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-60
17355866-1	2007	The cancer drug imatinib inhibits the tyrosine kinases c-Abl, c-Kit, and the PDGF receptor.	Imatinib Mesylate	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-60
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 Mesylate	0-8	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 Mesylate	109-117	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 Mesylate	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-103
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 Mesylate	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 Mesylate	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 Mesylate	54-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
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 Mesylate	123-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
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.	Sirolimus	145-154	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
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 Mesylate	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
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 Mesylate	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
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 Mesylate	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 Mesylate	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 Mesylate	81-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
17305499-6	2007	Imatinib induces high response rates in patients associated with constitutive activation of ABL, PDGFRalpha, PDGFRbeta and some KIT mutants.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-95
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 Mesylate	198-206	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
17301549-4	2007	Quite recently we successfully developed the novel Bcr-Abl/Lyn dual inhibitor INNO-406 (NS-187) which shows unique profile to overcome this resistance.	bafetinib	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
17301549-4	2007	Quite recently we successfully developed the novel Bcr-Abl/Lyn dual inhibitor INNO-406 (NS-187) which shows unique profile to overcome this resistance.	bafetinib	88-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
17364993-3	2007	Imatinib blocks proliferation and induces apoptosis of BCR-ABL-expression in CML.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
17132628-7	2007	Inhibition of Bcr-Abl by the chemical inhibitor STI571 resulted in activation of FOXO3a and down-regulation of Id1 expression.	Imatinib Mesylate	48-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
17254966-3	2007	A conserved tyrosine residue (Y88) in the Cdk-binding domain of p27 can be phosphorylated by the Src-family kinase Lyn and the oncogene product BCR-ABL.	Tyrosine	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
16954505-8	2007	Tetracycline-inducible expression of KLF4 in B-cell progenitors of transgenic mice blocks transformation by BCR-ABL and depletes leukemic pre-B cells in vivo.	Tetracycline	0-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
16990603-0	2007	MK-0457, a novel kinase inhibitor, is active in patients with chronic myeloid leukemia or acute lymphocytic leukemia with the T315I BCR-ABL mutation.	VX680	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
16990603-2	2007	The T315I BCR-ABL mutation mediates resistance to imatinib, nilotinib, and dasatinib.	Imatinib Mesylate	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
16990603-2	2007	The T315I BCR-ABL mutation mediates resistance to imatinib, nilotinib, and dasatinib.	nilotinib	60-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
16990603-2	2007	The T315I BCR-ABL mutation mediates resistance to imatinib, nilotinib, and dasatinib.	Dasatinib	75-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
17003374-1	2007	SHP-2 phosphatase forms a stable protein complex with and is heavily tyrosine-phosphorylated by the oncogenic tyrosine kinase Bcr-Abl.	Tyrosine	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
17112510-3	2007	The data suggest that c-Abl binds to tyrosine phosphorylated Shb via a concerted effort involving both the c-Abl SH3 and SH2 domains.	Tyrosine	37-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-27
17126298-0	2007	Tyrosine 311 is phosphorylated by c-Abl and promotes the apoptotic effect of PKCdelta in glioma cells.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-39
17126298-2	2007	We found that c-Abl phosphorylated PKCdelta on tyrosine 311 in response to H2O2 and that this phosphorylation contributed to the apoptotic effect of H2O2.	Tyrosine	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
17126298-2	2007	We found that c-Abl phosphorylated PKCdelta on tyrosine 311 in response to H2O2 and that this phosphorylation contributed to the apoptotic effect of H2O2.	Hydrogen Peroxide	75-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
17126298-2	2007	We found that c-Abl phosphorylated PKCdelta on tyrosine 311 in response to H2O2 and that this phosphorylation contributed to the apoptotic effect of H2O2.	Hydrogen Peroxide	149-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
17126298-6	2007	These results suggest an important role of tyrosine 311 in the apoptotic function of PKCdelta and implicate c-Abl as the kinase that phosphorylates this tyrosine.	Tyrosine	153-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-113
17112510-3	2007	The data suggest that c-Abl binds to tyrosine phosphorylated Shb via a concerted effort involving both the c-Abl SH3 and SH2 domains.	Tyrosine	37-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-112
17112510-4	2007	The biological significance of the Shb/c-Abl interaction was presently tested in overexpression experiments and was found to promote hydrogen peroxide-induced cell death.	Hydrogen Peroxide	133-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-44
17112510-5	2007	We also show by Shb knockdown experiments that Shb regulates c-Abl activity and modulates cell death in response to the genotoxic agent cisplatin and the endoplasmic reticulum stress-inducer tunicamycin.	Cisplatin	136-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-66
17112510-5	2007	We also show by Shb knockdown experiments that Shb regulates c-Abl activity and modulates cell death in response to the genotoxic agent cisplatin and the endoplasmic reticulum stress-inducer tunicamycin.	Tunicamycin	191-202	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-66
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 Mesylate	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
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 Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
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 Mesylate	8-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
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 Mesylate	67-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
17957275-3	2007	We investigated the potential benefit of using STI571 to down-regulate Bcr-Abl activity for the enhancement of doxorubicin anti-proliferative action in K562 cell line derived from blast crisis of CML.	Doxorubicin	111-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
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 Mesylate	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 Mesylate	41-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
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 Mesylate	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 Mesylate	49-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
17404031-7	2007	Erufosine caused decreases of pAkt and CML fusion protein p210 (BCR-ABL) protein expression, but induced the Rb protein expression in K-562 cells.	erucylphospho-N,N,N-trimethylpropylammonium	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
16960151-0	2007	Durable responses to imatinib in patients with PDGFRB fusion gene-positive and BCR-ABL-negative chronic myeloproliferative disorders.	Imatinib Mesylate	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
17184589-0	2007	Curcumin synergistically augments bcr/abl phosphorothioate antisense oligonucleotides to inhibit growth of chronic myelogenous leukemia cells.	Curcumin	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
17184589-0	2007	Curcumin synergistically augments bcr/abl phosphorothioate antisense oligonucleotides to inhibit growth of chronic myelogenous leukemia cells.	Parathion	42-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
17184589-1	2007	AIM: To investigate the growth inhibition effect of the combination of bcr/abl phosphorothioate antisense oligonucleotides (PS-ASODN) and curcumin (cur), and the possible mechanisms of cur on the chronic myelogenous leukemia cell line K562.	Parathion	79-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
17184589-1	2007	AIM: To investigate the growth inhibition effect of the combination of bcr/abl phosphorothioate antisense oligonucleotides (PS-ASODN) and curcumin (cur), and the possible mechanisms of cur on the chronic myelogenous leukemia cell line K562.	ps-asodn	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
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 Mesylate	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 Mesylate	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
17394086-5	2007	Inhibition of Src activity using the Src/Abl inhibitor AZD0530 reduced FAK activity, suppressed cell spreading on matrix-coated surfaces and significantly inhibited cell migration.	saracatinib	55-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-44
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 Mesylate	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	239-244
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 Mesylate	147-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-173
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	157-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
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 Mesylate	102-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-167
17292738-6	2007	These include: dasatinib, a potent dual Bcr-Abl and Src inhibitor; nilotinib, a selective, potent Bcr-Abl inhibitor; bosutinib (SKI-606) and INNO-406 (NS-187), which are both Src-Abl inhibitors; and others.	nilotinib	67-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
17179059-4	2006	Imatinib, a selective inhibitor of BCR-ABL, represents a major success in the era of target-directed cancer chemotherapy.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
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 Mesylate	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 Mesylate	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 Mesylate	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185
17164333-0	2006	Phosphorylation of the ATP-binding loop directs oncogenicity of drug-resistant BCR-ABL mutants.	Adenosine Triphosphate	23-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
17164333-6	2006	Through global phosphoproteome analysis, we identified a unique phosphosubstrate signature associated with each drug-resistant allele, including a shift in phosphorylation of two tyrosines (Tyr253 and Tyr257) in the ATP binding loop (P-loop) of BCR-ABL when Thr315 is Ile or Ala.	phosphosubstrate	64-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	245-252
17164333-6	2006	Through global phosphoproteome analysis, we identified a unique phosphosubstrate signature associated with each drug-resistant allele, including a shift in phosphorylation of two tyrosines (Tyr253 and Tyr257) in the ATP binding loop (P-loop) of BCR-ABL when Thr315 is Ile or Ala.	Tyrosine	179-188	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	245-252
17164333-6	2006	Through global phosphoproteome analysis, we identified a unique phosphosubstrate signature associated with each drug-resistant allele, including a shift in phosphorylation of two tyrosines (Tyr253 and Tyr257) in the ATP binding loop (P-loop) of BCR-ABL when Thr315 is Ile or Ala.	Adenosine Triphosphate	216-219	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	245-252
17164333-6	2006	Through global phosphoproteome analysis, we identified a unique phosphosubstrate signature associated with each drug-resistant allele, including a shift in phosphorylation of two tyrosines (Tyr253 and Tyr257) in the ATP binding loop (P-loop) of BCR-ABL when Thr315 is Ile or Ala.	Isoleucine	268-271	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	245-252
17164333-6	2006	Through global phosphoproteome analysis, we identified a unique phosphosubstrate signature associated with each drug-resistant allele, including a shift in phosphorylation of two tyrosines (Tyr253 and Tyr257) in the ATP binding loop (P-loop) of BCR-ABL when Thr315 is Ile or Ala.	Alanine	275-278	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	245-252
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 Mesylate	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
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 Mesylate	2-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-57
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 Mesylate	2-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
21901078-3	2007	Imatinib mesylate inhibits the activation of PDGF receptor as well as c-Abl, Bcr-Abl and c-Kit tyrosine kinases.	Imatinib Mesylate	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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
17315048-1	2007	Dasatinib is an orally bioavailable potent inhibitor of multiple tyrosine kinases, including ABL and SRC.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-96
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.	Dasatinib	31-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
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.	Dasatinib	31-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-173
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 Mesylate	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
18024654-5	2007	For patients treated with imatinib, a rising level of BCR-ABL is a trigger for kinase domain mutation analysis.	Imatinib Mesylate	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
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 Mesylate	142-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-74
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 Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-169
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 Mesylate	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-168
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 Mesylate	112-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
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.	Hydrogen Peroxide	71-88	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 Mesylate	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 Mesylate	129-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-145
17006667-0	2006	Not all imatinib resistance in CML are BCR-ABL kinase domain mutations.	Imatinib Mesylate	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 Mesylate	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 Mesylate	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
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 Mesylate	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
17106015-13	2006	The most common mechanism for imatinib resistance is the presence of a mutated BCR-ABL kinase.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
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 Mesylate	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
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 Mesylate	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
17106016-5	2006	Nilotinib inhibits BCR-ABL at 20-50 times more potency than imatinib.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
17145844-3	2006	To improve treatment options, dasatinib (BMS-354825) was developed as a novel, oral, multi-targeted kinase inhibitor of BCR-ABL and SRC family kinases.	Dasatinib	30-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
17145844-7	2006	RESULTS: Following a single oral administration of dasatinib at a preclinical efficacious dose of 1.25 or 2.5 mg/kg, tumoral phospho-BCR-ABL/phospho-CrkL were maximally inhibited at approximately 3 hours and recovered to basal levels by 24 hours.	Dasatinib	51-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
17145844-9	2006	Pharmacokinetic/biomarker modeling predicted that the plasma concentration of dasatinib required to inhibit 90% of phospho-BCR-ABL in vivo was 10.9 ng/mL in mice and 14.6 ng/mL in humans, which is within the range of concentrations achieved in CML patients who responded to dasatinib treatment in the clinic.	Dasatinib	78-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-130
17145844-10	2006	CONCLUSIONS: Phospho-BCR-ABL/phospho-CrkL are likely to be useful clinical biomarkers for the assessment of BCR-ABL kinase inhibition by dasatinib.	Dasatinib	137-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
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 Mesylate	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
17085043-4	2006	A mechanism-based bisubstrate analog strategy has given X-ray crystallographic insights into how several topical PTKs, including the insulin receptor, Abl and epidermal growth factor receptor, interact with tyrosine-containing peptide substrates.	Tyrosine	207-215	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-154
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 Mesylate	20-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
17155893-0	2006	Targeting ABL and SRC kinases in chronic myeloid leukemia: experience with dasatinib.	Dasatinib	75-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-13
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 Mesylate	145-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-24
17155893-2	2006	The development of agents with dual inhibitory activity against SRC and ABL kinases is one approach to overcome imatinib resistance.	Imatinib Mesylate	112-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-75
17155893-3	2006	One such agent, dasatinib (formerly BMS-354825), is approximately 300-fold more potent against BCR-ABL than imatinib, and is active against all tested ABL mutant isoforms, except for T315I.	Dasatinib	16-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
17155893-3	2006	One such agent, dasatinib (formerly BMS-354825), is approximately 300-fold more potent against BCR-ABL than imatinib, and is active against all tested ABL mutant isoforms, except for T315I.	Dasatinib	16-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-102
17155893-5	2006	Studies exploring the efficacy of dasatinib as front-line therapy in patients with BCR-ABL-expressing hematologic malignancies are underway.	Dasatinib	34-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	146-154	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	205-212
17145844-10	2006	CONCLUSIONS: Phospho-BCR-ABL/phospho-CrkL are likely to be useful clinical biomarkers for the assessment of BCR-ABL kinase inhibition by dasatinib.	Dasatinib	137-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
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 Mesylate	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.	fludarabine	204-211	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-28
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 Mesylate	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 Mesylate	145-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-65
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 Mesylate	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 Mesylate	129-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	270-274
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 Mesylate	160-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
17108134-5	2006	In this study, flavopiridol, an inhibitor of transcription, homoharringtonine (HHT), a protein synthesis inhibitor, and imatinib were used singly and in combination against the Bcr-Abl-positive human CML cell line K562.	alvocidib	15-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	177-184
17108134-6	2006	Flavopiridol alone inhibited phosphorylation of the RNA polymerase II COOH-terminal domain, specifically reduced RNA polymerase II-directed mRNA synthesis, and decreased the Bcr-Abl transcript levels.	alvocidib	0-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-181
17108134-8	2006	Imatinib directly inhibited the kinase activity of Bcr-Abl.	Imatinib Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
17121903-8	2006	Arsenic trioxide also reduced the phosphorylation of BCR/ABL and FLT3 with corresponding decreased STAT5 phosphorylation.	Arsenic Trioxide	0-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
17064066-2	2006	We report here a novel subseries of C-5-substituted anilinoquinazolines that display high affinity and specificity for the tyrosine kinase domain of the c-Src and Abl enzymes.	c-5-substituted anilinoquinazolines	36-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-166
17064066-4	2006	N-(5-Chloro-1,3-benzodioxol-4-yl)-7-[2-(4-methylpiperazin-1-yl)ethoxy]-5-(tetrahydro-2H-pyran-4-yloxy)quinazolin-4-amine (AZD0530) inhibits c-Src and Abl enzymes at low nanomolar concentrations and is highly selective over a range of kinases.	saracatinib	122-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-153
17085669-3	2006	EXPERIMENTAL DESIGN: In this study, we investigated the effects of CT32228, a specific LPAAT-beta inhibitor, on BCR-ABL-transformed cell lines and primary cells from patients with chronic myelogenous leukemia.	CT-32228	67-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
17085669-6	2006	Importantly, CT32228 was highly active in cell lines resistant to the Bcr-Abl kinase inhibitor imatinib.	CT-32228	13-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
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 Mesylate	197-205	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	222-225
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 Mesylate	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 Mesylate	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
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 Mesylate	6-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-112
16546254-0	2006	In vivo antiproliferative effect of NS-187, a dual Bcr-Abl/Lyn tyrosine kinase inhibitor, on leukemic cells harbouring Abl kinase domain mutations.	bafetinib	36-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
16546254-0	2006	In vivo antiproliferative effect of NS-187, a dual Bcr-Abl/Lyn tyrosine kinase inhibitor, on leukemic cells harbouring Abl kinase domain mutations.	bafetinib	36-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-58
16546254-1	2006	Advanced-phase chronic myeloid leukemia patients treated with imatinib often relapse due to point mutations in the Abl kinase domain.	Imatinib Mesylate	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-118
16546254-3	2006	NS-187 inhibited both Tyr393-phosphorylated and Tyr393-unphosphorylated Abl, resulting in significant in vitro growth inhibition of cells expressing six of seven mutated Bcr-Abl kinases, though not T315I.	bafetinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-75
16546254-3	2006	NS-187 inhibited both Tyr393-phosphorylated and Tyr393-unphosphorylated Abl, resulting in significant in vitro growth inhibition of cells expressing six of seven mutated Bcr-Abl kinases, though not T315I.	bafetinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-177
17008892-0	2006	A novel Bcr-Abl splice isoform is associated with the L248V mutation in CML patients with acquired resistance to imatinib.	Imatinib Mesylate	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-15
17146202-0	2006	Dose modification of imatinib by monitoring the level of BCR-ABL transcript in chronic myelogenous leukemia.	Imatinib Mesylate	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 Mesylate	10-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
17114651-0	2006	Presence or the emergence of a F317L BCR-ABL mutation may be associated with resistance to dasatinib in Philadelphia chromosome-positive leukemia.	Dasatinib	91-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
17121928-0	2006	Activation of mammalian target of rapamycin and the p70 S6 kinase by arsenic trioxide in BCR-ABL-expressing cells.	Arsenic Trioxide	69-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
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 Mesylate	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 Mesylate	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 Mesylate	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-30
18221045-4	2006	To override resistance, several second generation ATP competitive Abl kinase inhibitors such as dasatinib, nilotinib and INNO-406 have been developed.	Adenosine Triphosphate	50-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-69
18221045-4	2006	To override resistance, several second generation ATP competitive Abl kinase inhibitors such as dasatinib, nilotinib and INNO-406 have been developed.	Dasatinib	96-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-69
18221045-4	2006	To override resistance, several second generation ATP competitive Abl kinase inhibitors such as dasatinib, nilotinib and INNO-406 have been developed.	nilotinib	107-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-69
18221045-4	2006	To override resistance, several second generation ATP competitive Abl kinase inhibitors such as dasatinib, nilotinib and INNO-406 have been developed.	bafetinib	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-69
17294703-2	2006	Imatinib (STI571) is a highly selective inhibitor of BCR/ABL oncogenic tyrosine kinase used in leukemia treatment.	Imatinib Mesylate	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 Mesylate	10-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
16943190-6	2006	Moreover, we show that activated Abl phosphorylates the EGFR primarily on tyrosine 1173, and that mutation of this site to phenylalanine restores ligand-dependent endocytosis of the EGFR in the presence of activated Abl.	Tyrosine	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-36
16943190-6	2006	Moreover, we show that activated Abl phosphorylates the EGFR primarily on tyrosine 1173, and that mutation of this site to phenylalanine restores ligand-dependent endocytosis of the EGFR in the presence of activated Abl.	Phenylalanine	123-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	216-219
16702947-0	2006	c-Abl phosphorylates Hdm2 at tyrosine 276 in response to DNA damage and regulates interaction with ARF.	Tyrosine	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
16702947-3	2006	As part of this mechanism ATM itself, and the ATM-activated protein tyrosine kinase, c-Abl, inhibit Hdm2 function through phosphorylation of serine 395 and tyrosine 394 (Y394), respectively.	Serine	141-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-90
16702947-3	2006	As part of this mechanism ATM itself, and the ATM-activated protein tyrosine kinase, c-Abl, inhibit Hdm2 function through phosphorylation of serine 395 and tyrosine 394 (Y394), respectively.	Tyrosine	68-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-90
16702947-4	2006	In the present study, we have identified a novel target of c-Abl in the Hdm2 protein, tyrosine 276 (Y276).	Tyrosine	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-64
16702947-4	2006	In the present study, we have identified a novel target of c-Abl in the Hdm2 protein, tyrosine 276 (Y276).	y276	100-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-64
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
16702947-5	2006	We show that c-Abl phosphorylates this residue in vitro and confirm that Y394 is a target of c-Abl.	y394	73-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-18
16702947-5	2006	We show that c-Abl phosphorylates this residue in vitro and confirm that Y394 is a target of c-Abl.	y394	73-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-98
16702947-6	2006	We also show that Y276 is phosphorylated in a c-Abl-dependent manner in cultured cells and provide evidence that Y276 is phosphorylated in response to DNA damage coincident with the activation of c-Abl.	y276	18-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-51
16702947-6	2006	We also show that Y276 is phosphorylated in a c-Abl-dependent manner in cultured cells and provide evidence that Y276 is phosphorylated in response to DNA damage coincident with the activation of c-Abl.	y276	18-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	196-201
16702947-6	2006	We also show that Y276 is phosphorylated in a c-Abl-dependent manner in cultured cells and provide evidence that Y276 is phosphorylated in response to DNA damage coincident with the activation of c-Abl.	y276	113-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-51
16702947-6	2006	We also show that Y276 is phosphorylated in a c-Abl-dependent manner in cultured cells and provide evidence that Y276 is phosphorylated in response to DNA damage coincident with the activation of c-Abl.	y276	113-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	196-201
16702947-8	2006	These data establish Y276 as a physiological target of c-Abl that contributes functionally to the induction of p53.	y276	21-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-60
16772610-1	2006	BMS-354825 (dasatinib) and AMN107 (nilotinib) are potent alternate Abl inhibitors with activity against many imatinib mesylate-resistant BCR-ABL kinase domain (KD) mutants, except T315I.	Dasatinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-70
16772610-1	2006	BMS-354825 (dasatinib) and AMN107 (nilotinib) are potent alternate Abl inhibitors with activity against many imatinib mesylate-resistant BCR-ABL kinase domain (KD) mutants, except T315I.	Dasatinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-144
16772610-1	2006	BMS-354825 (dasatinib) and AMN107 (nilotinib) are potent alternate Abl inhibitors with activity against many imatinib mesylate-resistant BCR-ABL kinase domain (KD) mutants, except T315I.	nilotinib	27-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-70
16772610-1	2006	BMS-354825 (dasatinib) and AMN107 (nilotinib) are potent alternate Abl inhibitors with activity against many imatinib mesylate-resistant BCR-ABL kinase domain (KD) mutants, except T315I.	nilotinib	27-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-144
16772610-1	2006	BMS-354825 (dasatinib) and AMN107 (nilotinib) are potent alternate Abl inhibitors with activity against many imatinib mesylate-resistant BCR-ABL kinase domain (KD) mutants, except T315I.	nilotinib	35-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-70
16772610-1	2006	BMS-354825 (dasatinib) and AMN107 (nilotinib) are potent alternate Abl inhibitors with activity against many imatinib mesylate-resistant BCR-ABL kinase domain (KD) mutants, except T315I.	nilotinib	35-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-144
16772610-3	2006	Although ENU is expected to induce mutations in multiple proteins, resistant clones were almost exclusively BCR-ABL KD mutant at relevant concentrations of nilotinib and dasatinib, consistent with a central role of KD mutations for resistance to these drugs.	Dasatinib	170-179	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-115
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
16969080-1	2006	Patients with blast crisis (BC) CML frequently become resistant to Imatinib, a Bcr-Abl tyrosine kinase-targeting agent.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
17020995-3	2006	RESULTS: Treatment with dasatinib attenuated the levels of autophosphorylated Bcr-Abl, p-CrkL, phospho-signal transducer and activator of transcription 5 (p-STAT5), p-c-Src, and p-Lyn; inhibited the activity of Lyn and c-Src; and induced apoptosis of the cultured CML cells.	Dasatinib	24-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-85
17020995-4	2006	Combined treatment of cultured human CML and BaF3 cells with vorinostat and dasatinib induced more apoptosis than either agent alone, as well as synergistically induced loss of clonogenic survival, which was associated with greater depletion of Bcr-Abl, p-CrkL, and p-STAT5 levels.	Vorinostat	61-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	249-252
17020995-4	2006	Combined treatment of cultured human CML and BaF3 cells with vorinostat and dasatinib induced more apoptosis than either agent alone, as well as synergistically induced loss of clonogenic survival, which was associated with greater depletion of Bcr-Abl, p-CrkL, and p-STAT5 levels.	Dasatinib	76-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	249-252
17020995-5	2006	Cotreatment with dasatinib and vorinostat also attenuated the levels of Bcr-AblE255K and Bcr-AblT315I and induced apoptosis of BaF3 cells with ectopic expression of the mutant forms of Bcr-Abl.	Dasatinib	17-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-79
17020995-5	2006	Cotreatment with dasatinib and vorinostat also attenuated the levels of Bcr-AblE255K and Bcr-AblT315I and induced apoptosis of BaF3 cells with ectopic expression of the mutant forms of Bcr-Abl.	Vorinostat	31-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-79
17020995-6	2006	Finally, cotreatment of the primary CML cells with vorinostat and dasatinib induced more loss of cell viability and depleted Bcr-Abl or Bcr-AblT315I, p-STAT5, and p-CrkL levels than either agent alone.	Vorinostat	51-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-132
17020995-6	2006	Finally, cotreatment of the primary CML cells with vorinostat and dasatinib induced more loss of cell viability and depleted Bcr-Abl or Bcr-AblT315I, p-STAT5, and p-CrkL levels than either agent alone.	Dasatinib	66-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-132
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 Mesylate	139-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
16899465-5	2006	We have demonstrated that Abl-dependent phosphorylation of WAVE2 is necessary for its activation in vivo, which is highlighted by the findings that RNA interference of WAVE2 expression in Abl/Arg-/- cells has no additive effect on the amount of membrane ruffling.	Arginine	192-195	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-29
16899465-6	2006	Furthermore, Abl phosphorylates WAVE2 on tyrosine 150, and WAVE2-deficient cells rescued with a Y150F mutant fail to regain their ability to ruffle and form microspikes, unlike cells rescued with wild-type WAVE2.	Tyrosine	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
16899465-7	2006	Together, these data show that c-Abl activates WAVE2 via tyrosine phosphorylation to promote actin remodeling in vivo and that Abi-1 forms the crucial link between these two factors.	Tyrosine	57-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-36
16912036-6	2006	Substitution of the SH3-SH2 tyrosine phosphorylation sites with phenylalanine substantially reduced Bcr-Abl-mediated transformation of TF-1 myeloid cells to cytokine independence.	Tyrosine	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
16912036-6	2006	Substitution of the SH3-SH2 tyrosine phosphorylation sites with phenylalanine substantially reduced Bcr-Abl-mediated transformation of TF-1 myeloid cells to cytokine independence.	Phenylalanine	64-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
16912036-7	2006	The positions of these tyrosines in the crystal structure of the c-Abl core and the transformation defect of the corresponding Bcr-Abl mutants together suggest that phosphorylation of the SH3-SH2 region by Src family kinases impacts Bcr-Abl protein conformation and signaling.	Tyrosine	23-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-70
16912036-7	2006	The positions of these tyrosines in the crystal structure of the c-Abl core and the transformation defect of the corresponding Bcr-Abl mutants together suggest that phosphorylation of the SH3-SH2 region by Src family kinases impacts Bcr-Abl protein conformation and signaling.	Tyrosine	23-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
16912036-7	2006	The positions of these tyrosines in the crystal structure of the c-Abl core and the transformation defect of the corresponding Bcr-Abl mutants together suggest that phosphorylation of the SH3-SH2 region by Src family kinases impacts Bcr-Abl protein conformation and signaling.	Tyrosine	23-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	233-240
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-144
17076652-4	2006	Inhibitors of Abl tyrosine kinase are divided into two main groups, namely, ATP-competitive and ATP non-competitive inhibitors.	Adenosine Triphosphate	76-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-17
17076652-4	2006	Inhibitors of Abl tyrosine kinase are divided into two main groups, namely, ATP-competitive and ATP non-competitive inhibitors.	Adenosine Triphosphate	96-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-17
17076652-5	2006	Moreover, ATP-competitive inhibitors are fall into two subclasses, i.e. the Src/Abl inhibitors, and 2-phenylaminopyrimidin-based compounds.	Adenosine Triphosphate	10-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
17076652-6	2006	Dasatinib (formerly BMS-354825), AP23464, SKI-606 and PD166326 are classified as Src/Abl inhibitors while AMN107 and NS-187 (INNO-406) belong to the latter subclass of inhibitors.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-88
17076652-6	2006	Dasatinib (formerly BMS-354825), AP23464, SKI-606 and PD166326 are classified as Src/Abl inhibitors while AMN107 and NS-187 (INNO-406) belong to the latter subclass of inhibitors.	PD 166326	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-88
17076652-10	2006	However, to date, an ATP-competitive inhibitor that can inhibit the phosphorylation of T315I Bcr-Abl has not yet been developed.	Adenosine Triphosphate	21-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
17030193-0	2006	Acetaldehyde inhibits PPARgamma via H2O2-mediated c-Abl activation in human hepatic stellate cells.	Acetaldehyde	0-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-55
17030193-0	2006	Acetaldehyde inhibits PPARgamma via H2O2-mediated c-Abl activation in human hepatic stellate cells.	Hydrogen Peroxide	36-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-55
17030193-9	2006	CONCLUSIONS: Our results showed that the induction of collagen expression by AcCHO in stellate cells is dependent on PPARgamma phosphorylation induced by a hydrogen peroxide-mediated activation of the profibrogenic c-Abl signaling pathway.	Hydrogen Peroxide	156-173	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	215-220
16481037-0	2006	Adaphostin and bortezomib induce oxidative injury and apoptosis in imatinib mesylate-resistant hematopoietic cells expressing mutant forms of Bcr/Abl.	NSC 680410	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
16481037-0	2006	Adaphostin and bortezomib induce oxidative injury and apoptosis in imatinib mesylate-resistant hematopoietic cells expressing mutant forms of Bcr/Abl.	Bortezomib	15-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
16481037-0	2006	Adaphostin and bortezomib induce oxidative injury and apoptosis in imatinib mesylate-resistant hematopoietic cells expressing mutant forms of Bcr/Abl.	Imatinib Mesylate	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.	NSC 680410	29-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
16481037-5	2006	These findings indicate that adaphostin+/-bortezomib circumvent imatinib resistance due to Bcr/Abl point mutations most likely through ROS generation.	Bortezomib	42-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
16481037-5	2006	These findings indicate that adaphostin+/-bortezomib circumvent imatinib resistance due to Bcr/Abl point mutations most likely through ROS generation.	Imatinib Mesylate	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
16481037-5	2006	These findings indicate that adaphostin+/-bortezomib circumvent imatinib resistance due to Bcr/Abl point mutations most likely through ROS generation.	ros	135-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
16855631-0	2006	Frequency and clinical significance of BCR-ABL mutations in patients with chronic myeloid leukemia treated with imatinib mesylate.	Imatinib Mesylate	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 Mesylate	79-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
17054420-5	2006	Signal transduction pathways that are activated in cancers, such as those mediated by the receptor tyrosine kinases breakpoint cluster region-abelson (Bcr-Abl), c-KIT or epidermal growth factor receptor (EGFR), correlate with the alterations in choline phospholipid metabolism of cancers, and also offer molecular targets for specific anticancer therapies.	Choline	245-252	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-158
17054420-5	2006	Signal transduction pathways that are activated in cancers, such as those mediated by the receptor tyrosine kinases breakpoint cluster region-abelson (Bcr-Abl), c-KIT or epidermal growth factor receptor (EGFR), correlate with the alterations in choline phospholipid metabolism of cancers, and also offer molecular targets for specific anticancer therapies.	Phospholipids	253-265	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-158
16970408-1	2006	Pyrrolo[1,2-b][1,2,5]benzothiadiazepine 5,5-dioxides (PBTDs) induced apoptosis in human BCR-ABL-expressing leukemia cells.	pyrrolo[1,2-b][1,2,5]benzothiadiazepine 5,5-dioxides	0-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
16970408-1	2006	Pyrrolo[1,2-b][1,2,5]benzothiadiazepine 5,5-dioxides (PBTDs) induced apoptosis in human BCR-ABL-expressing leukemia cells.	pbtds	54-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
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 Mesylate	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-167
16670264-5	2006	Northern and Western blotting plus immunocytochemical analysis confirmed CCN3 expression is decreased and is tyrosine-phosphorylated in BCR-ABL kinase active FDCP-Mix cells.	Tyrosine	109-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-143
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 Mesylate	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
16670264-8	2006	Cells from patients responding to imatinib showed a similar decrease in BCR-ABL and increase in CCN3.	Imatinib Mesylate	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
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).	Tyrphostins	16-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
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 Mesylate	196-213	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
16959615-3	2006	Oncogenic transformation of ovarian epithelial cells with H-Ras(V12) or expression of Bcr-Abl in hematopoietic cells causes elevated ROS generation and renders the malignant cells highly sensitive to PEITC, which effectively disables the glutathione antioxidant system and causes severe ROS accumulation preferentially in the transformed cells due to their active ROS output.	Reactive Oxygen Species	133-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
16959615-3	2006	Oncogenic transformation of ovarian epithelial cells with H-Ras(V12) or expression of Bcr-Abl in hematopoietic cells causes elevated ROS generation and renders the malignant cells highly sensitive to PEITC, which effectively disables the glutathione antioxidant system and causes severe ROS accumulation preferentially in the transformed cells due to their active ROS output.	Glutathione	238-249	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
16959615-3	2006	Oncogenic transformation of ovarian epithelial cells with H-Ras(V12) or expression of Bcr-Abl in hematopoietic cells causes elevated ROS generation and renders the malignant cells highly sensitive to PEITC, which effectively disables the glutathione antioxidant system and causes severe ROS accumulation preferentially in the transformed cells due to their active ROS output.	Reactive Oxygen Species	287-290	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
16959615-3	2006	Oncogenic transformation of ovarian epithelial cells with H-Ras(V12) or expression of Bcr-Abl in hematopoietic cells causes elevated ROS generation and renders the malignant cells highly sensitive to PEITC, which effectively disables the glutathione antioxidant system and causes severe ROS accumulation preferentially in the transformed cells due to their active ROS output.	Reactive Oxygen Species	287-290	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
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 Mesylate	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
16507320-4	2006	Treatment with the ABL tyrosine kinase inhibitor Imatinib mesylate increased PDCD5 expression in K562 and MEG-01 cells.	Imatinib Mesylate	49-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-22
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 Mesylate	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 Mesylate	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 Mesylate	29-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
16888623-4	2006	The results demonstrate that c-Abl phosphorylates MUC1 on Tyr-60 and forms a complex with MUC1 by binding of the c-Abl SH2 domain to the pTyr-60 site.	Tyrosine	58-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-34
16888623-4	2006	The results demonstrate that c-Abl phosphorylates MUC1 on Tyr-60 and forms a complex with MUC1 by binding of the c-Abl SH2 domain to the pTyr-60 site.	Tyrosine	58-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-118
16888623-4	2006	The results demonstrate that c-Abl phosphorylates MUC1 on Tyr-60 and forms a complex with MUC1 by binding of the c-Abl SH2 domain to the pTyr-60 site.	Phosphotyrosine	137-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-34
16888623-4	2006	The results demonstrate that c-Abl phosphorylates MUC1 on Tyr-60 and forms a complex with MUC1 by binding of the c-Abl SH2 domain to the pTyr-60 site.	Phosphotyrosine	137-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-118
16888623-5	2006	Binding of MUC1 to c-Abl attenuates phosphorylation of c-Abl on Thr-735 and the interaction between c-Abl and cytosolic 14-3-3.	Threonine	64-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-24
16888623-5	2006	Binding of MUC1 to c-Abl attenuates phosphorylation of c-Abl on Thr-735 and the interaction between c-Abl and cytosolic 14-3-3.	Threonine	64-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-60
16888623-6	2006	We also show that expression of MUC1 with a mutation at Tyr-60 (i) disrupts the interaction between MUC1 and c-Abl, (ii) relieves the MUC1-induced block of c-Abl phosphorylation on Thr-735 and binding to 14-3-3, and (iii) attenuates the MUC1 antiapoptotic function.	Tyrosine	56-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-114
16888623-6	2006	We also show that expression of MUC1 with a mutation at Tyr-60 (i) disrupts the interaction between MUC1 and c-Abl, (ii) relieves the MUC1-induced block of c-Abl phosphorylation on Thr-735 and binding to 14-3-3, and (iii) attenuates the MUC1 antiapoptotic function.	Tyrosine	56-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-161
16888623-6	2006	We also show that expression of MUC1 with a mutation at Tyr-60 (i) disrupts the interaction between MUC1 and c-Abl, (ii) relieves the MUC1-induced block of c-Abl phosphorylation on Thr-735 and binding to 14-3-3, and (iii) attenuates the MUC1 antiapoptotic function.	Threonine	181-184	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-114
16888623-6	2006	We also show that expression of MUC1 with a mutation at Tyr-60 (i) disrupts the interaction between MUC1 and c-Abl, (ii) relieves the MUC1-induced block of c-Abl phosphorylation on Thr-735 and binding to 14-3-3, and (iii) attenuates the MUC1 antiapoptotic function.	Threonine	181-184	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-161
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
16614241-0	2006	Bcr-Abl resistance screening predicts a limited spectrum of point mutations to be associated with clinical resistance to the Abl kinase inhibitor nilotinib (AMN107).	nilotinib	146-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
16614241-0	2006	Bcr-Abl resistance screening predicts a limited spectrum of point mutations to be associated with clinical resistance to the Abl kinase inhibitor nilotinib (AMN107).	nilotinib	157-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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 Mesylate	64-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
16614241-5	2006	In contrast to imatinib mesylate, resistance to nilotinib was associated with a limited spectrum of Bcr-Abl kinase mutations.	nilotinib	48-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
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 Mesylate	199-207	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
16904383-8	2006	Further, we provided evidence of apoptosis inhibition in BCR/ABL-positive cells using caspase-3 activity colorimetric assay and DAPI nuclear staining for chromatin condensation.	DAPI	128-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
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 Mesylate	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 Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-112
16840500-8	2006	The association between L-selectin and c-Abl was reduced by cytochalasin B.	Cytochalasin B	60-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-44
16880519-0	2006	Kinase domain mutants of Bcr-Abl exhibit altered transformation potency, kinase activity, and substrate utilization, irrespective of sensitivity to imatinib.	Imatinib Mesylate	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 Mesylate	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 Mesylate	110-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
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 Mesylate	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
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 Mesylate	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
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 Mesylate	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 Mesylate	18-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-48
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 Mesylate	18-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-112
16926141-2	2006	Upon detection of BCR-ABL transcripts after PBSCT, the patient received imatinib, leading to molecular remission.	Imatinib Mesylate	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
16966279-1	2006	Imatinib mesylate suppresses phosphorylation of its kinase target, Bcr-Abl.	Imatinib Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
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 Mesylate	96-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
16858728-4	2006	By metabolically labeling proteins with light or heavy tyrosine, we are able to quantify the change in phosphorylation of BCR-ABL kinase and its substrates in response to drug treatment in human CML cells.	Tyrosine	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
16858728-5	2006	In this study, we observed that BCR-ABL kinase is phosphorylated at tyrosines 393 and 644, and that SH2-domain containing inositol phosphatase (SHIP)-2 and downstream of kinase (Dok)-2 are phosphorylated at tyrosine 1135 and 299, respectively.	Tyrosine	68-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
16858728-5	2006	In this study, we observed that BCR-ABL kinase is phosphorylated at tyrosines 393 and 644, and that SH2-domain containing inositol phosphatase (SHIP)-2 and downstream of kinase (Dok)-2 are phosphorylated at tyrosine 1135 and 299, respectively.	Tyrosine	68-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
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 Mesylate	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 Mesylate	203-211	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	237-244
16537804-0	2006	Combined effects of novel tyrosine kinase inhibitor AMN107 and histone deacetylase inhibitor LBH589 against Bcr-Abl-expressing human leukemia cells.	nilotinib	52-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
16537804-0	2006	Combined effects of novel tyrosine kinase inhibitor AMN107 and histone deacetylase inhibitor LBH589 against Bcr-Abl-expressing human leukemia cells.	Panobinostat	93-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
16537804-2	2006	Treatment with the histone deacetylase inhibitor LBH589 (Novartis) depletes Bcr-Abl levels.	Panobinostat	49-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
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.	nilotinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
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 Mesylate	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 Mesylate	38-46	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 Mesylate	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 Mesylate	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
16543472-2	2006	We investigated cellular resistance to imatinib in BCR-ABL-expressing cells transduced and selected to overexpress BCRP (K562/BCRP-MX10).	Imatinib Mesylate	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
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 Mesylate	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
16597591-6	2006	IC50 values for the more potent BCR-ABL inhibitor nilotinib (AMN107) did not correlate with IC50(imatinib) (R(2) =-0.0561, P > .05).	nilotinib	50-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
16678414-0	2006	3-Benzimidazol-2-yl-1H-indazoles as potent c-ABL inhibitors.	3-benzimidazol-2-yl-1h-indazoles	0-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-48
16831266-1	2006	BACKGROUND & OBJECTIVE: The abnormal expression of poly(rC)-binding protein E2 (hnRNP E2) induced by BCR/ABL plays an important role in blast crisis of chronic myeloid leukemia (CML).	Adenosine Monophosphate	12-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-112
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
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.	Adenosine Triphosphate	100-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
16434489-3	2006	Dasatinib (BMS-354825) is a novel orally bioavailable SRC/ABL inhibitor that has activity against multiple imatinib-resistant BCR-ABL isoforms in vitro that is presently showing considerable promise in early-phase clinical trials of chronic myeloid leukemia (CML).	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-61
16434489-3	2006	Dasatinib (BMS-354825) is a novel orally bioavailable SRC/ABL inhibitor that has activity against multiple imatinib-resistant BCR-ABL isoforms in vitro that is presently showing considerable promise in early-phase clinical trials of chronic myeloid leukemia (CML).	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
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 Mesylate	27-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
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 Mesylate	27-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
16648821-7	2006	Indeed, acetylation on Lys 730 drives c-Abl accumulation in the cytoplasm and promotes differentiation.	Lysine	23-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-43
16648821-8	2006	Thus, Lys 730 acetylation is a novel post-translational modification of c-Abl and a novel mechanism for modulating its subcellular localization that contributes to myogenic differentiation.	Lysine	6-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-77
16825513-5	2006	We also examined expression of the control genes in BCR-ABL-positive K562 cells in response to Gleevec treatment.	Imatinib Mesylate	95-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
16891454-4	2006	In this work, we used locked nucleic acid (LNA)-modified oligonucleotides to silence BCR/ABL and reduce CML cell proliferation, as these oligonucleotides are resistant to nucleases and exhibit an exceptional affinity for cognate RNA.	Oligonucleotides	57-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
16891454-5	2006	The anti-BCR/ABL oligonucleotides were designed as LNA-DNA gapmers, consisting of end blocks of 3/4 LNA monomers and a central DNA stretch of 13/14 deoxyribonucleotides.	Deoxyribonucleotides	148-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
16721371-0	2006	AMN107 (nilotinib): a novel and selective inhibitor of BCR-ABL.	nilotinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
16721371-0	2006	AMN107 (nilotinib): a novel and selective inhibitor of BCR-ABL.	nilotinib	8-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
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 Mesylate	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 Mesylate	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.	nilotinib	40-46	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.	nilotinib	40-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
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.	Adenosine Triphosphate	77-80	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.	Adenosine Triphosphate	77-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
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 Mesylate	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 Mesylate	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 Mesylate	96-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
16721371-9	2006	Dasatinib (BMS-354825), which inhibits Abl and Src family kinases, is another promising new clinical candidate for CML that has shown good efficacy in CML patients.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-42
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 Mesylate	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 Mesylate	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 Mesylate	216-224	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
16775234-2	2006	We evaluated dasatinib, a BCR-ABL inhibitor that targets most imatinib-resistant BCR-ABL mutations, in patients with chronic myelogenous leukemia (CML) or Ph-positive acute lymphoblastic leukemia (ALL).	Dasatinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
16775234-2	2006	We evaluated dasatinib, a BCR-ABL inhibitor that targets most imatinib-resistant BCR-ABL mutations, in patients with chronic myelogenous leukemia (CML) or Ph-positive acute lymphoblastic leukemia (ALL).	Dasatinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
16754879-1	2006	Mutation in the ABL kinase domain is the principal mechanism of imatinib resistance in patients with chronic myelogenous leukemia.	Imatinib Mesylate	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-19
16754879-7	2006	The analogue AP23846 inhibited both native and T315I variants of BCR/ABL with submicromolar potency but showed nonspecific cellular toxicity.	AP23846	13-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-72
16680752-0	2006	Induction chemotherapy and post-remission imatinib therapy for de Novo BCR-ABL-positive AML.	Imatinib Mesylate	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
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 Mesylate	114-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
16469872-1	2006	Dasatinib (BMS-354825), a novel dual SRC/BCR-ABL kinase inhibitor, exhibits greater potency than imatinib mesylate (IM) and inhibits the majority of kinase mutations in IM-resistant chronic myeloid leukemia (CML).	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
16740718-0	2006	The structure of Dasatinib (BMS-354825) bound to activated ABL kinase domain elucidates its inhibitory activity against imatinib-resistant ABL mutants.	Dasatinib	17-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-62
16497976-0	2006	A common phosphotyrosine signature for the Bcr-Abl kinase.	Phosphotyrosine	9-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
16497976-3	2006	However, resistance to imatinib arises in later disease stages primarily because of a Bcr-Abl mutation.	Imatinib Mesylate	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 Mesylate	89-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
16740718-0	2006	The structure of Dasatinib (BMS-354825) bound to activated ABL kinase domain elucidates its inhibitory activity against imatinib-resistant ABL mutants.	Dasatinib	17-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-142
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 Mesylate	120-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-62
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 Mesylate	120-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-142
16740718-2	2006	Current frontline therapy for CML is imatinib, an inhibitor of BCR-ABL.	Imatinib Mesylate	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 Mesylate	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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
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 Mesylate	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 Mesylate	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.	Dasatinib	37-46	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.	Dasatinib	37-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-216
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 Mesylate	200-217	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-130
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 Mesylate	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 Mesylate	19-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-81
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.	Dasatinib	112-121	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.	Dasatinib	112-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-216
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 Mesylate	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 Mesylate	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.	Dasatinib	63-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
16740718-7	2006	The structure also provides an explanation for the activity of dasatinib against imatinib-resistant BCR-ABL mutants.	Imatinib Mesylate	81-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
16495075-7	2006	ALA-PDT led to the perturbation of the Hsp90/p23 multichaperone complex of which the Bcr-Abl is the client protein.	5-amino levulinic acid	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
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 Mesylate	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
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 Mesylate	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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	240-247
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.	Adenosine Triphosphate	144-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	240-247
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 Mesylate	81-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-20
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.	rottlerin	96-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-20
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.	Reactive Oxygen Species	169-192	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-20
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 Mesylate	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 Mesylate	156-164	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-78
16686543-5	2006	Moreover, it was active on both multidrug resistance and Bcr-Abl-expressing cells that were resistant to resveratrol.	Resveratrol	105-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
16469868-0	2006	Bcr-Abl reduces endoplasmic reticulum releasable calcium levels by a Bcl-2-independent mechanism and inhibits calcium-dependent apoptotic signaling.	Calcium	49-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
16469868-0	2006	Bcr-Abl reduces endoplasmic reticulum releasable calcium levels by a Bcl-2-independent mechanism and inhibits calcium-dependent apoptotic signaling.	Calcium	110-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
16469868-6	2006	Bcr-Abl-expressing cells exhibit a decreased amount of free releasable calcium in the ER as well as a weaker capacitative calcium entry response, relative to parental cells.	Calcium	71-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
16469868-6	2006	Bcr-Abl-expressing cells exhibit a decreased amount of free releasable calcium in the ER as well as a weaker capacitative calcium entry response, relative to parental cells.	Calcium	122-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
16469868-10	2006	The ability to negate calcium-dependent apoptotic signaling is likely to be a major prosurvival mechanism in Bcr-Abl-expressing cells.	Calcium	22-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
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 Mesylate	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
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.	lauric acid	30-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
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.	Adenosine Triphosphate	34-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
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 Mesylate	155-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-162
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 Mesylate	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
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 Mesylate	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
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 Mesylate	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 Mesylate	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 Mesylate	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
16678104-2	2006	The present study demonstrates that c-Abl and Arg (abl-related gene) tyrosine kinases associate with and phosphorylate the proteasome PSMA7 (alpha4) subunit at Tyr-153.	Tyrosine	160-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-41
16827161-0	2006	Combination treatment of imatinib-sensitive and -resistant BCR-ABL-positive CML cells with imatinib and farnesyltransferase inhibitors.	Imatinib Mesylate	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
16827161-0	2006	Combination treatment of imatinib-sensitive and -resistant BCR-ABL-positive CML cells with imatinib and farnesyltransferase inhibitors.	Imatinib Mesylate	91-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
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 Mesylate	38-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
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 Mesylate	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
16636310-5	2006	In addition, the observed reductions of nuclear c-Abl in ZD0.2 and ZD0.4 cells to 50% and 60% of ZN cells, respectively, may be a cellular response attempting to normalize nuclear p53 accumulation because nuclear c-Abl is known to down-regulate ubiquitination and nuclear export of p53.	Zinc	97-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-53
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 Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-144
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 Mesylate	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 Mesylate	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 Mesylate	91-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
16260034-0	2006	RNA interference targeting of Bcr-Abl increases chronic myeloid leukemia cell killing by 17-allylamino-17-demethoxygeldanamycin.	tanespimycin	89-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
16260034-1	2006	17-Allylamino-17-demethoxygeldanamycin (17-AAG) induces degradation of Hsp90 client proteins, including Bcr-Abl, however, its clinical use as an anti-tumor agent may be limited by toxicity and modest efficacy.	tanespimycin	0-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
16260034-1	2006	17-Allylamino-17-demethoxygeldanamycin (17-AAG) induces degradation of Hsp90 client proteins, including Bcr-Abl, however, its clinical use as an anti-tumor agent may be limited by toxicity and modest efficacy.	tanespimycin	40-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
16260034-2	2006	We reasoned that Bcr-Abl targeting by RNA interference (RNAi) might selectively increase the activity of 17-AAG against Bcr-Abl+ leukemia cells.	tanespimycin	105-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
16260034-2	2006	We reasoned that Bcr-Abl targeting by RNA interference (RNAi) might selectively increase the activity of 17-AAG against Bcr-Abl+ leukemia cells.	tanespimycin	105-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
16260034-3	2006	17-AAG in combination with targeting small interfering RNAs (siRNAs) reduced Bcr-Abl protein levels, triggered increases in markers of apoptosis and decreased cell viability more effectively than did control siRNA and 17-AAG together, or Bcr-Abl targeting siRNA alone.	tanespimycin	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
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.	DFG peptide	87-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
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.	1,3-Diphenylguanidine	100-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
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 Mesylate	237-245	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
16494624-0	2006	Bcr-abl positive blast crisis of chronic myeloid leukemia emerging in a case of metastatic colorectal cancer 3 months after completion of an 8-month course of cetuximab and irinotecan.	Irinotecan	173-183	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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 Mesylate	59-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
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 Mesylate	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 Mesylate	199-207	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
16639034-5	2006	Therefore, tyrosine phosphorylation-dependent signaling involving receptor tyrosine kinases, mitogen-activated protein kinases, Abl, Src, and Pyk2 is known to be initiated or amplified by reactive oxidants.	Tyrosine	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-131
16640460-4	2006	We present a structure of the kinase domain of Abl, determined in complex with an ATP-peptide conjugate, in which the protein adopts an inactive conformation that resembles closely that of the Src kinases.	Adenosine Triphosphate	82-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
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 Mesylate	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 Mesylate	159-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-33
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 Mesylate	100-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-193
16484222-5	2006	In contrast, we present evidence that RET/PTC3 acts on Erk8 through Tyr(981)-mediated activation of c-Abl.	Tyrosine	68-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-105
16443209-6	2006	RESULTS: The presence of lithium heparin at 100 units/mL in blood caused a significant negative bias of 2-3 mmol/L in sodium concentration with the ABL 725, but no significant bias occurred when the corresponding plasma fraction was analyzed on the VITROS 950.	lithium heparin	25-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	148-151
16443209-6	2006	RESULTS: The presence of lithium heparin at 100 units/mL in blood caused a significant negative bias of 2-3 mmol/L in sodium concentration with the ABL 725, but no significant bias occurred when the corresponding plasma fraction was analyzed on the VITROS 950.	Sodium	118-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	148-151
16609011-0	2006	Inhibition of phosphotyrosine phosphatase 1B causes resistance in BCR-ABL-positive leukemia cells to the ABL kinase inhibitor STI571.	Imatinib Mesylate	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 Mesylate	90-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
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 Mesylate	26-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-193
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 Mesylate	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 Mesylate	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
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 Mesylate	91-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	184-191
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 Mesylate	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 Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-103
16689455-7	2006	Imatinib mesylate (Glivec) is a small molecule that binds to the ATP pocket of ABL and blocks downstream signalling events.	Imatinib Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-82
16689455-7	2006	Imatinib mesylate (Glivec) is a small molecule that binds to the ATP pocket of ABL and blocks downstream signalling events.	Adenosine Triphosphate	65-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-82
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 Mesylate	100-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-193
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.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	33-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-107
16609040-1	2006	PURPOSE: To characterize interactions between the heat shock protein 90 antagonist 17-dimethylaminoethylamino-17-demethoxygeldanamycin (DMAG) and the mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) kinase 1/2 inhibitor PD184352 in Bcr/abl(+) leukemia cells sensitive and resistant to imatinib mesylate.	dimethylaminoethylamino	86-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	260-267
16609040-1	2006	PURPOSE: To characterize interactions between the heat shock protein 90 antagonist 17-dimethylaminoethylamino-17-demethoxygeldanamycin (DMAG) and the mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) kinase 1/2 inhibitor PD184352 in Bcr/abl(+) leukemia cells sensitive and resistant to imatinib mesylate.	demethoxygeldanamycin	113-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	260-267
16609040-1	2006	PURPOSE: To characterize interactions between the heat shock protein 90 antagonist 17-dimethylaminoethylamino-17-demethoxygeldanamycin (DMAG) and the mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) kinase 1/2 inhibitor PD184352 in Bcr/abl(+) leukemia cells sensitive and resistant to imatinib mesylate.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	136-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	260-267
16410245-0	2006	Activation of Bak and Bax through c-abl-protein kinase Cdelta-p38 MAPK signaling in response to ionizing radiation in human non-small cell lung cancer cells.	bakuchiol	14-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-39
16410245-3	2006	In this study, we showed that c-Abl-PKCdelta-Rac1-p38 MAPK signaling is required for the conformational changes of Bak and Bax during ionizing radiation-induced apoptotic cell death in human non-small cell lung cancer cells.	bakuchiol	115-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-35
16410245-12	2006	Moreover, siRNA targeting of c-Abl attenuated radiation-induced PKCdelta and p38 MAPK activations, and Bak and Bax modulations.	bakuchiol	103-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-34
16410245-13	2006	These data support a notion that activation of the c-Abl-PKCdelta-Rac1-p38 MAPK pathway in response to ionizing radiation signals conformational changes of Bak and Bax, resulting in mitochondrial activation-mediated apoptotic cell death in human non-small cell lung cancer cells.	bakuchiol	156-159	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-56
16291594-0	2006	Adaphostin-induced oxidative stress overcomes BCR/ABL mutation-dependent and -independent imatinib resistance.	Imatinib Mesylate	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
16291594-1	2006	The BCR/ABL kinase has been targeted for the treatment of chronic myelogenous leukemia (CML) by imatinib mesylate.	Imatinib Mesylate	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 Mesylate	109-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
16291594-4	2006	Adaphostin is a tyrphostin that was originally intended to inhibit the BCR/ABL kinase by competing with its peptide substrates.	Tyrphostins	16-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
16403813-0	2006	Prediction of response to imatinib by prospective quantitation of BCR-ABL transcript in late chronic phase chronic myeloid leukemia patients.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
16332440-0	2006	Design and synthesis of 3-substituted benzamide derivatives as Bcr-Abl kinase inhibitors.	3-substituted benzamide	24-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
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.	3-substituted benzamide	12-35	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.	3-substituted benzamide	12-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	253-260
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 Mesylate	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 Mesylate	72-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	253-260
16332440-2	2006	About ten 3-halogenated and 3-trifluoromethylated benzamide derivatives were identified as highly potent Bcr-Abl kinase inhibitors.	3-trifluoromethylated benzamide	28-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-112
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.	bafetinib	14-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
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 Mesylate	93-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
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 Mesylate	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
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.	mafosfamide	49-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
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.	Valproic Acid	133-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185
16689455-13	2006	Additional BCR-ABL independent chromosomal abnormalities are common in advanced phase CML and result in resistance to imatinib.	Imatinib Mesylate	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 Mesylate	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 Mesylate	122-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	132-140	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.	Dasatinib	202-211	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.	Dasatinib	202-211	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-43
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
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 Mesylate	10-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
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 Mesylate	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 Mesylate	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-90
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 Mesylate	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 Mesylate	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 Mesylate	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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 Mesylate	170-187	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-148
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 Mesylate	170-187	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-148
16609040-4	2006	RESULTS: Cotreatment of Bcr/abl(+) cells with minimally toxic concentrations of DMAG and PD184352 resulted in synergistic induction of mitochondrial injury (cytochrome c release and Bax conformational change), events associated with the pronounced and sustained inactivation of ERK1/2 accompanied by down-regulation of Bcl-x(L).	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	80-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-31
16609040-4	2006	RESULTS: Cotreatment of Bcr/abl(+) cells with minimally toxic concentrations of DMAG and PD184352 resulted in synergistic induction of mitochondrial injury (cytochrome c release and Bax conformational change), events associated with the pronounced and sustained inactivation of ERK1/2 accompanied by down-regulation of Bcl-x(L).	2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide	89-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-31
16609040-7	2006	CONCLUSIONS: A regimen combining the heat shock protein 90 antagonist DMAG and the mitogen-activated protein kinase/ERK kinase 1/2 inhibitor potently induces apoptosis in Bcr/abl(+) cells, including those resistant to imatinib mesylate through various mechanisms including Bcr/abl kinase mutations, through a process that may involve sustained ERK1/2 inactivation and Bcl-x(L) down-regulation.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	70-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-178
16609040-7	2006	CONCLUSIONS: A regimen combining the heat shock protein 90 antagonist DMAG and the mitogen-activated protein kinase/ERK kinase 1/2 inhibitor potently induces apoptosis in Bcr/abl(+) cells, including those resistant to imatinib mesylate through various mechanisms including Bcr/abl kinase mutations, through a process that may involve sustained ERK1/2 inactivation and Bcl-x(L) down-regulation.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	70-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-178
16611216-0	2006	Phosphoinositide, phosphopeptide and pyridone interactions of the Abl SH2 domain.	Phosphatidylinositols	0-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-69
16611216-0	2006	Phosphoinositide, phosphopeptide and pyridone interactions of the Abl SH2 domain.	Pyridones	37-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-69
16611216-3	2006	Here, the Abl Src homology 2 domain"s binding sites and affinities for phosphotyrosine- and phosphoserine-containing motifs, phosphoinositides as well as a pyridone-based peptidomimetic inhibitor were determined using nuclear magnetic resonance spectroscopy in order to define their roles.	Phosphotyrosine	71-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-13
16611216-3	2006	Here, the Abl Src homology 2 domain"s binding sites and affinities for phosphotyrosine- and phosphoserine-containing motifs, phosphoinositides as well as a pyridone-based peptidomimetic inhibitor were determined using nuclear magnetic resonance spectroscopy in order to define their roles.	Phosphoserine	92-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-13
16611216-3	2006	Here, the Abl Src homology 2 domain"s binding sites and affinities for phosphotyrosine- and phosphoserine-containing motifs, phosphoinositides as well as a pyridone-based peptidomimetic inhibitor were determined using nuclear magnetic resonance spectroscopy in order to define their roles.	Phosphatidylinositols	125-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-13
16611216-3	2006	Here, the Abl Src homology 2 domain"s binding sites and affinities for phosphotyrosine- and phosphoserine-containing motifs, phosphoinositides as well as a pyridone-based peptidomimetic inhibitor were determined using nuclear magnetic resonance spectroscopy in order to define their roles.	Pyridones	156-164	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-13
16611216-7	2006	Thus the Src homology 2 domain of Abl, a myristoylated and membrane-localized protein, is able to interact directly with phosphoinositides through a multifunctional basic site that overlaps the phosphotyrosine pocket.	Phosphatidylinositols	121-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-37
16611216-7	2006	Thus the Src homology 2 domain of Abl, a myristoylated and membrane-localized protein, is able to interact directly with phosphoinositides through a multifunctional basic site that overlaps the phosphotyrosine pocket.	Phosphotyrosine	194-209	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-37
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 Mesylate	103-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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.	leptomycin B	125-137	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 Mesylate	72-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
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.	leptomycin B	128-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
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.	leptomycin B	142-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
16249386-5	2006	Furthermore, nested reverse transcriptase-polymerase chain reaction (RT-PCR) analysis on colonies representative of each experimental condition demonstrated that the combination of IM and LMB was the most effective regimen in reducing the number of BCR-ABL-positive colonies.	leptomycin B	188-191	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	249-256
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 Mesylate	93-101	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 Mesylate	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 Mesylate	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 Mesylate	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
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 Mesylate	196-204	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185
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 Mesylate	208-216	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185
16444746-5	2006	Coexposure of cells to valproate and imatinib was associated with repression of several genes involved in Bcr-Abl transformation.	Valproic Acid	23-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
16444746-5	2006	Coexposure of cells to valproate and imatinib was associated with repression of several genes involved in Bcr-Abl transformation.	Imatinib Mesylate	37-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
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.	Valproic Acid	31-40	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 Mesylate	41-49	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 Mesylate	166-174	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
16505115-9	2006	RNA interference studies show that nucleoside-induced p73 increases are independent of c-Abl, a nucleoside-activated kinase recently implicated in p73 stabilization.	Nucleosides	35-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-92
16267043-2	2006	Activated Abl phosphorylates tyrosine 221 of c-CrkII (Crk; Crk-Y221-P), which prevents Crk from binding to the docking protein p130(CAS) (CAS).	Tyrosine	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-13
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 Mesylate	91-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
16505115-0	2006	c-Abl-independent p73 stabilization during gemcitabine- or 4"-thio-beta-D-arabinofuranosylcytosine-induced apoptosis in wild-type and p53-null colorectal cancer cells.	gemcitabine	43-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
16505115-0	2006	c-Abl-independent p73 stabilization during gemcitabine- or 4"-thio-beta-D-arabinofuranosylcytosine-induced apoptosis in wild-type and p53-null colorectal cancer cells.	4'-thio-arabinofuranosylcytosine	59-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
16505115-11	2006	Together, these studies indicate that c-Abl-independent p73 stabilization pathways could account for the p53-independent mechanisms in nucleoside-induced apoptosis.	Nucleosides	135-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-43
16158058-3	2006	We show that Rb is constitutively phosphorylated at tyrosine in Abl-dependent tumor cells, and that Abl phosphorylates Rb specifically at Y805 within the C-terminal domain of the molecule.	Tyrosine	52-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-67
16158058-3	2006	We show that Rb is constitutively phosphorylated at tyrosine in Abl-dependent tumor cells, and that Abl phosphorylates Rb specifically at Y805 within the C-terminal domain of the molecule.	Tyrosine	52-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-103
16158058-6	2006	Thus, our findings suggest that Abl-catalysed tyrosine phosphorylation of Rb is necessary for survival of Abl-dependent human tumor cells, and raises the possibility that this phosphorylated Rb can be a molecular target for cancer therapy aimed at inducing apoptosis of Abl-dependent tumor cells, such as Bcr/Abl-positive CML.	Tyrosine	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-35
16158058-6	2006	Thus, our findings suggest that Abl-catalysed tyrosine phosphorylation of Rb is necessary for survival of Abl-dependent human tumor cells, and raises the possibility that this phosphorylated Rb can be a molecular target for cancer therapy aimed at inducing apoptosis of Abl-dependent tumor cells, such as Bcr/Abl-positive CML.	Tyrosine	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-109
16158058-6	2006	Thus, our findings suggest that Abl-catalysed tyrosine phosphorylation of Rb is necessary for survival of Abl-dependent human tumor cells, and raises the possibility that this phosphorylated Rb can be a molecular target for cancer therapy aimed at inducing apoptosis of Abl-dependent tumor cells, such as Bcr/Abl-positive CML.	Tyrosine	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-109
16158058-6	2006	Thus, our findings suggest that Abl-catalysed tyrosine phosphorylation of Rb is necessary for survival of Abl-dependent human tumor cells, and raises the possibility that this phosphorylated Rb can be a molecular target for cancer therapy aimed at inducing apoptosis of Abl-dependent tumor cells, such as Bcr/Abl-positive CML.	Tyrosine	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-109
16286457-4	2006	Tyr-161 shares similarity to the consensus sequence for phosphorylation by the nonreceptor tyrosine kinases Abl and Arg.	Tyrosine	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-111
16286457-6	2006	Moreover, treatment of neurons with two structurally distinct and highly selective Abl inhibitors, PD173955 and Gleevec, blocks HK-induced phosphorylation of IkappaB-beta at Tyr-161 and induces neuronal apoptosis.	PD 173955	99-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-86
16286457-6	2006	Moreover, treatment of neurons with two structurally distinct and highly selective Abl inhibitors, PD173955 and Gleevec, blocks HK-induced phosphorylation of IkappaB-beta at Tyr-161 and induces neuronal apoptosis.	Tyrosine	174-177	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-86
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	9-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
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 Mesylate	139-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
16415863-5	2006	We propose that this new class of compounds inhibits Bcr-abl kinase activity through an allosteric non-ATP competitive mechanism.	Adenosine Triphosphate	103-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
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 Mesylate	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 Mesylate	19-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
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.	G(M1) Ganglioside	55-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
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 Mesylate	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
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 Mesylate	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 Mesylate	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
16397263-0	2006	Dasatinib (BMS-354825), a dual SRC/ABL kinase inhibitor, inhibits the kinase activity of wild-type, juxtamembrane, and activation loop mutant KIT isoforms associated with human malignancies.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
16397263-4	2006	Dasatinib (formerly BMS-354825) is a small-molecule, ATP-competitive inhibitor of SRC and ABL tyrosine kinases with potency in the low nanomolar range.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-93
16397263-4	2006	Dasatinib (formerly BMS-354825) is a small-molecule, ATP-competitive inhibitor of SRC and ABL tyrosine kinases with potency in the low nanomolar range.	Adenosine Triphosphate	53-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-93
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 Mesylate	139-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
16732964-4	2006	Expression of bcr-abl mRNA was detected by RT-PCR and tyrosine phosphorylation of BCR-ABL fusion protein by Western blot.	Tyrosine	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
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 Mesylate	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 Mesylate	17-25	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.	Tyrosine	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
16468238-4	2006	The median of relative quantity of BCR-ABL in the blood before imatinib therapy was 2.55%.	Imatinib Mesylate	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
16468238-8	2006	Three patients were primarily resistant to imatinib with the BCR-ABL range of 0.13%-11.7% during the treatment.	Imatinib Mesylate	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
16172030-2	2005	Imatinib targets the tyrosine kinase activity of Bcr-Abl and is a first-line therapy for this malignancy.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
16958604-2	2006	Our purpose was to verify if determination of total bilirubin (TBIL) in whole blood on an ABL 735 blood gas analyzer with a spectrophotometer module could provide an analytical alternative to chemical methods of TBIL measurement.	Bilirubin	52-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-93
16958604-2	2006	Our purpose was to verify if determination of total bilirubin (TBIL) in whole blood on an ABL 735 blood gas analyzer with a spectrophotometer module could provide an analytical alternative to chemical methods of TBIL measurement.	Bilirubin	63-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-93
16958604-14	2006	CONCLUSIONS: The ABL 735 instrument is reliable for measuring TBIL in 70-microL whole blood samples from neonates.	Bilirubin	62-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-20
16755775-4	2006	Imatinib Mesylate (Glivec) is a specific inhibitor of Bcr-Abl kinase.	Imatinib Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
16755775-4	2006	Imatinib Mesylate (Glivec) is a specific inhibitor of Bcr-Abl kinase.	Imatinib Mesylate	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
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 Mesylate	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 Mesylate	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-123
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 Mesylate	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
16542059-1	2006	Dasatinib [BMS 354825] is an orally active, small molecule, dual inhibitor of both SRC and ABL kinases that is under development with Bristol-Myers Squibb for the treatment of patients with chronic myelogenous leukaemia (CML) and imatinib-acquired resistance/intolerance.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-94
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 Mesylate	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-148
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 Mesylate	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 Mesylate	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
16434384-0	2006	The role of the K247R substitution in the ABL tyrosine kinase domain in sensitivity to imatinib.	Imatinib Mesylate	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-45
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-134
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 Mesylate	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	229-236
17124064-5	2006	Still newer inhibitors active against T315I mutant BCR-ABL may overcome primary and secondary resistance to dasatinib and nilotinib.	Dasatinib	108-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
17124064-5	2006	Still newer inhibitors active against T315I mutant BCR-ABL may overcome primary and secondary resistance to dasatinib and nilotinib.	nilotinib	122-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
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 Mesylate	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-87
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.	Arginine	48-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-87
16205964-10	2006	We show here for the first time in a large series of glioblastomas that PDGFR-alpha, -beta, c-kit, c-abl and arg expression is immunohistochemically detectable in a fraction of cases.	Arginine	38-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-104
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
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 Mesylate	193-201	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
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 Mesylate	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
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 Mesylate	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 Mesylate	211-219	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-159
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 Mesylate	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 Mesylate	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
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 Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
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 Mesylate	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 Mesylate	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 Mesylate	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-164
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 Mesylate	141-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
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 Mesylate	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 Mesylate	184-192	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
16319529-0	2005	BCR-ABL kinase domain mutations in chronic myeloid leukemia: not quite enough to cause resistance to imatinib therapy?	Imatinib Mesylate	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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 Mesylate	144-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	226-233
16226710-15	2005	STI-571 binds to Kit and Bcr-Abl (the oncoprotein of chronic myelogenous leukemia) at their ATP-binding sites.	Imatinib Mesylate	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
16226710-15	2005	STI-571 binds to Kit and Bcr-Abl (the oncoprotein of chronic myelogenous leukemia) at their ATP-binding sites.	Adenosine Triphosphate	92-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
16236241-0	2005	Assaying Bcr-Abl kinase activity and inhibition in whole cell extracts by phosphorylation of substrates immobilized on agarose beads.	Sepharose	119-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
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 Mesylate	83-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-42
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 Mesylate	83-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
15927253-0	2005	Treatment of elderly patients with acute lymphoblastic leukemia--evidence for a benefit of imatinib in BCR-ABL positive patients.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	137-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-181
16224487-0	2005	Selecting and deselecting imatinib-resistant clones: observations made by longitudinal, quantitative monitoring of mutated BCR-ABL.	Imatinib Mesylate	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-130
16105974-0	2005	NS-187, a potent and selective dual Bcr-Abl/Lyn tyrosine kinase inhibitor, is a novel agent for imatinib-resistant leukemia.	bafetinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	53-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
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.	bafetinib	54-60	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 Mesylate	134-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
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 Mesylate	49-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
16105974-5	2005	The inhibitory effect of NS-187 extends to 12 of 13 Bcr-Abl proteins with mutations in their kinase domain but not to T315I.	Nitrogen	25-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
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 Mesylate	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-22
16405837-0	2005	[Analysis of ABL tyrosine kinase point mutations in imatinib treated chronic myelogenous leukemia patients].	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-35
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	10-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
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 Mesylate	3-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
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 Mesylate	177-185	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	211-218
16242052-2	2005	Imatinib was first shown to inhibit the causative molecular translocation in chronic myelogenous leukemia, BCR-ABL.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
16305488-2	2005	Imatinib mesylate binds to the inactive conformation of BCR-ABL tyrosine kinase suppressing the Philadelphia chromosome positive clone in CML.	Imatinib Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
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 Mesylate	169-177	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
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 Mesylate	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-135
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.	Adenosine Triphosphate	154-157	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-135
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 Mesylate	103-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
16151465-0	2005	A single nucleotide polymorphism in the coding region of ABL and its effects on sensitivity to imatinib.	Imatinib Mesylate	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-60
16151465-1	2005	We have identified a gene polymorphism (K247R) within or close to the P-loop of BCR-ABL, which leads to the substitution of arginine for lysine.	Lysine	137-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-87
16151468-0	2005	Coexistence of AML1/RUNX1 and BCR-ABL point mutations in an imatinib-resistant form of CML.	Imatinib Mesylate	60-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
16167056-3	2005	Bisphosphonates, such as zoledronate, have been shown to inhibit the oncogenicity of Ras, an important downstream effector of Bcr-Abl.	Diphosphonates	0-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
16167056-3	2005	Bisphosphonates, such as zoledronate, have been shown to inhibit the oncogenicity of Ras, an important downstream effector of Bcr-Abl.	Zoledronic Acid	25-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
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 Mesylate	22-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
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 Mesylate	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 Mesylate	438-446	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
16151465-1	2005	We have identified a gene polymorphism (K247R) within or close to the P-loop of BCR-ABL, which leads to the substitution of arginine for lysine.	Arginine	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-87
16264277-0	2005	Detection of single nucleotide insertion of BCR/ABL region in imatinib-resistant human myelogenous leukemia SR-1 cells.	Imatinib Mesylate	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 Mesylate	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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-103
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 Mesylate	179-187	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
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 Mesylate	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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
16157305-2	2005	Imatinib mesylate inhibits Bcr-Abl tyrosine kinase, resulting in a blockage of tyrosine phosphorylation in its downstream pathways.	Tyrosine	35-43	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 Mesylate	56-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
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 Mesylate	69-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
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 Mesylate	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
16230377-2	2005	The novel SFK/Abl inhibitor, dasatinib (BMS-354825), is a promising therapeutic agent with oral bioavailability.	Dasatinib	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-17
16230377-3	2005	Dasatinib has been shown to inhibit growth of Bcr-Abl-dependent chronic myeloid leukemia xenografts in nude mice.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-53
16230407-4	2005	The BCR/ABL inhibitors imatinib and AMN107 were found to promote expression of Bim in CML cells.	Imatinib Mesylate	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
16230407-6	2005	The BCR/ABL-induced decrease in expression of Bim was found to be a posttranscriptional event that depended on signaling through the mitogen-activated protein kinase pathway and was abrogated by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	220-225	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
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 Mesylate	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 Mesylate	270-278	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
16334201-3	2005	A new targeted therapy, imatinib mesylate (Gleevec), inhibits of the dysregulated kinase activity of BCR-ABL.	Imatinib Mesylate	24-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
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 Mesylate	36-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-126
15956284-5	2005	Patients with low IC50imatinib (IC50 < or = 0.6 microM; n = 36) had a 36% probability of achieving 2-log reduction in BCR-ABL (breakpoint cluster region-abelson) by 3 months compared with 8% in patients with high IC50imatinib (n = 26) (P = .01).	ic50imatinib	18-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
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 Mesylate	203-211	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
15887238-1	2005	Imatinib mesylate is a tyrosine kinase inhibitor of the ABL, platelet-derived growth factor receptor (PDGFR), and c-kit kinases.	Imatinib Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-59
16204063-0	2005	Bcr-Abl expression levels determine the rate of development of resistance to imatinib mesylate in chronic myeloid leukemia.	Imatinib Mesylate	77-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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 Mesylate	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 Mesylate	159-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
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 Mesylate	53-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-152
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 Mesylate	27-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
16203792-0	2005	Combined Abl inhibitor therapy for minimizing drug resistance in chronic myeloid leukemia: Src/Abl inhibitors are compatible with imatinib.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-116
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 Mesylate	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 Mesylate	81-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
16078266-0	2005	AMN107, a novel aminopyrimidine inhibitor of p190 Bcr-Abl activation and of in vitro proliferation of Philadelphia-positive acute lymphoblastic leukemia cells.	nilotinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
16078266-0	2005	AMN107, a novel aminopyrimidine inhibitor of p190 Bcr-Abl activation and of in vitro proliferation of Philadelphia-positive acute lymphoblastic leukemia cells.	2-aminopyrimidine	16-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
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 Mesylate	161-178	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
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 Mesylate	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 Mesylate	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
16109618-0	2005	E6a2 BCR-ABL fusion with BCR exon 5-deleted transcript in a Philadelphia positive CML responsive to Imatinib.	Imatinib Mesylate	100-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	5-12
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.	ephrin-a	68-76	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.	ephrin-a	68-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-130
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 Mesylate	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 Mesylate	142-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-130
16170025-10	2005	PIN1, FEN1, and cABL up-regulation and LMNB1, AREG, RhoB, CCNG, TYMS, F3, and MGMT down-regulation suggest that methionine stress sensitizes the tumor cells to DNA-alkylating drugs, 5-fluorouracil, and radiation.	Methionine	112-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-20
16285507-4	2005	Specifically, the c-Abl SH3 domain binds to a proline-rich motif at amino acids 958-982 in the c-Abl C-terminal region.	Proline	46-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-23
16285507-4	2005	Specifically, the c-Abl SH3 domain binds to a proline-rich motif at amino acids 958-982 in the c-Abl C-terminal region.	Proline	46-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-100
15993098-2	2005	In the present study, we conducted a microarray analysis using an inducible model of BCR-ABL expression based on the TET-OFF system, and we found that osteopontin (OPN), a component of stem cell niche, is overexpressed in BCR-ABL-expressing cells.	tetramethylenedisulfotetramine	117-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
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 Mesylate	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.	Gefitinib	120-129	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.	Erlotinib Hydrochloride	135-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
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.	VX680	42-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-130
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.	doramapimod	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-130
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 Mesylate	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-130
15914012-5	2005	The ATP binding pocket of the active form of c-Src is similar to that of the c-Abl kinase in which the activation loop resembles that of an active form.	Adenosine Triphosphate	4-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-82
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 Mesylate	193-201	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	249-256
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 Mesylate	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
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 Mesylate	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 Mesylate	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 Mesylate	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
16157201-0	2005	Quantitative molecular monitoring of BCR-ABL and MDR1 transcripts in patients with chronic myeloid leukemia during Imatinib treatment.	Imatinib Mesylate	115-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
16203604-3	2005	Imatinib mesylate (IM) is one such therapy that also targets Abl, c-kit and PDGF-R tyrosine kinases.	Imatinib Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-64
16136169-1	2005	BCR/ABL-kinase mutations frequently mediate clinical resistance to the selective tyrosine kinase inhibitor Imatinib mesylate (IM, Gleevec).	Imatinib Mesylate	107-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
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 Mesylate	45-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
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 Mesylate	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-113
15878840-0	2005	Pterostilbene and 3"-hydroxypterostilbene are effective apoptosis-inducing agents in MDR and BCR-ABL-expressing leukemia cells.	pterostilbene	0-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
15878840-0	2005	Pterostilbene and 3"-hydroxypterostilbene are effective apoptosis-inducing agents in MDR and BCR-ABL-expressing leukemia cells.	3'-hydroxypterostilbene	18-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
15978941-2	2005	Phorbol ester-induced maturation of K562 cells was accompanied by repositioning of down-regulated BCR/ABL genes closer to the nuclear membrane.	Phorbol Esters	0-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-105
15978941-6	2005	Decreased expression of BCR/ABL gene was also found after cell stimulation by selectively pro-apoptotic agent etoposide and by ABL-RNAi leading to apoptosis.	Etoposide	110-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
15978941-6	2005	Decreased expression of BCR/ABL gene was also found after cell stimulation by selectively pro-apoptotic agent etoposide and by ABL-RNAi leading to apoptosis.	Etoposide	110-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-31
16093432-0	2005	T315I-mutated Bcr-Abl in chronic myeloid leukemia and imatinib: insights from a computational study.	Imatinib Mesylate	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
16014719-7	2005	Tyrosine phosphorylation of tau was inhibited by PP2 (4-amino-5-(4-chlorophenyl-7-(t-butyl)pyrazolo[3,4-d]pyrimidine), which is known to inhibit Src-family kinases and c-Abl.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	168-173
15937340-7	2005	Conversely, the ectopic overexpression of HDAC6 inhibited LAQ824-induced acetylation of HSP90 and alpha-tubulin and reduced LAQ824-mediated depletion of Bcr-Abl, AKT, and c-Raf.	LAQ824	124-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
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 Mesylate	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
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 Mesylate	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 Mesylate	127-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-15
16014719-0	2005	Tyrosine 394 is phosphorylated in Alzheimer"s paired helical filament tau and in fetal tau with c-Abl as the candidate tyrosine kinase.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-101
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 Mesylate	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 Mesylate	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 Mesylate	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
15917650-2	2005	It specifically suppresses the growth of bcr-abl expressing CML progenitor cells by blocking the ATP-binding site of the kinase domain of bcr-abl.	Adenosine Triphosphate	97-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
15917650-2	2005	It specifically suppresses the growth of bcr-abl expressing CML progenitor cells by blocking the ATP-binding site of the kinase domain of bcr-abl.	Adenosine Triphosphate	97-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-32
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-32
16000593-0	2005	AMN107, a novel aminopyrimidine inhibitor of Bcr-Abl, has in vitro activity against imatinib-resistant chronic myeloid leukemia.	nilotinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
16000593-0	2005	AMN107, a novel aminopyrimidine inhibitor of Bcr-Abl, has in vitro activity against imatinib-resistant chronic myeloid leukemia.	2-aminopyrimidine	16-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
16000593-0	2005	AMN107, a novel aminopyrimidine inhibitor of Bcr-Abl, has in vitro activity against imatinib-resistant chronic myeloid leukemia.	Imatinib Mesylate	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 Mesylate	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-179
16000593-2	2005	AMN107 is a novel, orally bioavailable ATP-competitive inhibitor of Bcr-Abl.	nilotinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
16000593-2	2005	AMN107 is a novel, orally bioavailable ATP-competitive inhibitor of Bcr-Abl.	Adenosine Triphosphate	39-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
16000593-6	2005	AMN107 inhibited autophosphorylation of Bcr-Abl kinase more effectively than imatinib in all cell lines.	nilotinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
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 Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
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 Mesylate	46-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
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 Mesylate	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 Mesylate	152-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
16014719-7	2005	Tyrosine phosphorylation of tau was inhibited by PP2 (4-amino-5-(4-chlorophenyl-7-(t-butyl)pyrazolo[3,4-d]pyrimidine), which is known to inhibit Src-family kinases and c-Abl.	AG 1879	54-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	168-173
16014719-8	2005	Cotransfection of tau and kinases showed that Tyr-18 was the major site for Fyn phosphorylation, but Tyr-394 was the main residue for Abl.	Tyrosine	101-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-137
16014719-11	2005	These results show that phosphorylation of tau on Tyr-394 is a physiological event that is potentially part of a signal relay and suggest that Abl could have a pathogenic role in Alzheimer"s disease.	Tyrosine	50-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-146
15858616-0	2005	Abl inhibitor BMS354825 binding mode in Abelson kinase revealed by molecular docking studies.	Dasatinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
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 Mesylate	24-32	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 Mesylate	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
15902298-1	2005	Overexpression of BCR-ABL and P-glycoprotein (Pgp) are two of the known mechanisms of imatinib resistance.	Imatinib Mesylate	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
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 Mesylate	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
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.	cev	25-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-55
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.	cev	25-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-137
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 Mesylate	112-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-137
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 Mesylate	110-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	148-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-114
15893754-6	2005	The phosphorylation sites of BCAP by c-Abl were mapped to five tyrosine residues in the C-terminal region that are well conserved in mammals.	Tyrosine	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-42
15942030-7	2005	C-Abl tyrosine phosphorylates OGG1 in vitro; however, this phosphorylation event does not affect OGG1 8-oxoG/C incision activity.	Tyrosine	6-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
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 Mesylate	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 Mesylate	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 Mesylate	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-159
15899391-0	2005	BCR-ABL gene amplification and overexpression in a patient with chronic myeloid leukemia treated with imatinib.	Imatinib Mesylate	102-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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 Mesylate	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 Mesylate	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 Mesylate	168-176	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
15930265-0	2005	In vitro activity of Bcr-Abl inhibitors AMN107 and BMS-354825 against clinically relevant imatinib-resistant Abl kinase domain mutants.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	140-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
15930265-5	2005	Two such Bcr-Abl inhibitors are currently being evaluated in clinical trials: the improved potency, selective Abl inhibitor AMN107 and the highly potent dual Src/Abl inhibitor BMS-354825.	nilotinib	124-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
15930265-5	2005	Two such Bcr-Abl inhibitors are currently being evaluated in clinical trials: the improved potency, selective Abl inhibitor AMN107 and the highly potent dual Src/Abl inhibitor BMS-354825.	nilotinib	124-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
15784722-1	2005	The mammalian target of rapamycin (mTOR) has recently been described to be constitutively activated in Bcr-Abl-transformed cells and to mediate rapamycin-induced inhibition of growth in respective cell lines.	Sirolimus	24-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
15784722-4	2005	Rapamycin dose dependently inhibited growth of primary CML cells obtained from patients with imatinib-responsive or imatinib-resistant disease as well as growth of Bcr-Abl-transformed imatinib-resistant cell lines.	Sirolimus	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	164-171
15784722-5	2005	Moreover, we observed potent cytoreductive effects of rapamycin in a patient with imatinib-resistant Bcr-Abl+ leukemia.	Sirolimus	54-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
15784722-5	2005	Moreover, we observed potent cytoreductive effects of rapamycin in a patient with imatinib-resistant Bcr-Abl+ leukemia.	Imatinib Mesylate	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
15755509-0	2005	Cytokinetics and mechanism of action of AKO4: a novel nitrogen mustard targeted to bcr-abl.	Mechlorethamine	54-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
15972123-9	2005	Berbamine down-regulated the expression levels of bcr/abl gene and P210 in K562 cells in a time- and concentration-dependent manner.	berbamine	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
15972123-10	2005	The bcr/abl expression decreased from (1.38 +/- 0.02) to (0.97 +/- 0.01) after exposure of the cells to 8.0 microg/ml berbamine for 0 and 72 hours (P < 0.01).	berbamine	118-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
15972123-12	2005	In vivo, after treatment for 4 weeks, the tumor weight of berbamine-treated group was also lower than that of untreated group [(1.46 +/- 0.43) g vs (2.90 +/- 0.94) g, P < 0.01] and the inhibition rate was 49.66%, moreover, berbamine down-regulated the expression level of bcr/abl gene of tumor cells.	berbamine	58-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	275-282
15972123-14	2005	The mechanisms of berbamine-induced apoptosis may be involved in down-regulation of bcr/abl gene expression and P210 level.	berbamine	18-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
15972123-15	2005	In vivo, berbamine can aslo display a better antileukemic effect and down-regulate expression of bcr/abl gene.	berbamine	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
15972123-16	2005	Berbamine extracted from Chinese herb may be a promising candidate of new drug for clinical anticancer treatment, especially for bcr-abl(+) diseases.	berbamine	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-136
15870711-1	2005	Imatinib mesylate (IM) is a tyrosine kinase inhibitor, which inhibits phosphorylation of downstream proteins involved in BCR-ABL signal transduction.	Imatinib Mesylate	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 Mesylate	19-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
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 Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-94
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 Mesylate	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-32
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 Mesylate	134-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-181
15815728-1	2005	Imatinib mesylate, a Bcr-Abl kinase inhibitor, has been very successful in the treatment of chronic myelogenous leukemia (CML).	Imatinib Mesylate	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 Mesylate	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
15850559-4	2005	c-Abl was associated with RNA polymerase II (RNAP II) in vivo and augmented the tyrosine phosphorylation of the largest subunit of RNAP II.	Tyrosine	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
15850559-6	2005	The combined results suggest that c-Abl plays an important role in the transcriptional regulation of c-fos gene and the tyrosine phosphorylation of the largest subunit of RNAP II by c-Abl is involved in the regulating process.	Tyrosine	120-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-187
15665113-9	2005	Together these data provide a novel therapeutic strategy to overcome imatinib mesylate resistance, especially with the Abl mutant T315I.	Imatinib Mesylate	69-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-122
15735728-5	2005	In both IL-3- treated cells and those expressing Bcr-Abl, high rates of hexose uptake were associated with the retention at the cell surface of approximately 80% of the total cellular content of the GLUT1 glucose transporter.	Hexoses	72-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
15735728-6	2005	In contrast, treatment of Bcr-Abl-expressing cells for 6 h with the Bcr-Abl kinase inhibitor Glivec (10 muM), in the absence of IL-3, led to internalization of approximately 90% of the cell-surface transporters and drastically decreased (4.4+/-0.9 (mean+/-s.e.m., 4)-fold) the V(max) for hexose uptake, without significant effect on the K(m) for this process or on the total cellular transporter content.	Hexoses	288-294	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
15735728-6	2005	In contrast, treatment of Bcr-Abl-expressing cells for 6 h with the Bcr-Abl kinase inhibitor Glivec (10 muM), in the absence of IL-3, led to internalization of approximately 90% of the cell-surface transporters and drastically decreased (4.4+/-0.9 (mean+/-s.e.m., 4)-fold) the V(max) for hexose uptake, without significant effect on the K(m) for this process or on the total cellular transporter content.	Hexoses	288-294	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
15890005-6	2005	c-Abl and Arg nonreceptor protein tyrosine kinases associate with catalase in cells treated with H(2)O(2) by mechanisms involving the SH3 domains of the kinases and the Pro(293)PheAsnPro motif of catalase and activate catalase by phosphorylating it on Tyr(231) and Tyr(386).	Water	97-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
15890005-6	2005	c-Abl and Arg nonreceptor protein tyrosine kinases associate with catalase in cells treated with H(2)O(2) by mechanisms involving the SH3 domains of the kinases and the Pro(293)PheAsnPro motif of catalase and activate catalase by phosphorylating it on Tyr(231) and Tyr(386).	pheasnpro	177-186	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
15890005-6	2005	c-Abl and Arg nonreceptor protein tyrosine kinases associate with catalase in cells treated with H(2)O(2) by mechanisms involving the SH3 domains of the kinases and the Pro(293)PheAsnPro motif of catalase and activate catalase by phosphorylating it on Tyr(231) and Tyr(386).	Tyrosine	252-255	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
15890005-6	2005	c-Abl and Arg nonreceptor protein tyrosine kinases associate with catalase in cells treated with H(2)O(2) by mechanisms involving the SH3 domains of the kinases and the Pro(293)PheAsnPro motif of catalase and activate catalase by phosphorylating it on Tyr(231) and Tyr(386).	Tyrosine	265-268	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	237-245	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
15992353-8	2005	Recently accumulating evidence suggest a role of the long patch DNA mismatch repair system in sensing cisplatin-damaged DNA and in triggering cell death through a c-Abl- and p73-dependent cascade; two other important pathways have been unravelled that are the mitogen-activated protein kinase cascade and the tumor suppressor p53.	Cisplatin	102-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-168
15755509-5	2005	More importantly, AK04 was 12-32-fold more potent than chlorambucil in all bcr-abl+ cells of our cell panel.	Chlorambucil	55-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
15755509-9	2005	These results suggest that AK04 is a nitrogen mustard with binary bcr-abl/DNA targeting effects, a property that may account for its superior potency when compared with the classical mustard chlorambucil.	Nitrogen	37-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
15878500-0	2005	Synthesis and in vitro examination of [124I]-, [125I]- and [131I]-2-(4-iodophenylamino) pyrido[2,3-d]pyrimidin-7-one radiolabeled Abl kinase inhibitors.	2-(4-iodophenylamino)pyrido(2,3-d)pyrimidin-7-one	66-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-133
15878500-1	2005	The pyridopyrimidinones are a potent class of inhibitors of c-Abl kinase and Bcr-Abl kinase, the causative fusion protein in chronic myelogenous leukemia and Src family kinases.	pyridopyrimidinones	4-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-65
15878500-1	2005	The pyridopyrimidinones are a potent class of inhibitors of c-Abl kinase and Bcr-Abl kinase, the causative fusion protein in chronic myelogenous leukemia and Src family kinases.	pyridopyrimidinones	4-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
15878500-6	2005	The 4-iodophenylpyridopyrimidinone 2 inhibited recombinant Abl kinase activity with an IC(50) of 2.0 nM.	4-iodophenylpyridopyrimidinone	4-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-62
15878500-8	2005	Rapid cellular uptake and equilibrium were observed within 10-15 min using [(131)I]-4-iodophenylpyridopyrimidinone 6c in K562 and A431 cells and demonstrated a 2.8-fold uptake selectivity for the Bcr-Abl-expressing K562 cells at 60 min.	iodophenylpyridopyrimidinone 6c	86-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	196-203
15878500-9	2005	These results suggest that pyridopyrimidinone radiotracers may be useful in imaging Abl-, Bcr-Abl- or Src-expressing malignancies.	Pyrido[3,2-d]pyrimidin-2(1H)-one	27-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-87
15878500-9	2005	These results suggest that pyridopyrimidinone radiotracers may be useful in imaging Abl-, Bcr-Abl- or Src-expressing malignancies.	Pyrido[3,2-d]pyrimidin-2(1H)-one	27-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
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 Mesylate	31-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
15626746-4	2005	The BCR/ABL inhibitor imatinib (=STI571) decreased the expression of MCL-1 in these cells.	Imatinib Mesylate	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 Mesylate	33-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
15626746-6	2005	BCR/ABL-dependent expression of MCL-1 in Ba/F3 cells was counteracted by the mitogen-activated protein-kinase/extracellular signal-regulated kinase (MEK) inhibitor, PD98059, but not by the phosphoinositide 3-kinase inhibitor, LY294002.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	165-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
15626746-6	2005	BCR/ABL-dependent expression of MCL-1 in Ba/F3 cells was counteracted by the mitogen-activated protein-kinase/extracellular signal-regulated kinase (MEK) inhibitor, PD98059, but not by the phosphoinositide 3-kinase inhibitor, LY294002.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	226-234	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-32
15604220-0	2005	Synergy between imatinib and mycophenolic acid in inducing apoptosis in cell lines expressing Bcr-Abl.	Imatinib Mesylate	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
15604220-0	2005	Synergy between imatinib and mycophenolic acid in inducing apoptosis in cell lines expressing Bcr-Abl.	Mycophenolic Acid	29-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
15604220-4	2005	We have demonstrated that mycophenolic acid (MPA), a specific inosine monophosphate dehydrogenase (IMPDH) inhibitor that results in depletion of intracellular guanine nucleotides, is synergistic with imatinib in inducing apoptosis in Bcr-Abl-expressing cell lines.	Mycophenolic Acid	26-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	234-241
15604220-4	2005	We have demonstrated that mycophenolic acid (MPA), a specific inosine monophosphate dehydrogenase (IMPDH) inhibitor that results in depletion of intracellular guanine nucleotides, is synergistic with imatinib in inducing apoptosis in Bcr-Abl-expressing cell lines.	Mycophenolic Acid	45-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	234-241
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 Mesylate	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
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 Mesylate	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
15840387-0	2005	Imatinib (STI571) induces DNA damage in BCR/ABL-expressing leukemic cells but not in normal lymphocytes.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	46-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	298-305
15735735-6	2005	The results further demonstrate that c-Abl-mediated phosphorylation of Arg on Y-261 similarly confers Arg stabilization.	Arginine	71-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-42
15735735-6	2005	The results further demonstrate that c-Abl-mediated phosphorylation of Arg on Y-261 similarly confers Arg stabilization.	Arginine	102-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-42
15540985-0	2005	Modulation of the p38 MAPK (mitogen-activated protein kinase) pathway through Bcr/Abl: implications in the cellular response to Ara-C.	Cytarabine	128-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
15540985-9	2005	Our results demonstrate that the involvement of Bcr/Abl in the p38 MAPK pathway is a key mechanism for explaining resistance to Ara-C, and could provide a clue for new therapeutic approaches based on the use of specific Abl inhibitors.	Cytarabine	128-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
15540985-9	2005	Our results demonstrate that the involvement of Bcr/Abl in the p38 MAPK pathway is a key mechanism for explaining resistance to Ara-C, and could provide a clue for new therapeutic approaches based on the use of specific Abl inhibitors.	Cytarabine	128-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-55
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 Mesylate	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 Mesylate	38-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
15846067-0	2005	Kinase-addiction and bi-phasic sensitivity-resistance of Bcr-Abl- and Raf-1-expressing cells to imatinib and geldanamycin.	Imatinib Mesylate	96-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
15846067-0	2005	Kinase-addiction and bi-phasic sensitivity-resistance of Bcr-Abl- and Raf-1-expressing cells to imatinib and geldanamycin.	geldanamycin	109-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
15846067-1	2005	By activating anti-apoptotic factors (e.g., Hsp70, Raf-1, Bcl-xL), Bcr-Abl blocks apoptotic pathways at multiple levels, thus rendering leukemia cells resistant to chemotherapeutic agents such as doxorubicin (DOX).	Doxorubicin	196-207	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
15846067-1	2005	By activating anti-apoptotic factors (e.g., Hsp70, Raf-1, Bcl-xL), Bcr-Abl blocks apoptotic pathways at multiple levels, thus rendering leukemia cells resistant to chemotherapeutic agents such as doxorubicin (DOX).	Doxorubicin	209-212	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
15846067-3	2005	The Bcr-Abl inhibitor imatinib (Gleevec, STI-571) released the apoptotic stream.	Imatinib Mesylate	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
15846067-3	2005	The Bcr-Abl inhibitor imatinib (Gleevec, STI-571) released the apoptotic stream.	Imatinib Mesylate	41-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
15846067-4	2005	Also, HL/Bcr-Abl cells were hyper-sensitive to geldanamycin (GA), which depletes Bcr-Abl and Raf-1.	geldanamycin	47-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
15846067-4	2005	Also, HL/Bcr-Abl cells were hyper-sensitive to geldanamycin (GA), which depletes Bcr-Abl and Raf-1.	geldanamycin	47-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
15846067-4	2005	Also, HL/Bcr-Abl cells were hyper-sensitive to geldanamycin (GA), which depletes Bcr-Abl and Raf-1.	geldanamycin	61-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
15846067-4	2005	Also, HL/Bcr-Abl cells were hyper-sensitive to geldanamycin (GA), which depletes Bcr-Abl and Raf-1.	geldanamycin	61-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
15846067-5	2005	Raf-1 and Bcr-Abl-transfected FDC-P1 hematopoietic cells were selectively sensitive to GA and imatinib, respectively.	geldanamycin	87-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
15846067-5	2005	Raf-1 and Bcr-Abl-transfected FDC-P1 hematopoietic cells were selectively sensitive to GA and imatinib, respectively.	Imatinib Mesylate	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 Mesylate	126-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
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 Mesylate	157-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	98-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-148
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 Mesylate	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
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.	suberanoylanilide hydroxamic acid	17-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
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.	suberanoylanilide hydroxamic acid	17-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	239-246
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.	tanespimycin	55-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
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.	tanespimycin	55-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	239-246
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 Mesylate	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).	tanespimycin	176-214	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	246-253
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
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 Mesylate	182-190	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
15657060-4	2005	We show that c-Abl phosphorylates caspase-9 on Tyr-153 in vitro and in cells treated with DNA damaging agents.	Tyrosine	47-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-18
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 Mesylate	35-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-29
15632178-3	2005	We report here that Abl from mitotic cells or cells treated with the protein phosphatase inhibitor okadaic acid remains active when detached from the extracellular matrix.	Okadaic Acid	99-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-23
15632178-4	2005	Aspartic acid substitution of Thr(566), which is phosphorylated in mitotic or okadaic acid-treated cells, is sufficient to abolish F-actin-mediated inhibition and to maintain Abl activity despite cell detachment.	Aspartic Acid	0-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-178
15632178-4	2005	Aspartic acid substitution of Thr(566), which is phosphorylated in mitotic or okadaic acid-treated cells, is sufficient to abolish F-actin-mediated inhibition and to maintain Abl activity despite cell detachment.	Threonine	30-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-178
15632178-4	2005	Aspartic acid substitution of Thr(566), which is phosphorylated in mitotic or okadaic acid-treated cells, is sufficient to abolish F-actin-mediated inhibition and to maintain Abl activity despite cell detachment.	Okadaic Acid	78-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-178
15632178-7	2005	Immediately following the kinase domain in Abl is a proline-rich linker (PRL) that binds to several SH3 adaptor proteins.	Proline	52-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-46
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	233-241	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-59
15649617-3	2005	Present study describes the cytotoxicity of BA on human CML cell line K-562, positive for Bcr-Abl.	betulinic acid	44-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
15649617-7	2005	RT-PCR confirmed the expression levels of Bcr-Abl in controls and K-562 cells treated with BA.	betulinic acid	91-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
15649617-8	2005	The rapid loss of MMP of K-562 cells upon treatment with BA shows the direct activation of apoptosis at the level of mitochondria, overcoming the resistance of the high levels of expression of Bcr-Abl.	betulinic acid	57-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	193-200
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 Mesylate	133-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
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 Mesylate	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 Mesylate	91-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
15345592-8	2005	These BCR-ABL mutations were associated with varying levels of imatinib resistance.	Imatinib Mesylate	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 Mesylate	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-60
15721630-1	2005	The BCR/ABL tyrosine kinase inhibitor imatinib has shown remarkable efficacy in treating patients with chronic myelogenous leukemia (CML).	Imatinib Mesylate	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 Mesylate	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
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.	Tyrosine	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
15803362-1	2005	BACKGROUND: Imatinib mesylate is a potent inhibitor of Abl, KIT, and PDGFR tyrosine kinases.	Imatinib Mesylate	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-58
15738656-2	2005	In chronic myeloid leukaemia (CML), the Bcr-Abl kinase inhibitor imatinib (STI571, Gleevec) induces impressive response rates.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	0-17	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 Mesylate	19-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-134
15791812-3	2005	Imatinib mesylate, a selective BCR-ABL tyrosine kinase inhibitor, was first given to a patient with CML in June 1998.	Imatinib Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
15696159-5	2005	Phosphorylation of c-Abl on Thr 735 functions as a site for direct binding to 14-3-3 proteins.	Threonine	28-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-24
15659698-0	2005	Effects of 17-allylamino-17-demethoxygeldanamycin (17-AAG) on pediatric acute lymphoblastic leukemia (ALL) with respect to Bcr-Abl status and imatinib mesylate sensitivity.	tanespimycin	11-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-130
15659698-5	2005	We describe experiments in which 17-allylamino-17-demethoxygeldanamycin (17-AAG) was evaluated in the context of Bcr-Abl and resistance to imatinib mesylate.	tanespimycin	33-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
15659698-5	2005	We describe experiments in which 17-allylamino-17-demethoxygeldanamycin (17-AAG) was evaluated in the context of Bcr-Abl and resistance to imatinib mesylate.	tanespimycin	73-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
15659698-12	2005	We describe an experimental approach to investigate the complex interaction between Bcr-Abl status, imatinib mesylate sensitivity, and 17-AAG in pediatric ALL.	tanespimycin	135-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-148
15716362-2	2005	Here, we report highly sensitive and label-free direct electrical detection of small-molecule inhibitors of ATP binding to Abl by using silicon nanowire field-effect transistor devices.	Adenosine Triphosphate	108-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-126
15716362-2	2005	Here, we report highly sensitive and label-free direct electrical detection of small-molecule inhibitors of ATP binding to Abl by using silicon nanowire field-effect transistor devices.	Silicon	136-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-126
15716362-3	2005	Abl, which is a protein tyrosine kinase whose constitutive activity is responsible for chronic myelogenous leukemia, was covalently linked to the surfaces of silicon nanowires within microfluidic channels to create active electrical devices.	Silicon	158-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
15499612-1	2005	STI571, or imatinib, selectively inhibits BCR/ABL, PDGFR and c-kit kinase activity.	Imatinib Mesylate	0-6	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 Mesylate	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
15459011-0	2005	A cell-based screen for resistance of Bcr-Abl-positive leukemia identifies the mutation pattern for PD166326, an alternative Abl kinase inhibitor.	PD 166326	100-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
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 Mesylate	138-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
15459011-7	2005	In addition, PD166326 produced a distinct pattern of Bcr-Abl mutations.	PD 166326	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
15514006-3	2005	In K562 cells, exposure to LBH589 attenuated Bcr-Abl, p-AKT, and p-ERK1/2.	Panobinostat	27-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
15514006-5	2005	The hsp90 inhibitor 17-allyl-amino-demethoxy geldanamycin (17-AAG) also induced polyubiquitylation and proteasomal degradation of FLT-3 and Bcr-Abl by reducing their chaperone association with hsp90.	17-allyl-amino-demethoxy geldanamycin	20-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
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 Mesylate	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 Mesylate	7-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-174
15677719-0	2005	A non-ATP-competitive inhibitor of BCR-ABL overrides imatinib resistance.	Adenosine Triphosphate	6-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
15677719-0	2005	A non-ATP-competitive inhibitor of BCR-ABL overrides imatinib resistance.	Imatinib Mesylate	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
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 Mesylate	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 Mesylate	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	234-242	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
15681433-6	2005	Further analysis revealed that Shc is required for v-Abl-mediated Raf tyrosine 340 and 341 phosphorylation, an event associated with Erk phosphorylation.	Tyrosine	70-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-56
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
15388581-1	2005	Bcr-Abl-expressing primary or cultured leukemia cells display high levels of the antiapoptotic heat shock protein (hsp) 70 and are resistant to cytarabine (Ara-C), etoposide, or Apo-2L/TRAIL (TNF-related apoptosis-inducing ligand)-induced apoptosis.	Cytarabine	144-154	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
15388581-1	2005	Bcr-Abl-expressing primary or cultured leukemia cells display high levels of the antiapoptotic heat shock protein (hsp) 70 and are resistant to cytarabine (Ara-C), etoposide, or Apo-2L/TRAIL (TNF-related apoptosis-inducing ligand)-induced apoptosis.	Cytarabine	156-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
15388581-1	2005	Bcr-Abl-expressing primary or cultured leukemia cells display high levels of the antiapoptotic heat shock protein (hsp) 70 and are resistant to cytarabine (Ara-C), etoposide, or Apo-2L/TRAIL (TNF-related apoptosis-inducing ligand)-induced apoptosis.	Etoposide	164-173	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
15710324-1	2005	The Abl inhibitor imatinib is a highly effective therapy for patients with chronic myeloid leukemia.	Imatinib Mesylate	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 Mesylate	49-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
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 Mesylate	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 Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-144
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 Mesylate	15-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	212-215
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 Mesylate	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 Mesylate	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-158
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.	methyl-thiazol-tetrazolium	235-261	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-158
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.	monooxyethylene trimethylolpropane tristearate	263-266	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-158
15659545-0	2005	The Abl/Arg substrate ArgBP2/nArgBP2 coordinates the function of multiple regulatory mechanisms converging on the actin cytoskeleton.	Arginine	8-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
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 Mesylate	15-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	240-243
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.	Arsenic	27-34	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.	Arsenic	27-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	240-243
15748444-0	2005	[Effect of tetrandrine combined with Droloxifen on the expression of bcr/abl of K562 at both mRNA and protein levels].	tetrandrine	11-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
15748444-0	2005	[Effect of tetrandrine combined with Droloxifen on the expression of bcr/abl of K562 at both mRNA and protein levels].	droloxifen	37-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
15659545-6	2005	At least two of the ArgBP2/nArgBP2 binding partners, synaptojanin 2B and WAVE2, undergo ubiquitination and Abl-dependent tyrosine phosphorylation.	Tyrosine	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-110
15677719-4	2005	In our quest to develop new BCR-ABL inhibitors, we chose to target regions outside the ATP-binding site of this enzyme because these compounds offer the potential to be unaffected by mutations that make CML cells resistant to imatinib.	Adenosine Triphosphate	87-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
15677719-5	2005	Here we describe the activity of one compound, ON012380, that can specifically inhibit BCR-ABL and induce cell death of Ph+ CML cells at a concentration of <10 nM.	ON012380	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
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 Mesylate	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 Mesylate	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
15748444-1	2005	To observe the effect of Tetrandrine (tet) combined with Droloxifen (DRL) on the expression of bcr/abl mRNA and P(210) BCR/ABL protein of K562 cell line, after K562 cells were cultured in the medium containing Tet (1 micromol/L), DRL (5 micromol/L) separately or in their combination for some time, the changes of bcr/abl mRNA and protein expression were detected by RT-PCR and Western blot respectively.	tetrandrine	25-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
15748444-1	2005	To observe the effect of Tetrandrine (tet) combined with Droloxifen (DRL) on the expression of bcr/abl mRNA and P(210) BCR/ABL protein of K562 cell line, after K562 cells were cultured in the medium containing Tet (1 micromol/L), DRL (5 micromol/L) separately or in their combination for some time, the changes of bcr/abl mRNA and protein expression were detected by RT-PCR and Western blot respectively.	tetrandrine	25-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-126
15748444-1	2005	To observe the effect of Tetrandrine (tet) combined with Droloxifen (DRL) on the expression of bcr/abl mRNA and P(210) BCR/ABL protein of K562 cell line, after K562 cells were cultured in the medium containing Tet (1 micromol/L), DRL (5 micromol/L) separately or in their combination for some time, the changes of bcr/abl mRNA and protein expression were detected by RT-PCR and Western blot respectively.	tet	38-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
15748444-1	2005	To observe the effect of Tetrandrine (tet) combined with Droloxifen (DRL) on the expression of bcr/abl mRNA and P(210) BCR/ABL protein of K562 cell line, after K562 cells were cultured in the medium containing Tet (1 micromol/L), DRL (5 micromol/L) separately or in their combination for some time, the changes of bcr/abl mRNA and protein expression were detected by RT-PCR and Western blot respectively.	tet	38-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-126
15748444-1	2005	To observe the effect of Tetrandrine (tet) combined with Droloxifen (DRL) on the expression of bcr/abl mRNA and P(210) BCR/ABL protein of K562 cell line, after K562 cells were cultured in the medium containing Tet (1 micromol/L), DRL (5 micromol/L) separately or in their combination for some time, the changes of bcr/abl mRNA and protein expression were detected by RT-PCR and Western blot respectively.	droloxifen	57-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
15748444-1	2005	To observe the effect of Tetrandrine (tet) combined with Droloxifen (DRL) on the expression of bcr/abl mRNA and P(210) BCR/ABL protein of K562 cell line, after K562 cells were cultured in the medium containing Tet (1 micromol/L), DRL (5 micromol/L) separately or in their combination for some time, the changes of bcr/abl mRNA and protein expression were detected by RT-PCR and Western blot respectively.	droloxifen	57-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-126
15748444-1	2005	To observe the effect of Tetrandrine (tet) combined with Droloxifen (DRL) on the expression of bcr/abl mRNA and P(210) BCR/ABL protein of K562 cell line, after K562 cells were cultured in the medium containing Tet (1 micromol/L), DRL (5 micromol/L) separately or in their combination for some time, the changes of bcr/abl mRNA and protein expression were detected by RT-PCR and Western blot respectively.	tetramethylenedisulfotetramine	25-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
15748444-1	2005	To observe the effect of Tetrandrine (tet) combined with Droloxifen (DRL) on the expression of bcr/abl mRNA and P(210) BCR/ABL protein of K562 cell line, after K562 cells were cultured in the medium containing Tet (1 micromol/L), DRL (5 micromol/L) separately or in their combination for some time, the changes of bcr/abl mRNA and protein expression were detected by RT-PCR and Western blot respectively.	tetramethylenedisulfotetramine	25-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-126
15748444-3	2005	However, Tet in combination with DRL began to downregulate bcr/abl mRNA and P(210) BCR/ABL expression of K562 cells at 48 h and 72 h, respectively.	tetramethylenedisulfotetramine	9-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
15748444-3	2005	However, Tet in combination with DRL began to downregulate bcr/abl mRNA and P(210) BCR/ABL expression of K562 cells at 48 h and 72 h, respectively.	tetramethylenedisulfotetramine	9-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
15748444-4	2005	It is concluded that tetrandrine in combination with Droloxifen can downregulate the expression of bcr/abl mRNA and P(210) BCR/ABL protein and the combination may be involved in the mechanism underlying the reverse effects on multidrug resistance in leukemia.	tetrandrine	21-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
15748444-4	2005	It is concluded that tetrandrine in combination with Droloxifen can downregulate the expression of bcr/abl mRNA and P(210) BCR/ABL protein and the combination may be involved in the mechanism underlying the reverse effects on multidrug resistance in leukemia.	tetrandrine	21-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-130
15748444-4	2005	It is concluded that tetrandrine in combination with Droloxifen can downregulate the expression of bcr/abl mRNA and P(210) BCR/ABL protein and the combination may be involved in the mechanism underlying the reverse effects on multidrug resistance in leukemia.	droloxifen	53-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
15748444-4	2005	It is concluded that tetrandrine in combination with Droloxifen can downregulate the expression of bcr/abl mRNA and P(210) BCR/ABL protein and the combination may be involved in the mechanism underlying the reverse effects on multidrug resistance in leukemia.	droloxifen	53-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-130
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 Mesylate	23-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
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 Mesylate	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 Mesylate	163-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
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 Mesylate	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	220-227
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 Mesylate	148-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
15558795-0	2005	Overproduction of BCR-ABL induces apoptosis in imatinib mesylate-resistant cell lines.	Imatinib Mesylate	47-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
15558795-1	2005	BACKGROUND: Imatinib mesylate, a BCR-ABL tyrosine kinase inhibitor, induces apoptosis in chronic myeloid leukemia cells.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	145-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
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 Mesylate	32-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
15583844-0	2005	The histone deacetylase inhibitor suberoylanilide hydroxamic acid down-regulates expression levels of Bcr-abl, c-Myc and HDAC3 in chronic myeloid leukemia cell lines.	Vorinostat	34-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
16304378-1	2005	The treatment of chronic myeloid leukemia (CML) has been revolutionized by the small molecule BCR-ABL-selective kinase inhibitor imatinib.	Imatinib Mesylate	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 Mesylate	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.	Dasatinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
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.	Dasatinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-177
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 Mesylate	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 Mesylate	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
15583844-2	2005	In the present study, we show that the histone deacetylase inhibitor SAHA (suberoylanilide hydroxamic acid) markedly decreases protein expression levels of Bcr-Abl and c-Myc in BV-173 cells, while in K562 cells only a minor decrease of Bcr-Abl protein levels is observed while a considerable reduction of c-Myc protein expression may only be achieved at higher concentrations of SAHA.	Vorinostat	69-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
15583844-2	2005	In the present study, we show that the histone deacetylase inhibitor SAHA (suberoylanilide hydroxamic acid) markedly decreases protein expression levels of Bcr-Abl and c-Myc in BV-173 cells, while in K562 cells only a minor decrease of Bcr-Abl protein levels is observed while a considerable reduction of c-Myc protein expression may only be achieved at higher concentrations of SAHA.	Vorinostat	69-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	236-243
15583844-2	2005	In the present study, we show that the histone deacetylase inhibitor SAHA (suberoylanilide hydroxamic acid) markedly decreases protein expression levels of Bcr-Abl and c-Myc in BV-173 cells, while in K562 cells only a minor decrease of Bcr-Abl protein levels is observed while a considerable reduction of c-Myc protein expression may only be achieved at higher concentrations of SAHA.	Vorinostat	75-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
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 Mesylate	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 Mesylate	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
15583844-2	2005	In the present study, we show that the histone deacetylase inhibitor SAHA (suberoylanilide hydroxamic acid) markedly decreases protein expression levels of Bcr-Abl and c-Myc in BV-173 cells, while in K562 cells only a minor decrease of Bcr-Abl protein levels is observed while a considerable reduction of c-Myc protein expression may only be achieved at higher concentrations of SAHA.	Vorinostat	75-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	236-243
15583844-2	2005	In the present study, we show that the histone deacetylase inhibitor SAHA (suberoylanilide hydroxamic acid) markedly decreases protein expression levels of Bcr-Abl and c-Myc in BV-173 cells, while in K562 cells only a minor decrease of Bcr-Abl protein levels is observed while a considerable reduction of c-Myc protein expression may only be achieved at higher concentrations of SAHA.	Vorinostat	379-383	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
15583844-5	2005	In conclusion, our results imply a molecular mechanism for SAHA-induced apoptosis in BV-173 cells, which involves decreased protein expression levels of Bcr-Abl, c-Myc and HDAC3.	Vorinostat	59-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
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 Mesylate	34-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-141
15864744-9	2005	In summary, we have demonstrated that denbinobin displays anticancer effects in K562 cells through the increase of levels of tubulin polymerization and deregulation of Bcr-Abl signaling.	denbinobin	38-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	168-175
15510211-0	2005	Evidence for D276G and L364I Bcr-Abl mutations in Ph+ leukaemic cells obtained from patients resistant to Imatinib.	Imatinib Mesylate	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
16416674-0	2005	c-Abl is required for staurosporine-induced caspase activity.	Staurosporine	22-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
16416674-6	2005	Here, we report c-Abl dependent caspase-3 and caspase-8 activity in response to staurosporine.	Staurosporine	80-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-21
15610007-6	2004	The anti-b2a2 siRNAs promoted biological effects on KYO-1 cells, because the bcr/abl suppression resulted in the inhibition of cell growth and colony formation in agar and activation of apoptosis and upregulation of the cell-cycle inhibitor p27 protein.	Agar	163-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
15592617-0	2004	Synthesis of N3- and 2-NH2-substituted 6,7-diphenylpterins and their use as intermediates for the preparation of oligonucleotide conjugates designed to target photooxidative damage on single-stranded DNA representing the bcr-abl chimeric gene.	n3- and 2-nh2-substituted 6,7-diphenylpterins	13-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	221-228
15592617-0	2004	Synthesis of N3- and 2-NH2-substituted 6,7-diphenylpterins and their use as intermediates for the preparation of oligonucleotide conjugates designed to target photooxidative damage on single-stranded DNA representing the bcr-abl chimeric gene.	Oligonucleotides	113-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	221-228
15592617-1	2004	Two 17-mer oligodeoxynucleotide-5"-linked-(6,7-diphenylpterin) conjugates, 2 and 3, were prepared as photosensitisers for targeting photooxidative damage to a 34-mer DNA oligodeoxynucleotide (ODN) fragment 1 representing the chimeric bcr-abl gene that is implicated in the pathogenesis of chronic myeloid leukaemia (CML).	6,7-Diphenylpterin	43-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	234-241
15604256-3	2004	PKD2 was found to be the major isoform of the PKD family expressed in chronic myeloid leukemia cells and is tyrosine phosphorylated by Bcr-Abl in its pleckstrin homology domain.	Tyrosine	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
15604256-5	2004	Furthermore, our data show that Bcr-Abl-induced activation of the nuclear factor kappaB cascade in LAMA84 cells is largely mediated by tyrosine-phosphorylated PKD2.	Tyrosine	135-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
15604256-7	2004	Targeting PKD2 tyrosine phosphorylation, not its kinase activity, could be a novel therapeutic approach for the treatment of Bcr-Abl(+) myeloid leukemia.	Tyrosine	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
15448168-0	2004	Phosphorylation of DNA topoisomerase I by the c-Abl tyrosine kinase confers camptothecin sensitivity.	Camptothecin	76-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-51
15448168-10	2004	In addition, loss of topo I phosphorylation in c-Abl-deficient cells conferred resistance to camptothecin-induced apoptosis.	Camptothecin	93-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-52
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-189
15505216-4	2004	We have produced a mutant allele of BCR-ABL (T315A) that is uniquely inhibitable by the small molecule 4-amino-1-tert-butyl-3-(1-naphthyl)pyrazolo[3,4-d]pyrimidine and used it to demonstrate that sole suppression of BCR-ABL activity was insufficient to eliminate BCR-ABL(+) KIT(+)-expressing immature murine myeloid leukemic cells.	4-amino-1-tert-butyl-3-(1-naphthyl)pyrazolo[3,4-d]pyrimidine	103-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
15505216-5	2004	In contrast, imatinib mesylate effectively eliminated BCR-ABL(+) KIT(+)-expressing leukemic cells.	Imatinib Mesylate	13-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
15501042-0	2004	Urea derivatives of STI571 as inhibitors of Bcr-Abl and PDGFR kinases.	Urea	0-4	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
15501042-0	2004	Urea derivatives of STI571 as inhibitors of Bcr-Abl and PDGFR kinases.	Imatinib Mesylate	20-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
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.	Urea	0-4	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-164
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 Mesylate	64-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-164
15501042-3	2004	In particular a dimethylamino-aniline derivative (18) inhibited c-Abl transphosphorylation with an IC(50) value of 56 nM.	dimethylamino-aniline	16-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-69
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 Mesylate	272-280	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-144
15304390-2	2004	We find that BCR/ABL-induced reactive oxygen species (ROSs) cause chronic oxidative DNA damage resulting in double-strand breaks (DSBs) in S and G(2)/M cell cycle phases.	Reactive Oxygen Species	29-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
15304390-2	2004	We find that BCR/ABL-induced reactive oxygen species (ROSs) cause chronic oxidative DNA damage resulting in double-strand breaks (DSBs) in S and G(2)/M cell cycle phases.	Reactive Oxygen Species	54-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
15304390-2	2004	We find that BCR/ABL-induced reactive oxygen species (ROSs) cause chronic oxidative DNA damage resulting in double-strand breaks (DSBs) in S and G(2)/M cell cycle phases.	dsbs	130-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
15496979-6	2004	Synergy between NVP-LAQ824 and imatinib was demonstrated against BCR/ABL-expressing K562 myeloid leukemia cell lines.	Imatinib Mesylate	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
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 Mesylate	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 Mesylate	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
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 Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
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 Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-181
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 Mesylate	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-141
15678915-8	2004	On the other hand, 8 patients who received imatinib without SCT showed a remarkable decrease in bcr-abl/abl ratios.	Imatinib Mesylate	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
15678915-8	2004	On the other hand, 8 patients who received imatinib without SCT showed a remarkable decrease in bcr-abl/abl ratios.	Imatinib Mesylate	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-82
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 Mesylate	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-75
15631652-0	2004	[Identification bcr-abl fusion gene in leukemia cells with oligonucleotide microarray].	Oligonucleotides	59-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
15730714-1	2004	OBJECTIVES: To investigate targeted blockage of BCR/ABL oncoprotein mediated cell transformation by STAT5 decoy oligodeoxynucleotide (ODN), its effect on the growth and proliferation inhibition of K562 cells and the related molecular mechanisms.	Oligodeoxyribonucleotides	112-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
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 Mesylate	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 Mesylate	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
15494718-0	2004	Tyrosine kinase inhibitor AG1024 exerts antileukaemic effects on STI571-resistant Bcr-Abl expressing cells and decreases AKT phosphorylation.	tyrphostin AG 1024	26-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
15494718-0	2004	Tyrosine kinase inhibitor AG1024 exerts antileukaemic effects on STI571-resistant Bcr-Abl expressing cells and decreases AKT phosphorylation.	Imatinib Mesylate	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 Mesylate	61-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
15494718-5	2004	To this end, the TK inhibitor Tyrphostin AG1024 was used to evaluate effect on regulation of BCR-ABL expression, inhibition of cell proliferation and tumour formation in vivo in human and murine BCR-ABL expressing cell lines.	Tyrphostins	30-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
15494718-5	2004	To this end, the TK inhibitor Tyrphostin AG1024 was used to evaluate effect on regulation of BCR-ABL expression, inhibition of cell proliferation and tumour formation in vivo in human and murine BCR-ABL expressing cell lines.	tyrphostin AG 1024	41-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
15494718-6	2004	Tyrphostin AG1024 was shown to downregulate expression of BCR-ABL and P-Akt, and to upregulate DNA-PKcs expression.	Tyrphostins	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
15494718-9	2004	Interestingly, Tyrphostin AG1024 was also effective against cells resistant to STI571 by distinct mechanisms including Bcr-Abl mutation.	Tyrphostins	15-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-126
15372471-2	2004	Imatinib mesylate is a tyrosine kinase inhibitor targeting platelet-derived growth factor receptor-beta (PDGFRB), BCR-ABL, and KIT.	Imatinib Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
15468123-1	2004	BACKGROUND: Constitutive tyrosine phosphorylation derived from Bcr-Abl kinase activity is the major characteristic of Bcr-Abl positive cells.	Tyrosine	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
15468123-1	2004	BACKGROUND: Constitutive tyrosine phosphorylation derived from Bcr-Abl kinase activity is the major characteristic of Bcr-Abl positive cells.	Tyrosine	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
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.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-179
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 Mesylate	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-179
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 Mesylate	25-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
15509806-8	2004	Furthermore, silencing of FoxO3a and BCL6 in BCR-ABL-expressing cells abolishes STI571-mediated effects on cyclin D2.	Imatinib Mesylate	80-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
15179523-0	2004	[Regression of the Philadelphia chromosome (bcr/abl)-positive myelo- and megakaryopoiesis after Imatinib (STI571) therapy in chronic myelogenous leukemia (CML)].	Imatinib Mesylate	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 Mesylate	106-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
15226183-0	2004	Chlorogenic acid inhibits Bcr-Abl tyrosine kinase and triggers p38 mitogen-activated protein kinase-dependent apoptosis in chronic myelogenous leukemic cells.	Chlorogenic Acid	0-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
15226183-1	2004	We report that chlorogenic acid (Chl) induces apoptosis of several Bcr-Abl-positive chronic myelogenous leukemia (CML) cell lines and primary cells from CML patients in vitro and destroys Bcr-Abl-positive K562 cells in vivo.	Chlorogenic Acid	15-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
15226183-1	2004	We report that chlorogenic acid (Chl) induces apoptosis of several Bcr-Abl-positive chronic myelogenous leukemia (CML) cell lines and primary cells from CML patients in vitro and destroys Bcr-Abl-positive K562 cells in vivo.	Chlorogenic Acid	15-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	188-195
15226183-1	2004	We report that chlorogenic acid (Chl) induces apoptosis of several Bcr-Abl-positive chronic myelogenous leukemia (CML) cell lines and primary cells from CML patients in vitro and destroys Bcr-Abl-positive K562 cells in vivo.	Chlorogenic Acid	33-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
15226183-1	2004	We report that chlorogenic acid (Chl) induces apoptosis of several Bcr-Abl-positive chronic myelogenous leukemia (CML) cell lines and primary cells from CML patients in vitro and destroys Bcr-Abl-positive K562 cells in vivo.	Chlorogenic Acid	33-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	188-195
15226183-5	2004	NaChl inhibits autophosphorylation of p210(Bcr-Abl) fusion protein rapidly.	nachl	0-5	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
15226183-6	2004	We demonstrate that p38 phosphorylation is increased in Bcr-Abl-positive cells after treatment with NaChl and closely paralleled the inhibition of Bcr-Abl phosphorylation.	nachl	100-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
15226183-6	2004	We demonstrate that p38 phosphorylation is increased in Bcr-Abl-positive cells after treatment with NaChl and closely paralleled the inhibition of Bcr-Abl phosphorylation.	nachl	100-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-154
15256422-0	2004	Inhibition of wild-type and mutant Bcr-Abl by AP23464, a potent ATP-based oncogenic protein kinase inhibitor: implications for CML.	AP23464	46-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
15256422-2	2004	Imatinib mesylate (Gleevec, STI571), a Bcr-Abl kinase inhibitor, selectively inhibits proliferation and promotes apoptosis of CML cells.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	16-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
15256422-5	2004	AP23464, a potent adenosine 5"-triphosphate (ATP)-based inhibitor of Src and Abl kinases, displays antiproliferative activity against a human CML cell line and Bcr-Abl-transduced Ba/F3 cells (IC(50) = 14 nM; imatinib mesylate IC(50) = 350 nM).	AP23464	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-80
15256422-5	2004	AP23464, a potent adenosine 5"-triphosphate (ATP)-based inhibitor of Src and Abl kinases, displays antiproliferative activity against a human CML cell line and Bcr-Abl-transduced Ba/F3 cells (IC(50) = 14 nM; imatinib mesylate IC(50) = 350 nM).	AP23464	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-167
15256422-5	2004	AP23464, a potent adenosine 5"-triphosphate (ATP)-based inhibitor of Src and Abl kinases, displays antiproliferative activity against a human CML cell line and Bcr-Abl-transduced Ba/F3 cells (IC(50) = 14 nM; imatinib mesylate IC(50) = 350 nM).	Adenosine Triphosphate	45-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-80
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 Mesylate	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
15389905-3	2004	The BCR/ABL fusion gene was detected on a paraffin-embedded tissue section of the lymph node by double-color fluorescence in situ hybridization, indicating an extramedullary hematopoietic tumor of CML origin.	Paraffin	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
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 Mesylate	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 Mesylate	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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-93
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 Mesylate	140-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
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 Mesylate	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
15475456-0	2004	Imatinib (STI571)-mediated changes in glucose metabolism in human leukemia BCR-ABL-positive cells.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
15475456-0	2004	Imatinib (STI571)-mediated changes in glucose metabolism in human leukemia BCR-ABL-positive cells.	Imatinib Mesylate	10-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
15475456-0	2004	Imatinib (STI571)-mediated changes in glucose metabolism in human leukemia BCR-ABL-positive cells.	Glucose	38-45	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 Mesylate	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.	Glucose	39-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
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 Mesylate	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 Mesylate	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 Mesylate	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
15455301-0	2004	[An alternative Abl-kinase inhibitor overcomes imatinib resistance mutations of Bcr-Abl oncogenes].	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	117-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
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.	pyrido(3,2-d)pyrimidine	133-150	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 Mesylate	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 Mesylate	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
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 Mesylate	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 Mesylate	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 Mesylate	56-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
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 Mesylate	9-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-94
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
15361874-7	2004	The constitutively phosphorylated tyrosine kinase NUP214-ABL1 is sensitive to the tyrosine kinase inhibitor imatinib.	Imatinib Mesylate	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 Mesylate	110-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	7-11
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 Mesylate	98-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-86
15456825-6	2004	Biochemical assays using a glutathione S-transferase pull-down method to determine GTP-bound active Rho GTPases demonstrate that Abl inhibition increases RhoA activity but has no effect on the activity of Rac1 or Cdc42.	Glutathione	27-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-132
15456825-6	2004	Biochemical assays using a glutathione S-transferase pull-down method to determine GTP-bound active Rho GTPases demonstrate that Abl inhibition increases RhoA activity but has no effect on the activity of Rac1 or Cdc42.	Guanosine Triphosphate	83-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-132
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 Mesylate	64-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-178
15456825-10	2004	The CA-Abl phenotype is not affected by destabilization of microtubules but is reversed partially when actin filaments are stabilized with jasplakinolide.	jasplakinolide	139-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	7-10
15368327-6	2004	RESULTS: Two of the designed ds/siRNAs decreased the target mRNA levels markedly (determined by reverse transcriptase-polymerase chain reaction analysis) and bcr-abl/c-abl oncoproteins (determined by flow cytometry using Fluor-488-labeled, anti-c-abl antibody as well as by Western blot analysis).	fluor-488	221-230	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-165
15368327-6	2004	RESULTS: Two of the designed ds/siRNAs decreased the target mRNA levels markedly (determined by reverse transcriptase-polymerase chain reaction analysis) and bcr-abl/c-abl oncoproteins (determined by flow cytometry using Fluor-488-labeled, anti-c-abl antibody as well as by Western blot analysis).	fluor-488	221-230	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	245-250
15313630-11	2004	Furthermore, the mutation by Tyr of two proline residues in APP-RP1, which are essential for the binding of some linear peptides to Abl-SH3, demonstrates the effectiveness of the scaffold in enhancing the variability in the design of high-affinity and high-specificity ligands for any SH3 domain.	Tyrosine	29-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-135
15313630-11	2004	Furthermore, the mutation by Tyr of two proline residues in APP-RP1, which are essential for the binding of some linear peptides to Abl-SH3, demonstrates the effectiveness of the scaffold in enhancing the variability in the design of high-affinity and high-specificity ligands for any SH3 domain.	Proline	40-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-135
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
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 Mesylate	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 Mesylate	85-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-105
15548364-3	2004	Using a p73-specific antibody, we confirmed that c-Abl is required for cisplatin-induced p73 upregulation, and further demonstrate that the p73 protein is upregulated by UV irradiation and other stress stimuli including sorbitol, hydrogen peroxide, nocodazol, and taxol.	Cisplatin	71-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-54
15548364-3	2004	Using a p73-specific antibody, we confirmed that c-Abl is required for cisplatin-induced p73 upregulation, and further demonstrate that the p73 protein is upregulated by UV irradiation and other stress stimuli including sorbitol, hydrogen peroxide, nocodazol, and taxol.	Sorbitol	220-228	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-54
15548364-3	2004	Using a p73-specific antibody, we confirmed that c-Abl is required for cisplatin-induced p73 upregulation, and further demonstrate that the p73 protein is upregulated by UV irradiation and other stress stimuli including sorbitol, hydrogen peroxide, nocodazol, and taxol.	Hydrogen Peroxide	230-247	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-54
15548364-3	2004	Using a p73-specific antibody, we confirmed that c-Abl is required for cisplatin-induced p73 upregulation, and further demonstrate that the p73 protein is upregulated by UV irradiation and other stress stimuli including sorbitol, hydrogen peroxide, nocodazol, and taxol.	Nocodazole	249-258	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-54
15548364-3	2004	Using a p73-specific antibody, we confirmed that c-Abl is required for cisplatin-induced p73 upregulation, and further demonstrate that the p73 protein is upregulated by UV irradiation and other stress stimuli including sorbitol, hydrogen peroxide, nocodazol, and taxol.	Paclitaxel	264-269	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-54
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 Mesylate	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	2-9
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 Mesylate	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 Mesylate	42-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-103
15289338-9	2004	Expression of BCR/ABL genes with deletions of either the COOH-terminal actin binding or proline-rich domains resulted in enhanced adhesion and chemotaxis compared with wild-type BCR/ABL but did not affect progenitor proliferation.	Proline	88-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
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 Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	146-149
15175272-3	2004	We show that YT521-B is tyrosine phosphorylated by c-Abl in the nucleus.	Tyrosine	24-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-56
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 Mesylate	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-96
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 Mesylate	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-57
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-100
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 Mesylate	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
15197326-2	2004	The p53-family members, p63 and p73, are highly similar to p53, yet are differentially activated by IR, UV and cis-platinum via ATM and c-abl/ATR signaling pathways.	Cisplatin	111-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-141
15324693-1	2004	The ABL inhibitor imatinib is a highly effective therapy for patients with chronic myeloid leukemia.	Imatinib Mesylate	18-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
15256422-6	2004	AP23464 ablates Bcr-Abl tyrosine phosphorylation, blocks cell cycle progression, and promotes apoptosis of Bcr-Abl-expressing cells.	AP23464	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
15256422-6	2004	AP23464 ablates Bcr-Abl tyrosine phosphorylation, blocks cell cycle progression, and promotes apoptosis of Bcr-Abl-expressing cells.	AP23464	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
15256422-6	2004	AP23464 ablates Bcr-Abl tyrosine phosphorylation, blocks cell cycle progression, and promotes apoptosis of Bcr-Abl-expressing cells.	Tyrosine	24-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
15256422-7	2004	Biochemical assays with purified glutathione S transferase (GST)-Abl kinase domain confirmed that AP23464 directly inhibits Abl activity.	AP23464	98-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-68
15256422-7	2004	Biochemical assays with purified glutathione S transferase (GST)-Abl kinase domain confirmed that AP23464 directly inhibits Abl activity.	AP23464	98-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-127
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.	AP23464	81-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-154
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 Mesylate	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.	AP23464	15-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
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 Mesylate	31-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
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 Mesylate	52-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-41
15289456-4	2004	c-abl-/- osteoblasts displayed enhanced Prx I induction, elevated Nrf2 levels, and hypersusceptibility to arsenate, which were reinstated by reconstitution of c-Abl; Atm-/- osteoblasts showed the opposite.	arsenic acid	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
15289456-4	2004	c-abl-/- osteoblasts displayed enhanced Prx I induction, elevated Nrf2 levels, and hypersusceptibility to arsenate, which were reinstated by reconstitution of c-Abl; Atm-/- osteoblasts showed the opposite.	arsenic acid	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-164
15201856-0	2004	Efficacy of dual-specific Bcr-Abl and Src-family kinase inhibitors in cells sensitive and resistant to imatinib mesylate.	Imatinib Mesylate	103-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
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 Mesylate	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.	pyrido[2,3-d] pyrimidines	25-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	123-130	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).	PD 166326	143-151	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).	ok171	203-208	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-41
15039284-0	2004	Bortezomib and flavopiridol interact synergistically to induce apoptosis in chronic myeloid leukemia cells resistant to imatinib mesylate through both Bcr/Abl-dependent and -independent mechanisms.	Bortezomib	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-158
15363137-3	2004	All patients with stable MC (90% </= DC < 95%) and bcr/abl negative had a probability of long-term survival with molecular remission, however the result of bcr/abl positivity was not always associated with leukemia relapse, only the patient with decreasing values of donor chimerism as well as bcr/abl positive proved to be in a higher risk of relapse or graft failure.	Methylcholanthrene	25-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-23
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 Mesylate	210-216	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	192-199
15039284-0	2004	Bortezomib and flavopiridol interact synergistically to induce apoptosis in chronic myeloid leukemia cells resistant to imatinib mesylate through both Bcr/Abl-dependent and -independent mechanisms.	alvocidib	15-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-158
15039284-1	2004	Interactions between the cyclin-dependent kinase (CDK) inhibitor flavopiridol and the proteasome inhibitor bortezomib were examined in Bcr/Abl(+) human leukemia cells.	Bortezomib	107-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
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 Mesylate	3-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
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 Mesylate	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 Mesylate	89-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-9
15256671-0	2004	Overriding imatinib resistance with a novel ABL kinase inhibitor.	Imatinib Mesylate	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-47
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-121
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 Mesylate	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.	Bortezomib	83-93	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.	Bortezomib	83-93	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.	alvocidib	94-106	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.	alvocidib	94-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	185-192
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 Mesylate	35-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
15039284-7	2004	The capacity of flavopiridol to promote bortezomib-mediated Bcr/Abl down-regulation and apoptosis was mimicked by the positive transcription elongation factor-b (P-TEFb) inhibitor DRB (5,6-dichloro 1-beta-d-ribofuranosylbenzinida-sole).	alvocidib	16-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
15039284-7	2004	The capacity of flavopiridol to promote bortezomib-mediated Bcr/Abl down-regulation and apoptosis was mimicked by the positive transcription elongation factor-b (P-TEFb) inhibitor DRB (5,6-dichloro 1-beta-d-ribofuranosylbenzinida-sole).	Bortezomib	40-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
15039284-7	2004	The capacity of flavopiridol to promote bortezomib-mediated Bcr/Abl down-regulation and apoptosis was mimicked by the positive transcription elongation factor-b (P-TEFb) inhibitor DRB (5,6-dichloro 1-beta-d-ribofuranosylbenzinida-sole).	Dichlororibofuranosylbenzimidazole	180-183	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
15039284-7	2004	The capacity of flavopiridol to promote bortezomib-mediated Bcr/Abl down-regulation and apoptosis was mimicked by the positive transcription elongation factor-b (P-TEFb) inhibitor DRB (5,6-dichloro 1-beta-d-ribofuranosylbenzinida-sole).	5,6-dichloro 1-beta-d-ribofuranosylbenzinida	185-229	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
15039284-8	2004	Finally, the bortezomib/flavopiridol regimen also potently induced apoptosis in Bcr/Abl(-) human leukemia cells.	Bortezomib	13-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
15039284-8	2004	Finally, the bortezomib/flavopiridol regimen also potently induced apoptosis in Bcr/Abl(-) human leukemia cells.	alvocidib	24-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
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).	Adenosine Monophosphate	12-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
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 Mesylate	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 Mesylate	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 Mesylate	149-157	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	168-175
15194504-0	2004	The two major imatinib resistance mutations E255K and T315I enhance the activity of BCR/ABL fusion kinase.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
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.	Tyrosine	200-208	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
15107311-0	2004	Denaturing-HPLC-based assay for detection of ABL mutations in chronic myeloid leukemia patients resistant to Imatinib.	Imatinib Mesylate	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 Mesylate	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 Mesylate	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
15293570-1	2004	Imatinib mesylate and rituximab are molecularly targeted drugs against the BCR-ABL fusion protein and the CD20 antigen, respectively.	Imatinib Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
15359647-8	2004	Moreover, in response to Imatinib, BCR/ABL transcripts decreased and were no longer detectable after 6 months.	Imatinib Mesylate	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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.	NSC 680410	75-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
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.	U 0126	179-184	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
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.	geldanamycin	201-213	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
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 Mesylate	259-267	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
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 Mesylate	110-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
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 Mesylate	23-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
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 Mesylate	217-225	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-67
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 Mesylate	217-225	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	196-199
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 Mesylate	160-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
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 Mesylate	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
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 Mesylate	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	389-396
15143164-2	2004	Here, we demonstrate direct binding of Grb2 to the Tel-Abl (ETV6-Abl) fusion protein, the product of complex (9;12) chromosomal translocations in human leukemia, via tyrosine 314 encoded by TEL exon 5.	Tyrosine	166-174	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-58
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 Mesylate	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
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 Mesylate	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 Mesylate	123-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
15031292-6	2004	Here, we show that active c-Abl stimulates APP/Fe65-mediated gene transcription and that this effect is mediated by phosphorylation of Fe65 on tyrosine 547 within its second PTB domain.	Tyrosine	143-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-31
15067724-1	2004	The basolateral amygdala (ABL) is essential for the amnestic effects of benzodiazepines in aversive learning tasks.	Benzodiazepines	72-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-29
15067724-10	2004	The activation of alpha1-containing GABA(A) receptors in the ABL by benzodiazepines may disrupt rhythmic oscillations critical for memory consolidation.	Benzodiazepines	68-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-64
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 Mesylate	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 Mesylate	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 Mesylate	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
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 Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
15126367-2	2004	Targeting hsp90 by the ansamycins geldanamycin and 17-allyl-amino-demethoxygeldanamycin (17-AAG) promotes degradation of several proteins through the ubiquitin-proteasome pathway, including oncogenic Raf, v-Src, erbB2, and BCR-ABL.	Lactams, Macrocyclic	23-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	223-230
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 Mesylate	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 Mesylate	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	189-196
15126367-2	2004	Targeting hsp90 by the ansamycins geldanamycin and 17-allyl-amino-demethoxygeldanamycin (17-AAG) promotes degradation of several proteins through the ubiquitin-proteasome pathway, including oncogenic Raf, v-Src, erbB2, and BCR-ABL.	17-allyl-amino-demethoxygeldanamycin	51-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	223-230
15126367-2	2004	Targeting hsp90 by the ansamycins geldanamycin and 17-allyl-amino-demethoxygeldanamycin (17-AAG) promotes degradation of several proteins through the ubiquitin-proteasome pathway, including oncogenic Raf, v-Src, erbB2, and BCR-ABL.	geldanamycin	34-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	223-230
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 Mesylate	65-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
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 Mesylate	59-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	5-12
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 Mesylate	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 Mesylate	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 Mesylate	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-86
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 Mesylate	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
15126530-4	2004	Reports suggest that imatinib may also be effective against ABL and platelet-derived growth factor receptor kinase-dependent pathological conditions.	Imatinib Mesylate	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-63
15014531-0	2004	Dendritic cells become BCR-ABL negative in chronic myeloid leukaemia patients successfully treated with imatinib.	Imatinib Mesylate	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
15036938-0	2004	Mechanisms of transformation by the BCR-ABL oncogene: new perspectives in the post-imatinib era.	Imatinib Mesylate	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
15042680-0	2004	Changes associated with the development of resistance to imatinib (STI571) in two leukemia cell lines expressing p210 Bcr/Abl protein.	Imatinib Mesylate	57-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-125
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 Mesylate	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	241-248
15070699-0	2004	BCR/ABL kinase inhibition by imatinib mesylate enhances MAP kinase activity in chronic myelogenous leukemia CD34+ cells.	Imatinib Mesylate	29-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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 Mesylate	70-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-33
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 Mesylate	70-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
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 Mesylate	70-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-33
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 Mesylate	70-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
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 Mesylate	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 Mesylate	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 Mesylate	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
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 Mesylate	10-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
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 Mesylate	27-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
15135086-3	2004	The latter cells express the BCR/ABL fusion protein, which can be a target of the tyrosine kinase inhibitor STI571.	Imatinib Mesylate	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.	Cisplatin	120-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
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 Mesylate	134-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
15135086-12	2004	Our results suggest also that aside from the BCR/ABL other factors such as p53 level, signal transduction pathways and DNA repair processes can be responsible for the increased sensitivity of K562 cells to cisplatin compared with normal lymphocytes.	Cisplatin	206-215	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
15087031-1	2004	BACKGROUND & OBJECTIVE: The aberrant regulation of the protein tyrosine kinase (PTK) activity of P210(BCR-ABL), which is the protein product of Bcr-Abl fusion gene leads to the pathogenesis of chronic myeloid leukemia (CML).	Adenosine Monophosphate	12-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-113
15087031-1	2004	BACKGROUND & OBJECTIVE: The aberrant regulation of the protein tyrosine kinase (PTK) activity of P210(BCR-ABL), which is the protein product of Bcr-Abl fusion gene leads to the pathogenesis of chronic myeloid leukemia (CML).	Adenosine Monophosphate	12-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	148-155
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	213-216
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.	Adenosine Triphosphate	139-142	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.	Adenosine Triphosphate	139-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
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 Mesylate	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 Mesylate	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 Mesylate	339-347	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	234-241
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.	N-phenylpyrimidin-2-amine	60-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	234-241
15024053-7	2004	Tyrosine phosphorylation in the PH domain at Tyr463, mediated by the Src-Abl pathway, which in turn facilitates the phosphorylation of Ser738/Ser742 in the activation loop, mediated by the Src-PKCdelta pathway.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-76
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 Mesylate	30-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	165-172
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 Mesylate	38-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	165-172
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 Mesylate	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
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.	N-phenylpyrimidin-2-amine	4-27	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 Mesylate	39-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-125
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 Mesylate	88-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-24
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 Mesylate	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 Mesylate	88-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	220-223
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 Mesylate	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-162
15109541-0	2004	Imatinib mesylate (STI571) prevents the mutator phenotype of Bcr-Abl in hematopoietic cell lines.	Imatinib Mesylate	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 Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
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 Mesylate	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 Mesylate	118-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
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 Mesylate	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-29
15171550-7	2004	In cell-based assays of ABL tyrosine phosphorylation, the ability of two kinds of novel, structurally diverse, lead compounds to inhibit ABL kinase activity was observed.	Tyrosine	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-27
15160936-5	2004	Mutations in the ATP binding site of ABL are frequent events which counteract the antileukemic effect of STI571.	Adenosine Triphosphate	17-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-40
15175998-2	2004	These receptor tyrosine kinases, as well as ABL and BCR-ABL, are inhibited by imatinib.	Imatinib Mesylate	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 Mesylate	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
15171550-7	2004	In cell-based assays of ABL tyrosine phosphorylation, the ability of two kinds of novel, structurally diverse, lead compounds to inhibit ABL kinase activity was observed.	Tyrosine	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-140
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 Mesylate	229-236	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-143
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 Mesylate	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 Mesylate	22-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
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 Mesylate	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-102
14670960-2	2004	We demonstrated previously that atypical PKCiota is required for Bcr-Abl-mediated resistance of human K562 chronic myelogenous leukemia (CML) cells to Taxol-induced apoptosis.	Paclitaxel	151-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
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 Mesylate	26-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
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 Mesylate	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 Mesylate	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 Mesylate	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.	Sirolimus	0-9	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 Mesylate	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 Mesylate	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
15050919-4	2004	Furthermore, BCR/ABL increases DNA double-strand damage after etoposide treatment and leads to a defect in an intra-S phase checkpoint, causing a radioresistant DNA synthesis (RDS) phenotype.	Etoposide	62-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
14657961-6	2004	Cells in which c-Abl expression was knocked down by RNA interference resisted cisplatin- but not TNFalpha-induced apoptosis.	Cisplatin	78-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-20
14657961-7	2004	A similar selective resistance against cisplatin-induced apoptosis was observed when cleavage resistant c-Abl was overexpressed in treated cells.	Cisplatin	39-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-109
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 Mesylate	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-71
14993293-2	2004	Here, we show that the related kinase Arg is activated downstream of PDGFRs in a manner dependent on Src family kinases and phospholipase C gamma1 (PLC-gamma1)-mediated phosphatidylinositol 4,5-bisphosphate (PIP2) hydrolysis, as we showed previously for c-Abl.	Arginine	38-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	254-259
14993293-2	2004	Here, we show that the related kinase Arg is activated downstream of PDGFRs in a manner dependent on Src family kinases and phospholipase C gamma1 (PLC-gamma1)-mediated phosphatidylinositol 4,5-bisphosphate (PIP2) hydrolysis, as we showed previously for c-Abl.	Phosphatidylinositol 4,5-Diphosphate	169-206	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	254-259
14993293-2	2004	Here, we show that the related kinase Arg is activated downstream of PDGFRs in a manner dependent on Src family kinases and phospholipase C gamma1 (PLC-gamma1)-mediated phosphatidylinositol 4,5-bisphosphate (PIP2) hydrolysis, as we showed previously for c-Abl.	Phosphatidylinositol 4,5-Diphosphate	208-212	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	254-259
14757063-3	2004	We present here a complete thermodynamic analysis of the binding energetics of the p41 proline-rich decapeptide (APSYSPPPPP) to the SH3 domain of the c-Abl oncogene.	Proline	87-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-155
14993293-3	2004	PIP2, a highly abundant phosphoinositide known to regulate cytoskeletal and membrane proteins, inhibits the tyrosine kinase activities of both Arg and c-Abl in vitro and in cells.	Phosphatidylinositol 4,5-Diphosphate	0-4	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-156
14993293-3	2004	PIP2, a highly abundant phosphoinositide known to regulate cytoskeletal and membrane proteins, inhibits the tyrosine kinase activities of both Arg and c-Abl in vitro and in cells.	Phosphatidylinositols	24-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-156
14993293-7	2004	Reintroduction of c-Abl into Arg-Abl double-null fibroblasts rescues the ability of PLC-gamma1 to increase PDGF-mediated chemotaxis, while reexpression of Arg fails to rescue the chemotaxis defect.	arg-abl	29-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-23
14993293-7	2004	Reintroduction of c-Abl into Arg-Abl double-null fibroblasts rescues the ability of PLC-gamma1 to increase PDGF-mediated chemotaxis, while reexpression of Arg fails to rescue the chemotaxis defect.	Arginine	29-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-23
15039778-0	2004	Abl-dependent tyrosine phosphorylation of Sos-1 mediates growth-factor-induced Rac activation.	Tyrosine	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
15039778-5	2004	We show that Sos-1, a dual guanine nucleotide-exchange factor (GEF), is phosphorylated on tyrosine, after activation of RTKs, in an Abl-dependent manner.	Tyrosine	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-135
15039778-6	2004	Sos-1 and Abl interact in vivo, and Abl-induced tyrosine phosphorylation of Sos-1 is sufficient to elicit its Rac-GEF activity in vitro.	Tyrosine	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-39
15039778-7	2004	Genetic or pharmacological interference with Abl (and the related kinase Arg) resulted in a marked decrease in Rac activation induced by physiological doses of growth factors.	Arginine	73-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-48
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 Mesylate	45-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
14712293-3	2004	Here, we describe the establishment and phenotypic characterization of U937 cells in which P210 BCR/ABL can be conditionally expressed using tetracycline.	Tetracycline	141-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
14712293-5	2004	Phenotypic characterization of the clones revealed that BCR/ABL induces a slight decrease in the proliferation and viability, without a marked effect on cell cycle distribution, the rate of apoptosis or on cellular differentiation, as judged by several cell surface markers and capacity to reduce nitro blue tetrazolium.	Nitroblue Tetrazolium	297-319	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
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 Mesylate	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
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 Mesylate	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 Mesylate	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
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 Mesylate	10-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
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 Mesylate	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
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 Mesylate	23-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-99
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 Mesylate	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 Mesylate	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 Mesylate	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.	apicidin	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
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 Mesylate	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.	apicidin	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
14687026-2	2004	We examined whether apicidin potentiates the imatinib-induced apoptosis of Bcr-Abl-positive human leukaemia cells.	Imatinib Mesylate	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
14687026-7	2004	Imatinib/apicidin co-treatment for 48 h produced a prominent decrease in Bcr-Abl protein levels in a caspase-dependent manner.	apicidin	9-17	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.	apicidin	37-45	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.	apicidin	37-45	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 Mesylate	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 Mesylate	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	256-263
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.	apicidin	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
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 Mesylate	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
14755375-0	2004	Chronic myeloid leukemia with an e13a3 BCR-ABL fusion: benign course responsive to imatinib with an RT-PCR advisory.	Imatinib Mesylate	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
14605878-1	2004	Imatinib (STI571), a 2-phenylaminopyrimidine, specifically inhibits the tyrosine kinase activity of Abl, Kit, and platelet-derived growth factor receptor.	Imatinib Mesylate	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 Mesylate	10-16	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.	N-phenylpyrimidin-2-amine	21-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-103
14737178-4	2004	One such example is imatinib mesylate, which targets the BCR-ABL kinase as well as a few structurally related kinases.	Imatinib Mesylate	20-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
15101726-0	2004	Triptolide down-regulates bcr-abl expression and induces apoptosis in chronic myelogenous leukemia cells.	triptolide	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
15101726-8	2004	Significantly, triptolide-induced apoptosis of K562 cells was associated with a decline in bcr-abl expression levels, at the concentrations of 20 ng/ml, 40 ng/ml and 80 ng/ml, triptolide was able to decrease the expression of bcr-abl down to 50%, 30% and 20% respectively of the basal value after 72 h. Our findings strongly suggest that triptolide might be an effective therapeutic agent against CML cells.	triptolide	15-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
15101726-8	2004	Significantly, triptolide-induced apoptosis of K562 cells was associated with a decline in bcr-abl expression levels, at the concentrations of 20 ng/ml, 40 ng/ml and 80 ng/ml, triptolide was able to decrease the expression of bcr-abl down to 50%, 30% and 20% respectively of the basal value after 72 h. Our findings strongly suggest that triptolide might be an effective therapeutic agent against CML cells.	triptolide	15-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	226-233
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
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 Mesylate	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.	Adenosine Triphosphate	159-181	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-94
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 Mesylate	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 Mesylate	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 Mesylate	36-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	146-153
14744784-0	2004	Imatinib mesylate resistance through BCR-ABL independence in chronic myelogenous leukemia.	Imatinib Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
14736495-8	2004	Significantly, woodfordin I-induced apoptosis was associated with a decline in the levels of c-Abl, Bcr-Abl, and cellular protein tyrosine phosphorylation.	Woodfordin I	15-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-98
14736495-8	2004	Significantly, woodfordin I-induced apoptosis was associated with a decline in the levels of c-Abl, Bcr-Abl, and cellular protein tyrosine phosphorylation.	Woodfordin I	15-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
14736495-10	2004	Furthermore, because CML is a malignancy of pleuripotent hematopoietic cells caused by the dysregulated tyrosine kinase activity of Bcr-Abl, these findings suggest that woodfordin I may be a potential lead compound against CML.	Woodfordin I	169-181	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
14710199-2	2004	The leading drug in this area is imatinib mesylate, which targets ABL, KIT and PDGFR.	Imatinib Mesylate	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-69
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 Mesylate	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 Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
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 Mesylate	144-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
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 Mesylate	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.	Cytarabine	68-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
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 Mesylate	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 Mesylate	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 Mesylate	18-24	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.	Cytarabine	106-126	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.	Cytarabine	128-133	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 Mesylate	31-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
15032571-4	2004	Imatinib mesylate (Gleevec, STI571, or CP57148B) is a direct inhibitor of ABL (ABL1), ARG (ABL2), KIT, and PDGFR tyrosine kinases.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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.	cp57148b	39-47	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.	cp57148b	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-83
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 Mesylate	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 Mesylate	61-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-45
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 Mesylate	42-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-99
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 Mesylate	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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-46
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.	Adenosine Triphosphate	74-77	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.	Adenosine Triphosphate	74-77	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 Mesylate	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 Mesylate	162-170	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
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 Mesylate	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
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 Mesylate	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 Mesylate	60-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
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 Mesylate	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
14676625-0	2004	Mechanisms and implications of imatinib resistance mutations in BCR-ABL.	Imatinib Mesylate	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
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 Mesylate	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 Mesylate	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.	Adenosine Triphosphate	153-156	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 Mesylate	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 Mesylate	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
14676627-7	2004	Similar to BCR-ABL-positive leukemias, resistance to imatinib due to point mutations in the PDGFRalpha kinase domain may develop.	Imatinib Mesylate	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-18
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
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 Mesylate	120-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
14725908-0	2004	Coexistence of phosphotyrosine-dependent and -independent interactions between Cbl and Bcr-Abl.	Phosphotyrosine	15-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
14725908-1	2004	Cbl is one of the major tyrosine-phosphorylated proteins in Bcr-Abl-expressing cells.	Tyrosine	24-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
14725908-2	2004	A direct association between the SH2 domain of Bcr-Abl and tyrosine-phosphorylated Cbl has been demonstrated.	Tyrosine	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
14725908-6	2004	Bcr-Abl did, however, associate with Grb2, an adaptor protein that binds tyrosine 177 of Bcr-Abl.	Tyrosine	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
14725908-6	2004	Bcr-Abl did, however, associate with Grb2, an adaptor protein that binds tyrosine 177 of Bcr-Abl.	Tyrosine	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
14725908-10	2004	In cells expressing Bcr-Abl with a mutation in the Grb2 binding site, binding of Cbl to Bcr-Abl was significantly reduced, but Cbl tyrosine phosphorylation was maintained.	Tyrosine	131-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
14725908-14	2004	Following this initial interaction, Cbl can then become tyrosine phosphorylated and interact with the SH2 domain of Bcr-Abl, further stabilizing the complex.	Chlorambucil	36-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
14725908-14	2004	Following this initial interaction, Cbl can then become tyrosine phosphorylated and interact with the SH2 domain of Bcr-Abl, further stabilizing the complex.	Tyrosine	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
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 Mesylate	158-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-41
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 Mesylate	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 Mesylate	115-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-49
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 Mesylate	15-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
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 Mesylate	15-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-82
14654952-7	2004	Site-directed mutagenesis of Y881 aa within the RAFTK sequence abolished the binding of RAFTK to c-Abl, indicating that the tyrosine residue 881 of RAFTK is the c-Abl binding site within the RAFTK molecule.	Tyrosine	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-102
14654952-7	2004	Site-directed mutagenesis of Y881 aa within the RAFTK sequence abolished the binding of RAFTK to c-Abl, indicating that the tyrosine residue 881 of RAFTK is the c-Abl binding site within the RAFTK molecule.	Tyrosine	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-166
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 Mesylate	75-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
15579919-0	2004	Serial monitoring of BCR-ABL transcripts in chronic myelogenous leukemia (CML) treated with imatinib mesylate.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
14730159-11	2004	The average ABL(net) (i.e. ABL reduced by the amount of CS returned) was 1,794 +/- 806 cm(3).	Cesium	56-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-15
14730159-11	2004	The average ABL(net) (i.e. ABL reduced by the amount of CS returned) was 1,794 +/- 806 cm(3).	Cesium	56-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-30
15015226-2	2004	Imatinib potently inhibits several protein tyrosine kinases, including BCR-ABL, c-Kit, and PDGF receptor.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
12881321-2	2003	Imatinib mesylate (STI-571 or Gleevec) is a potent inhibitor of the BCR/ABL and c-KIT tyrosine kinases.	Imatinib Mesylate	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 Mesylate	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 Mesylate	4-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
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 Mesylate	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.	Adenosine	30-39	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.	Adenosine Triphosphate	54-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
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 Mesylate	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
15025410-6	2003	Imatinib mesylate is an orally available tyrosine kinase inhibitor that specifically blocks Bcr-Abl function.	Imatinib Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
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 Mesylate	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-15
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	19-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-103
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 Mesylate	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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.	Adenosine Triphosphate	42-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-36
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 Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
15243647-2	2004	Point mutations have been detected in ATP-binding domain of ABL gene which disturbs the binding of Gleevec to this target leading to resistance.	Adenosine Triphosphate	38-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-63
14738154-2	2003	STI571 inhibits tyrosine kinase activity of ABL and induces apoptosis of CML cells.	Imatinib Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-47
14638869-2	2003	Imatinib mesylate (STI571, Gleevec), a therapeutically used inhibitor of Bcr-Abl, causes apoptosis of Bcr-Abl-positive cells.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
14624253-7	2003	Inhibition of Abl by the drug STI-571 or inhibition of signaling events upstream of Erk increases RAG-1 expression.	Imatinib Mesylate	30-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-17
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-157
14581377-0	2003	Induction of apoptosis by apicidin, a histone deacetylase inhibitor, via the activation of mitochondria-dependent caspase cascades in human Bcr-Abl-positive leukemia cells.	apicidin	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
14581377-2	2003	The aim of this study was to examine the potential of apicidin to induce apoptosis in human Bcr-Abl-positive leukemia cells and to assess the mechanism of apicidin-induced apoptosis.	apicidin	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
14581377-13	2003	The p210 Bcr-Abl protein levels were notably decreased after the apicidin treatment, with near complete loss after 48 h. Reverse transcription-PCR assay demonstrated that the Bcr-Abl mRNA level was also remarkably decreased in a time-dependent manner.	apicidin	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
14581377-13	2003	The p210 Bcr-Abl protein levels were notably decreased after the apicidin treatment, with near complete loss after 48 h. Reverse transcription-PCR assay demonstrated that the Bcr-Abl mRNA level was also remarkably decreased in a time-dependent manner.	apicidin	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-182
14581377-14	2003	CONCLUSIONS: These results indicate that apicidin effectively induces the apoptosis of Bcr-Abl-positive leukemia cells through the activation of the mitochondrial pathway-dependent caspase cascades.	apicidin	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
14581377-15	2003	The down-regulation of Bcr-Abl mRNA might also be one of the mechanisms implicated in the apicidin-mediated apoptosis in the K562 cells.	apicidin	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
14581377-16	2003	This study provides the rationale to additionally investigate apicidin as a potential therapeutic agent for the drug-resistant Bcr-Abl-positive leukemia cells.	apicidin	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
12893824-3	2003	The c-Abl and Arg SH3 domains bind directly to a proline-rich site in GPx1 at amino acids 132-145.	Proline	49-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-9
12893824-4	2003	GPx1 also functions as a substrate for c-Abl- and Arg-mediated phosphorylation on Tyr-96.	Tyrosine	82-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-44
12951113-0	2003	Synthesis of pyrimidinopyridine-triazene conjugates targeted to abl tyrosine kinase.	pyrimidinopyridine-triazene	13-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-67
12951113-1	2003	The synthesis and abl tyrosine kinase inhibitory activities of alkyltriazenes conjugated to phenylaminopyrimidines are described.	alkyltriazenes	63-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-21
12951113-1	2003	The synthesis and abl tyrosine kinase inhibitory activities of alkyltriazenes conjugated to phenylaminopyrimidines are described.	phenylaminopyrimidines	92-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-21
12951113-2	2003	Significant abl inhibitory activities were observed only when a benzamido spacer was inserted between the 1,2,3-triazene chain and the 2-phenyaminopyridopyrimidine moiety.	1,2,3-triazene	106-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-15
12951113-2	2003	Significant abl inhibitory activities were observed only when a benzamido spacer was inserted between the 1,2,3-triazene chain and the 2-phenyaminopyridopyrimidine moiety.	2-phenyaminopyridopyrimidine	135-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-15
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 Mesylate	181-189	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
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).	Cytarabine	255-265	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 Mesylate	161-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
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.	Cytarabine	221-231	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
14534537-3	2003	The response to As2O3 is genetically determined by the t(15;17)-or the t(9;22)-specific fusion proteins PML/RARalpha or BCR/ABL.	Arsenic Trioxide	16-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
14534537-8	2003	Therefore, we hypothesized that BCR/ABL could increase sensitivity to As2O2-induced apoptosis by modifying PML expression.	as2o2	70-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
13679030-1	2003	STI-571 (imatinib, Gleevec, Glivec, CGP 57148) is an inhibitor of the Abl group of protein-tyrosine kinases.	Imatinib Mesylate	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-73
13679030-1	2003	STI-571 (imatinib, Gleevec, Glivec, CGP 57148) is an inhibitor of the Abl group of protein-tyrosine kinases.	Imatinib Mesylate	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-73
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.	Tetradecanoylphorbol Acetate	15-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	187-194
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 Mesylate	205-213	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	187-194
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.	bim-el	91-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	187-194
14510940-9	2003	In Bcr-Abl-expressing cells, p21WAF-1 rapidly diminishes as the cells are sensitized to apoptosis, using the inhibitor STI571.	Imatinib Mesylate	119-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	3-10
14559829-3	2003	Point mutations within the BCR-ABL kinase domain emerged as a major mechanism of resistance toward imatinib.	Imatinib Mesylate	99-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
14559829-6	2003	We screened 13 different pyrido-pyrimidine with cells expressing wild-type and mutant BCR-ABL.	pyrido(3,2-d)pyrimidine	25-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
14559829-12	2003	This observation is consistent with the hypothesis that unlike imatinib, pyrido-pyrimidine inhibitors bind Bcr-Abl regardless of the conformation of the activation loop.	pyrido(3,2-d)pyrimidine	73-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
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 Mesylate	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 Mesylate	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 Mesylate	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	187-194
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 Mesylate	239-245	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	205-212
14639002-4	2003	STI571 competitively binds to the ATP binding site of Bcr-Abl kinase and inhibits Abl tyrosine kinase activity.	Imatinib Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
14639002-4	2003	STI571 competitively binds to the ATP binding site of Bcr-Abl kinase and inhibits Abl tyrosine kinase activity.	Adenosine Triphosphate	34-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
14639002-11	2003	Certain point mutations in the ATP binding site were found to be a cause of resistance to STI571 in both Bcr-Abl and c-Kit kinases.	Adenosine Triphosphate	31-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-112
14706143-0	2003	[The reverse effect on drug-resistance against tyrosine kinase inhibitor STI571 in mdr1 and bcr-abl positive leukemic cells].	Imatinib Mesylate	73-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
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 Mesylate	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 Mesylate	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.	monooxyethylene trimethylolpropane tristearate	233-236	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
14506255-5	2003	We characterized the substrate specificity of ACK1 using synthetic peptides, and we show that the specificity of the ACK1 catalytic domain most closely resembles that of Abl.	Peptides	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-173
14599548-1	2003	The Abl tyrosine kinase inhibitor imatinb is becoming a standard for the treatment of chronic myelogenous leukemia (CML).	imatinb	34-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
14633726-0	2003	Arsenic trioxide inhibits translation of mRNA of bcr-abl, resulting in attenuation of Bcr-Abl levels and apoptosis of human leukemia cells.	Arsenic Trioxide	0-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
14633726-0	2003	Arsenic trioxide inhibits translation of mRNA of bcr-abl, resulting in attenuation of Bcr-Abl levels and apoptosis of human leukemia cells.	Arsenic Trioxide	0-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
14633726-1	2003	Present studies demonstrate that treatment with arsenic trioxide (AT) lowered ectopically expressed or endogenous levels of Bcr-Abl protein, as well as induced apoptosis of Bcr-Abl-expressing cultured and primary chronic myeloid leukemia cells, including those refractory to imatinib mesylate.	Arsenic Trioxide	48-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
14633726-1	2003	Present studies demonstrate that treatment with arsenic trioxide (AT) lowered ectopically expressed or endogenous levels of Bcr-Abl protein, as well as induced apoptosis of Bcr-Abl-expressing cultured and primary chronic myeloid leukemia cells, including those refractory to imatinib mesylate.	Arsenic Trioxide	48-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	173-180
14552760-7	2003	Two promising compounds showed inhibition in further ABL tyrosine phosphorylation assay.	Tyrosine	57-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
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 Mesylate	34-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
14529384-2	2003	In the mid 1980s, it was found that the benzoquinone ansamycin antibiotics (herbimycin A, geldanamycin, and macbecin) reversed v-Src transformed cells to normal phenotypes, and Bcr-abl was subsequently suggested to be the molecular target for the treatment of chronic myelogenous leukemia through a study using herbimycin A for its selective antioncogenic activity.	herbimycin	76-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	177-184
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 Mesylate	5-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
14529384-2	2003	In the mid 1980s, it was found that the benzoquinone ansamycin antibiotics (herbimycin A, geldanamycin, and macbecin) reversed v-Src transformed cells to normal phenotypes, and Bcr-abl was subsequently suggested to be the molecular target for the treatment of chronic myelogenous leukemia through a study using herbimycin A for its selective antioncogenic activity.	geldanamycin	90-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	177-184
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 Mesylate	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
14529384-2	2003	In the mid 1980s, it was found that the benzoquinone ansamycin antibiotics (herbimycin A, geldanamycin, and macbecin) reversed v-Src transformed cells to normal phenotypes, and Bcr-abl was subsequently suggested to be the molecular target for the treatment of chronic myelogenous leukemia through a study using herbimycin A for its selective antioncogenic activity.	Macbecin	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	177-184
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 Mesylate	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
14529384-2	2003	In the mid 1980s, it was found that the benzoquinone ansamycin antibiotics (herbimycin A, geldanamycin, and macbecin) reversed v-Src transformed cells to normal phenotypes, and Bcr-abl was subsequently suggested to be the molecular target for the treatment of chronic myelogenous leukemia through a study using herbimycin A for its selective antioncogenic activity.	herbimycin	311-323	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	177-184
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.	Cytarabine	133-138	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 Mesylate	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
14529387-9	2003	Radicicol oxime showed potent antitumor activity against ER negative/ErbB2 overexpressing breast cancer and Bcr-Abl expressing CML.	radicicol oxime	0-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
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 Mesylate	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 Mesylate	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 Mesylate	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	179-186
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 Mesylate	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 Mesylate	86-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
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 Mesylate	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.	Tyrosine	37-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
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 Mesylate	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 Mesylate	173-190	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
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 Mesylate	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	189-196
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 Mesylate	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 Mesylate	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 Mesylate	79-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	286-293
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 Mesylate	91-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-168
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].	Adenosine Triphosphate	141-144	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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
14527680-1	2003	The myristoylated N-terminal latching to the C-terminal lobe of c-Abl was recently demonstrated to be an important regulatory element for the kinase, playing a role similar to that of the tyrosine-phosphorylated C-terminal tail of c-Src.	Tyrosine	188-196	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-69
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	138-146	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
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 Mesylate	41-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
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 Mesylate	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
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 Mesylate	68-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
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 Mesylate	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 Mesylate	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
12824179-3	2003	Under these conditions p73 is tyrosine-phosphorylated by c-Abl, a prerequisite modification for p73 to elicit cell death in fibroblasts.	Tyrosine	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-62
12824179-6	2003	Moreover, STI-571, a specific c-Abl kinase inhibitor, is sufficient to block significantly p73 alpha nuclear matrix association.	Imatinib Mesylate	10-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-35
12824179-8	2003	Under these conditions p73 alpha but not p53 is specifically tyrosine-phosphorylated by c-Abl.	Tyrosine	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-93
12928501-4	2003	In this study, we show that c-Abl mediates a second pathway by which adhesion to extracellular matrix regulates cell killing by chemotherapeutic agents 5-arabinofuranosylcytosine, cisplatin, and camptothecin.	5-arabinofuranosylcytosine	152-178	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-33
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 Mesylate	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
12928501-4	2003	In this study, we show that c-Abl mediates a second pathway by which adhesion to extracellular matrix regulates cell killing by chemotherapeutic agents 5-arabinofuranosylcytosine, cisplatin, and camptothecin.	Cisplatin	180-189	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-33
12928501-4	2003	In this study, we show that c-Abl mediates a second pathway by which adhesion to extracellular matrix regulates cell killing by chemotherapeutic agents 5-arabinofuranosylcytosine, cisplatin, and camptothecin.	Camptothecin	195-207	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-33
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 Mesylate	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 Mesylate	33-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-94
14666657-0	2003	The hepoxilin analog PBT-3 induces apoptosis in BCR-ABL-positive K562 leukemia cells.	8-hydroxy-11,12-epoxyeicosa-5,9,14-trienoic acid	4-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
12955086-3	2003	c-Abl phosphorylates the cytoskeleton-associated adaptor protein, Crk, at tyrosine 221, causing disassociation of Crk from the Crk-associated substrate (CAS) and disassembly of Crk/CAS complexes.	Tyrosine	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
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 Mesylate	39-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
14614324-2	2003	Exposure of K562 cells to greater or less than 3.0 mM SB or 3.0 mM SAHA for 24-48 hr resulted in a marked induction of mitchondrial damage (e.g., cytochrome c release) and apoptosis, events associated with downregulation of Bcr/Abl and Raf-1, induction of p21CIP1, inactivation of MEK1/2, ERK1/2, and p70S6K, and a dramatic increase in JNK activation.	Butyric Acid	54-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	224-231
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 Mesylate	36-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
14614324-8	2003	Together, these findings support a model in which induction of apoptosis in Bcr/Abl+ cells by HDIs involves coordinate inactivation of the cytoprotective Raf/MEK/ERK pathway in conjunction with the ROS-dependent activation of JNK.	ros	198-201	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
14614324-2	2003	Exposure of K562 cells to greater or less than 3.0 mM SB or 3.0 mM SAHA for 24-48 hr resulted in a marked induction of mitchondrial damage (e.g., cytochrome c release) and apoptosis, events associated with downregulation of Bcr/Abl and Raf-1, induction of p21CIP1, inactivation of MEK1/2, ERK1/2, and p70S6K, and a dramatic increase in JNK activation.	Vorinostat	67-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	224-231
12944467-4	2003	After bleomycin treatment in culture, WRN and c-Abl are dissociated and followed by an Abl kinase-dependent WRN relocalization to the nucleoplasm.	Bleomycin	6-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-51
12960692-0	2003	Multiplex RT-PCR for the detection of common BCR-ABL fusion transcripts in paraffin-embedded tissues from patients with chronic myeloid leukemia and acute lymphoblastic leukemia.	Paraffin	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
12960692-3	2003	Histopathologists, who usually use formalin-fixed tissues, may be confronted with the need to investigate the BCR-ABL rearrangement when evaluating tumor forming infiltrates and bone marrow trephines from patients presenting with chronic myeloproliferative disorders.	Formaldehyde	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
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 Mesylate	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 Mesylate	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	232-239
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.	Adenosine Triphosphate	191-194	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
12869662-3	2003	Imatinib, an ATP-competitive selective inhibitor of Bcr-Abl, has unprecedented efficacy for the treatment of CML.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
12869662-3	2003	Imatinib, an ATP-competitive selective inhibitor of Bcr-Abl, has unprecedented efficacy for the treatment of CML.	Adenosine Triphosphate	13-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
12902478-3	2003	We now report that direct activation of protein kinase C (PKC) by the phorbol ester PMA in the BCR-ABL(+) CML cell line K562 and primary CML blasts induced nonterminal differentiation into cells with typical DC morphology (cytoplasmic dendrites), characteristic surface markers (MHC class I, MHC class II, CD86, CD40), chemokine and transcription factor expression, and ability to stimulate T cell proliferation (equivalent to normal monocyte-derived DC).	Phorbol Esters	70-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
12941844-0	2003	Histone deacetylase inhibitor LAQ824 both lowers expression and promotes proteasomal degradation of Bcr-Abl and induces apoptosis of imatinib mesylate-sensitive or -refractory chronic myelogenous leukemia-blast crisis cells.	LAQ824	30-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
12941844-1	2003	Treatment with LAQ824 (Novartis Pharmaceutical, Inc.), a cinnamyl hydroxamic acid analogue inhibitor of histone deacetylases, depleted the mRNA and protein expression of Bcr-Abl in human chronic myeloid leukemia blast crisis (CML-BC) cells.	LAQ824	15-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-177
12941844-1	2003	Treatment with LAQ824 (Novartis Pharmaceutical, Inc.), a cinnamyl hydroxamic acid analogue inhibitor of histone deacetylases, depleted the mRNA and protein expression of Bcr-Abl in human chronic myeloid leukemia blast crisis (CML-BC) cells.	cinnamyl hydroxamic acid	57-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-177
12777400-4	2003	The results show that H2O2 induced binding of c-Abl and Arg to catalase.	Hydrogen Peroxide	22-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-51
12777400-6	2003	c-Abl and Arg phosphorylated catalase at Tyr231 and Tyr386 in vitro and in the response of cells to H2O2.	Hydrogen Peroxide	100-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
12777400-7	2003	The functional significance of the interaction is supported by the demonstration that cells deficient in both c-Abl and Arg exhibit substantial increases in H2O2 levels.	Hydrogen Peroxide	157-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-115
12777400-8	2003	In addition, c-abl-/- arg-/- cells exhibited a marked increase in H2O2-induced apoptosis compared with that found in the absence of either kinase.	Arginine	22-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-18
12777400-8	2003	In addition, c-abl-/- arg-/- cells exhibited a marked increase in H2O2-induced apoptosis compared with that found in the absence of either kinase.	Hydrogen Peroxide	66-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-18
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-103
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 Mesylate	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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
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.	Adenosine Triphosphate	74-77	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.	Adenosine Triphosphate	124-127	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.	Adenosine Triphosphate	124-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
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.	Tyrosine	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
12815263-2	2003	The method was applied to the selective labeling of the catalytic domain of c-Abl kinase with (15)N-phenylalanine, (15)N-glycine, (15)N-tyrosine or (15)N-valine.	n-glycine	119-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-81
12815263-2	2003	The method was applied to the selective labeling of the catalytic domain of c-Abl kinase with (15)N-phenylalanine, (15)N-glycine, (15)N-tyrosine or (15)N-valine.	n-tyrosine	134-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-81
12815263-2	2003	The method was applied to the selective labeling of the catalytic domain of c-Abl kinase with (15)N-phenylalanine, (15)N-glycine, (15)N-tyrosine or (15)N-valine.	n-valine	152-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-81
12663457-0	2003	Presence of the BCR-ABL mutation Glu255Lys prior to STI571 (imatinib) treatment in patients with Ph+ acute lymphoblastic leukemia.	glu255lys	33-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
12663457-0	2003	Presence of the BCR-ABL mutation Glu255Lys prior to STI571 (imatinib) treatment in patients with Ph+ acute lymphoblastic leukemia.	Imatinib Mesylate	52-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
12663457-0	2003	Presence of the BCR-ABL mutation Glu255Lys prior to STI571 (imatinib) treatment in patients with Ph+ acute lymphoblastic leukemia.	Imatinib Mesylate	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 Mesylate	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 Mesylate	38-46	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.	Adenosine Triphosphate	75-97	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.	Adenosine Triphosphate	99-102	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 Mesylate	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 Mesylate	36-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
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 Mesylate	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
12777393-3	2003	Here we show that Dok-R associates with c-Abl directly via a constitutive SH3-mediated interaction and that this binding requires a PMMP motif in the proline-rich tail of Dok-R.	pmmp	132-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-45
12777393-3	2003	Here we show that Dok-R associates with c-Abl directly via a constitutive SH3-mediated interaction and that this binding requires a PMMP motif in the proline-rich tail of Dok-R.	Proline	150-157	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-45
12777393-5	2003	Interaction of Dok-R with c-Abl also results in an increase in c-Abl tyrosine phosphorylation and kinase activity.	Tyrosine	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-31
12777393-5	2003	Interaction of Dok-R with c-Abl also results in an increase in c-Abl tyrosine phosphorylation and kinase activity.	Tyrosine	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-68
12777400-1	2003	The Abl family of mammalian non-receptor tyrosine kinases includes c-Abl and Arg.	Arginine	77-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
12777400-3	2003	This work demonstrates that catalase, a major effector of the cellular defense against H2O2, interacts with c-Abl and Arg.	Hydrogen Peroxide	87-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-113
12879454-0	2003	Immunoreactivity of Stat5 phosphorylated on tyrosine as a cell-based measure of Bcr/Abl kinase activity.	Tyrosine	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-87
12823349-0	2003	Clinical and genetic studies of ETV6/ABL1-positive chronic myeloid leukaemia in blast crisis treated with imatinib mesylate.	Imatinib Mesylate	106-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-41
12623848-1	2003	Imatinib-treated chronic myeloid leukemia (CML) patients with acquired resistance commonly have detectable BCR-ABL kinase domain mutations.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
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 Mesylate	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 Mesylate	14-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-138
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 Mesylate	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
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 Mesylate	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-42
12821944-4	2003	The enforced expression of BCR-ABL in an ES cell line, engineered to express a tetracycline-inducible dominant-negative form of a STAT3, triggered ES cell differentiation with an increased generation of hematopoietic cells expressing erythroid and megakaryocytic phenotypes.	Tetracycline	79-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
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 Mesylate	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 Mesylate	66-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-11
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 Mesylate	76-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-47
12810679-6	2003	Consequence to the phosphorylation is a marked increase of the association between c-Abl and p73 via the binding of tyrosine-phosphorylated p73 to the c-Abl Src homology 2 (SH2) domain.	Tyrosine	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-88
12810679-6	2003	Consequence to the phosphorylation is a marked increase of the association between c-Abl and p73 via the binding of tyrosine-phosphorylated p73 to the c-Abl Src homology 2 (SH2) domain.	Tyrosine	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-156
12810679-8	2003	Importantly, expression of the c-Abl SH2 domain peptide also leads to an efficient inhibition of cisplatin-induced accumulation of endogenous p73, highlighting the biological significance.	Cisplatin	97-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-36
12672821-0	2003	Abl interactor 1 promotes tyrosine 296 phosphorylation of mammalian enabled (Mena) by c-Abl kinase.	Tyrosine	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-91
12672821-7	2003	Importantly, Abi-1 dramatically promoted c-Abl-mediated tyrosine phosphorylation of Mena but not other substrates such as c-Cbl.	Tyrosine	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-46
12576318-0	2003	Several Bcr-Abl kinase domain mutants associated with imatinib mesylate resistance remain sensitive to imatinib.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	44-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	176-183
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.	Adenosine Triphosphate	74-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	176-183
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.	Adenosine Triphosphate	98-101	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 Mesylate	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-79
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 Mesylate	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
12824882-1	2003	STI571, an Abl-specific tyrosine kinase inhibitor, selectively kills Bcr-Abl-containing cells in vitro and in vivo.	Imatinib Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-14
12824882-1	2003	STI571, an Abl-specific tyrosine kinase inhibitor, selectively kills Bcr-Abl-containing cells in vitro and in vivo.	Imatinib Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-76
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	41-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
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 Mesylate	9-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
12738983-3	2003	Overexpression of kinase active c-Abl can overcome RB-induced growth arrest in Saos-2 cells.	Rubidium	51-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-37
12748290-2	2003	Following the breakdown of inhibitory intramolecular interactions, Abl activation requires phosphorylation on several tyrosine residues, including a tyrosine in its activation loop.	Tyrosine	118-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-70
12748290-2	2003	Following the breakdown of inhibitory intramolecular interactions, Abl activation requires phosphorylation on several tyrosine residues, including a tyrosine in its activation loop.	Tyrosine	149-157	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-70
12748290-4	2003	We show here that these two pathways mediate phosphorylation at distinct sites in Abl and Arg and have additive effects on Abl and Arg kinase activation.	Arginine	90-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-126
12637538-5	2003	This phosphorylation is mediated by a pathway that consists of the Src and Abl tyrosine kinases and occurs in response to stimulation with pervanadate and oxidative stress.	pervanadate	139-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-78
12637538-6	2003	Mutational analysis revealed three tyrosine phosphorylation sites (Tyr(432), Tyr(463), and Tyr(502)), which are regulated by the Src-Abl pathway, and phosphorylation of only one of these (Tyr(463)) leads to PKD activation.	Tyrosine	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-136
12637538-6	2003	Mutational analysis revealed three tyrosine phosphorylation sites (Tyr(432), Tyr(463), and Tyr(502)), which are regulated by the Src-Abl pathway, and phosphorylation of only one of these (Tyr(463)) leads to PKD activation.	Tyrosine	67-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-136
12637538-6	2003	Mutational analysis revealed three tyrosine phosphorylation sites (Tyr(432), Tyr(463), and Tyr(502)), which are regulated by the Src-Abl pathway, and phosphorylation of only one of these (Tyr(463)) leads to PKD activation.	Tyrosine	77-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-136
12637538-6	2003	Mutational analysis revealed three tyrosine phosphorylation sites (Tyr(432), Tyr(463), and Tyr(502)), which are regulated by the Src-Abl pathway, and phosphorylation of only one of these (Tyr(463)) leads to PKD activation.	Tyrosine	77-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-136
12637538-6	2003	Mutational analysis revealed three tyrosine phosphorylation sites (Tyr(432), Tyr(463), and Tyr(502)), which are regulated by the Src-Abl pathway, and phosphorylation of only one of these (Tyr(463)) leads to PKD activation.	Tyrosine	77-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-136
12637538-7	2003	By using a phospho-specific antibody, we show that Abl directly phosphorylates PKD at Tyr(463) in vitro, and in cells phosphorylation of this site is sufficient to mediate full activation of PKD.	Tyrosine	86-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-54
12521991-5	2003	Inhibition of p38 MAPK by the small molecule inhibitor SB203580 expanded ES-derived hematopoietic progenitors by an antiapoptotic mechanism and is sufficient to expand ES-derived hematopoietic progenitors to levels approaching 80% of that seen following BCR-ABL expression.	SB 203580	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	254-261
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 Mesylate	52-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
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 Mesylate	71-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
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 Mesylate	81-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
12752112-0	2003	Cross-resistance of imatinib mesylate and 17-AAG in imatinib-resistant cells that overexpress BCR-ABL.	Imatinib Mesylate	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 Mesylate	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 Mesylate	39-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
12727828-0	2003	Histone deacetylase inhibitors promote STI571-mediated apoptosis in STI571-sensitive and -resistant Bcr/Abl+ human myeloid leukemia cells.	Imatinib Mesylate	68-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
12727828-5	2003	Coexposure of Bcr/Abl(+) cells to STI571 also blocked SAHA-mediated induction of p21(CIP1) and resulted in down-regulation of Bcr/Abl protein expression.	Vorinostat	54-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
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 Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
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.	Vorinostat	11-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
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 Mesylate	71-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
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 Mesylate	101-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
12781364-2	2003	Imatinib is a potent inhibitor of ABL, ARG, PDGFRalpha, PDGFRbeta, and KIT and induces durable hematologic responses in HES patients.	Imatinib Mesylate	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 Mesylate	102-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
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.	herbimycin	100-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
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.	Genistein	114-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
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 Mesylate	127-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
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 Mesylate	273-279	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-158
12857554-1	2003	BACKGROUND AND OBJECTIVES: Imatinib mesylate inhibits ABL tyrosine kinase.	Imatinib Mesylate	27-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-57
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 Mesylate	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 Mesylate	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-147
12775773-6	2003	Among the tyrosine kinases, c-Abl and its relative Arg are unique in binding directly to F-actin.	Arginine	51-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-33
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).	sh2-cd	138-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
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 Mesylate	197-205	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
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 Mesylate	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
12692682-3	2003	By combining peptide nucleic acid (PNA)-based DNA clamping with a fluorescence hybridization probe assay, we developed a new and highly sensitive technique for the detection of known mutations within the Bcr/Abl kinase domain.	Peptide Nucleic Acids	35-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	204-211
12739051-8	2003	Imatinib (STI571/Glivec) is a selective inhibitor of BCR/ABL, PDGFR and KIT receptor-tyrosine kinases.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
12714574-0	2003	Imatinib restores expression of CD62L in BCR-ABL-positive cells.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	85-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
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 Mesylate	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
12833568-5	2003	High-resolution affinity panning coupled with mass spectrometric readout allows for quick identification of Trp as the preferred fourth residue in the decapeptide ligand APTWSPPPPP, which binds to Abl SH3 four times stronger than does the decapeptide containing Tyr or Phe in the fourth position.	Tryptophan	108-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	197-200
12833568-5	2003	High-resolution affinity panning coupled with mass spectrometric readout allows for quick identification of Trp as the preferred fourth residue in the decapeptide ligand APTWSPPPPP, which binds to Abl SH3 four times stronger than does the decapeptide containing Tyr or Phe in the fourth position.	Tyrosine	262-265	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	197-200
12833568-5	2003	High-resolution affinity panning coupled with mass spectrometric readout allows for quick identification of Trp as the preferred fourth residue in the decapeptide ligand APTWSPPPPP, which binds to Abl SH3 four times stronger than does the decapeptide containing Tyr or Phe in the fourth position.	Phenylalanine	269-272	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	197-200
12833568-6	2003	This finding is in contrast to several reports that Tyr is the only residue selected from phage displayed peptide libraries that interacts with the specificity pocket of Abl SH3.	Tyrosine	52-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-173
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 Mesylate	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 Mesylate	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 Mesylate	296-302	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
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.	Vorinostat	51-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
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.	Vorinostat	84-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
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 Mesylate	99-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
12446442-1	2003	Here we demonstrate that treatment with SAHA (suberoylanilide hydroxamic acid), a known inhibitor of histone deacetylases (HDACs), alone induced p21 and/or p27 expressions but decreased the mRNA and protein levels of Bcr-Abl, which was associated with apoptosis of Bcr-Abl-expressing K562 and LAMA-84 cells.	Vorinostat	40-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	217-224
12446442-1	2003	Here we demonstrate that treatment with SAHA (suberoylanilide hydroxamic acid), a known inhibitor of histone deacetylases (HDACs), alone induced p21 and/or p27 expressions but decreased the mRNA and protein levels of Bcr-Abl, which was associated with apoptosis of Bcr-Abl-expressing K562 and LAMA-84 cells.	Vorinostat	40-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	265-272
12446442-1	2003	Here we demonstrate that treatment with SAHA (suberoylanilide hydroxamic acid), a known inhibitor of histone deacetylases (HDACs), alone induced p21 and/or p27 expressions but decreased the mRNA and protein levels of Bcr-Abl, which was associated with apoptosis of Bcr-Abl-expressing K562 and LAMA-84 cells.	Vorinostat	46-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	217-224
12446442-1	2003	Here we demonstrate that treatment with SAHA (suberoylanilide hydroxamic acid), a known inhibitor of histone deacetylases (HDACs), alone induced p21 and/or p27 expressions but decreased the mRNA and protein levels of Bcr-Abl, which was associated with apoptosis of Bcr-Abl-expressing K562 and LAMA-84 cells.	Vorinostat	46-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	265-272
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).	Vorinostat	17-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
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 Mesylate	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
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).	Tyrosine	96-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
12446442-4	2003	Significantly, treatment with SAHA also down-regulated Bcr-Abl levels and induced apoptosis of CD34(+) leukemia blast progenitor cells derived from patients who had developed progressive blast crisis (BC) of chronic myelocytic leukemia (CML) while receiving therapy with imatinib.	Vorinostat	30-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
12694868-2	2003	The present study shows that ML formation occurs at two different stages of apoptosis induced in human erythroleukemia K562 cells by a brief (3 hr) exposure to paclitaxel (Taxol), an antitumour drug with a stabilising effect on microtubules, or to paclitaxel plus tyrphostin AG957, a selective inhibitor of the p210(BCR-ABL) tyrosine kinase activity.	Paclitaxel	160-170	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	316-323
12694868-2	2003	The present study shows that ML formation occurs at two different stages of apoptosis induced in human erythroleukemia K562 cells by a brief (3 hr) exposure to paclitaxel (Taxol), an antitumour drug with a stabilising effect on microtubules, or to paclitaxel plus tyrphostin AG957, a selective inhibitor of the p210(BCR-ABL) tyrosine kinase activity.	Paclitaxel	172-177	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	316-323
12569093-1	2003	The Abl family of mammalian nonreceptor tyrosine kinases consists of c-Abl and Arg.	Arginine	79-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
12569093-3	2003	The present studies demonstrate that reactive oxygen species (ROS) induce the formation of c-Abl and Arg heterodimers.	Reactive Oxygen Species	37-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-96
12569093-3	2003	The present studies demonstrate that reactive oxygen species (ROS) induce the formation of c-Abl and Arg heterodimers.	Reactive Oxygen Species	62-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-96
12569093-4	2003	The results show that the c-Abl SH3 domain binds directly to a proline-rich site (amino acids 567-576) in the Arg C-terminal region.	Proline	63-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-31
12569093-4	2003	The results show that the c-Abl SH3 domain binds directly to a proline-rich site (amino acids 567-576) in the Arg C-terminal region.	Arginine	110-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-31
12569093-5	2003	Formation of c-Abl.Arg heterodimers also involves direct binding of the Arg Src homology 3 domain to the C-terminal region of c-Abl.	Arginine	19-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-18
12569093-5	2003	Formation of c-Abl.Arg heterodimers also involves direct binding of the Arg Src homology 3 domain to the C-terminal region of c-Abl.	Arginine	19-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-131
12569093-5	2003	Formation of c-Abl.Arg heterodimers also involves direct binding of the Arg Src homology 3 domain to the C-terminal region of c-Abl.	Arginine	72-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-18
12569093-5	2003	Formation of c-Abl.Arg heterodimers also involves direct binding of the Arg Src homology 3 domain to the C-terminal region of c-Abl.	Arginine	72-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-131
12569093-6	2003	The results further demonstrate that the interaction between c-Abl and Arg involves c-Abl-mediated phosphorylation of Arg.	Arginine	71-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-66
12569093-6	2003	The results further demonstrate that the interaction between c-Abl and Arg involves c-Abl-mediated phosphorylation of Arg.	Arginine	71-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-89
12569093-6	2003	The results further demonstrate that the interaction between c-Abl and Arg involves c-Abl-mediated phosphorylation of Arg.	Arginine	118-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-66
12569093-6	2003	The results further demonstrate that the interaction between c-Abl and Arg involves c-Abl-mediated phosphorylation of Arg.	Arginine	118-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-89
12569093-7	2003	The functional significance of the c-Abl-Arg interaction is supported by the demonstration that both c-Abl and Arg are required for ROS-induced apoptosis.	Arginine	41-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-40
12569093-7	2003	The functional significance of the c-Abl-Arg interaction is supported by the demonstration that both c-Abl and Arg are required for ROS-induced apoptosis.	Arginine	41-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-106
12569093-7	2003	The functional significance of the c-Abl-Arg interaction is supported by the demonstration that both c-Abl and Arg are required for ROS-induced apoptosis.	Reactive Oxygen Species	132-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-40
12569093-7	2003	The functional significance of the c-Abl-Arg interaction is supported by the demonstration that both c-Abl and Arg are required for ROS-induced apoptosis.	Reactive Oxygen Species	132-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-106
12569093-8	2003	These findings indicate that ROS induce c-Abl.Arg heterodimers and that both c-Abl and Arg are necessary as effectors in the apoptotic response to oxidative stress.	Reactive Oxygen Species	29-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-45
12824897-6	2003	Imatinib mesylate inhibits BCR-ABL fused tyrosine kinase that causes CML.	Imatinib Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
12684394-0	2003	A novel pyridopyrimidine inhibitor of abl kinase is a picomolar inhibitor of Bcr-abl-driven K562 cells and is effective against STI571-resistant Bcr-abl mutants.	pyrido(3,2-d)pyrimidine	8-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-41
12684394-0	2003	A novel pyridopyrimidine inhibitor of abl kinase is a picomolar inhibitor of Bcr-abl-driven K562 cells and is effective against STI571-resistant Bcr-abl mutants.	pyrido(3,2-d)pyrimidine	8-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
12684394-0	2003	A novel pyridopyrimidine inhibitor of abl kinase is a picomolar inhibitor of Bcr-abl-driven K562 cells and is effective against STI571-resistant Bcr-abl mutants.	pyrido(3,2-d)pyrimidine	8-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-152
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 Mesylate	71-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
12684394-3	2003	We have screened a family of TK inhibitors of the pyrido [2,3-d]pyrimidine class, unrelated to STI571, and describe here a compound with substantial activity against STI-resistant mutant Bcr-abl proteins.	pyrido [2,3-d]pyrimidine	50-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	187-194
12684394-4	2003	This compound, PD166326, is a dual specificity TK inhibitor and inhibits src and abl in vitro with IC(50)s of 6 and 8 nM respectively.	PD 166326	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-84
12684394-6	2003	We tested the effects of PD166326 on two of the clinically observed STI571-resistant Bcr-abl mutants.	PD 166326	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
12684394-7	2003	PD166326 potently inhibits the E255K mutant Bcr-abl protein and the growth of Bcr-ablE255K-driven cells.	PD 166326	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
12684394-8	2003	The T315I mutant Bcr-abl protein, which is mutated within the ATP-binding pocket, is resistant to PD166326; however, the growth of Bcr-ablT315I-driven cells is partially sensitive to this compound, likely through the inhibition of Bcr-abl effector pathways.	Adenosine Triphosphate	62-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
12684394-8	2003	The T315I mutant Bcr-abl protein, which is mutated within the ATP-binding pocket, is resistant to PD166326; however, the growth of Bcr-ablT315I-driven cells is partially sensitive to this compound, likely through the inhibition of Bcr-abl effector pathways.	Adenosine Triphosphate	62-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
12684394-8	2003	The T315I mutant Bcr-abl protein, which is mutated within the ATP-binding pocket, is resistant to PD166326; however, the growth of Bcr-ablT315I-driven cells is partially sensitive to this compound, likely through the inhibition of Bcr-abl effector pathways.	PD 166326	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
12684394-10	2003	PD166326 is a prototype of a new generation of anti-Bcr-abl compounds with picomolar potency and substantial activity against STI571-resistant mutants.	PD 166326	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
12656747-0	2003	Double minutes containing amplified bcr-abl fusion gene in a case of chronic myeloid leukemia treated by imatinib.	Imatinib Mesylate	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 Mesylate	89-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
12663768-6	2003	These data indicate that the central portion of the COOH terminus is not essential for lymphoid transformation and reveal that one important function of the COOH terminus is to stabilize the v-Abl protein in lymphoid cells.	Carbonic Acid	52-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	191-196
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 Mesylate	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 Mesylate	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
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.	Adenosine Triphosphate	100-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
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.	Adenosine Triphosphate	100-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
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 Mesylate	51-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-15
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 Mesylate	86-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-73
12663768-6	2003	These data indicate that the central portion of the COOH terminus is not essential for lymphoid transformation and reveal that one important function of the COOH terminus is to stabilize the v-Abl protein in lymphoid cells.	Carbonic Acid	157-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	191-196
12665579-7	2003	Transient-transfection experiments show that cleavage of c-Abl may affect the efficiency of Fas-induced cell death.	ammonium ferrous sulfate	92-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-62
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 Mesylate	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 Mesylate	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 Mesylate	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
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 Mesylate	29-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	29-35	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).	Adenosine Triphosphate	63-87	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).	Adenosine Triphosphate	89-92	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 Mesylate	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 Mesylate	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 Mesylate	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
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 Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-126
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 Mesylate	30-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-80
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 Mesylate	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 Mesylate	205-213	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-116
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	145-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
12654250-0	2003	A myristoyl/phosphotyrosine switch regulates c-Abl.	myristoyl/phosphotyrosine	2-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-50
12654250-3	2003	We found that like Src kinases, c-Abl 1b is activated by phosphotyrosine ligands.	Phosphotyrosine	57-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-37
12654250-4	2003	Ligand-activated c-Abl is particularly sensitive to the anti-cancer drug STI-571/Gleevec/imatinib (STI-571).	Imatinib Mesylate	89-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-22
12654250-6	2003	Functional studies coupled with structural analysis define a myristoyl/phosphotyrosine switch in c-Abl that regulates docking and accessibility of the SH2 domain.	myristoyl	61-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-102
12654250-6	2003	Functional studies coupled with structural analysis define a myristoyl/phosphotyrosine switch in c-Abl that regulates docking and accessibility of the SH2 domain.	Phosphotyrosine	71-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-102
12654250-7	2003	This mechanism offers an explanation for the observed cellular activation of c-Abl by tyrosine-phosphorylated proteins, the intracellular mobility of c-Abl, and it provides new insights into the mechanism of action of STI-571.	Tyrosine	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-82
12654251-2	2003	The details of this mechanism have been elusive because c-Abl lacks a phosphotyrosine residue that triggers the assembly of the autoinhibited form of the closely related Src kinases by internally engaging the SH2 domain.	Phosphotyrosine	70-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-61
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 Mesylate	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 Mesylate	177-184	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-19
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 Mesylate	193-201	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 Mesylate	193-201	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-19
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 Mesylate	203-210	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 Mesylate	203-210	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-19
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 Mesylate	135-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
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 Mesylate	144-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
12531427-2	2003	Tyrosine 14 is a consensus Abl phosphorylation site suggesting that caveolin-1 may be an Abl substrate.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-30
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 Mesylate	115-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
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.	Verapamil	161-170	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
12633758-4	2003	For lactate ABL (y) = 1.13 Vitros (x) -0.43 with a CI (slope) of 1.10 to 1.16, CI (int) of -0.61 to -0.28.	Lactic Acid	4-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-15
12633758-8	2003	CONCLUSION: The ABL 700 series gave comparable results for lactate, bilirubin and hemoglobin F with laboratory methods and may be used in patient care.	Lactic Acid	59-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-19
12633758-8	2003	CONCLUSION: The ABL 700 series gave comparable results for lactate, bilirubin and hemoglobin F with laboratory methods and may be used in patient care.	Bilirubin	68-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-19
12527798-0	2003	Abrogation of the cell death response to oxidative stress by the c-Abl tyrosine kinase inhibitor STI571.	Imatinib Mesylate	97-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-70
12527798-3	2003	ROS-induced apoptosis and necrosis involves activation of the cytoplasmic c-Abl tyrosine kinase and thereby signaling to mitochondria.	Reactive Oxygen Species	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-79
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 Mesylate	85-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-137
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%.	Hydrogen Peroxide	102-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-137
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 Mesylate	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 Mesylate	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 Mesylate	78-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-42
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	171-179	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-67
12646934-5	2003	The median duration of imatinib treatment before the identification of cytogenetic abnormalities in BCR-ABL-negative cells was 13 months.	Imatinib Mesylate	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
12644574-0	2003	Phosphotyrosine mapping in Bcr/Abl oncoprotein using phosphotyrosine-specific immonium ion scanning.	Phosphotyrosine	0-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-34
12644574-0	2003	Phosphotyrosine mapping in Bcr/Abl oncoprotein using phosphotyrosine-specific immonium ion scanning.	Phosphotyrosine	53-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-34
12644574-2	2003	The tyrosine-phosphorylated fraction of the p185 form of Bcr/Abl was isolated by immunoprecipitation with an anti-phosphotyrosine antibody and SDS-PAGE.	Tyrosine	4-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
12644574-2	2003	The tyrosine-phosphorylated fraction of the p185 form of Bcr/Abl was isolated by immunoprecipitation with an anti-phosphotyrosine antibody and SDS-PAGE.	Sodium Dodecyl Sulfate	143-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
12657715-0	2003	Efficacy of SCH66336, a farnesyl transferase inhibitor, in conjunction with imatinib against BCR-ABL-positive cells.	lonafarnib	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
12657715-0	2003	Efficacy of SCH66336, a farnesyl transferase inhibitor, in conjunction with imatinib against BCR-ABL-positive cells.	Imatinib Mesylate	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 Mesylate	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.	lonafarnib	0-8	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 Mesylate	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 Mesylate	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
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 Mesylate	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 Mesylate	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 Mesylate	147-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	179-186
12592388-4	2003	By contrast, Bcr-Abl-positive K562 cells were resistant to the induction of apoptosis by beta-HIVS and this compound did not suppress the kinase activity of PLK1 in these cells.	beta-hydroxyisovalerylshikonin	89-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
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 Mesylate	30-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
12547280-7	2003	Amifostine at 14 mM decreased the level of DNA damage in normal lymphocytes, had no effect on the HL-60 cells and potentiated the DNA-damaging effect of the drug in BCR/ABL-transformed cells.	Amifostine	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	165-172
12552081-1	2003	We established a quantitative real-time RT-PCR assay for the detection of chimeric BCR-ABL transcripts in archival formalin-fixed bone marrow trephines, both acrylate-embedded and paraffin-embedded.	Formaldehyde	115-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
12552081-1	2003	We established a quantitative real-time RT-PCR assay for the detection of chimeric BCR-ABL transcripts in archival formalin-fixed bone marrow trephines, both acrylate-embedded and paraffin-embedded.	acrylic acid	158-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
12552081-1	2003	We established a quantitative real-time RT-PCR assay for the detection of chimeric BCR-ABL transcripts in archival formalin-fixed bone marrow trephines, both acrylate-embedded and paraffin-embedded.	Paraffin	180-188	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
12531427-2	2003	Tyrosine 14 is a consensus Abl phosphorylation site suggesting that caveolin-1 may be an Abl substrate.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-92
12531427-6	2003	Oxidative stress-induced tyrosine phosphorylation of caveolin-1 occurs only at the Abl site, tyrosine 14.	Tyrosine	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-86
12531427-6	2003	Oxidative stress-induced tyrosine phosphorylation of caveolin-1 occurs only at the Abl site, tyrosine 14.	Tyrosine	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-86
12531427-7	2003	Caveolin-1 is also a major phosphotyrosine signal detected in cells over-expressing c-Abl.	Phosphotyrosine	27-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-89
12560071-0	2003	BCR-ABL binds to IRS-1 and IRS-1 phosphorylation is inhibited by imatinib in K562 cells.	Imatinib Mesylate	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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 Mesylate	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
12522270-4	2003	We used this methodology to follow changes in tyrosine phosphorylation patterns that occur over time during either the activation of human T cells or the inhibition of the oncogenic BCR-ABL fusion product in chronic myelogenous leukemia cells in response to treatment with STI571 (Gleevec).	Tyrosine	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-189
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 Mesylate	111-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-25
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 Mesylate	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 Mesylate	136-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
12509383-1	2003	Clinical studies have shown that the tyrosine kinase inhibitor STI571 effectively controls BCR-ABL-positive chronic myelogenous leukemia (CML).	Imatinib Mesylate	63-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
12393636-2	2003	Mutations at the IBP may lead to resistance of the Abl kinase against imatinib mesylate.	Imatinib Mesylate	70-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-54
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	125-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-164
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 Mesylate	273-290	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	245-252
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-115
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 Mesylate	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	217-224
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 Mesylate	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
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 Mesylate	30-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-154
12680254-0	2003	The actinomycin D-induced apoptosis in BCR-ABL-positive K562 cells is associated with cytoplasmic translocation and cleavage of RNA helicase A.	Dactinomycin	4-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
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 Mesylate	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 Mesylate	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 Mesylate	25-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
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 Mesylate	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 Mesylate	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
12673129-0	2003	Imatinib (ST1571) provides only limited selectivity for CML cells and treatment might be complicated by silent BCR-ABL genes.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
12673129-5	2003	About half of these treated colonies also displayed methylation of the internal ABL Pa promoter, a CML-specific epigenetic alteration, which was used in this study as a marker for BCR-ABL translocation-containing cells.	Protactinium	84-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	180-187
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 Mesylate	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 Mesylate	100-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	255-258
12898363-4	2003	STI571 selectively inhibits c-Kit, BCR-ABL, and PDGFR tyrosine kinases.	Imatinib Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
14657531-6	2003	STI571 (imatinib mesylate) inhibits the Bcr-Abl TK, blocks the growth of these leukemia cells, and induces apoptosis.	Imatinib Mesylate	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 Mesylate	8-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
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 Mesylate	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 Mesylate	55-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
12743326-1	2003	The BCR/ABL tyrosine kinase inhibitor, imatinib, has shown substantial effects in blast crises of chronic myelogenous leukemia.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	169-177	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
12499247-4	2002	Recently, a novel pyrido[2,3-d]pyrimidine derivative, PD180970, has been shown to potently inhibit Bcr-Abl and induce apoptosis in Bcr-Abl-expressing leukemic cells.	Pyrido[2,3-d]pyrimidine	18-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
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).	PD 180970	41-49	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).	PD 180970	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
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 Mesylate	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 Mesylate	120-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
12379650-4	2002	We show here that c-Abl tyrosine kinase associates with and phosphorylates Rad52 on tyrosine 104.	Tyrosine	24-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-23
12476302-3	2002	Another consequence of this Bcr-Abl fusion is the extensive autophosphorylation of the cis Bcr protein sequences on tyrosine residues.	Tyrosine	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
12476302-4	2002	This review will summarize the effects of Bcr-Abl autophosphorylation on tyrosines as they relate to the oncogenic activity of Bcr-Abl, and as a means to inactivate the serine/threonine kinase activity of the Bcr protein.	Tyrosine	73-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
12476302-4	2002	This review will summarize the effects of Bcr-Abl autophosphorylation on tyrosines as they relate to the oncogenic activity of Bcr-Abl, and as a means to inactivate the serine/threonine kinase activity of the Bcr protein.	Tyrosine	73-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
12476302-5	2002	The review also discusses our findings that show that phosphoserine Bcr by means of a unique structure, binds to the Abl SH2 domain of the Bcr-Abl oncoprotein, and as a result this SH2 binding inhibits the oncogenic effects of the oncoprotein.	Phosphoserine	54-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-120
12476302-5	2002	The review also discusses our findings that show that phosphoserine Bcr by means of a unique structure, binds to the Abl SH2 domain of the Bcr-Abl oncoprotein, and as a result this SH2 binding inhibits the oncogenic effects of the oncoprotein.	Phosphoserine	54-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-146
12476302-8	2002	In the case of Bcr(64-413), serine 354 is required for the formation of the unique Bcr structure that binds to the Abl SH2 domain.	Serine	28-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-118
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 Mesylate	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 Mesylate	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 Mesylate	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
12476305-7	2002	Small molecule inhibitors that downregulate the levels of Bcr-Abl by inhibiting its translation, e.g., arsenic trioxide, or promoting its proteasomal degradation, e.g., geldanamycin analogues, have also been identified.	Arsenic Trioxide	103-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
12476305-7	2002	Small molecule inhibitors that downregulate the levels of Bcr-Abl by inhibiting its translation, e.g., arsenic trioxide, or promoting its proteasomal degradation, e.g., geldanamycin analogues, have also been identified.	geldanamycin	169-181	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
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 Mesylate	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 Mesylate	58-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-21
12483533-3	2002	We recently identified PD180970 as a new and highly potent inhibitor of Bcr-Abl kinase.	PD 180970	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
12483533-10	2002	Moreover, PD180970 blocked Stat5 signaling and induced apoptosis of STI-571 (Gleevec, Imatinib)-resistant Bcr-Abl-positive cells.	Imatinib Mesylate	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 Mesylate	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
12445832-4	2002	In this report we describe for the first time that c-Abl and Btk physically interact and that c-Abl can phosphorylate tyrosine 223 in the SH3 domain of Btk.	Tyrosine	118-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-56
12445832-4	2002	In this report we describe for the first time that c-Abl and Btk physically interact and that c-Abl can phosphorylate tyrosine 223 in the SH3 domain of Btk.	Tyrosine	118-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-99
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 Mesylate	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 Mesylate	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 Mesylate	90-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-26
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 Mesylate	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 Mesylate	83-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-22
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 Mesylate	98-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-29
12495909-0	2002	Combination of imatinib and established antileukemic treatment modalities for otherwise refractory BCR-ABL positive lymphoblastic leukemia.	Imatinib Mesylate	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
12807155-0	2002	In vitro resistance of leukaemic blasts to prednisolone in bcr-abl positive childhood acute lymphoblastic leukaemia.	Prednisolone	43-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
12807155-5	2002	We studied the association between the presence of bcr-abl fusion gene and in vitro prednisolone resistance in children with B-lineage acute lymphoblastic leukaemia at diagnosis.	Prednisolone	84-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
12807155-8	2002	RESULTS: A median LD50 (lethal dose for 50% cells) for prednisolone in bcr-abl positive children (n=7) was 1.6 mg/ml (range: 0.25-5.0 mg/ml) and that of bcr-abl negative children (n=16) was 0.35 mg/ml (range 0.62-1.0 mg/ml).	Prednisolone	55-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
12807155-8	2002	RESULTS: A median LD50 (lethal dose for 50% cells) for prednisolone in bcr-abl positive children (n=7) was 1.6 mg/ml (range: 0.25-5.0 mg/ml) and that of bcr-abl negative children (n=16) was 0.35 mg/ml (range 0.62-1.0 mg/ml).	Prednisolone	55-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
12807155-9	2002	The median LD50 for prednisolone differed significantly between the bcr-abl positive and negative groups of children with acute lymphoblastic leukaemia (P<0.005).	Prednisolone	20-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
12807155-10	2002	INTERPRETATION & CONCLUSION: This is probably the first report to show that leukaemic blasts of bcr-abl positive children with ALL are about four-fold resistant to prednisolone as compared to blasts from bcr-abl negative children.	Prednisolone	168-180	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
12807155-11	2002	This suggests that one of the reasons for the poor prognosis of bcr-abl positive ALL could be a lower steroid sensitivity.	Steroids	102-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
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 Mesylate	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 Mesylate	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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-43
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 Mesylate	111-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
12661602-0	2002	Targeting of photooxidative damage on single-stranded DNA representing the bcr-abl chimeric gene using oligonucleotide-conjugates containing [Ru(phen)3](2+)-like photosensitiser groups.	Oligonucleotides	103-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
12661602-0	2002	Targeting of photooxidative damage on single-stranded DNA representing the bcr-abl chimeric gene using oligonucleotide-conjugates containing [Ru(phen)3](2+)-like photosensitiser groups.	tris-(1,10-phenanthroline)ruthenium	141-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
12297496-4	2002	In DU-145 cells, RB-mediated apoptosis involved biphasic activation of ABL kinase.	Rubidium	17-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-74
12444544-0	2002	Selective pyrrolo-pyrimidine inhibitors reveal a necessary role for Src family kinases in Bcr-Abl signal transduction and oncogenesis.	pyrrolopyrimidine	10-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
12444544-8	2002	In contrast, the phosphotyrosine content of Bcr-Abl and its endogenous substrate CrkL was unchanged at inhibitor concentrations that induced apoptosis, blocked oncogenic signaling and inhibited Src kinases.	Phosphotyrosine	17-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
12393646-7	2002	BCR/ABL-induced VEGF gene expression was counteracted by the phosphoinositide 3-kinase (PI3-kinase) inhibitor LY294002 and rapamycin, an antagonist of mammalian target of rapamycin (mTOR), but not by inhibition of the mitogen-activated protein kinase pathway.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	110-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
12393646-7	2002	BCR/ABL-induced VEGF gene expression was counteracted by the phosphoinositide 3-kinase (PI3-kinase) inhibitor LY294002 and rapamycin, an antagonist of mammalian target of rapamycin (mTOR), but not by inhibition of the mitogen-activated protein kinase pathway.	Sirolimus	123-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
12393646-8	2002	Similarly, BCR/ABL-dependent HIF-1alpha expression was inhibited by the addition of LY294002 and rapamycin.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-18
12421474-12	2002	The decline of the Bcr-Abl protein and its PTK activity may play an important role in the apoptotic effect of As2S2.	Arsenic(II) sulfide	110-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
12410571-0	2002	Resistance of bcr-abl-positive acute lymphoblastic leukemia to daunorubicin is not mediated by mdr1 gene expression.	Daunorubicin	63-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
12410571-9	2002	The median LD(50) of daunorubicin (concentration lethal to 50% of the leukemic blasts) differed significantly between bcr-abl-positive and -negative patients (P = 0.018).	Daunorubicin	21-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
12410571-10	2002	This in vitro study suggests that bcr-abl-positive ALL is relatively resistant to daunorubicin, but this resistance is not mediated through mdr1 gene expression.	Daunorubicin	82-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
12439339-0	2002	DNA damage and repair in BCR/ABL-expressing cells after combined action of idarubicin, STI571 and amifostine.	Idarubicin	75-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
12439339-0	2002	DNA damage and repair in BCR/ABL-expressing cells after combined action of idarubicin, STI571 and amifostine.	Imatinib Mesylate	87-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
12439339-0	2002	DNA damage and repair in BCR/ABL-expressing cells after combined action of idarubicin, STI571 and amifostine.	Amifostine	98-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
12439339-1	2002	STI571 is a specific ABL family tyrosine kinases inhibitor approved for treatment of leukemias.	Imatinib Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-24
12439339-4	2002	In the present work we investigated DNA damage and repair induced by idarubicin in the presence of STI571 and amifostine, a normal cell protector, in the BCR/ABL fusion tyrosine kinase-expressing cell line.	Idarubicin	69-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-161
12439339-4	2002	In the present work we investigated DNA damage and repair induced by idarubicin in the presence of STI571 and amifostine, a normal cell protector, in the BCR/ABL fusion tyrosine kinase-expressing cell line.	Amifostine	110-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-161
12439339-8	2002	In the absence of STI571 amifostine decreased the DNA-damaging effect of idarubicin in normal cells and increased it in BCR/ABL-positive cells.	Amifostine	25-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
12439339-10	2002	These results suggest that amifostine should be applied with special caution in idarubicin-based chemotherapies of BCR/ABL-positive leukemias involving STI571 inhibitor.	Amifostine	27-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
12439339-10	2002	These results suggest that amifostine should be applied with special caution in idarubicin-based chemotherapies of BCR/ABL-positive leukemias involving STI571 inhibitor.	Idarubicin	80-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
12414617-0	2002	Mutation in the ATP-binding pocket of the ABL kinase domain in an STI571-resistant BCR/ABL-positive cell line.	Adenosine Triphosphate	16-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-45
12414617-0	2002	Mutation in the ATP-binding pocket of the ABL kinase domain in an STI571-resistant BCR/ABL-positive cell line.	Adenosine Triphosphate	16-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-90
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 Mesylate	33-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-110
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.	Adenosine Triphosphate	79-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-110
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 Mesylate	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 Mesylate	35-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	184-191
12547154-0	2002	BCR/ABL amplification in chronic myelocytic leukemia blast crisis following imatinib mesylate administration.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	86-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
12642693-5	2002	Coadminstration of UCN-01 with U0126 produced multiple perturbations in signal transduction/cell cycle regulatory pathways, including diminished expression of Bcr/Abl, Mcl-1, cylin D(1), and activation of JNK and p34(cdc2).	U 0126	31-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-166
12429620-0	2002	Inhibition of human telomerase enhances the effect of the tyrosine kinase inhibitor, imatinib, in BCR-ABL-positive leukemia cells.	Imatinib Mesylate	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 Mesylate	161-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	243-250
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 Mesylate	199-207	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
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 Mesylate	128-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
12499247-4	2002	Recently, a novel pyrido[2,3-d]pyrimidine derivative, PD180970, has been shown to potently inhibit Bcr-Abl and induce apoptosis in Bcr-Abl-expressing leukemic cells.	Pyrido[2,3-d]pyrimidine	18-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
12499247-4	2002	Recently, a novel pyrido[2,3-d]pyrimidine derivative, PD180970, has been shown to potently inhibit Bcr-Abl and induce apoptosis in Bcr-Abl-expressing leukemic cells.	PD 180970	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
12499247-4	2002	Recently, a novel pyrido[2,3-d]pyrimidine derivative, PD180970, has been shown to potently inhibit Bcr-Abl and induce apoptosis in Bcr-Abl-expressing leukemic cells.	PD 180970	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
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 Mesylate	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
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 Mesylate	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
12384576-2	2002	Conformational changes induced by phosphotyrosine recognition promote the binding of the Src homology 3 (SH3) domain of the Abl tyrosine kinase to a proline-rich loop located between the betaD and betaE strands of the SH2 domain (DE loop).	Phosphotyrosine	34-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-127
12384576-2	2002	Conformational changes induced by phosphotyrosine recognition promote the binding of the Src homology 3 (SH3) domain of the Abl tyrosine kinase to a proline-rich loop located between the betaD and betaE strands of the SH2 domain (DE loop).	Proline	149-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-127
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.	Adenosine Triphosphate	18-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
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 Mesylate	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
12397549-13	2002	They can be detected by sequencing of the ATP binding site of BCR-ABL in specialized laboratories.	Adenosine Triphosphate	42-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
12440260-5	2002	The specific inhibitor of BCR-ABL TK, STI571 was developed by Brian Druker and his co-workers in 1996.	Imatinib Mesylate	38-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
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 Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
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.	Adenosine Triphosphate	101-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
12370803-1	2002	We have previously shown that the Jak2 tyrosine kinase is activated in Bcr-Abl positive cell lines and blood cells from CML blast crisis patients by tyrosine phosphorylation.	Tyrosine	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
12370803-9	2002	Treatment of 32Dp210 Bcr-Abl cells with both the proteasome inhibitor MG132 and AG490 blocked the reduction of the c-Myc protein observed by AG490 alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
12370803-11	2002	In this regard we showed that the Jak2/Bcr-Abl complex contains SH2-Bbeta.	sh2-bbeta	64-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
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 Mesylate	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 Mesylate	50-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-148
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 Mesylate	46-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
12384536-5	2002	The decline in Bcr-Abl expression and TK activity in K562 R (-Bcr-Abl) cells was associated with reduced AKT kinase and signal transducers and activators of transcription-5 DNA binding activities and increased sensitivity to the death ligand Apo-2 ligand/tumor necrosis factor-related apoptosis-inducing ligand and 1-beta-D-arabinofuranosylcytosine-induced apoptosis.	Deuterium	173-174	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
12384536-5	2002	The decline in Bcr-Abl expression and TK activity in K562 R (-Bcr-Abl) cells was associated with reduced AKT kinase and signal transducers and activators of transcription-5 DNA binding activities and increased sensitivity to the death ligand Apo-2 ligand/tumor necrosis factor-related apoptosis-inducing ligand and 1-beta-D-arabinofuranosylcytosine-induced apoptosis.	Deuterium	173-174	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
12384536-5	2002	The decline in Bcr-Abl expression and TK activity in K562 R (-Bcr-Abl) cells was associated with reduced AKT kinase and signal transducers and activators of transcription-5 DNA binding activities and increased sensitivity to the death ligand Apo-2 ligand/tumor necrosis factor-related apoptosis-inducing ligand and 1-beta-D-arabinofuranosylcytosine-induced apoptosis.	Cytarabine	324-348	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
12384536-5	2002	The decline in Bcr-Abl expression and TK activity in K562 R (-Bcr-Abl) cells was associated with reduced AKT kinase and signal transducers and activators of transcription-5 DNA binding activities and increased sensitivity to the death ligand Apo-2 ligand/tumor necrosis factor-related apoptosis-inducing ligand and 1-beta-D-arabinofuranosylcytosine-induced apoptosis.	Cytarabine	324-348	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
12384536-6	2002	All Gleevec-resistant cell types were sensitive to 17-allylamino-17-demethoxygeldanamycin (17-AAG)- and PD180970 (a SRC and Bcr-Abl TK inhibitor)-induced apoptosis.	PD 180970	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
12384536-9	2002	These findings also support the rationale to test the in vivo efficacy of 17-AAG and PD180970 against STI-571-resistant Bcr-Abl-positive acute leukemias.	tanespimycin	74-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	251-254
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 Mesylate	228-235	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
12358910-0	2002	Mutation in the ATP-binding site of BCR-ABL in a patient with chronic myeloid leukaemia with increasing resistance to STI571.	Adenosine Triphosphate	16-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
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 Mesylate	56-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
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 Mesylate	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
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 Mesylate	31-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-121
12200353-3	2002	Imatinib is an orally administered, potent inhibitor of the Bcr-Abl tyrosine kinase.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
12176881-2	2002	Imatinib mesylate (STI571), a selective inhibitor of the Bcr-Abl tyrosine kinase, has significant activity in AP CML.	Imatinib Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
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 Mesylate	65-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
12176881-2	2002	Imatinib mesylate (STI571), a selective inhibitor of the Bcr-Abl tyrosine kinase, has significant activity in AP CML.	Imatinib Mesylate	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
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 Mesylate	129-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
12231544-0	2002	Flavopiridol potentiates STI571-induced mitochondrial damage and apoptosis in BCR-ABL-positive human leukemia cells.	alvocidib	0-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
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 Mesylate	36-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	225-232
12231544-7	2002	Finally, STI571/flavopiridol effectively induced apoptosis in STI571-resistant K562 cells displaying amplification of the Bcr/Abl protein.	Imatinib Mesylate	9-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
12208881-6	2002	Inhibition of BCR/ABL tyrosine kinase with STI571 restores Lyn responsiveness to SDF-1 signaling.	Imatinib Mesylate	43-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
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 Mesylate	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 Mesylate	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
12528770-3	2002	Based on these observations, imatinib was developed as a specific inhibitor for the Bcr-Abl protein tyrosine kinase.	Imatinib Mesylate	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
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 Mesylate	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 Mesylate	121-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	226-233
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	94-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	294-302	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-182
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 Mesylate	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 Mesylate	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 Mesylate	131-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
12200668-5	2002	We report here three new pyrido[2,3-d]pyrimidine Bcr-Abl tyrosine kinase inhibitors, PD164199, PD173952, PD173958, that induced apoptosis of Bcr-Abl-dependent hematopoietic cells.	Pyrido[2,3-d]pyrimidine	25-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
12200668-5	2002	We report here three new pyrido[2,3-d]pyrimidine Bcr-Abl tyrosine kinase inhibitors, PD164199, PD173952, PD173958, that induced apoptosis of Bcr-Abl-dependent hematopoietic cells.	Pyrido[2,3-d]pyrimidine	25-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-148
12200668-5	2002	We report here three new pyrido[2,3-d]pyrimidine Bcr-Abl tyrosine kinase inhibitors, PD164199, PD173952, PD173958, that induced apoptosis of Bcr-Abl-dependent hematopoietic cells.	pd164199	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
12200668-5	2002	We report here three new pyrido[2,3-d]pyrimidine Bcr-Abl tyrosine kinase inhibitors, PD164199, PD173952, PD173958, that induced apoptosis of Bcr-Abl-dependent hematopoietic cells.	pd164199	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-148
12359059-6	2002	(2) An inhibitor of the nuclear transport of GSTpi, edible mushroom lectin (Agaricus bisporus lectin, ABL), increased the sensitivity of the cancer cells to DOX and CDDP, and partially to CPT-11.	Doxorubicin	157-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-105
12359059-6	2002	(2) An inhibitor of the nuclear transport of GSTpi, edible mushroom lectin (Agaricus bisporus lectin, ABL), increased the sensitivity of the cancer cells to DOX and CDDP, and partially to CPT-11.	Cisplatin	165-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-105
12359059-6	2002	(2) An inhibitor of the nuclear transport of GSTpi, edible mushroom lectin (Agaricus bisporus lectin, ABL), increased the sensitivity of the cancer cells to DOX and CDDP, and partially to CPT-11.	Irinotecan	188-194	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-105
12167702-3	2002	Interestingly, the association of c-Abl with IkappaBalpha, which is detectable in the form of nonphosphorylated proteins, is remarkably enhanced by an inducible binding of tyrosine-phosphorylated IkappaBalpha to the c-Abl SH2 domain.	Tyrosine	172-180	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-39
12167702-3	2002	Interestingly, the association of c-Abl with IkappaBalpha, which is detectable in the form of nonphosphorylated proteins, is remarkably enhanced by an inducible binding of tyrosine-phosphorylated IkappaBalpha to the c-Abl SH2 domain.	Tyrosine	172-180	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	216-221
12167702-4	2002	In contrast to the serine 32/34 phosphorylation that triggers ubiquitination and degradation of IkappaBalpha, c-Abl-mediated phosphorylation at tyrosine 305 is associated with an increase of the IkappaBalpha protein stability.	Serine	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-115
12167702-4	2002	In contrast to the serine 32/34 phosphorylation that triggers ubiquitination and degradation of IkappaBalpha, c-Abl-mediated phosphorylation at tyrosine 305 is associated with an increase of the IkappaBalpha protein stability.	Tyrosine	144-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-115
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
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 Mesylate	15-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-148
12077114-0	2002	Analysis of the structural basis of specificity of inhibition of the Abl kinase by STI571.	Imatinib Mesylate	83-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-72
12077114-1	2002	STI571, a selective inhibitor of Bcr-Abl, has been a successful therapeutic agent in clinical trials for chronic myelogenous leukemia.	Imatinib Mesylate	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 Mesylate	125-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-33
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.	Threonine	199-202	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	177-183	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-166
12185586-2	2002	STI571 (Gleevec), a novel anti-leukemia drug targeting BCR/ABL kinase can induce remissions of the Ph(1)-positive leukemias.	Imatinib Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-62
12173041-10	2002	Finally, we compared leukemic cell killing by RNAi to that caused by the ABL kinase tyrosine inhibitor, STI 571, Imatinib.	Imatinib Mesylate	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-76
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 Mesylate	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 Mesylate	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-145
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 Mesylate	0-6	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 Mesylate	8-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
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 Mesylate	44-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-113
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.	Tyrosine	95-98	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 Mesylate	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 Mesylate	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 Mesylate	183-190	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
12149456-2	2002	Mutations of Thr-315 in the Abl kinase domain to Ile (T315I) were previously described in STI-571-resistant patients and likely cause resistance from steric interference with drug binding.	Threonine	13-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-31
12149456-2	2002	Mutations of Thr-315 in the Abl kinase domain to Ile (T315I) were previously described in STI-571-resistant patients and likely cause resistance from steric interference with drug binding.	Isoleucine	49-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-31
12149456-3	2002	Here we identify mutations of Tyr-253 in the nucleotide-binding (P) loop of the Abl kinase domain to Phe or His in patients with advanced CML and acquired STI-571 resistance.	Tyrosine	30-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
12149456-3	2002	Here we identify mutations of Tyr-253 in the nucleotide-binding (P) loop of the Abl kinase domain to Phe or His in patients with advanced CML and acquired STI-571 resistance.	Phenylalanine	101-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
12149456-3	2002	Here we identify mutations of Tyr-253 in the nucleotide-binding (P) loop of the Abl kinase domain to Phe or His in patients with advanced CML and acquired STI-571 resistance.	Histidine	108-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
12149456-5	2002	The response of Abl proteins to STI-571 was influenced by the regulatory state of the kinase and by tyrosine phosphorylation.	Tyrosine	100-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-19
12149456-6	2002	The sensitivity of purified c-Abl to STI-571 was increased by a dysregulating mutation (P112L) in the Src homology 3 domain of Abl but decreased by phosphorylation at the regulatory Tyr-393.	Tyrosine	182-185	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-33
12149456-6	2002	The sensitivity of purified c-Abl to STI-571 was increased by a dysregulating mutation (P112L) in the Src homology 3 domain of Abl but decreased by phosphorylation at the regulatory Tyr-393.	Tyrosine	182-185	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-33
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 Mesylate	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 Mesylate	61-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
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.	lonafarnib	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
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.	lonafarnib	85-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
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 Mesylate	127-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
12154025-0	2002	Crystal structures of the kinase domain of c-Abl in complex with the small molecule inhibitors PD173955 and imatinib (STI-571).	PD 173955	95-103	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	118-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
12154025-6	2002	In contrast, PD173955 binds to a conformation of Abl in which the activation loop resembles that of an active kinase.	PD 173955	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-52
12154026-4	2002	During studies of signal transduction, we observed that the pyrido[2,3-d]pyrimidine src tyrosine kinase inhibitor PD173955 inhibited Bcr-Abl-dependent cell growth.	Pyrido[2,3-d]pyrimidine	60-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
12154026-4	2002	During studies of signal transduction, we observed that the pyrido[2,3-d]pyrimidine src tyrosine kinase inhibitor PD173955 inhibited Bcr-Abl-dependent cell growth.	PD 173955	114-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
12154026-5	2002	Subsequently, a related compound, PD180970, was reported as a potent inhibitor of Bcr-Abl.	PD 180970	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
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 Mesylate	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
12154026-9	2002	PD173955 has an IC(50) of 1-2 nM in kinase inhibition assays of Bcr-Abl, and in cellular growth assays it inhibits Bcr-Abl-dependent substrate tyrosine phosphorylation.	Tyrosine	143-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
12154026-10	2002	Of the six pyrido[2,3-d]pyrimidine analogues studied, PD166326 was the most potent inhibitor of Bcr-Abl-dependent cell growth.	Pyrido[2,3-d]pyrimidine	11-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
12154026-10	2002	Of the six pyrido[2,3-d]pyrimidine analogues studied, PD166326 was the most potent inhibitor of Bcr-Abl-dependent cell growth.	PD 166326	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
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 Mesylate	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	228-233
12204529-2	2002	Imatinib, a potent inhibitor of Bcr-Abl, has shown impressive clinical activity in CML patients.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	103-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-16
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 Mesylate	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 Mesylate	254-262	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-126
12204532-7	2002	Our data support a clonal selection model of preexisting BCR-ABL mutations that confer imatinib resistance.	Imatinib Mesylate	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
12110584-0	2002	Tyrosine phosphorylation of Mdm2 by c-Abl: implications for p53 regulation.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-41
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 Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
12135670-6	2002	Western blot analysis was performed to detect Bcr-Abl protein levels in K562 cells exposed to As2O3 at graded concentrations.	Arsenic Trioxide	94-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
12135670-7	2002	Bcr-Abl protein level kinetics were correlated with cell viability (trypan blue count) and activated caspase-3 detected by flow cytometry.	Trypan Blue	68-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
12135670-11	2002	Treatment of K562 cells with As2O3 alone led to down-regulation of Bcr-Abl protein within 24 hours, even at low doses.	Arsenic Trioxide	29-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
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.	Arsenic Trioxide	158-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
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.	Arsenic Trioxide	158-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
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 Mesylate	218-226	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
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 Mesylate	218-226	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
12138893-4	2002	We have developed an in vitro system that mirrors the chronic phase of CML with a combination of in vitro embryonic stem cell differentiation and tetracycline-inducible Bcr-Abl expression.	Tetracycline	146-158	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	169-176
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 Mesylate	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 Mesylate	96-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
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 Mesylate	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
12231544-7	2002	Finally, STI571/flavopiridol effectively induced apoptosis in STI571-resistant K562 cells displaying amplification of the Bcr/Abl protein.	alvocidib	16-28	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 Mesylate	62-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
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.	alvocidib	90-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-181
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 Mesylate	159-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-181
12231544-0	2002	Flavopiridol potentiates STI571-induced mitochondrial damage and apoptosis in BCR-ABL-positive human leukemia cells.	Imatinib Mesylate	25-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
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 Mesylate	102-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
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 Mesylate	102-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-174
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.	alvocidib	151-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
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.	alvocidib	151-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-174
12080468-8	2002	Based upon these results it is concluded that ARG can be activated as an oncogene in human malignancy and that the ETV6/ARG oncoprotein triggers some of the same signaling pathways associated with activated ABL oncogenes.	Arginine	46-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	207-210
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 Mesylate	25-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
12023887-4	2002	Indeed, in ascorbate-supplemented cells, increased cisplatin-induced apoptosis was seen, involving activation of the MLH1/c-Abl/p73 signalling cascade.	Ascorbic Acid	11-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-127
12023887-4	2002	Indeed, in ascorbate-supplemented cells, increased cisplatin-induced apoptosis was seen, involving activation of the MLH1/c-Abl/p73 signalling cascade.	Cisplatin	51-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-127
12023887-6	2002	The increased sensitivity to cisplatin observed in ascorbate-loaded cells appeared to be dependent exclusively on MLH1 and c-Abl expression, and independent of p53.	Cisplatin	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-128
12023887-6	2002	The increased sensitivity to cisplatin observed in ascorbate-loaded cells appeared to be dependent exclusively on MLH1 and c-Abl expression, and independent of p53.	Ascorbic Acid	51-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-128
12124177-3	2002	The autophosphorylation site tyrosine 177 binds the adaptor Grb2 and helps determine the lineage and severity of BCR/ABL disease: Tyr177 mutation (BCR/ABL-Y177F) dramatically impairs myeloid leukemogenesis, while diminishing lymphoid leukemogenesis.	Tyrosine	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
12124177-6	2002	Compared to BCR/ABL-expressing Ba/F3 cells, BCR/ABL-Y177F cells exhibit markedly reduced Gab2 tyrosine phosphorylation and association of phosphatidylinositol-3 kinase (PI3K) and Shp2 with Gab2 and BCR/ABL, and decreased PI3K/Akt and Ras/Erk activation, cell proliferation, and spontaneous migration.	Tyrosine	94-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
11929862-2	2002	This phage-displayed library was screened by affinity selection for SH3 domains that bind to the synthetic peptides, APTYPPPLPP and LSSRPLPTLPSP, which are peptide ligands for the human Abl or Src SH3 domains, respectively.	Peptides	107-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-189
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 Mesylate	109-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	168-175
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 Mesylate	49-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
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.	Cytarabine	128-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
12021410-1	2002	The response of myeloid leukemia cells to treatment with 1-beta-D-arabinofuranosylcytosine (ara-C) includes activation of the c-Abl protein tyrosine kinase and the stress-activated protein kinase (SAPK).	Cytarabine	57-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-131
12021410-1	2002	The response of myeloid leukemia cells to treatment with 1-beta-D-arabinofuranosylcytosine (ara-C) includes activation of the c-Abl protein tyrosine kinase and the stress-activated protein kinase (SAPK).	Cytarabine	92-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-131
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 Mesylate	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 Mesylate	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.	Cytarabine	118-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-49
12021410-4	2002	In concert with these effects of STI571, similar findings were obtained in c-Abl-deficient cells.	Imatinib Mesylate	33-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-80
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 Mesylate	32-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-59
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.	Cytarabine	135-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-59
12082821-2	2002	STI571 (signal transduction inhibition number 571) is a potent and selective inhibitor of the BCR-ABL tyrosine kinase.	serum sodium transport inhibitor	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
12411057-1	2002	OBJECTIVE: To investigate the mechanism of STI571 inducing apoptosis of K562 cells which express P210(BCR/ABL).	Imatinib Mesylate	43-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
12513785-9	2002	Bcr-abl fusion gene prevented apoptosis induced by etoposide or camptothecin, but did not prevent apoptosis induced by CIK cells.	Etoposide	51-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
12513785-9	2002	Bcr-abl fusion gene prevented apoptosis induced by etoposide or camptothecin, but did not prevent apoptosis induced by CIK cells.	Camptothecin	64-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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 Mesylate	55-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
12049868-3	2002	Clinical trials have confirmed the efficacy of imatinib, which has toxic effects in cells that express BCR-ABL.	Imatinib Mesylate	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
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 Mesylate	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
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 Mesylate	37-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-26
11986785-2	2002	The tyrosine kinase inhibitor imatinib (formerly STI571) was reported to selectively suppress the proliferation of BCR-ABL-positive cells.	Imatinib Mesylate	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 Mesylate	49-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
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 Mesylate	210-217	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-173
11964320-0	2002	Transient response to imatinib mesylate (STI571) in a patient with the ETV6-ABL t(9;12) translocation.	Imatinib Mesylate	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 Mesylate	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 Mesylate	189-195	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-161
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.	Adenosine Triphosphate	55-77	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 Mesylate	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 Mesylate	212-218	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
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 Mesylate	92-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
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).	Adenosine Triphosphate	34-56	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).	Adenosine Triphosphate	58-61	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 Mesylate	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 Mesylate	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 Mesylate	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
11964322-4	2002	Thus we confirm a high frequency of mutations clustered within the ATP-binding region of BCR/ABL in resistant patients.	Adenosine Triphosphate	67-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-79
12367580-1	2002	Imatinib mesylate (imatinib) inhibits Bcr/Abl, an oncogenic fusion protein.	Imatinib Mesylate	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 Mesylate	19-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
11971963-5	2002	c-Abl phosphorylates the Rad9 Bcl-2 homology 3 domain (Tyr-28) in vitro and in cells exposed to DNA-damaging agents.	Tyrosine	55-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
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 Mesylate	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 Mesylate	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
11790798-7	2002	Furthermore, we show tyrosine phosphorylation of Vav by Bcr-Abl.	Tyrosine	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
11999362-4	2002	The diagnosis of ABL depended on the following: (1) metachromasia with toluidine blue stain, (2) intracytoplasmic theta granules identified by electron microscopy, and (3) findings obtained from extensive immunophenotypic analysis.	Tolonium Chloride	71-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-20
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 Mesylate	29-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
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 Mesylate	14-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
11983100-0	2002	High-dose hydroxyurea plus G-CSF mobilize BCR-ABL-negative progenitor cells (CFC, LTC-IC) into the blood of newly diagnosed CML patients at any time of hematopoietic regeneration.	Hydroxyurea	10-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
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 Mesylate	35-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
11960322-1	2002	Geldanamycin (GA), herbimycin A and radicicol bind heat-shock protein-90 (Hsp90) and destabilize its client proteins including v-Src, Bcr-Abl, Raf-1, ErbB2, some growth factor receptors and steroid receptors.	geldanamycin	0-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
11960322-1	2002	Geldanamycin (GA), herbimycin A and radicicol bind heat-shock protein-90 (Hsp90) and destabilize its client proteins including v-Src, Bcr-Abl, Raf-1, ErbB2, some growth factor receptors and steroid receptors.	geldanamycin	14-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
11960322-1	2002	Geldanamycin (GA), herbimycin A and radicicol bind heat-shock protein-90 (Hsp90) and destabilize its client proteins including v-Src, Bcr-Abl, Raf-1, ErbB2, some growth factor receptors and steroid receptors.	herbimycin	19-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
11960322-1	2002	Geldanamycin (GA), herbimycin A and radicicol bind heat-shock protein-90 (Hsp90) and destabilize its client proteins including v-Src, Bcr-Abl, Raf-1, ErbB2, some growth factor receptors and steroid receptors.	monorden	36-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
11960353-0	2002	Nitric oxide induces the apoptosis of human BCR-ABL-positive myeloid leukemia cells: evidence for the chelation of intracellular iron.	Nitric Oxide	0-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
11960353-7	2002	The simultaneous addition of exogenous iron reversed NO-mediated inhibition of cell growth, caspase activation and apoptosis in all BCR-ABL(+) cells tested.	Iron	39-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
12014917-5	2002	FITC-labelled lectin was used to study cell binding and internalization of ABL.ABL caused a dose-dependent inhibition of proliferation and lattice contraction without significant toxicity.	Fluorescein-5-isothiocyanate	0-4	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-82
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 Mesylate	97-114	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 Mesylate	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 Mesylate	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 Mesylate	116-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	199-206
11861307-0	2002	Ph(+) acute lymphoblastic leukemia resistant to the tyrosine kinase inhibitor STI571 has a unique BCR-ABL gene mutation.	Imatinib Mesylate	78-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
11861307-2	2002	To identify mechanisms of resistance to STI571, 30 complementary DNAs (including 9 matched samples) obtained from the bone marrow of individuals with Ph(+) ALL were analyzed by direct sequencing of a 714-base pair region of ABL encoding for the adenosine triphosphate (ATP)-binding site and the kinase activation loop.	Adenosine Triphosphate	245-267	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	224-227
11861307-5	2002	Glu255Lys is within the motif important for forming the pocket of the ATP-binding site in ABL and it is highly conserved across species.	Adenosine Triphosphate	70-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-93
12054102-2	2002	Novartis has launched imatinib, an inhibitor of tyrosine kinases, including Bcr-Abl, for the treatment of chronic myeloid leukemia (CML).	Imatinib Mesylate	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
12054102-6	2002	Futhermore, Bcr-Abl-expressing cells treated with imatinib undergo apoptosis.	Imatinib Mesylate	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
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 Mesylate	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
11937320-1	2002	Improving etoposide efficacy in BCR-ABL-positive CML cells.	Etoposide	10-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
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 Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
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.	Adenosine Triphosphate	39-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
11853795-5	2002	METHODS: We analysed clinical samples from eight patients resistant to STI571-who had advanced-stage Ph+ leukaemia-for mutations within the ATP-binding site and activation loop of BCR-ABL.	Adenosine Triphosphate	140-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	180-187
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 Mesylate	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-181
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 Mesylate	24-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-132
11707430-8	2002	Finally, MGO and cisplatin induced c-Abl activation and c-Abl:PKCdelta association.	Pyruvaldehyde	9-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-40
11707430-8	2002	Finally, MGO and cisplatin induced c-Abl activation and c-Abl:PKCdelta association.	Pyruvaldehyde	9-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-61
11707430-8	2002	Finally, MGO and cisplatin induced c-Abl activation and c-Abl:PKCdelta association.	Cisplatin	17-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-40
11707430-8	2002	Finally, MGO and cisplatin induced c-Abl activation and c-Abl:PKCdelta association.	Cisplatin	17-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-61
11707430-9	2002	Rottlerin blocked c-Abl activation, but the c-Abl inhibitor STI-571 increased MGO and cisplatin-induced apoptosis by 50%.	rottlerin	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-23
11707430-9	2002	Rottlerin blocked c-Abl activation, but the c-Abl inhibitor STI-571 increased MGO and cisplatin-induced apoptosis by 50%.	Imatinib Mesylate	60-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-49
11707430-9	2002	Rottlerin blocked c-Abl activation, but the c-Abl inhibitor STI-571 increased MGO and cisplatin-induced apoptosis by 50%.	Pyruvaldehyde	78-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-49
11707430-9	2002	Rottlerin blocked c-Abl activation, but the c-Abl inhibitor STI-571 increased MGO and cisplatin-induced apoptosis by 50%.	Cisplatin	86-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-49
11781088-0	2002	Antigene effect in K562 cells of a PEG-conjugated triplex-forming oligonucleotide targeted to the bcr/abl oncogene.	Polyethylene Glycols	35-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
11840343-4	2002	Here, we present evidence that c-Abl induces the phosphorylation of p73 in threonine residues adjacent to prolines, and that the p38 MAP kinase pathway mediates this response.	Threonine	75-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-36
11840343-4	2002	Here, we present evidence that c-Abl induces the phosphorylation of p73 in threonine residues adjacent to prolines, and that the p38 MAP kinase pathway mediates this response.	Proline	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-36
11781088-6	2002	It was found that PEG ODN(13) specifically downregulated the transcription of bcr/abl mRNA at 65 +/- 5% with respect to control and inhibited cell growth by 32 +/- 3% in a 3 day liquid culture assay.	Polyethylene Glycols	18-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
11781088-0	2002	Antigene effect in K562 cells of a PEG-conjugated triplex-forming oligonucleotide targeted to the bcr/abl oncogene.	triplex-forming oligonucleotide	50-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
11781088-4	2002	Band-shift and footprinting experiments showed that PEG ODN(13) forms a stable triple helix (apparent K(d) between 10(-6) and 10(-7) M in 50 mM Tris-acetate, 10 mM MgCl(2), pH 7.4, 37 degrees C) with a natural polypurine-polypyrimidine target located in the 5" flanking region of the human bcr/abl oncogene.	Polyethylene Glycols	52-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	290-297
11809685-0	2002	Inhibition of the Bcr-Abl oncoprotein by Bcr requires phosphoserine 354.	Phosphoserine	54-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
11809685-2	2002	This inhibition is believed to be the result of binding to the SH2 domain of Bcr-Abl in a non-phosphotyrosine-dependent manner.	Phosphotyrosine	94-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
11809685-12	2002	This altered phosphoserine form of the Bcr protein selectively binds to the Abl SH2 domain of the oncoprotein, which we propose down-regulates the activity of the Bcr-Abl tyrosine kinase.	Phosphoserine	13-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-79
11809685-12	2002	This altered phosphoserine form of the Bcr protein selectively binds to the Abl SH2 domain of the oncoprotein, which we propose down-regulates the activity of the Bcr-Abl tyrosine kinase.	Phosphoserine	13-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-170
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 Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
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.	Adenosine Triphosphate	54-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
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 Mesylate	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-157
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 Mesylate	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 Mesylate	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 Mesylate	30-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
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 Mesylate	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.	2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide	57-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	204-211
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.	2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	205-212
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 Mesylate	124-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	205-212
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 Mesylate	95-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
11991666-7	2002	We hypothesize that this observed increase in the efficacy of repair in BCR/ABL- positive cells is involved in their resistance to idarubicin.	Idarubicin	131-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-79
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 Mesylate	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 Mesylate	22-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-166
11739186-9	2001	As expected, growth of BaF3/BCR-ABL was inhibited by STI571 but not by SU5402.	Imatinib Mesylate	53-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
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 Mesylate	30-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
11726515-0	2001	Tyrosine phosphorylation of Grb2 by Bcr/Abl and epidermal growth factor receptor: a novel regulatory mechanism for tyrosine kinase signaling.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
30147592-0	2001	Pyrrolo-1,5-Benzoxazepines Induce Apoptosis in Chronic Myeloid Leukemia (CML) Cells by Bypassing the Apoptotic Suppressor BCR-ABL.	pyrrolo-1,5-benzoxazepines	0-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
11726515-2	2001	We found that Grb2 was tyrosine-phosphorylated in cells expressing BCR/ABL and in A431 cells stimulated with epidermal growth factor (EGF).	Tyrosine	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
11726515-3	2001	Phosphorylation of Grb2 by Bcr/Abl or EGF receptor reduced its SH3-dependent binding to Sos in vivo, but not its SH2-dependent binding to Bcr/Abl.	sulfur monoxide	88-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-34
11726515-3	2001	Phosphorylation of Grb2 by Bcr/Abl or EGF receptor reduced its SH3-dependent binding to Sos in vivo, but not its SH2-dependent binding to Bcr/Abl.	sulfur monoxide	88-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
11781820-3	2001	Here we report tyrosine phosphorylation of endogenous c-Abl and a concomitant increase in catalytic activity.	Tyrosine	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-59
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 Mesylate	74-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-25
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 Mesylate	65-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-34
11781820-9	2001	These mutations resulted in tyrosine phosphorylation and activation of c-Abl, as if relieving c-Abl from inhibition.	Tyrosine	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-99
11751479-1	2001	STI571 is a 2-phenylalaminopyrimidine derivative that inhibits c-abl, Bcr-Abl, and platelet-derived growth factor receptor tyrosine kinases.	Imatinib Mesylate	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 Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
11751479-1	2001	STI571 is a 2-phenylalaminopyrimidine derivative that inhibits c-abl, Bcr-Abl, and platelet-derived growth factor receptor tyrosine kinases.	2-phenylalaminopyrimidine	12-37	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.	2-phenylalaminopyrimidine	12-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
11695992-2	2001	In cells transformed by the src, crk or BCR-Abl oncogenes, the phosphotyrosine content of paxillin is elevated.	Phosphotyrosine	63-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
11753652-5	2001	Abl was regulated efficiently when its SH3 domain was replaced with a heterologous SH3 from c-Src that binds a different spectrum of proline-rich ligands, but not by substitution of a modular WW domain with similar ligand-binding specificity.	Proline	133-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
11698276-6	2001	Here, it is shown that JAK2 is constitutively tyrosine phosphorylated in cultured and primary erythroid cells expressing BCR-ABL.	Tyrosine	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
11746976-8	2001	Transcription regulation of BACH2 in BCR/ABL-positive cells was exerted via the MEK pathways, as shown by their responses to the U0126-specific inhibitor.	U 0126	129-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-44
11681425-0	2001	Marked ploidy and BCR-ABL gene amplification in vivo in a patient treated with STI571.	Imatinib Mesylate	79-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
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 Mesylate	0-8	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 Mesylate	10-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
11489902-3	2001	In response to 0.68 and 6.8 microm STI571, proliferation of Bcr-Abl-positive K562 cells showed a 57% and 74% decrease, respectively, whereas glucose label incorporation into RNA decreased by 13.4% and 30.1%, respectively, through direct glucose oxidation, as indicated by the decrease in the m1/Sigma(m)n ratio in RNA.	Glucose	237-244	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
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 Mesylate	0-17	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-124
11680792-4	2001	Imatinib also has substantial activity in Philadelphia chromosome-positive acute lymphoblastic leukaemia expressing the BCR-ABL fusion protein.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
11587211-0	2001	The Hsp90 inhibitor geldanamycin selectively sensitizes Bcr-Abl-expressing leukemia cells to cytotoxic chemotherapy.	geldanamycin	20-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
11587211-4	2001	Furthermore, GA sensitized Bcr-Abl-expressing cells to doxorubicin (DOX) and paclitaxel (PTX).	Paclitaxel	89-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
11587211-6	2001	Like GA, STI 571 (an inhibitor of the Abl kinase) sensitized Bcr-Abl-expressing cells to DOX.	Imatinib Mesylate	9-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-41
11587211-6	2001	Like GA, STI 571 (an inhibitor of the Abl kinase) sensitized Bcr-Abl-expressing cells to DOX.	Imatinib Mesylate	9-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
11587211-6	2001	Like GA, STI 571 (an inhibitor of the Abl kinase) sensitized Bcr-Abl-expressing cells to DOX.	Doxorubicin	89-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-41
11587211-6	2001	Like GA, STI 571 (an inhibitor of the Abl kinase) sensitized Bcr-Abl-expressing cells to DOX.	Doxorubicin	89-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
11684015-2	2001	Here we demonstrate that RAD51 is important for resistance to cisplatin and mitomycin C in cells expressing the BCR/ABL oncogenic tyrosine kinase.	Cisplatin	62-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
11684015-2	2001	Here we demonstrate that RAD51 is important for resistance to cisplatin and mitomycin C in cells expressing the BCR/ABL oncogenic tyrosine kinase.	Mitomycin	76-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
11684015-5	2001	Phosphorylation of the RAD51 Tyr-315 residue by BCR/ABL appears essential for enhanced DSB repair and drug resistance.	Tyrosine	29-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-55
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	121-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	318-325
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 Mesylate	30-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
11593427-0	2001	Involvement of Jak2 tyrosine phosphorylation in Bcr-Abl transformation.	Tyrosine	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-55
11593427-1	2001	We have previously reported that the Jak2 tyrosine kinase but not Jak1 is tyrosine phosphorylated in the absence of IL-3 in Bcr-Abl positive M3.16 cells, which are rendered IL-3 independent by BCR-ABL gene expression.	Tyrosine	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
11593427-1	2001	We have previously reported that the Jak2 tyrosine kinase but not Jak1 is tyrosine phosphorylated in the absence of IL-3 in Bcr-Abl positive M3.16 cells, which are rendered IL-3 independent by BCR-ABL gene expression.	Tyrosine	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	193-200
11593427-3	2001	Our results indicate that Jak2 became tyrosine-phosphorylated in a number of cell lines expressing Bcr-Abl, when maintained in medium lacking IL-3, whereas Bcr-Abl negative cells lacked Jak2 tyrosine phosphorylation.	Tyrosine	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
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.	Tyrosine	10-18	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.	Tyrosine	10-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-53
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 Mesylate	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 Mesylate	106-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-53
11559572-9	2001	Furthermore, the percentage of BCR-ABL RNA-positive colonies was almost same among the colonies not displaying Pa methylation as among the colonies in which this methylation was found.	Protactinium	111-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
11587132-8	2001	We conclude that the Radiometer ABL 735 bilirubin assay is suitable for near-patient assessment of neonatal jaundice using whole blood, thus eliminating the need for sample centrifugation.	Bilirubin	40-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-35
11709051-6	2001	RB inhibits E2F and the nuclear c-Abl tyrosine kinase.	Rubidium	0-2	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-37
11709051-8	2001	Because of RB, the c-Abl/p73 apoptosis pathway is activated in S/G(2) cells but not in G(1) cells.	Rubidium	11-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-24
11509666-5	2001	The results also demonstrate that induction of ER stress with calcium ionophore A23187, brefeldin A, or tunicamycin is associated with translocation of ER-associated c-Abl to mitochondria.	Calcium	62-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-171
11509666-5	2001	The results also demonstrate that induction of ER stress with calcium ionophore A23187, brefeldin A, or tunicamycin is associated with translocation of ER-associated c-Abl to mitochondria.	Calcimycin	80-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-171
11509666-5	2001	The results also demonstrate that induction of ER stress with calcium ionophore A23187, brefeldin A, or tunicamycin is associated with translocation of ER-associated c-Abl to mitochondria.	Brefeldin A	88-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-171
11509666-5	2001	The results also demonstrate that induction of ER stress with calcium ionophore A23187, brefeldin A, or tunicamycin is associated with translocation of ER-associated c-Abl to mitochondria.	Tunicamycin	104-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-171
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.	2-Phenylpyrimidine	4-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-79
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.	2-Phenylpyrimidine	4-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
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 Mesylate	34-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-79
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 Mesylate	34-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
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.	Adenosine Triphosphate	139-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-79
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.	Adenosine Triphosphate	139-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
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 Mesylate	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 Mesylate	23-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	658-661
11587211-2	2001	Geldanamycin (GA), a drug which destabilizes Hsp90-associated proteins, depletes cells of Bcr-Abl, an Hsp90 client, but not of Abl.	geldanamycin	0-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
11587211-2	2001	Geldanamycin (GA), a drug which destabilizes Hsp90-associated proteins, depletes cells of Bcr-Abl, an Hsp90 client, but not of Abl.	geldanamycin	0-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-97
11587211-2	2001	Geldanamycin (GA), a drug which destabilizes Hsp90-associated proteins, depletes cells of Bcr-Abl, an Hsp90 client, but not of Abl.	geldanamycin	14-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
11587211-2	2001	Geldanamycin (GA), a drug which destabilizes Hsp90-associated proteins, depletes cells of Bcr-Abl, an Hsp90 client, but not of Abl.	geldanamycin	14-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-97
11587211-3	2001	Both HL60 cells transfected with Bcr-Abl and naturally Ph1-positive K562 leukemia cells are resistant to most cytotoxic drugs, but were found to be sensitive to GA.	geldanamycin	161-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
11587211-4	2001	Furthermore, GA sensitized Bcr-Abl-expressing cells to doxorubicin (DOX) and paclitaxel (PTX).	Doxorubicin	55-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
11587211-4	2001	Furthermore, GA sensitized Bcr-Abl-expressing cells to doxorubicin (DOX) and paclitaxel (PTX).	Doxorubicin	68-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
11587211-4	2001	Furthermore, GA sensitized Bcr-Abl-expressing cells to doxorubicin (DOX) and paclitaxel (PTX).	Paclitaxel	77-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
11521190-2	2001	We showed previously that human erythroleukemia K562 cells are resistant to antineoplastic drug (taxol)-induced apoptosis through the atypical protein kinase C iota isozyme (PKC iota), a kinase downstream of Bcr-Abl.	Paclitaxel	97-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	208-215
11387320-0	2001	Deletion of the Src homology 3 domain and C-terminal proline-rich sequences in Bcr-Abl prevents Abl interactor 2 degradation and spontaneous cell migration and impairs leukemogenesis.	Proline	53-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
11387320-5	2001	We report here that the Src homology 3 domain and C-terminal proline-rich sequences of Bcr-Abl are required for its binding to Abl interactor 2 as well as for the induction of Abl interactor 2 degradation.	Proline	61-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
11337505-6	2001	Under similar conditions, nuclear c-ABL was only exported after the addition of cytosolic extract, and the export was blocked by the CRM1-specific inhibitor, leptomycin B.	leptomycin B	158-170	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-39
11521190-11	2001	Our results indicate that RelA transactivation is an important downstream target of the PKC iota-mediated Bcr-Abl signaling pathway and is required for resistance to taxol-induced apoptosis.	iota	92-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
11521190-11	2001	Our results indicate that RelA transactivation is an important downstream target of the PKC iota-mediated Bcr-Abl signaling pathway and is required for resistance to taxol-induced apoptosis.	Paclitaxel	166-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
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 Mesylate	17-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
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 Mesylate	17-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
11494128-6	2001	The SH2 domains of Abl and Arg bind to tyrosine-phosphorylated motifs in the juxtamembrane region of EphB2.	Tyrosine	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-22
11494128-8	2001	A third interaction between Abl and EphB2 is probably mediated by an intermediary protein because it requires tyrosine phosphorylation of EphB2, but not the binding sites for the Abl SH2 domain.	Tyrosine	110-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-31
11494128-10	2001	Activated EphB2 causes tyrosine phosphorylation of Abl and Arg, and vice versa.	Tyrosine	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-54
11494134-6	2001	The major proline-rich region of Cbl was required for its phosphorylation by c-Abl, but not by a constitutively activated Abl mutant, suggesting Cbl activates c-Abl by engaging its SH3 domain.	Proline	10-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-82
11494134-6	2001	The major proline-rich region of Cbl was required for its phosphorylation by c-Abl, but not by a constitutively activated Abl mutant, suggesting Cbl activates c-Abl by engaging its SH3 domain.	Proline	10-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-82
11494134-6	2001	The major proline-rich region of Cbl was required for its phosphorylation by c-Abl, but not by a constitutively activated Abl mutant, suggesting Cbl activates c-Abl by engaging its SH3 domain.	Proline	10-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-164
11494134-7	2001	Efficient phosphorylation of Cbl and its stable association with Abl required the SH2 domain of Abl, suggesting that SH2-phosphotyrosine interactions prevent dissociation of active Abl from Cbl.	Phosphotyrosine	121-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-68
11494134-7	2001	Efficient phosphorylation of Cbl and its stable association with Abl required the SH2 domain of Abl, suggesting that SH2-phosphotyrosine interactions prevent dissociation of active Abl from Cbl.	Phosphotyrosine	121-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-99
11494134-7	2001	Efficient phosphorylation of Cbl and its stable association with Abl required the SH2 domain of Abl, suggesting that SH2-phosphotyrosine interactions prevent dissociation of active Abl from Cbl.	Phosphotyrosine	121-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-99
11494134-9	2001	Studies with Nck mutants suggested that the Nck SH2 domain is responsible for inhibiting the activity of Abl toward both Cbl and Nck itself, most likely by competing with the Abl SH2 for tyrosine-phosphorylated binding sites.	Tyrosine	187-195	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-108
11494134-9	2001	Studies with Nck mutants suggested that the Nck SH2 domain is responsible for inhibiting the activity of Abl toward both Cbl and Nck itself, most likely by competing with the Abl SH2 for tyrosine-phosphorylated binding sites.	Tyrosine	187-195	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-178
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.	N-phenylpyrimidin-2-amine	18-41	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.	N-phenylpyrimidin-2-amine	18-41	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 Mesylate	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 Mesylate	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.	serum sodium transport inhibitor	102-108	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.	serum sodium transport inhibitor	102-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-162
11504279-5	2001	STI571, an Abl-specific tyrosine kinase inhibitor, has shown remarkable activity in all phases of CML.	Imatinib Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-14
11454136-2	2001	Signal transduction inhibitor (STI571) (formerly CGP57 148B), is an ABL specific, tyrosine kinase inhibitor.	Imatinib Mesylate	31-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-71
11526595-3	2001	A tetracycline-regulated promoter was developed to drive Bcr-Abl expression in differentiating embryonal stem cells.	Tetracycline	2-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
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 Mesylate	30-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-168
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	18-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-178
11279131-0	2001	The beta-amyloid precursor protein APP is tyrosine-phosphorylated in cells expressing a constitutively active form of the Abl protoncogene.	Tyrosine	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-125
11279131-6	2001	Furthermore, in cells expressing the active form of Abl, APP is tyrosine-phosphorylated.	Tyrosine	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-55
11279131-8	2001	Co-immunoprecipitation experiments demonstrate that active Abl and tyrosine-phosphorylated APP also form a stable complex, which could result from the interaction of the pYENP motif of the APP cytodomain with the SH2 domain of Abl.	Tyrosine	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	227-230
11409908-4	2001	Several compounds have now been identified as relatively selective inhibitors of BCR-ABL, including members of the tyrphostin family, herbimycin A and most importantly the 2-phenylaminopyrimidine ST1571.	Tyrphostins	115-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
11409908-4	2001	Several compounds have now been identified as relatively selective inhibitors of BCR-ABL, including members of the tyrphostin family, herbimycin A and most importantly the 2-phenylaminopyrimidine ST1571.	herbimycin	134-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
11409908-4	2001	Several compounds have now been identified as relatively selective inhibitors of BCR-ABL, including members of the tyrphostin family, herbimycin A and most importantly the 2-phenylaminopyrimidine ST1571.	N-phenylpyrimidin-2-amine	172-195	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
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 Mesylate	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 Mesylate	40-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
11278340-7	2001	Overexpression of c-Abl(K-R) inhibits HPK1-induced activation of SAPK/JNK.	Krypton	24-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-23
11350980-2	2001	The present study demonstrates that reactive oxygen species (ROS) induce targeting of c-Abl to mitochondria.	Reactive Oxygen Species	36-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-91
11350980-2	2001	The present study demonstrates that reactive oxygen species (ROS) induce targeting of c-Abl to mitochondria.	Reactive Oxygen Species	61-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-91
11350980-3	2001	We show that ROS-induced localization of c-Abl to mitochondria is dependent on activation of protein kinase C (PKC)delta and the c-Abl kinase function.	Reactive Oxygen Species	13-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-46
11350980-3	2001	We show that ROS-induced localization of c-Abl to mitochondria is dependent on activation of protein kinase C (PKC)delta and the c-Abl kinase function.	Reactive Oxygen Species	13-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-134
11350980-4	2001	Targeting of c-Abl to mitochondria is associated with ROS-induced loss of mitochondrial transmembrane potential.	Reactive Oxygen Species	54-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-18
11350980-5	2001	The results also demonstrate that c-Abl is necessary for ROS-induced depletion of ATP and the activation of a necrosis-like cell death.	Reactive Oxygen Species	57-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-39
11350980-5	2001	The results also demonstrate that c-Abl is necessary for ROS-induced depletion of ATP and the activation of a necrosis-like cell death.	Adenosine Triphosphate	82-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-39
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.	N-phenylpyrimidin-2-amine	4-27	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 Mesylate	39-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-79
11342454-6	2001	By contrast, STI571 is unique among c-Abl-specific tyrosine kinase inhibitors in modulating the pharmacologic activity of ATRA.	Imatinib Mesylate	13-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-41
11342454-6	2001	By contrast, STI571 is unique among c-Abl-specific tyrosine kinase inhibitors in modulating the pharmacologic activity of ATRA.	Tretinoin	122-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-41
11342454-8	2001	All this is accompanied by inhibition of c-Abl tyrosine phosphorylation and retardation of the retinoid-dependent degradation of PML-RARalpha and RARalpha.	Tyrosine	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-46
11339833-0	2001	Caveolin-1 and a 29-kDa caveolin-associated protein are phosphorylated on tyrosine in cells expressing a temperature-sensitive v-Abl kinase.	Tyrosine	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-132
11339833-4	2001	We found that caveolin-1 is also phosphorylated on tyrosine in v-Abl-transformed cells.	Tyrosine	51-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-68
11339833-8	2001	Caveolin-1 is phosphorylated at tyrosine 14 in v-Abl-expressing cells as has been observed previously in v-Src-expressing cells.	Tyrosine	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-52
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 Mesylate	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
11313280-8	2001	However, neither IL-3 nor GM-CSF could reactivate Stat-5 after the STI-571-mediated inhibition of bcr-abl.	Imatinib Mesylate	67-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
11380621-4	2001	The interaction of the amino-terminal Src-homology (SH) 3 domain of c-Crk and the proline-rich motifs of c-Abl is an essential step for the phosphorylation of c-Crk by c-Abl, as well as the activation of c-Abl by c-Crk.	Proline	82-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-110
11380621-4	2001	The interaction of the amino-terminal Src-homology (SH) 3 domain of c-Crk and the proline-rich motifs of c-Abl is an essential step for the phosphorylation of c-Crk by c-Abl, as well as the activation of c-Abl by c-Crk.	Proline	82-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	168-173
11380621-4	2001	The interaction of the amino-terminal Src-homology (SH) 3 domain of c-Crk and the proline-rich motifs of c-Abl is an essential step for the phosphorylation of c-Crk by c-Abl, as well as the activation of c-Abl by c-Crk.	Proline	82-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	168-173
11380621-5	2001	The activation of c-Abl by c-Crk is negatively regulated by phosphorylation of the tyrosine 221 of c-Crk.	Tyrosine	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-23
11383207-1	2001	STI571 selectively inhibits the ABL-tyrosine kinase, the activity of which is activated by the formation of chimeric BCR/ABL.	Imatinib Mesylate	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 Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
11368438-2	2001	Treatment with arsenic trioxide (As2O3) lowers Bcr-Abl protein levels and induces apoptosis of the Bcr-Abl-positive leukemic blasts (Blood 2000; 95: 1014).	Arsenic Trioxide	15-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
11368438-2	2001	Treatment with arsenic trioxide (As2O3) lowers Bcr-Abl protein levels and induces apoptosis of the Bcr-Abl-positive leukemic blasts (Blood 2000; 95: 1014).	Arsenic Trioxide	15-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
11368438-2	2001	Treatment with arsenic trioxide (As2O3) lowers Bcr-Abl protein levels and induces apoptosis of the Bcr-Abl-positive leukemic blasts (Blood 2000; 95: 1014).	Arsenic Trioxide	33-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
11368438-2	2001	Treatment with arsenic trioxide (As2O3) lowers Bcr-Abl protein levels and induces apoptosis of the Bcr-Abl-positive leukemic blasts (Blood 2000; 95: 1014).	Arsenic Trioxide	33-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
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).	Arsenic Trioxide	142-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	206-213
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 Mesylate	152-159	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	206-213
11368438-6	2001	These data demonstrate that a treatment strategy which combines an agent that lowers Bcr-Abl levels, eg As2O3, with an agent that inhibits Bcr-Abl TK activity, eg STI-571, can potently induce apoptosis and differentiation of Bcr-Abl-positive human leukemic cells.	Arsenic Trioxide	104-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
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 Mesylate	53-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
21189610-1	2001	AIM: To study the effect of bcr-abl fusion gene antisense phosphorothioate oligodeoxynucleotide (Aspo) on bcr-abl mRNA and apoptosis of K562 cells.	phosphorothioate oligodeoxynucleotide	58-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
21189610-1	2001	AIM: To study the effect of bcr-abl fusion gene antisense phosphorothioate oligodeoxynucleotide (Aspo) on bcr-abl mRNA and apoptosis of K562 cells.	phosphorothioate oligodeoxynucleotide	58-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
21189610-1	2001	AIM: To study the effect of bcr-abl fusion gene antisense phosphorothioate oligodeoxynucleotide (Aspo) on bcr-abl mRNA and apoptosis of K562 cells.	aspo	97-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
21189610-1	2001	AIM: To study the effect of bcr-abl fusion gene antisense phosphorothioate oligodeoxynucleotide (Aspo) on bcr-abl mRNA and apoptosis of K562 cells.	aspo	97-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
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 Mesylate	58-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
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.	57148b	88-94	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 Mesylate	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 Mesylate	51-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
11368361-7	2001	STI571 inhibited CA formation of BCR-ABL-positive ALL cells virtually 100% at 0.1-1.0 micromol/l.	Imatinib Mesylate	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 Mesylate	26-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
11280726-0	2001	Geldanamycin and its analogue 17-allylamino-17-demethoxygeldanamycin lowers Bcr-Abl levels and induces apoptosis and differentiation of Bcr-Abl-positive human leukemic blasts.	geldanamycin	0-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
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 Mesylate	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 Mesylate	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 Mesylate	8-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
11280726-0	2001	Geldanamycin and its analogue 17-allylamino-17-demethoxygeldanamycin lowers Bcr-Abl levels and induces apoptosis and differentiation of Bcr-Abl-positive human leukemic blasts.	geldanamycin	0-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-143
11280726-0	2001	Geldanamycin and its analogue 17-allylamino-17-demethoxygeldanamycin lowers Bcr-Abl levels and induces apoptosis and differentiation of Bcr-Abl-positive human leukemic blasts.	tanespimycin	30-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
11280726-0	2001	Geldanamycin and its analogue 17-allylamino-17-demethoxygeldanamycin lowers Bcr-Abl levels and induces apoptosis and differentiation of Bcr-Abl-positive human leukemic blasts.	tanespimycin	30-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-143
11280726-2	2001	Present studies demonstrate that treatment with ansamycin antibiotic geldanamycin (GA), or its less toxic analogue 17-allylamino-17-demethoxygeldanamycin (17-AAG), induces cytosolic accumulation of cytochrome c and cleavage and activities of caspase-9 and caspase-3, triggering apoptosis of HL-60/Bcr-Abl and K562 cells.	Rifabutin	48-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	297-304
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 Mesylate	71-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-35
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 Mesylate	45-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-18
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 Mesylate	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 Mesylate	43-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
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.	Dexrazoxane	114-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-18
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 Mesylate	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 Mesylate	34-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	177-180
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.	Cytarabine	45-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	177-180
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.	Hydroxyurea	97-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	177-180
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.	mafosfamide	110-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	177-180
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.	Etoposide	125-134	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 Mesylate	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 Mesylate	72-78	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.	Etoposide	81-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-161
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	17-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
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 Mesylate	53-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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.	2-aminopyrimidine	13-28	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.	Adenosine Triphosphate	64-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-112
11168864-1	2001	OBJECTIVES: Firstly, to determine the accuracy of the Radiometer ABL 625 lactate electrode (Radiometer Medical Pty Ltd, Nunawading, Victoria, Australia) by comparing the lactate values obtained by this method to those obtained with the Hitachi 917 lactate analyser (Boehringer Mannheim Corporation, Charlottetown, Prince Edward Island, Canada).	Lactic Acid	73-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-68
11168864-6	2001	RESULTS: The lactate levels obtained from the Radiometer ABL 625 lactate electrode were consistently lower than the levels obtained from the Hitachi 917 lactate analyser (mean difference - 0.24), but the correlation was high (r = 0.97).	Lactic Acid	13-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-60
11160680-6	2001	This mutant encodes a v-Abl protein in which the beta B5 arginine at the base of the phosphotyrosine-binding pocket has been replaced by a lysine.	beta b5 arginine	49-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-27
11160680-6	2001	This mutant encodes a v-Abl protein in which the beta B5 arginine at the base of the phosphotyrosine-binding pocket has been replaced by a lysine.	Phosphotyrosine	85-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-27
11160680-6	2001	This mutant encodes a v-Abl protein in which the beta B5 arginine at the base of the phosphotyrosine-binding pocket has been replaced by a lysine.	Lysine	139-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-27
11376433-6	2001	Using these antibodies, we established/confirmed the in vivo phosphorylation of Ser-354, Tyr-328, and Tyr-360 in Bcr and Bcr-Abl proteins.	Serine	80-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
11280917-6	2001	This case suggests that Ph/-7 ALL with major BCR/ABL gene rearrangement showing coexpression of myeloid antigens may be sensitive to intermediate- and high-dose ara-C.	Cytarabine	161-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
11196151-5	2001	Under these conditions, both Bcr-Abl-positive and -negative hematopoietic cells can be efficiently infected by adenovirus, as demonstrated by 5-bromo-4-chloro-3-indolyl-beta-D-galactopyranoside staining of cells infected by beta-galactosidase (beta-GAL) adenovirus.	5-bromo-4-chloro-3-indolyl beta-galactoside	142-193	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
11376433-6	2001	Using these antibodies, we established/confirmed the in vivo phosphorylation of Ser-354, Tyr-328, and Tyr-360 in Bcr and Bcr-Abl proteins.	Tyrosine	89-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
11376433-6	2001	Using these antibodies, we established/confirmed the in vivo phosphorylation of Ser-354, Tyr-328, and Tyr-360 in Bcr and Bcr-Abl proteins.	Tyrosine	102-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
11527146-6	2001	Interestingly, CEP treatment induced remarkable degradation of the Bcr-Abl protein in K562 cells, and this degradation was prevented partially by zVAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	146-154	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
11165139-4	2001	Moreover, we observed that TBZ-4-OCH3 was also active in cells expressing Bcr-Abl, an oncogene that confers resistance to apoptosis induced by several stimuli, including cytotoxic agents.	tbz-4-och3	27-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
11423669-1	2001	Therapeutic agent STI571 (signal transduction inhibitor number 571) is a rationally developed, potent, and selective inhibitor for abl tyrosine kinases, including bcr-abl, as well c-kit and the platelet-derived growth factor receptor tyrosine kinases.	serum sodium transport inhibitor	18-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
11280726-2	2001	Present studies demonstrate that treatment with ansamycin antibiotic geldanamycin (GA), or its less toxic analogue 17-allylamino-17-demethoxygeldanamycin (17-AAG), induces cytosolic accumulation of cytochrome c and cleavage and activities of caspase-9 and caspase-3, triggering apoptosis of HL-60/Bcr-Abl and K562 cells.	geldanamycin	69-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	297-304
11161255-0	2001	PBPC mobilization with chemotherapy and G-CSF in patients with chronic myeloid leukemia: quantification of bcr/abl-positive cells by interphase fluorescence in situ hybridization and competitive PCR.	PbPc	0-4	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-114
11280726-2	2001	Present studies demonstrate that treatment with ansamycin antibiotic geldanamycin (GA), or its less toxic analogue 17-allylamino-17-demethoxygeldanamycin (17-AAG), induces cytosolic accumulation of cytochrome c and cleavage and activities of caspase-9 and caspase-3, triggering apoptosis of HL-60/Bcr-Abl and K562 cells.	geldanamycin	83-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	297-304
11280726-2	2001	Present studies demonstrate that treatment with ansamycin antibiotic geldanamycin (GA), or its less toxic analogue 17-allylamino-17-demethoxygeldanamycin (17-AAG), induces cytosolic accumulation of cytochrome c and cleavage and activities of caspase-9 and caspase-3, triggering apoptosis of HL-60/Bcr-Abl and K562 cells.	tanespimycin	155-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	297-304
11280726-3	2001	GA or 17-AAG down-regulated intracellular Bcr-Abl and c-Raf protein levels, as well as reduced Akt kinase activity.	geldanamycin	0-2	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
11280726-3	2001	GA or 17-AAG down-regulated intracellular Bcr-Abl and c-Raf protein levels, as well as reduced Akt kinase activity.	tanespimycin	6-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
11280726-5	2001	By binding and inhibiting Hsp90, GA or 17-AAG treatment shifted the binding of Bcr-Abl from Hsp90 to Hsp70 and induced the proteasomal degradation of Bcr-Abl, because cotreatment with proteasome inhibitor PSC341 reduced both GA (or 17-AAG)-mediated down-regulation of Bcr-Abl levels and inhibited apoptosis of HL-60/Bcr-Abl and K562 cells.	tanespimycin	39-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
11280726-5	2001	By binding and inhibiting Hsp90, GA or 17-AAG treatment shifted the binding of Bcr-Abl from Hsp90 to Hsp70 and induced the proteasomal degradation of Bcr-Abl, because cotreatment with proteasome inhibitor PSC341 reduced both GA (or 17-AAG)-mediated down-regulation of Bcr-Abl levels and inhibited apoptosis of HL-60/Bcr-Abl and K562 cells.	tanespimycin	39-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
11280726-5	2001	By binding and inhibiting Hsp90, GA or 17-AAG treatment shifted the binding of Bcr-Abl from Hsp90 to Hsp70 and induced the proteasomal degradation of Bcr-Abl, because cotreatment with proteasome inhibitor PSC341 reduced both GA (or 17-AAG)-mediated down-regulation of Bcr-Abl levels and inhibited apoptosis of HL-60/Bcr-Abl and K562 cells.	tanespimycin	39-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
11280726-5	2001	By binding and inhibiting Hsp90, GA or 17-AAG treatment shifted the binding of Bcr-Abl from Hsp90 to Hsp70 and induced the proteasomal degradation of Bcr-Abl, because cotreatment with proteasome inhibitor PSC341 reduced both GA (or 17-AAG)-mediated down-regulation of Bcr-Abl levels and inhibited apoptosis of HL-60/Bcr-Abl and K562 cells.	tanespimycin	39-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
11280726-5	2001	By binding and inhibiting Hsp90, GA or 17-AAG treatment shifted the binding of Bcr-Abl from Hsp90 to Hsp70 and induced the proteasomal degradation of Bcr-Abl, because cotreatment with proteasome inhibitor PSC341 reduced both GA (or 17-AAG)-mediated down-regulation of Bcr-Abl levels and inhibited apoptosis of HL-60/Bcr-Abl and K562 cells.	tanespimycin	232-238	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
11280726-5	2001	By binding and inhibiting Hsp90, GA or 17-AAG treatment shifted the binding of Bcr-Abl from Hsp90 to Hsp70 and induced the proteasomal degradation of Bcr-Abl, because cotreatment with proteasome inhibitor PSC341 reduced both GA (or 17-AAG)-mediated down-regulation of Bcr-Abl levels and inhibited apoptosis of HL-60/Bcr-Abl and K562 cells.	tanespimycin	232-238	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
11280726-5	2001	By binding and inhibiting Hsp90, GA or 17-AAG treatment shifted the binding of Bcr-Abl from Hsp90 to Hsp70 and induced the proteasomal degradation of Bcr-Abl, because cotreatment with proteasome inhibitor PSC341 reduced both GA (or 17-AAG)-mediated down-regulation of Bcr-Abl levels and inhibited apoptosis of HL-60/Bcr-Abl and K562 cells.	tanespimycin	232-238	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
11280726-5	2001	By binding and inhibiting Hsp90, GA or 17-AAG treatment shifted the binding of Bcr-Abl from Hsp90 to Hsp70 and induced the proteasomal degradation of Bcr-Abl, because cotreatment with proteasome inhibitor PSC341 reduced both GA (or 17-AAG)-mediated down-regulation of Bcr-Abl levels and inhibited apoptosis of HL-60/Bcr-Abl and K562 cells.	tanespimycin	232-238	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
11280726-6	2001	These data establish the in vitro activity of GA and 17-AAG against Bcr-Abl-positive leukemic cells and support the in vivo investigation of 17-AAG against Bcr-Abl-positive leukemias.	geldanamycin	46-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
11280726-6	2001	These data establish the in vitro activity of GA and 17-AAG against Bcr-Abl-positive leukemic cells and support the in vivo investigation of 17-AAG against Bcr-Abl-positive leukemias.	tanespimycin	53-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
11280726-6	2001	These data establish the in vitro activity of GA and 17-AAG against Bcr-Abl-positive leukemic cells and support the in vivo investigation of 17-AAG against Bcr-Abl-positive leukemias.	tanespimycin	141-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
11121037-4	2000	Activation of gamma-PAK in human embryonic kidney 293T cells by cotransfection with constitutively active Cdc42 induces activation of c-Abl, resulting in increased phosphotyrosine levels.	Phosphotyrosine	164-179	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-139
11121037-5	2000	Cotransfection of c-Abl and gamma-PAK elicits phosphorylation of gamma-PAK on tyrosine and down-regulation of gamma-PAK activity, promoting accumulation of inactive gamma-PAK.	Tyrosine	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-23
11010972-5	2000	First, induction of BCR/ABL by a tetracycline-regulated promoter is associated with a reversible down-regulation of p27(Kip1).	Tetracycline	33-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
11010972-6	2000	Second, inhibition of BCR/ABL kinase activity with the Abl tyrosine kinase inhibitor STI571 rapidly increases p27(Kip1) levels.	Imatinib Mesylate	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 Mesylate	85-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-58
11010972-7	2000	The PI3K inhibitor LY-294002 blocks the ability of BCR/ABL to induce p27(Kip1) down-regulation and inhibits BCR/ABL-induced entry into S phase.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	19-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
11010972-7	2000	The PI3K inhibitor LY-294002 blocks the ability of BCR/ABL to induce p27(Kip1) down-regulation and inhibits BCR/ABL-induced entry into S phase.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	19-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
11167748-1	2000	We report the use of multiplex polymerase chain reaction (PCR), using 4% polyacrylamide gel electrophoresis (PAGE) for the detection of BCR-ABL transcripts in Philadelphia-positive disease.	polyacrylamide	73-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-143
11123359-0	2001	Pyrrolo-1,5-benzoxazepines induce apoptosis in chronic myelogenous leukemia (CML) cells by bypassing the apoptotic suppressor bcr-abl.	pyrrolo-1,5-benzoxazepines	0-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
11123359-1	2001	Expression of the transforming oncogene bcr-abl in chronic myelogenous leukemia (CML) cells is reported to confer resistance against apoptosis induced by many chemotherapeutic agents such as etoposide, ara-C, and staurosporine.	Etoposide	191-200	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
11123359-1	2001	Expression of the transforming oncogene bcr-abl in chronic myelogenous leukemia (CML) cells is reported to confer resistance against apoptosis induced by many chemotherapeutic agents such as etoposide, ara-C, and staurosporine.	Cytarabine	202-207	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
11123359-1	2001	Expression of the transforming oncogene bcr-abl in chronic myelogenous leukemia (CML) cells is reported to confer resistance against apoptosis induced by many chemotherapeutic agents such as etoposide, ara-C, and staurosporine.	Staurosporine	213-226	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
11905636-0	2000	STI571: an inhibitor of the BCR-ABL tyrosine kinase for the treatment of chronic myelogenous leukaemia.	Imatinib Mesylate	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 Mesylate	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 Mesylate	17-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
11087392-0	2000	Src-Abl tyrosine kinase chimeras: replacement of the adenine binding pocket of c-Abl with v-Src to swap nucleotide and inhibitor specificities.	Adenine	53-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	2-7
11087392-5	2000	Although many kinases can be similarly engineered using v-Src as a blueprint, we encountered one kinase, c-Abl, which when mutated, does not display the ability to accept unnatural ATP analogues.	Adenosine Triphosphate	181-184	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-110
10945997-9	2000	Binding of Abl and nSrc SH3 domains, but not profilin or other SH3 domains, was abolished by cAMP-dependent protein kinase phosphorylation of EVL.	Cyclic AMP	93-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-14
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 Mesylate	41-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
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 Mesylate	115-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
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 Mesylate	129-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-154
11080615-1	2000	c-Abl preferentially phosphorylates peptide substrates that contain proline at the P+3 site (relative to the phosphorylated tyrosine).	Proline	68-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
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 Mesylate	38-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
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 Mesylate	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 Mesylate	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 Mesylate	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-174
11003655-9	2000	Finally, we demonstrate that tyrosine phosphorylation of endogenous Abi-1 in fibroblasts is induced by both v-Abl and serum stimulation, further suggesting a role for Abi-1 in signal transduction initiated by v-Abl and growth factors.	Tyrosine	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-113
11003655-9	2000	Finally, we demonstrate that tyrosine phosphorylation of endogenous Abi-1 in fibroblasts is induced by both v-Abl and serum stimulation, further suggesting a role for Abi-1 in signal transduction initiated by v-Abl and growth factors.	Tyrosine	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-214
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 Mesylate	142-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
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 Mesylate	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 Mesylate	11-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
10979978-0	2000	Novel oxime derivatives of radicicol induce erythroid differentiation associated with preferential G(1) phase accumulation against chronic myelogenous leukemia cells through destabilization of Bcr-Abl with Hsp90 complex.	Oximes	6-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	193-200
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 Mesylate	104-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
10979978-0	2000	Novel oxime derivatives of radicicol induce erythroid differentiation associated with preferential G(1) phase accumulation against chronic myelogenous leukemia cells through destabilization of Bcr-Abl with Hsp90 complex.	monorden	27-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	193-200
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 Mesylate	104-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
10979978-6	2000	KF58333 treatment depleted p210(Bcr-Abl), Raf-1, and cellular tyrosine phosphorylated proteins in K562 cells, whereas radicicol and HA showed transient depletion of these proteins.	KF58333	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
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 Mesylate	104-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
10979978-8	2000	Immunoprecipitation analysis showed that p210(Bcr-Abl) formed multiple complexes with Hsp90, some containing p23 and others Hsp70; KF58333 treatment dissociated p210(Bcr-Abl) from Hsp90/p23 chaperone complexes.	KF58333	131-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
10979973-3	2000	Exposure to low-dose cytosine arabinoside (Ara-C; 10 nmol/L) increased hemoglobin levels in HL-60/Bcr-Abl and in the chronic myeloid leukemia (CML) blast crisis K562 cells, which express the p210 Bcr-Abl protein.	Cytarabine	21-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
10979978-8	2000	Immunoprecipitation analysis showed that p210(Bcr-Abl) formed multiple complexes with Hsp90, some containing p23 and others Hsp70; KF58333 treatment dissociated p210(Bcr-Abl) from Hsp90/p23 chaperone complexes.	KF58333	131-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-173
10979973-3	2000	Exposure to low-dose cytosine arabinoside (Ara-C; 10 nmol/L) increased hemoglobin levels in HL-60/Bcr-Abl and in the chronic myeloid leukemia (CML) blast crisis K562 cells, which express the p210 Bcr-Abl protein.	Cytarabine	21-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	196-203
10979978-10	2000	These results suggest that KF58333 may have therapeutic potential for the treatment of CML that involves abnormal cellular proliferation induced by p210(Bcr-Abl).	KF58333	27-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
10979973-3	2000	Exposure to low-dose cytosine arabinoside (Ara-C; 10 nmol/L) increased hemoglobin levels in HL-60/Bcr-Abl and in the chronic myeloid leukemia (CML) blast crisis K562 cells, which express the p210 Bcr-Abl protein.	Cytarabine	43-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
10979973-3	2000	Exposure to low-dose cytosine arabinoside (Ara-C; 10 nmol/L) increased hemoglobin levels in HL-60/Bcr-Abl and in the chronic myeloid leukemia (CML) blast crisis K562 cells, which express the p210 Bcr-Abl protein.	Cytarabine	43-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	196-203
10979973-4	2000	As compared with HL-60/neo, HL-60/Bcr-Abl and K562 cells were resistant to apoptosis induced by Ara-C, doxorubicin, or tumor necrosis factor-alpha (TNF-alpha), which was associated with reduced processing of caspase-8 and Bid protein and decreased cytosolic accumulation of cytochrome c (cyt c).	Cytarabine	96-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
10979973-4	2000	As compared with HL-60/neo, HL-60/Bcr-Abl and K562 cells were resistant to apoptosis induced by Ara-C, doxorubicin, or tumor necrosis factor-alpha (TNF-alpha), which was associated with reduced processing of caspase-8 and Bid protein and decreased cytosolic accumulation of cytochrome c (cyt c).	Doxorubicin	103-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
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 Mesylate	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 Mesylate	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 Mesylate	30-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
10979973-9	2000	Importantly, cotreatment with CGP57148B significantly increased Ara-C- or doxorubicin-induced apoptosis of HL-60/Bcr-Abl and K562 cells.	Cytarabine	64-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
10979973-9	2000	Importantly, cotreatment with CGP57148B significantly increased Ara-C- or doxorubicin-induced apoptosis of HL-60/Bcr-Abl and K562 cells.	Doxorubicin	74-85	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 Mesylate	50-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
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.	Cytarabine	91-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
10833515-0	2000	The BCR/ABL tyrosine kinase induces production of reactive oxygen species in hematopoietic cells.	Reactive Oxygen Species	50-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
10988075-2	2000	A small-molecule inhibitor of Abl (STI-571) is effective in the treatment of CML.	Imatinib Mesylate	35-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-33
10833515-2	2000	It is shown here that transformation of the hematopoietic cell lines Ba/F3, 32Dcl3, and MO7e with BCR/ABL results in an increase in reactive oxygen species (ROS) compared with quiescent, untransformed cells.	Reactive Oxygen Species	132-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
10833515-2	2000	It is shown here that transformation of the hematopoietic cell lines Ba/F3, 32Dcl3, and MO7e with BCR/ABL results in an increase in reactive oxygen species (ROS) compared with quiescent, untransformed cells.	Reactive Oxygen Species	157-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
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.	Reactive Oxygen Species	16-19	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.	Reactive Oxygen Species	16-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-47
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 Mesylate	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 Mesylate	117-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-47
10833515-5	2000	To understand the significance of increased production of ROS, a model system was established in which hydrogen peroxide (H(2)O(2)) was added to untransformed cells to mimic the increase in ROS induced constitutively by BCR/ABL.	Hydrogen Peroxide	103-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	220-227
10833515-5	2000	To understand the significance of increased production of ROS, a model system was established in which hydrogen peroxide (H(2)O(2)) was added to untransformed cells to mimic the increase in ROS induced constitutively by BCR/ABL.	Reactive Oxygen Species	190-193	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	220-227
10833515-7	2000	Further, stimulation of untransformed cells with H(2)O(2) or pervanadate increased tyrosine phosphorylation of each of the most prominent known substrates of BCR/ABL, including c-ABL, c-CBL, SHC, and SHP-2.	Hydrogen Peroxide	49-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-165
10833515-7	2000	Further, stimulation of untransformed cells with H(2)O(2) or pervanadate increased tyrosine phosphorylation of each of the most prominent known substrates of BCR/ABL, including c-ABL, c-CBL, SHC, and SHP-2.	Hydrogen Peroxide	49-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	177-182
10833515-7	2000	Further, stimulation of untransformed cells with H(2)O(2) or pervanadate increased tyrosine phosphorylation of each of the most prominent known substrates of BCR/ABL, including c-ABL, c-CBL, SHC, and SHP-2.	pervanadate	61-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-165
10833515-7	2000	Further, stimulation of untransformed cells with H(2)O(2) or pervanadate increased tyrosine phosphorylation of each of the most prominent known substrates of BCR/ABL, including c-ABL, c-CBL, SHC, and SHP-2.	pervanadate	61-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	177-182
10833515-7	2000	Further, stimulation of untransformed cells with H(2)O(2) or pervanadate increased tyrosine phosphorylation of each of the most prominent known substrates of BCR/ABL, including c-ABL, c-CBL, SHC, and SHP-2.	Tyrosine	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-165
10833515-7	2000	Further, stimulation of untransformed cells with H(2)O(2) or pervanadate increased tyrosine phosphorylation of each of the most prominent known substrates of BCR/ABL, including c-ABL, c-CBL, SHC, and SHP-2.	Tyrosine	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	177-182
10887132-2	2000	The Bcr/Abl fusion protein is a constitutively active tyrosine kinase that stimulates several intracellular signaling pathways, including activation of Ras through direct binding of the SH2-containing adapter protein Grb2 to Bcr tyrosine 177.	Tyrosine	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
10833515-8	2000	Treatment of the BCR/ABL-expressing cell line MO7/p210 with the reducing agents pyrrolidine dithiocarbamate or N-acetylcysteine reduced the accumulation of ROS and also decreased tyrosine phosphorylation of cellular proteins.	pyrrolidine dithiocarbamic acid	80-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
10833515-8	2000	Treatment of the BCR/ABL-expressing cell line MO7/p210 with the reducing agents pyrrolidine dithiocarbamate or N-acetylcysteine reduced the accumulation of ROS and also decreased tyrosine phosphorylation of cellular proteins.	Acetylcysteine	111-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
10833515-8	2000	Treatment of the BCR/ABL-expressing cell line MO7/p210 with the reducing agents pyrrolidine dithiocarbamate or N-acetylcysteine reduced the accumulation of ROS and also decreased tyrosine phosphorylation of cellular proteins.	Reactive Oxygen Species	156-159	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
10833515-8	2000	Treatment of the BCR/ABL-expressing cell line MO7/p210 with the reducing agents pyrrolidine dithiocarbamate or N-acetylcysteine reduced the accumulation of ROS and also decreased tyrosine phosphorylation of cellular proteins.	Tyrosine	179-187	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
10833515-9	2000	Further, treatment of MO7e cells with H(2)O(2) or pervanadate increased the tyrosine kinase activity of c-ABL.	Hydrogen Peroxide	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-109
10833515-9	2000	Further, treatment of MO7e cells with H(2)O(2) or pervanadate increased the tyrosine kinase activity of c-ABL.	pervanadate	50-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-109
10833515-10	2000	Drugs that alter ROS metabolism or reactivate PTPases may antagonize BCR/ABL transformation.	Reactive Oxygen Species	17-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
10770918-0	2000	Activation of the cytoplasmic c-Abl tyrosine kinase by reactive oxygen species.	Reactive Oxygen Species	55-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-35
10965789-0	2000	A case of chronic myeloid leukemia with minor bcr-abl transcript following fluorouracil therapy for esophageal carcinoma.	Fluorouracil	75-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
10965789-1	2000	We report here a very rare case of chronic myeloid leukemia (CML) with a minor bcr-abl transcript, which developed following long-term chemotherapy with fluorouracil for esophageal carcinoma.	Fluorouracil	153-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
10910048-0	2000	BCR-ABL mediates arsenic trioxide-induced apoptosis independently of its aberrant kinase activity.	Arsenic Trioxide	17-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
10910048-3	2000	Hence, we reasoned that As2O3 might have a selective inhibitory effect on proliferation of BCR-ABL-expressing cells.	Arsenic Trioxide	24-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
10910048-4	2000	Here, we report that: (a) As2O3 induced apoptosis in Ph+ but not in Ph- lymphoblasts; (b) enforced expression of BCR-ABL in U937 cells dramatically increased the sensitivity to As2O3; (c) the effect of As2O3 was independent of BCR-ABL kinase activity; and (d) As2O3 reduced proliferation of chronic myelogenous leukemia blasts but not of peripheral CD34+ progenitors.	Arsenic Trioxide	26-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
10910048-4	2000	Here, we report that: (a) As2O3 induced apoptosis in Ph+ but not in Ph- lymphoblasts; (b) enforced expression of BCR-ABL in U937 cells dramatically increased the sensitivity to As2O3; (c) the effect of As2O3 was independent of BCR-ABL kinase activity; and (d) As2O3 reduced proliferation of chronic myelogenous leukemia blasts but not of peripheral CD34+ progenitors.	Arsenic Trioxide	26-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	227-234
10910048-4	2000	Here, we report that: (a) As2O3 induced apoptosis in Ph+ but not in Ph- lymphoblasts; (b) enforced expression of BCR-ABL in U937 cells dramatically increased the sensitivity to As2O3; (c) the effect of As2O3 was independent of BCR-ABL kinase activity; and (d) As2O3 reduced proliferation of chronic myelogenous leukemia blasts but not of peripheral CD34+ progenitors.	Arsenic Trioxide	177-182	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
10910048-4	2000	Here, we report that: (a) As2O3 induced apoptosis in Ph+ but not in Ph- lymphoblasts; (b) enforced expression of BCR-ABL in U937 cells dramatically increased the sensitivity to As2O3; (c) the effect of As2O3 was independent of BCR-ABL kinase activity; and (d) As2O3 reduced proliferation of chronic myelogenous leukemia blasts but not of peripheral CD34+ progenitors.	Arsenic Trioxide	177-182	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
10910048-4	2000	Here, we report that: (a) As2O3 induced apoptosis in Ph+ but not in Ph- lymphoblasts; (b) enforced expression of BCR-ABL in U937 cells dramatically increased the sensitivity to As2O3; (c) the effect of As2O3 was independent of BCR-ABL kinase activity; and (d) As2O3 reduced proliferation of chronic myelogenous leukemia blasts but not of peripheral CD34+ progenitors.	Arsenic Trioxide	177-182	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
10829062-2	2000	Here we report that the kinase-deficient Src (SrcKD) directly inhibits the tyrosine phosphorylation of Cbl and other cellular proteins by Abl.	Tyrosine	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-141
10950939-0	2000	Detailed mapping of methylcytosine positions at the CpG island surrounding the Pa promoter at the bcr-abl locus in CML patients and in two cell lines, K562 and BV173.	1-methylcytosine	20-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
10950939-0	2000	Detailed mapping of methylcytosine positions at the CpG island surrounding the Pa promoter at the bcr-abl locus in CML patients and in two cell lines, K562 and BV173.	Protactinium	79-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
10896159-0	2000	Cables links Cdk5 and c-Abl and facilitates Cdk5 tyrosine phosphorylation, kinase upregulation, and neurite outgrowth.	Tyrosine	49-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-27
10896159-4	2000	Active c-Abl kinase leads to Cdk5 tyrosine phosphorylation, and this phosphorylation is enhanced by Cables.	Tyrosine	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	7-12
10896159-5	2000	Phosphorylation of Cdk5 by c-Abl occurs on tyrosine 15 (Y15), which is stimulatory for p35/Cdk5 kinase activity.	Tyrosine	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-32
10837221-7	2000	Moreover, our findings demonstrate that exposure of cells to ionizing radiation induces tyrosine phosphorylation of hTERT by a c-Abl-dependent mechanism.	Tyrosine	88-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-132
10779450-1	2000	We used a sensitive, quantitative bisulfite PCR assay, methylation sensitive single nucleotide primer extension (Ms-SNuPE), to measure methylation of the 5" CpG islands of c-abl and p15 in chronic myelogenous leukemia (CML) patients during progression.	hydrogen sulfite	34-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-177
10779450-2	2000	We found that the Pa promoter of c-abl was methylated in 81% (17/21) of the white blood cells (WBCs) of CML patients, which correlates with previous reports.	Protactinium	18-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-38
10815921-0	2000	The tyrosine kinase inhibitor CGP 57148 (ST1 571) induces apoptosis in BCR-ABL-positive cells by down-regulating BCL-X.	Imatinib Mesylate	30-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
10815921-11	2000	We conclude that the inhibition of the BCR-ABL kinase by CGP 57148 (a) preferentially inhibits the growth of immature leukemic precursor cells, (b) efficiently reverts the antiapoptotic effects of BCR-ABL by down-regulation of BCL-X, and (c) is more effective than the inhibition of the downstream signal transduction pathways of PI-3 kinase, mitogen-activated protein/extracellular signal-regulated kinase kinase, and Janus-activated kinase 2.	cgp	57-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
10815921-11	2000	We conclude that the inhibition of the BCR-ABL kinase by CGP 57148 (a) preferentially inhibits the growth of immature leukemic precursor cells, (b) efficiently reverts the antiapoptotic effects of BCR-ABL by down-regulation of BCL-X, and (c) is more effective than the inhibition of the downstream signal transduction pathways of PI-3 kinase, mitogen-activated protein/extracellular signal-regulated kinase kinase, and Janus-activated kinase 2.	cgp	57-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	197-204
10879451-7	2000	The correlations between the Lactate Pro and the ABL 700 Series Acid-Base analyser, YSI 2300 and Accusport were r = 0.98, r = 0.99, r = 0.97.	Lactic Acid	29-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-52
10879451-7	2000	The correlations between the Lactate Pro and the ABL 700 Series Acid-Base analyser, YSI 2300 and Accusport were r = 0.98, r = 0.99, r = 0.97.	Proline	37-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-52
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 Mesylate	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 Mesylate	45-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
10803516-5	2000	Tyrosine phosphorylation of cellular proteins was markedly reduced in BCR/ABL transformed cells after 16 h at 39 degrees C, whereas the expression of BCR/ABL was unchanged.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
11080615-1	2000	c-Abl preferentially phosphorylates peptide substrates that contain proline at the P+3 site (relative to the phosphorylated tyrosine).	Tyrosine	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
11080615-2	2000	We previously described a mutant form of the Abl catalytic domain (Y569W) with altered substrate specificity at the P+3 position, as measured using synthetic peptides.	Peptides	158-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-48
11080615-3	2000	In this study, we examine the phosphorylation of Crk, a protein substrate of Abl that is phosphorylated in the sequence Tyr221-Ala-Gln-Pro.	Glutamine	131-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-80
11080615-3	2000	In this study, we examine the phosphorylation of Crk, a protein substrate of Abl that is phosphorylated in the sequence Tyr221-Ala-Gln-Pro.	Proline	135-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-80
11080615-5	2000	Overexpression of Y569W mutant Abl in 293T kidney cells produces a similar overall pattern of tyrosine phosphorylation as wild-type Abl, indicating that not all cellular proteins depend on Pro at P+3 for Abl recognition.	Tyrosine	94-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-34
11080615-7	2000	A truncated form of Abl lacking the C-terminal polyproline region is not able to phosphorylate Crk in these assay conditions.	polyproline	47-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-23
11080615-8	2000	Thus, proper phosphorylation of Crk by Abl depends not only on the interaction of the Crk SH3 domain with the Abl polyproline region, but also on the recognition of amino acids surrounding tyrosine by the Abl catalytic domain.	polyproline	114-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-42
11080615-8	2000	Thus, proper phosphorylation of Crk by Abl depends not only on the interaction of the Crk SH3 domain with the Abl polyproline region, but also on the recognition of amino acids surrounding tyrosine by the Abl catalytic domain.	polyproline	114-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-113
11080615-8	2000	Thus, proper phosphorylation of Crk by Abl depends not only on the interaction of the Crk SH3 domain with the Abl polyproline region, but also on the recognition of amino acids surrounding tyrosine by the Abl catalytic domain.	polyproline	114-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-113
11080615-8	2000	Thus, proper phosphorylation of Crk by Abl depends not only on the interaction of the Crk SH3 domain with the Abl polyproline region, but also on the recognition of amino acids surrounding tyrosine by the Abl catalytic domain.	Tyrosine	189-197	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-42
10866298-2	2000	We found that PD180970 inhibited in vivo tyrosine phosphorylation of p210Bcr-Abl (IC50 = 170 nM) and the p210BcrAbl substrates Gab2 and CrkL (IC50 = 80 nM) in human K562 chronic myelogenous leukemic cells.	PD 180970	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-115
10828035-0	2000	Mechanism of resistance to the ABL tyrosine kinase inhibitor STI571 in BCR/ABL-transformed hematopoietic cell lines.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	54-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-107
10770918-4	2000	The results also demonstrate that mitochondrial cytochrome c is released in the cellular response to H(2)O(2) and that this effect is mediated by a c-Abl-dependent mechanism.	Hydrogen Peroxide	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	148-153
10770918-5	2000	In concert with these results, we show that H(2)O(2)-induced apoptosis is attenuated in c-Abl-deficient cells.	Hydrogen Peroxide	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-93
10763825-3	2000	In this study, the kinase specificities of the Bcr-Abl and Tel-Abl proteins were compared to the physiological Abl family kinases c-Abl and Arg (abl related gene).	Arginine	140-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-148
10727953-9	2000	The radioactivity in this extract reached a maximum after 10 h and declined after 20 h. Release of ABL from the cell, after pulse labelling, was assessed using both fluorescein isothiocyanate-labelled ABL and 125I-ABL and was slow, with a t1/2 of 48 h. Most of the 125I-ABL both inside cells and in the medium remained intact, as determined by trichloroacetic acid precipitation and SDS/PAGE, and after 48 h only 22 +/- 2% of ABL in the medium and 14 +/- 2% inside the cells was degraded.	Fluorescein-5-isothiocyanate	165-191	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-102
10727953-9	2000	The radioactivity in this extract reached a maximum after 10 h and declined after 20 h. Release of ABL from the cell, after pulse labelling, was assessed using both fluorescein isothiocyanate-labelled ABL and 125I-ABL and was slow, with a t1/2 of 48 h. Most of the 125I-ABL both inside cells and in the medium remained intact, as determined by trichloroacetic acid precipitation and SDS/PAGE, and after 48 h only 22 +/- 2% of ABL in the medium and 14 +/- 2% inside the cells was degraded.	Fluorescein-5-isothiocyanate	165-191	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	201-204
10727953-9	2000	The radioactivity in this extract reached a maximum after 10 h and declined after 20 h. Release of ABL from the cell, after pulse labelling, was assessed using both fluorescein isothiocyanate-labelled ABL and 125I-ABL and was slow, with a t1/2 of 48 h. Most of the 125I-ABL both inside cells and in the medium remained intact, as determined by trichloroacetic acid precipitation and SDS/PAGE, and after 48 h only 22 +/- 2% of ABL in the medium and 14 +/- 2% inside the cells was degraded.	Fluorescein-5-isothiocyanate	165-191	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	201-204
10727953-9	2000	The radioactivity in this extract reached a maximum after 10 h and declined after 20 h. Release of ABL from the cell, after pulse labelling, was assessed using both fluorescein isothiocyanate-labelled ABL and 125I-ABL and was slow, with a t1/2 of 48 h. Most of the 125I-ABL both inside cells and in the medium remained intact, as determined by trichloroacetic acid precipitation and SDS/PAGE, and after 48 h only 22 +/- 2% of ABL in the medium and 14 +/- 2% inside the cells was degraded.	Fluorescein-5-isothiocyanate	165-191	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	201-204
10727953-9	2000	The radioactivity in this extract reached a maximum after 10 h and declined after 20 h. Release of ABL from the cell, after pulse labelling, was assessed using both fluorescein isothiocyanate-labelled ABL and 125I-ABL and was slow, with a t1/2 of 48 h. Most of the 125I-ABL both inside cells and in the medium remained intact, as determined by trichloroacetic acid precipitation and SDS/PAGE, and after 48 h only 22 +/- 2% of ABL in the medium and 14 +/- 2% inside the cells was degraded.	Fluorescein-5-isothiocyanate	165-191	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	201-204
10727953-9	2000	The radioactivity in this extract reached a maximum after 10 h and declined after 20 h. Release of ABL from the cell, after pulse labelling, was assessed using both fluorescein isothiocyanate-labelled ABL and 125I-ABL and was slow, with a t1/2 of 48 h. Most of the 125I-ABL both inside cells and in the medium remained intact, as determined by trichloroacetic acid precipitation and SDS/PAGE, and after 48 h only 22 +/- 2% of ABL in the medium and 14 +/- 2% inside the cells was degraded.	Trichloroacetic Acid	344-364	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-102
10727953-9	2000	The radioactivity in this extract reached a maximum after 10 h and declined after 20 h. Release of ABL from the cell, after pulse labelling, was assessed using both fluorescein isothiocyanate-labelled ABL and 125I-ABL and was slow, with a t1/2 of 48 h. Most of the 125I-ABL both inside cells and in the medium remained intact, as determined by trichloroacetic acid precipitation and SDS/PAGE, and after 48 h only 22 +/- 2% of ABL in the medium and 14 +/- 2% inside the cells was degraded.	Sodium Dodecyl Sulfate	383-386	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-102
10763825-6	2000	In addition, c-Crk II and CRKL are tyrosine phosphorylated and complexed with numerous other tyrosine phosphorylated proteins in Tel-Abl expressing Ba/F3 cells.	Tyrosine	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-136
10706884-0	2000	A new ETV6/TEL partner gene, ARG (ABL-related gene or ABL2), identified in an AML-M3 cell line with a t(1;12)(q25;p13) translocation.	Arginine	29-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-37
10706884-3	2000	We identified a novel ETV6 partner gene, ARG (ABL-related gene or ABL2), another TK gene in a cell line established from a patient with acute myelogenous leukemia (AML-M3) with a t(15;17)(q22;q11.2) and a t(1;12)(q25;p13), which has the remarkable feature to differentiate to mature eosinophils in culture with all-trans retinoic acid and cytokines.	Arginine	41-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-49
10763825-6	2000	In addition, c-Crk II and CRKL are tyrosine phosphorylated and complexed with numerous other tyrosine phosphorylated proteins in Tel-Abl expressing Ba/F3 cells.	Tyrosine	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-136
10763825-7	2000	GTPase analysis with a Ras-GTP-specific precipitation assay showed constitutive elevation of GTP-loaded Ras in cells expressing the leukaemic Abl proteins.	Guanosine Triphosphate	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-145
10763825-7	2000	GTPase analysis with a Ras-GTP-specific precipitation assay showed constitutive elevation of GTP-loaded Ras in cells expressing the leukaemic Abl proteins.	Guanosine Triphosphate	27-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-145
10763825-9	2000	The results indicate that the leukaemic Abl-fusion proteins have catalytic specificities different from the normal kinases c-Abl and Arg and that Tel-Abl is capable to activate at least some pathways which are also upregulated by Bcr-Abl.	Arginine	133-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-43
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.	N-phenylpyrimidin-2-amine	4-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
10713049-2	2000	The present studies demonstrate that treatment of cells with hydrogen peroxide (H(2)O(2)) induces binding of the PKCdelta isoform and the c-Abl protein-tyrosine kinase.	Hydrogen Peroxide	61-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-143
10713049-2	2000	The present studies demonstrate that treatment of cells with hydrogen peroxide (H(2)O(2)) induces binding of the PKCdelta isoform and the c-Abl protein-tyrosine kinase.	Hydrogen Peroxide	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-143
10713049-5	2000	In cells, induction of c-Abl activity by H(2)O(2) is attenuated by the PKCdelta inhibitor, rottlerin, and by overexpression of the regulatory domain of PKCdelta.	Hydrogen Peroxide	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-28
10713049-5	2000	In cells, induction of c-Abl activity by H(2)O(2) is attenuated by the PKCdelta inhibitor, rottlerin, and by overexpression of the regulatory domain of PKCdelta.	rottlerin	91-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-28
10708759-5	2000	Furthermore, we show here that c-Abl binds to phosphotyrosine residue(s) in the kinase activation loop of TrkA.	Phosphotyrosine	46-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-36
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 Mesylate	39-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
10739005-6	2000	After the induction of the granulocytic differentiation of HL-60 cells with all trans retinoic acid (ATRA) or dimethylsulfoxide (DMSO), the abl and bcr homologous genes were repositioned closer to the nuclear periphery and the average distances between homologous abl-abl and bcr-bcr genes as well as between heterologous abl-bcr genes were elongated as compared with untreated human leukemic promyelocytic HL-60 cells.	Dimethyl Sulfoxide	110-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-143
10857905-3	2000	We designed the maxizyme in such a way that it was able to form an active core with which to capture the catalytically indispensable Mg2+ ions only in the presence of the BCR-ABL mRNA junction.	magnesium ion	133-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-178
10739005-6	2000	After the induction of the granulocytic differentiation of HL-60 cells with all trans retinoic acid (ATRA) or dimethylsulfoxide (DMSO), the abl and bcr homologous genes were repositioned closer to the nuclear periphery and the average distances between homologous abl-abl and bcr-bcr genes as well as between heterologous abl-bcr genes were elongated as compared with untreated human leukemic promyelocytic HL-60 cells.	Dimethyl Sulfoxide	110-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	264-267
10739005-6	2000	After the induction of the granulocytic differentiation of HL-60 cells with all trans retinoic acid (ATRA) or dimethylsulfoxide (DMSO), the abl and bcr homologous genes were repositioned closer to the nuclear periphery and the average distances between homologous abl-abl and bcr-bcr genes as well as between heterologous abl-bcr genes were elongated as compared with untreated human leukemic promyelocytic HL-60 cells.	Dimethyl Sulfoxide	110-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	264-267
10739005-6	2000	After the induction of the granulocytic differentiation of HL-60 cells with all trans retinoic acid (ATRA) or dimethylsulfoxide (DMSO), the abl and bcr homologous genes were repositioned closer to the nuclear periphery and the average distances between homologous abl-abl and bcr-bcr genes as well as between heterologous abl-bcr genes were elongated as compared with untreated human leukemic promyelocytic HL-60 cells.	Dimethyl Sulfoxide	110-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	264-267
10739005-6	2000	After the induction of the granulocytic differentiation of HL-60 cells with all trans retinoic acid (ATRA) or dimethylsulfoxide (DMSO), the abl and bcr homologous genes were repositioned closer to the nuclear periphery and the average distances between homologous abl-abl and bcr-bcr genes as well as between heterologous abl-bcr genes were elongated as compared with untreated human leukemic promyelocytic HL-60 cells.	Dimethyl Sulfoxide	129-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	264-267
10739005-6	2000	After the induction of the granulocytic differentiation of HL-60 cells with all trans retinoic acid (ATRA) or dimethylsulfoxide (DMSO), the abl and bcr homologous genes were repositioned closer to the nuclear periphery and the average distances between homologous abl-abl and bcr-bcr genes as well as between heterologous abl-bcr genes were elongated as compared with untreated human leukemic promyelocytic HL-60 cells.	Dimethyl Sulfoxide	129-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	264-267
10739005-6	2000	After the induction of the granulocytic differentiation of HL-60 cells with all trans retinoic acid (ATRA) or dimethylsulfoxide (DMSO), the abl and bcr homologous genes were repositioned closer to the nuclear periphery and the average distances between homologous abl-abl and bcr-bcr genes as well as between heterologous abl-bcr genes were elongated as compared with untreated human leukemic promyelocytic HL-60 cells.	Dimethyl Sulfoxide	129-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	264-267
10739005-8	2000	In the case of the monocytic maturation of HL-60 cells treated with phorbol esters (PMA), the abl and bcr homologous genes were repositioned closer to each other and closer to the nuclear centre.	Phorbol Esters	68-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-97
10739005-8	2000	In the case of the monocytic maturation of HL-60 cells treated with phorbol esters (PMA), the abl and bcr homologous genes were repositioned closer to each other and closer to the nuclear centre.	Tetradecanoylphorbol Acetate	84-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-97
10677527-6	2000	We utilized tetracycline-regulated expression of Bcr-Abl from a promoter engineered for robust expression in primitive stem cells through multilineage blood cell development in combination with the in vitro differentiation of embryonal stem cells into hematopoietic elements.	Tetracycline	12-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
10706884-7	2000	Although the ABL is known to be involved in various human malignancies, ARG has not been involved in human malignancies despite its high homology to ABL.	Arginine	72-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-152
10688886-6	2000	We have found that p62(dok) is directly tyrosine phosphorylated by p210(bcr-abl), and the sites of phosphorylation are located in the C-terminal half of the p62(dok) molecule.	Tyrosine	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
10706130-3	2000	In addition, Fes has been shown to associate with and phosphorylate Bcr on NH2-terminal sequences retained within Bcr-Abl.	Iron	13-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
10706130-6	2000	Similarly, tyrosine phosphorylation of kinase-inactive Fes was observed after coexpression with active Bcr-Abl.	Tyrosine	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
10706130-12	2000	The phosphotyrosine content of both wild-type and kinase-inactive Fes was strongly enhanced after coexpression with Bcr-Abl in DAGM cells, similar to the 293T result.	Phosphotyrosine	4-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
10648417-0	2000	Arsenic induces apoptosis of multidrug-resistant human myeloid leukemia cells that express Bcr-Abl or overexpress MDR, MRP, Bcl-2, or Bcl-x(L).	Arsenic	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
10648417-4	2000	Exposure to 2 micromol/L As(2)O(3) for 7 days induced apoptosis of all cell types, including HL-60/Bcr-Abl and K562 cells.	Aligeron	25-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
10607685-11	2000	The median ratio of BCR-ABL/ABL at maximal response was significantly higher in patients who relapsed than in those who remained in CR (0.49% versus 0.021%, P < 0.0001).	Chromium	21-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-27
10834406-7	2000	Quantitative competitive RT-PCR amplification of the ABL gene showed comparable results for RNA isolated with RNAzol and TRIzol.	rnazol	110-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
10834406-7	2000	Quantitative competitive RT-PCR amplification of the ABL gene showed comparable results for RNA isolated with RNAzol and TRIzol.	trizol	121-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
10637231-0	2000	A nuclear tyrosine phosphorylation circuit: c-Jun as an activator and substrate of c-Abl and JNK.	Tyrosine	10-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-96
10637231-3	2000	We found that active nuclear Abl efficiently phosphorylate c-Jun, a transcription factor not previously known to be tyrosine phosphorylated.	Tyrosine	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-32
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 Mesylate	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
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 Mesylate	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	194-201
11920195-0	2000	Role of early anthracycline dose-intensity according to expression of Philadelphia chromosome/BCR-ABL rearrangements in B-precursor adult acute lymphoblastic leukemia.	Anthracyclines	14-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
10565030-0	2000	Inhibition of c-ABL expression in hematopoietic progenitor cells using antisense oligodeoxynucleotides.	Oligodeoxyribonucleotides	81-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
10611245-6	2000	Finally, we show that the proline-rich region of ESX1 mediates interactions in vitro with the c-abl SH3 domain as well as with certain WW domains.	Proline	26-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-99
10441393-1	1999	We screened 1680 spatially separated compounds of a diverse combinatorial library of 1,4-benzodiazepines for their ability to inhibit the kinase activity of protein tyrosine kinases Src, Yes, Abl, Lck, Csk, and fibroblast growth factor receptor.	Bz-423	85-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	192-195
11721366-0	1999	[Effects of As2O3 on the BCR/ABL protein tyrosine phosphorylation in K562 cells].	Arsenic Trioxide	12-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
11721366-0	1999	[Effects of As2O3 on the BCR/ABL protein tyrosine phosphorylation in K562 cells].	Tyrosine	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
11721366-2	1999	METHODS: The effects of As2O3 on BCR/ABL protein tyrosine phosphorylation(PTP) and its signal transduction as well as the expression of apoptosis-related genes were studied by means of immunoprecipitation, Western blot, biochemical method and immunofluorescence.	Arsenic Trioxide	24-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
11721366-3	1999	RESULTS: Tyrosine phosphorylation of several cellular proteins especially BCR/ABL protein was decreased by 1 mumol/L As2O3, but not by 0.1 mumol/L As2O3.	Tyrosine	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
11721366-3	1999	RESULTS: Tyrosine phosphorylation of several cellular proteins especially BCR/ABL protein was decreased by 1 mumol/L As2O3, but not by 0.1 mumol/L As2O3.	Arsenic Trioxide	117-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
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 Mesylate	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.	serum sodium transport inhibitor	60-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
10588700-4	1999	We also show that EWS/WT1 can interact with, and is a substrate for, modification on tyrosine residues by c-Abl.	Tyrosine	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-111
10588700-5	1999	Tyrosine phosphorylation of EWS/WT1 by c-Abl negatively regulates its DNA binding properties.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-44
11721366-6	1999	CONCLUSION: As2O3 might induce K562 cell apoptosis and inhibit its growth by reducing tyrosine phosphorylation of cellular proteins especially BCR/ABL protein and/or by downregulating JAK2 protein expression to interfere with the BCR/ABL protein signal transduction.	Arsenic Trioxide	12-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-150
11721366-6	1999	CONCLUSION: As2O3 might induce K562 cell apoptosis and inhibit its growth by reducing tyrosine phosphorylation of cellular proteins especially BCR/ABL protein and/or by downregulating JAK2 protein expression to interfere with the BCR/ABL protein signal transduction.	Arsenic Trioxide	12-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	230-237
10583226-0	1999	BCR-ABL influences the antileukaemic efficacy of alkylphosphocholines.	alkylphosphocholines	49-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
10583226-5	1999	injectable APC, erucylphosphocholine, was more active against BCR-ABL-positive cell lines than the two reference APC.	erucylphosphocholine	16-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
10583226-13	1999	Transfection of K-562 cells with antisense oligonucleotides directed against bcr-abl caused a specific suppression of K-562 clonogenicity.	Oligonucleotides	43-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
10583226-15	1999	injectable alkylphosphocholines are potent inducers of apoptosis and display increased antileukaemic efficacy against BCR-ABL-positive blasts as compared with miltefosine and perifosine.	alkylphosphocholines	11-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
10583226-16	1999	The expression of BCR-ABL cannot prevent apoptosis but delays erucylphosphocholine-induced programmed cell death.	erucylphosphocholine	62-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
10583226-17	1999	Transfection with bcr-abl directed antisense oligonucleotides reduces the clonogenicity of K-562 cells.	Oligonucleotides	45-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
10441115-0	1999	Direct determination of changes of interdomain orientation on ligation: use of the orientational dependence of 15N NMR relaxation in Abl SH(32).	15n	111-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-136
10419896-7	1999	BCR-ABL peptide-specific T-cell clones did respond to autologous EBV cells transfected with invariant chain (li) cDNA in which the HLA class II-associated invariant chain peptide (CLIP) was replaced by a BCR-ABL b2a2 fusion oligonucleotide sequence, illustrating the potential of these T cells to recognize an endogenous BCR-ABL(b2a2) ligand.	Oligonucleotides	224-239	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
10419904-4	1999	In BCR-Abl transformed K562 cells, STAT5A and 5B are constitutively phosphorylated on tyrosine and are transcriptionally active.	Tyrosine	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	3-10
10391250-5	1999	Furthermore, p73 and c-Abl can associate with each other, andthis binding is mediated by a PxxP motif in p73 and the SH3 domain of c-Abl.	andthis	58-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-26
10391250-5	1999	Furthermore, p73 and c-Abl can associate with each other, andthis binding is mediated by a PxxP motif in p73 and the SH3 domain of c-Abl.	andthis	58-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-136
10391251-4	1999	c-Abl phosphorylates p73 on a tyrosine residue at position 99 both in vitro and in cells that have been exposed to ionizing radiation.	Tyrosine	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
10391678-0	1999	Tyrosine phosphorylation of C-Cbl facilitates adhesion and spreading while suppressing anchorage-independent growth of V-Abl-transformed NIH3T3 fibroblasts.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-124
10339507-4	1999	AG957, a member of the tyrphostin compounds, exerts a selective inhibition of p210(BCR/ABL) tyrosine phosphorylation.	Tyrphostins	23-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
10339507-4	1999	AG957, a member of the tyrphostin compounds, exerts a selective inhibition of p210(BCR/ABL) tyrosine phosphorylation.	Tyrosine	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
10414920-1	1999	Antisense oligodeoxyribonucleotides (ODN) targeted against the breakpoint in BCR-ABL mRNA will specifically decrease BCR-ABL mRNA, provided cells are first permeabilised with streptolysin-O (SL-O).	Oligodeoxyribonucleotides	10-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
10414920-1	1999	Antisense oligodeoxyribonucleotides (ODN) targeted against the breakpoint in BCR-ABL mRNA will specifically decrease BCR-ABL mRNA, provided cells are first permeabilised with streptolysin-O (SL-O).	Oligodeoxyribonucleotides	10-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
10392900-0	1999	Nuclear c-Abl is a COOH-terminal repeated domain (CTD)-tyrosine (CTD)-tyrosine kinase-specific for the mammalian RNA polymerase II: possible role in transcription elongation.	Tyrosine	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-13
10392900-1	1999	The c-Abl tyrosine kinase has been shown to interact with the COOH-terminal repeated domain (CTD) of mammalian RNA polymerase II and can phosphorylate the tyrosine residues in the CTD.	Tyrosine	10-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-9
10392900-5	1999	In vivo, coexpression of a full length CTD prevents c-Abl from inducing the tyrosine phosphorylation of endogenous RNA polymerase II, and such inhibitory effect was not observed with the coexpression of COOH-terminal-truncated CTD.	Tyrosine	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-57
10392900-9	1999	The activation of the HIV promoter required the nuclear localization of c-Abl and could be correlated with increased tyrosine phosphorylation of RNA polymerase II.	Tyrosine	117-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-77
10325413-8	1999	In contrast, c-Abl and HMG-D respond very differently to deletion or addition of the 5-methyl group of pyrimidine bases in the major groove.	pyrimidine	103-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-18
10325413-10	1999	Conversely, deleting the methyl group from thymines promotes the interaction of the DNA with HMG-D but diminishes its interaction with c-Abl.	Thymine	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-140
10325413-11	1999	The enhanced binding of c-Abl to DNA containing 5-methylcytosine residues may result from an increased propensity of the double helix to denature locally coupled with a protein-induced reduction in the base stacking interaction.	5-Methylcytosine	48-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-29
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 Mesylate	59-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
10098743-0	1999	Induction of JNK and c-Abl signalling by cisplatin and oxaliplatin in mismatch repair-proficient and -deficient cells.	Cisplatin	41-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-26
10098743-0	1999	Induction of JNK and c-Abl signalling by cisplatin and oxaliplatin in mismatch repair-proficient and -deficient cells.	Oxaliplatin	55-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-26
10098743-3	1999	To identify the signal transduction pathways with which the detector communicates, we investigated the effect of loss of DNA mismatch repair on activation of known damage-responsive pathways, and recently reported that cisplatin differentially activates c-Jun NH2-terminal kinase (JNK) and c-Abl in repair-proficient vs.-deficient cells.	Cisplatin	219-228	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	290-295
10098743-6	1999	)-fold more efficiently in DNA mismatch repair-proficient than repair-deficient cells, and that the c-Abl response to cisplatin is completely absent in DNA mismatch repair-deficient cells.	Cisplatin	118-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-105
10098743-9	1999	The DNA mismatch repair system plays an important part in the recognition of cisplatin adducts, and activation of both the JNK and c-Abl kinases in response to cisplatin damage is dependent on the detector function of the DNA mismatch repair proteins.	Cisplatin	77-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-136
10098743-9	1999	The DNA mismatch repair system plays an important part in the recognition of cisplatin adducts, and activation of both the JNK and c-Abl kinases in response to cisplatin damage is dependent on the detector function of the DNA mismatch repair proteins.	Cisplatin	160-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-136
10390076-5	1999	In oncohematology, a number of trials have been initiated with antisense oligonucleotides directed against molecular targets, including the bcl-2, c-myc, bcr-abl, c-myb or p53 oncogenes and tumor suppressor genes.	Oligonucleotides	73-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-161
10194128-2	1999	The amino terminal CRKL SH3 domain binds directly to a proline-rich region in the C-terminus of BCR-ABL.	Proline	55-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
10194128-4	1999	Yeast two-hybrid analysis and gel overlay assays show eradication of the direct interaction of CRKL with BCR-ABL in the proline deletion mutants.	Proline	120-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-112
10194128-5	1999	However, these BCR-ABL mutants transform myeloid cells to growth factor independence, and in these cells CRKL is tyrosine phosphorylated and associates with BCR-ABL.	Tyrosine	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
9988731-7	1999	In digitonin-permeabilized cells, nuclear uptake of bovine albumin conjugated to a nuclear localization sequence (NLS)-containing peptide was also inhibited by a 15-min preincubation with 40-100 micrograms/ml ABL.	Digitonin	3-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-212
9933579-8	1999	In contrast, Bcr-Abl-negative HL60 myeloid leukemia cells, which are sensitive to taxol-induced apoptosis, do not exhibit sustained PKCiota activation in response to taxol.	Paclitaxel	82-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
9933579-9	1999	Treatment of K562 cells with tyrphostin AG957, a selective Bcr-Abl inhibitor, blocks taxol-induced PKCiota activation and sensitizes these cells to taxol-induced apoptosis, indicating that PKCiota is a relevant downstream target of Bcr-Abl-mediated resistance.	Tyrphostins	29-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
9933579-9	1999	Treatment of K562 cells with tyrphostin AG957, a selective Bcr-Abl inhibitor, blocks taxol-induced PKCiota activation and sensitizes these cells to taxol-induced apoptosis, indicating that PKCiota is a relevant downstream target of Bcr-Abl-mediated resistance.	Tyrphostins	29-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	232-239
9933579-9	1999	Treatment of K562 cells with tyrphostin AG957, a selective Bcr-Abl inhibitor, blocks taxol-induced PKCiota activation and sensitizes these cells to taxol-induced apoptosis, indicating that PKCiota is a relevant downstream target of Bcr-Abl-mediated resistance.	Paclitaxel	85-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
9933579-9	1999	Treatment of K562 cells with tyrphostin AG957, a selective Bcr-Abl inhibitor, blocks taxol-induced PKCiota activation and sensitizes these cells to taxol-induced apoptosis, indicating that PKCiota is a relevant downstream target of Bcr-Abl-mediated resistance.	Paclitaxel	85-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	232-239
10022809-7	1999	Moreover, the caspase inhibitor Z-Asp suppressed c-Abl activation and the onset of apoptosis but not the JNK1/SAPK activation.	benzyloxycarbonyl-asparagine	32-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-54
10022809-8	1999	Interestingly, c-Abl tyrosine kinase inhibition by CGP 57148 reduced apoptosis without interfering with JNK1/SAPK activation.	cgp	51-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-20
10224280-5	1999	In a murine bone marrow transduction/transplantation model, the three forms of BCR/ABL were equally potent in the induction of a chronic myeloid leukemia (CML)-like myeloproliferative syndrome in recipient mice when 5-fluorouracil (5-FU)-treated donors were used.	Fluorouracil	216-230	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
10224280-5	1999	In a murine bone marrow transduction/transplantation model, the three forms of BCR/ABL were equally potent in the induction of a chronic myeloid leukemia (CML)-like myeloproliferative syndrome in recipient mice when 5-fluorouracil (5-FU)-treated donors were used.	Fluorouracil	232-236	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
10215653-9	1999	Furthermore, reduced Bcr-Abl expression is reflected in significantly attenuated Bcr-Abl-mediated protein tyrosine phosphorylation.	Tyrosine	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
10215653-9	1999	Furthermore, reduced Bcr-Abl expression is reflected in significantly attenuated Bcr-Abl-mediated protein tyrosine phosphorylation.	Tyrosine	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
10374889-3	1999	After cellular permeabilization and fixation, the mRNA BCR-ABL was reverse transcribed and amplified by PCR using digoxigenin-labelled dUTP.	Digoxigenin	114-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
10374889-3	1999	After cellular permeabilization and fixation, the mRNA BCR-ABL was reverse transcribed and amplified by PCR using digoxigenin-labelled dUTP.	deoxyuridine triphosphate	135-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
10212258-3	1999	Here we demonstrate that there is an I-R-induced Rad51 tyrosine phosphorylation, and this induction is dependent on both ATM and c-Abl.	Tyrosine	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-134
10194451-2	1999	We describe here the purification and mass spectrometric identification of a 155-kD tyrosine phosphorylated protein associated with src homologous and collagen gene (SHC) from p210(bcr/abl)-expressing hematopoietic cells as SHIP2, a recently reported, unique SH2-domain-containing protein closely related to phosphatidylinositol polyphosphate 5-phosphatase SHIP.	Tyrosine	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	185-188
10099134-2	1999	Various attempts to design antisense oligonucleotides that specifically cleave abnormal L6 BCR-ABL fusion mRNA have not been successful.	Oligonucleotides	37-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
10326252-1	1999	The stability and folding thermodynamics of two SH3-domains, belonging to Fyn and Abl proteins, have been studied by scanning calorimetry and urea-induced unfolding.	Urea	142-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-85
9874796-2	1999	The binding appeared to be required for XPB to be tyrosine-phosphorylated by BCR-ABL.	Tyrosine	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
9923858-8	1999	A single administration of CGP57148B caused substantial (>50%) but short-lived (2-5 hours) inhibition of Bcr/Abl kinase activity.	Imatinib Mesylate	27-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
10685045-2	1999	Using Src homology 3 domains from the proteins c-Abl and c-Crk as model systems, we show here that EPL can be performed in the presence of moderate concentrations of the chemical denaturant, guanidine hydrochloride, and the organic solvent dimethylsulfoxide.	denaturant	179-189	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-52
10685045-2	1999	Using Src homology 3 domains from the proteins c-Abl and c-Crk as model systems, we show here that EPL can be performed in the presence of moderate concentrations of the chemical denaturant, guanidine hydrochloride, and the organic solvent dimethylsulfoxide.	Guanidine	191-214	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-52
10685045-2	1999	Using Src homology 3 domains from the proteins c-Abl and c-Crk as model systems, we show here that EPL can be performed in the presence of moderate concentrations of the chemical denaturant, guanidine hydrochloride, and the organic solvent dimethylsulfoxide.	Dimethyl Sulfoxide	240-257	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-52
9872323-8	1998	Our results suggest that the unique structure of Gads regulates its interaction with downstream SH3 domain-binding proteins and that Gads may function to couple tyrosine-phosphorylated proteins such as Shc, Bcr-Abl and activated receptor tyrosine kinases to downstream effectors distinct from Sos and Ras.	Tyrosine	161-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	207-214
10500812-12	1999	These data suggest that in addition of the multidrug resistance phenotype, bcr-abl translocation and bcl-xL overexpression could also account for the development of resistance to cell death induced by anthracyclines in leukemic cells.	Anthracyclines	201-215	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
10883504-2	1999	We studied in this work normal endometrial tissue, with benign and malignant entities in search for the presence of the Galactose beta 1-3 N Acetylgalactosamine(Gal beta 1-3 GalNAC alpha and Galactose beta 1-3 N Acetylgalactosamine (Gal beta 1-3 alpha and beta) using the Lectins: Agaricus bisporus (ABL) and Arachis hipogea (PNA) respectively.	galactose beta 1-3 n acetylgalactosamine	120-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	300-303
10215768-2	1999	Peanut agglutinin (PNA) and the lectin from the edible mushroom (Agaricus bisporus, ABL) both bind to the disaccharide galactosyl beta-1,3-N-acetyl galactosamine alpha-.	Disaccharides	106-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-87
10215768-2	1999	Peanut agglutinin (PNA) and the lectin from the edible mushroom (Agaricus bisporus, ABL) both bind to the disaccharide galactosyl beta-1,3-N-acetyl galactosamine alpha-.	galactosyl beta-1,3-n-acetyl galactosamine	119-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-87
9837937-8	1998	Tyrosine-phosphorylated mammalian Disabled can recruit nonreceptor tyrosine kinases, such as src and abl, to the cytoplasmic tails of the receptors to which it binds, suggesting a molecular pathway by which receptor/ligand interaction on the cell surface could generate an intracellular signal.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-40
9858222-1	1998	We investigated whether inhibition of the BCR-ABL tyrosine kinase by the CGP57418B compound would render chronic myeloid leukaemia (CML) cells susceptible to Fas (CD95, Apo-1)-mediated cell death.	cgp57418b	73-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
9886328-6	1998	The presence of BCR-ABL provides an explanation for the constitutive tyrosine phosphorylation of CrkL in CML platelets.	Tyrosine	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
9886328-7	1998	As no correlation was observed between platelet counts and platelet BCR-ABL protein expression, thrombocytosis or thrombocythaemia in CML cannot be explained by constitutive BCR-ABL-mediated CrkL tyrosine phosphorylation.	Tyrosine	196-204	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-181
9858222-1	1998	We investigated whether inhibition of the BCR-ABL tyrosine kinase by the CGP57418B compound would render chronic myeloid leukaemia (CML) cells susceptible to Fas (CD95, Apo-1)-mediated cell death.	ammonium ferrous sulfate	158-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
10081494-8	1998	Since CDDP and carboplatin damage DNA and then activate c-abl and the JNK/SAPK pathway, EAT/mcl-1 may inhibit p53-independent apoptosis through a c-abl/JNK (SAPK)-dependent mechanism.	Cisplatin	6-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-61
10081494-8	1998	Since CDDP and carboplatin damage DNA and then activate c-abl and the JNK/SAPK pathway, EAT/mcl-1 may inhibit p53-independent apoptosis through a c-abl/JNK (SAPK)-dependent mechanism.	Cisplatin	6-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	146-151
10081494-8	1998	Since CDDP and carboplatin damage DNA and then activate c-abl and the JNK/SAPK pathway, EAT/mcl-1 may inhibit p53-independent apoptosis through a c-abl/JNK (SAPK)-dependent mechanism.	Carboplatin	15-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-61
9843217-4	1998	The proline-rich region has been shown to bind to the SH3 domain of c-Abl, which facilitates its phosphorylation and activation by ATM.	Proline	4-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-73
9823945-0	1998	Tyrphostin AG957, a tyrosine kinase inhibitor with anti-BCR/ABL tyrosine kinase activity restores beta1 integrin-mediated adhesion and inhibitory signaling in chronic myelogenous leukemia hematopoietic progenitors.	Tyrphostins	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
10049047-0	1999	Clonally unrelated BCR-ABL-negative acute myeloblastic leukemia masquerading as blast crisis after busulphan and interferon therapy for BCR-ABL-positive chronic myeloid leukemia.	Busulfan	99-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
9828110-3	1998	The C-terminal domains of Arg and c-abl, poorly similar to each other, may account for their different functions.	Arginine	26-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-39
9823945-5	1998	Incubation of CML marrow CD34+HLA-DR+ cells with Tyrphostin AG957 at concentrations that did not affect colony-forming cells (CFC) viability, but which partly inhibited p210BCR/ABL kinase activity, significantly increased CML CFC adhesion to stroma and alpha4beta1 and alpha5beta1 integrin binding fragments of fibronectin (FN).	Tyrphostins	49-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	177-180
9792313-4	1998	In the eighth position before the junctional region of BCR/ABL cDNA, a cytosine replaces thymine in these cases.	Cytosine	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-62
10211125-0	1998	Detection of the bcr/abl gene in bone marrow macrophages in CML and alterations during interferon therapy--a fluorescence in situ hybridization study on trephine biopsies.	trephine	153-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
9792313-4	1998	In the eighth position before the junctional region of BCR/ABL cDNA, a cytosine replaces thymine in these cases.	Thymine	89-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-62
9642287-2	1998	We examined whether tyrosine 221, which has been shown to be phosphorylated by c-Abl, was phosphorylated also by other tyrosine kinases, such as epidermal growth factor (EGF) receptor.	Tyrosine	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-84
9844818-3	1998	We demonstrate that despite this property, Bcr-Abl transformed cells (primitive hematopoietic progenitors or cell lines) remains sensitive to apoptosis induced by Ceramides analogues.	Ceramides	163-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
9844818-5	1998	In addition to the classical features of apoptosis, we observed that Ceramide-treated CML cells display a rapid and sequential activation of the Bcr-Abl and PI3 kinases.	Ceramides	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-152
9844818-6	1998	We then demonstrated the role of the Bcr-Abl kinase activity in the accelerated response observed in CML cells treated by Ceramide.	Ceramides	122-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
9844818-7	1998	The PI3 kinase seems to be partly involved in the accelerated Phosphatidyl-Serine exposure observed in Bcr-Abl transformed cells.	Phosphatidylserines	62-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
9844818-9	1998	Taken together these results support the hypothesis of at least two independent signaling pathways initiating programmed cell death: one will be involved in apoptosis mediated by signals such as cytokine-starving is blocked by the Bcr-Abl fusion protein while the other one initiated by Ceramide is accelerated by the Bcr-Abl protein.	Ceramides	287-295	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	231-238
9844818-9	1998	Taken together these results support the hypothesis of at least two independent signaling pathways initiating programmed cell death: one will be involved in apoptosis mediated by signals such as cytokine-starving is blocked by the Bcr-Abl fusion protein while the other one initiated by Ceramide is accelerated by the Bcr-Abl protein.	Ceramides	287-295	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	318-325
9740329-0	1998	c-Abl proto-oncoprotein is expressed and tyrosine phosphorylated in human sperm cell.	Tyrosine	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
9740329-2	1998	The c-Abl monoclonal antibody (mAb), against the protein tyrosine kinase domain of v-Abl protein, reacted specifically with the acrosomal region of methanol-fixed capacitated and non-capacitated human sperm cell in the indirect immunofluorescence technique.	Methanol	148-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-9
9740329-2	1998	The c-Abl monoclonal antibody (mAb), against the protein tyrosine kinase domain of v-Abl protein, reacted specifically with the acrosomal region of methanol-fixed capacitated and non-capacitated human sperm cell in the indirect immunofluorescence technique.	Methanol	148-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-88
9740329-3	1998	The c-Abl mAb predominantly recognized two protein bands of 145 kD and 95 kD in detergent-solubilized (Triton X-100 and NP-40) sperm and testes preparations in the Western blot procedure.	Octoxynol	103-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-9
9740329-3	1998	The c-Abl mAb predominantly recognized two protein bands of 145 kD and 95 kD in detergent-solubilized (Triton X-100 and NP-40) sperm and testes preparations in the Western blot procedure.	Nonidet P-40	120-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-9
9740329-5	1998	In the in vitro kinase assay using the Triton X-100-solubilized capacitated sperm preparation, the 95 kD protein was autophosphorylated at the tyrosine residues, which was inhibited in the presence of c-Abl mAb.	Octoxynol	39-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	201-206
9740329-5	1998	In the in vitro kinase assay using the Triton X-100-solubilized capacitated sperm preparation, the 95 kD protein was autophosphorylated at the tyrosine residues, which was inhibited in the presence of c-Abl mAb.	Tyrosine	143-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	201-206
9740329-7	1998	These findings suggest that the c-Abl or c-Abl-like proteins are present in mature sperm cells that are tyrosine autophosphorylated and may have a role in human sperm cell function.	Tyrosine	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-37
9740329-7	1998	These findings suggest that the c-Abl or c-Abl-like proteins are present in mature sperm cells that are tyrosine autophosphorylated and may have a role in human sperm cell function.	Tyrosine	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-46
9710592-1	1998	Crkl is an adapter protein and phosphotyrosine-containing substrate implicated in transformation by the bcr-abl oncogene and in signaling by cytokines.	Phosphotyrosine	31-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
9710592-6	1998	In vivo and in vitro tryptic phosphopeptide mapping studies show that Crkl is phosphorylated on multiple tyrosine residues when overexpressed or when activated by Bcr-Abl.	Tyrosine	105-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
10921025-2	1998	METHODS: Apoptosis of in vitro cultured K562 cells was observed after exposure to synthetic 18-mer antisense oligodeoxynucleotide complementary to the bcr-abl junction (b3a2).	Oligodeoxyribonucleotides	109-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-158
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 Mesylate	22-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-125
9636171-10	1998	The c-Abl NES function is sensitive to the nuclear export inhibitor leptomycin B.	leptomycin B	68-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-9
9616172-1	1998	The hybrid gene BCR-ABL that typifies chronic myeloid leukemia (CML) represents an attractive target for therapy with antisense oligodeoxyribonucleotides (ODN).	Oligodeoxyribonucleotides	128-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
9616172-1	1998	The hybrid gene BCR-ABL that typifies chronic myeloid leukemia (CML) represents an attractive target for therapy with antisense oligodeoxyribonucleotides (ODN).	Oligodeoxyribonucleotides	155-158	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
9616172-4	1998	We have shown that (1) BCR-ABL-directed ODN will specifically decrease the level of BCR-ABL mRNA, provided that cells are first permeabilized with Streptolysin-O (SL-O), and (2) chimeric methylphosphonodiester:phosphodiester ODN directed against 9 bases either side of the BCR-ABL junction are more efficient ODN effectors than structures composed solely of phosphodiester or phosphorothioate linkages.	Parathion	376-392	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
9616172-4	1998	We have shown that (1) BCR-ABL-directed ODN will specifically decrease the level of BCR-ABL mRNA, provided that cells are first permeabilized with Streptolysin-O (SL-O), and (2) chimeric methylphosphonodiester:phosphodiester ODN directed against 9 bases either side of the BCR-ABL junction are more efficient ODN effectors than structures composed solely of phosphodiester or phosphorothioate linkages.	Parathion	376-392	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
9616172-4	1998	We have shown that (1) BCR-ABL-directed ODN will specifically decrease the level of BCR-ABL mRNA, provided that cells are first permeabilized with Streptolysin-O (SL-O), and (2) chimeric methylphosphonodiester:phosphodiester ODN directed against 9 bases either side of the BCR-ABL junction are more efficient ODN effectors than structures composed solely of phosphodiester or phosphorothioate linkages.	Parathion	376-392	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
9603926-4	1998	Several proteins that were phosphorylated on tyrosine were found to transiently co-precipitate with c-Abl during cell adhesion, and one was identified as the focal adhesion protein paxillin.	Tyrosine	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-105
9639422-0	1998	Arginine butyrate downregulates p210 bcr-abl expression and induces apoptosis in chronic myelogenous leukemia cells.	arginine butyrate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
9639422-1	1998	Downregulation of bcr-abl expression in the chronic myelogenous leukemia cell line K562 using antisense oligonucleotides has been shown to enhance the sensitivity of the cells to apoptotic stimuli, suggesting that p210 bcr-abl, like bcl-2 functions as an anti-apoptosis factor (McGahon A et al, Blood 1994, 83: 1179).	Oligonucleotides	104-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
9639422-4	1998	To further explore the mechanisms of this effect, we examined expression of p210 bcr-abl after butyrate exposure and found a dose-related inhibition of p210 bcr-abl protein without concordant change in other phosphoproteins, including the JAK-1 kinase.	Butyrates	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
9639422-4	1998	To further explore the mechanisms of this effect, we examined expression of p210 bcr-abl after butyrate exposure and found a dose-related inhibition of p210 bcr-abl protein without concordant change in other phosphoproteins, including the JAK-1 kinase.	Butyrates	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-164
9639422-5	1998	Further analysis revealed that the inhibition of bcr-abl expression occurs due to transcriptional regulation of the bcr-abl gene by arginine butyrate.	arginine butyrate	132-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
9639422-5	1998	Further analysis revealed that the inhibition of bcr-abl expression occurs due to transcriptional regulation of the bcr-abl gene by arginine butyrate.	arginine butyrate	132-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
9639422-6	1998	These results suggest that arginine butyrate and other butyrate analogs alone or in combination may be useful in the therapy of patients with chronic myelogenous leukemia or bcr-abl expressing acute leukemias.	arginine butyrate	27-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-181
9639422-6	1998	These results suggest that arginine butyrate and other butyrate analogs alone or in combination may be useful in the therapy of patients with chronic myelogenous leukemia or bcr-abl expressing acute leukemias.	Butyrates	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-181
9636171-11	1998	Mutation of a single leucine (L1064A) in the c-Abl NES abrogates export function.	Leucine	21-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-50
9636171-13	1998	Treatment of cells with leptomycin B also leads to the nuclear accumulation of wild-type c-Abl protein.	leptomycin B	24-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-94
9558370-0	1998	BCR-ABL antisense oligodeoxynucleotide in vitro purging and autologous bone marrow transplantation for patients with chronic myelogenous leukemia in advanced phase.	Oligodeoxyribonucleotides	18-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
9558370-1	1998	BCR-ABL antisense oligodeoxynucleotides (ODN) have provided evidence of antileukemia effect when tested in vitro against Philadelphia-positive (Ph-pos) cells and in vivo when injected into leukemic mice.	Oligodeoxyribonucleotides	18-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
9558370-1	1998	BCR-ABL antisense oligodeoxynucleotides (ODN) have provided evidence of antileukemia effect when tested in vitro against Philadelphia-positive (Ph-pos) cells and in vivo when injected into leukemic mice.	Oligodeoxyribonucleotides	41-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
9558400-0	1998	Inhibition of BCR-ABL expression with antisense oligodeoxynucleotides restores beta1 integrin-mediated adhesion and proliferation inhibition in chronic myelogenous leukemia hematopoietic progenitors.	Oligodeoxyribonucleotides	48-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
9536079-0	1998	The BCR gene recombines preferentially with Alu elements in complex BCR-ABL translocations of chronic myeloid leukaemia.	METHYL HYDROGEN (S)-ACETYLPHOSPHONATE	44-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
9558345-6	1998	The c-Abl DNA-binding domain recognizes specific sequences and interacts with deformed DNA structures such as four-way junctions and bubble DNA containing a large single-stranded loop, as determined by electromobility shift assay, melting temperature studies, and binding to specific oligonucleotides covalently linked to beads.	Oligonucleotides	284-300	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-9
9525737-5	1998	Treatment with antisense oligonucleotides directed to bcr decreased the expression of the ectopic bcr - abl and restored susceptibility to apoptosis.	Oligonucleotides	25-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-107
9525737-6	1998	Double mutations affecting the autophosphorylation site and the phosphotyrosine-binding motif (FLVRES) have been previously shown to impair the transforming activity of Bcr - Abl in fibroblasts and hematopoietic cells, however HL-60 cells expressing this double mutant molecule exhibited the same level of resistance to apoptosis as those expressing the wild-type Bcr - Abl.	Phosphotyrosine	64-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	169-178
9525737-6	1998	Double mutations affecting the autophosphorylation site and the phosphotyrosine-binding motif (FLVRES) have been previously shown to impair the transforming activity of Bcr - Abl in fibroblasts and hematopoietic cells, however HL-60 cells expressing this double mutant molecule exhibited the same level of resistance to apoptosis as those expressing the wild-type Bcr - Abl.	Phosphotyrosine	64-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	364-373
9525737-10	1998	Bcr - Abl cells to staurosporine.	Staurosporine	19-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-9
9461559-5	1998	We show that c-Abl phosphorylates Rad51 on Tyr-54 in vitro.	Tyrosine	43-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-18
9461559-7	1998	Phosphorylation of Rad51 by c-Abl inhibits the binding of Rad51 to DNA and the function of Rad51 in ATP-dependent DNA strand exchange reactions.	Adenosine Triphosphate	100-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-33
9461588-0	1998	Modification of phosphatidylinositol 3-kinase SH2 domain binding properties by Abl- or Lck-mediated tyrosine phosphorylation at Tyr-688.	Tyrosine	100-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-82
9461588-0	1998	Modification of phosphatidylinositol 3-kinase SH2 domain binding properties by Abl- or Lck-mediated tyrosine phosphorylation at Tyr-688.	Tyrosine	128-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-82
9461588-1	1998	In cells expressing the oncogenic Bcr-Abl tyrosine kinase, the regulatory p85 subunit of phosphatidylinositol 3-kinase is phosphorylated on tyrosine residues.	Tyrosine	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
11243118-4	1998	RESULTS: As2O3 reduced the PTK activities of cytosol and membrane proteins and BCR/ABL and ABL proteins.	Arsenic Trioxide	9-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
11243118-4	1998	RESULTS: As2O3 reduced the PTK activities of cytosol and membrane proteins and BCR/ABL and ABL proteins.	Arsenic Trioxide	9-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-86
11243118-6	1998	CONCLUSION: As2O3 may interfere the signal transduction of BCR/ABL protein by reducing its PTK activity and induce K562 cell apoptosis.	Arsenic Trioxide	12-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
9516141-2	1998	Apoptotic DNA fragmentation is delayed in the bcr-abl+ K562 and KCL-22 compared with the bcr-abl- U937 and HL-60 cell lines when treated with etoposide concentrations that induce similar DNA damage in the four cell lines.	Etoposide	142-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
9516141-2	1998	Apoptotic DNA fragmentation is delayed in the bcr-abl+ K562 and KCL-22 compared with the bcr-abl- U937 and HL-60 cell lines when treated with etoposide concentrations that induce similar DNA damage in the four cell lines.	Etoposide	142-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
9516141-3	1998	By the use of a cell-free system, we show that nuclei from untreated cells that express p210(bcr-abl) remain sensitive to apoptotic DNA fragmentation induced by triton-soluble extracts from p210(bcr-abl-) cells treated with etoposide.	Etoposide	224-233	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
9516141-3	1998	By the use of a cell-free system, we show that nuclei from untreated cells that express p210(bcr-abl) remain sensitive to apoptotic DNA fragmentation induced by triton-soluble extracts from p210(bcr-abl-) cells treated with etoposide.	Etoposide	224-233	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	195-202
9516141-6	1998	The role of p210(bcr-abl) in this delay is confirmed by comparing the effect of etoposide on the granulocyte-macrophage colony-stimulating factor (GM-CSF)-dependent UT7 cells and the bcr-abl-transfected GM-CSF-independent UT7/9 clone.	Etoposide	80-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
9516141-7	1998	We conclude that the cytosolic pathway that leads to apoptotic DNA fragmentation in etoposide-treated leukemic cells is delayed upstream of procaspase-3-mediated events in bcr-abl+ cell lines.	Etoposide	84-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-179
9389683-13	1997	LasBD also rendered 20% to 30% of primary Ph- and Ph+ CD34(+) cells MTX-resistant and decreased BCR/ABL mRNA levels in MTX resistant Ph+ CD34(+) cells by 10-fold.	lasbd	0-5	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
9467953-2	1998	Tyrosine phosphorylated Bcr has dramatically reduced kinase activity, and tyrosine 360 of Bcr, which is one of the sites of phosphorylation by the Bcr-Abl oncoprotein, is required for transkinase activity (Liu et al., Mol.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-154
9467953-2	1998	Tyrosine phosphorylated Bcr has dramatically reduced kinase activity, and tyrosine 360 of Bcr, which is one of the sites of phosphorylation by the Bcr-Abl oncoprotein, is required for transkinase activity (Liu et al., Mol.	Tyrosine	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-154
9467953-7	1998	Taken together with the kinase inhibitory effects of tyrosine phosphorylation of Bcr by Bcr-Abl, our studies with tyrosine to phenylalanine Bcr mutants indicate that the hydroxyl residues of tyrosines 328 and 360 play crucial roles in Bcr"s kinase activity.	Tyrosine	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
9467953-7	1998	Taken together with the kinase inhibitory effects of tyrosine phosphorylation of Bcr by Bcr-Abl, our studies with tyrosine to phenylalanine Bcr mutants indicate that the hydroxyl residues of tyrosines 328 and 360 play crucial roles in Bcr"s kinase activity.	Tyrosine	191-200	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
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 Mesylate	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-126
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.	N-phenylpyrimidin-2-amine	31-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-126
9389713-4	1997	In cell-based assays of ABL tyrosine phosphorylation, inhibition of ABL kinase activity was observed at concentrations similar to that reported for p210BCR-ABL.	Tyrosine	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-27
9389713-4	1997	In cell-based assays of ABL tyrosine phosphorylation, inhibition of ABL kinase activity was observed at concentrations similar to that reported for p210BCR-ABL.	Tyrosine	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-71
9389713-4	1997	In cell-based assays of ABL tyrosine phosphorylation, inhibition of ABL kinase activity was observed at concentrations similar to that reported for p210BCR-ABL.	Tyrosine	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-71
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	190-197
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.	Adenosine Triphosphate	16-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-52
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 Mesylate	60-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-159
9464542-0	1998	BCR-ABL accelerates C2-ceramide-induced apoptosis.	N-acetylsphingosine	20-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
9464542-5	1998	Nevertheless, both primary CML cells and BCR-ABL+ BAF3 cells show the same dose-dependent sensitivity to TNF-alpha or ceramide-induced apoptosis as their respective normal counterparts.	Ceramides	118-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
9464542-6	1998	In fact, time course studies demonstrated an even faster onset of apoptosis in ceramide-treated BCR-ABL+ BAF3 cells as compared to normal controls.	Ceramides	79-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
9464542-7	1998	BCR-ABL+ cells treated with ceramide also showed a rapid and sequential increase in the tyrosine phosphorylation of p210(BCR-ABL), p46-56SHC and p120Cbl.	Ceramides	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
9464542-7	1998	BCR-ABL+ cells treated with ceramide also showed a rapid and sequential increase in the tyrosine phosphorylation of p210(BCR-ABL), p46-56SHC and p120Cbl.	Ceramides	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
9464542-7	1998	BCR-ABL+ cells treated with ceramide also showed a rapid and sequential increase in the tyrosine phosphorylation of p210(BCR-ABL), p46-56SHC and p120Cbl.	Tyrosine	88-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
9464542-7	1998	BCR-ABL+ cells treated with ceramide also showed a rapid and sequential increase in the tyrosine phosphorylation of p210(BCR-ABL), p46-56SHC and p120Cbl.	Tyrosine	88-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
9393882-6	1997	In hematopoietic cells transformed by the BCR/ABL oncogene, this phosphatase complex was found to be constitutively present with both components heavily tyrosine phosphorylated.	Tyrosine	153-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
9393882-8	1997	However, transformation by BCR/ABL was associated with a reduced SHIP protein expression, which could further affect the accumulation of various inositol polyphosphates in these leukemic cells.	inositol polyphosphates	145-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
9345054-0	1997	The tyrosine kinase inhibitor CGP57148B selectively inhibits the growth of BCR-ABL-positive cells.	Imatinib Mesylate	30-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
9345054-3	1997	CGP57148B, a 2-phenylaminopyrimidine derivative, has been shown to selectively inhibit the tyrosine kinase of ABL and BCR-ABL.	Imatinib Mesylate	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 Mesylate	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
9345054-3	1997	CGP57148B, a 2-phenylaminopyrimidine derivative, has been shown to selectively inhibit the tyrosine kinase of ABL and BCR-ABL.	N-phenylpyrimidin-2-amine	13-36	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.	N-phenylpyrimidin-2-amine	13-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
9389683-13	1997	LasBD also rendered 20% to 30% of primary Ph- and Ph+ CD34(+) cells MTX-resistant and decreased BCR/ABL mRNA levels in MTX resistant Ph+ CD34(+) cells by 10-fold.	Methotrexate	119-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
9355902-4	1997	At the end of the 6 months, the 21 patients of the Abl+Pm group who completed the study showed, in comparison with the 18 of the drug group, lower scores in the Living with Heart Failure Questionnaire (-51%, P=.0006), palpitations (-71%, P=.0000), effort dyspnea (-36%, P=.04), exercise intolerance score (-46%, P=.001), and easy fatigue (-51%, P=.02).	Promethium	55-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-54
9365241-0	1997	Pro-apoptotic effect of the c-Abl tyrosine kinase in the cellular response to 1-beta-D-arabinofuranosylcytosine.	Cytarabine	78-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-33
9365241-1	1997	Treatment of cells with the antimetabolite 1-beta-D-arabinofuranosylcytosine (ara-C) and other genotoxic agents is associated with activation of the c-Abl protein tyrosine kinase.	antimetabolite 1-beta-d-arabinofuranosylcytosine	28-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-154
9365241-1	1997	Treatment of cells with the antimetabolite 1-beta-D-arabinofuranosylcytosine (ara-C) and other genotoxic agents is associated with activation of the c-Abl protein tyrosine kinase.	Cytarabine	78-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-154
9365241-3	1997	The present studies demonstrate that cells expressing a dominant negative, kinase-inactive c-Abl (K-R) are resistant to killing by ara-C.	Krypton	98-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-96
9365241-3	1997	The present studies demonstrate that cells expressing a dominant negative, kinase-inactive c-Abl (K-R) are resistant to killing by ara-C.	Cytarabine	131-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-96
9365241-4	1997	The expression of c-Abl (K-R) blocked ara-C-induced apoptosis by a mechanism that is at least in part independent of the p53 tumor suppressor.	Krypton	25-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-23
9365241-4	1997	The expression of c-Abl (K-R) blocked ara-C-induced apoptosis by a mechanism that is at least in part independent of the p53 tumor suppressor.	Cytarabine	38-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-23
9202056-4	1997	p210(BCR/ABL) binds to actin, and several cytoskeletal proteins are tyrosine phosphorylated by this oncoprotein.	Tyrosine	68-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	5-12
9305594-1	1997	Antisense oligodeoxyribonucleotides (ODN) have been shown to produce a sequence-specific cleavage of BCR-ABL mRNA.	Oligodeoxyribonucleotides	10-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
9315092-8	1997	Shd was tyrosine phosphorylated in COS-7 cells co-transfected with Shd and c-Abl or Bcr-Abl.	Tyrosine	8-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-80
9315092-8	1997	Shd was tyrosine phosphorylated in COS-7 cells co-transfected with Shd and c-Abl or Bcr-Abl.	Tyrosine	8-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
9315092-8	1997	Shd was tyrosine phosphorylated in COS-7 cells co-transfected with Shd and c-Abl or Bcr-Abl.	carbonyl sulfide	35-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-80
21528234-6	1997	We found that SHP-1 was highly and constitutively tyrosine phosphorylated in 32DCl3 and TF-1 cells transfected with BCR-ABL expression vector.	Tyrosine	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
9242457-0	1997	Differential induction of c-Jun NH2-terminal kinase and c-Abl kinase in DNA mismatch repair-proficient and -deficient cells exposed to cisplatin.	Cisplatin	135-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-61
9242457-1	1997	The c-Abl nonreceptor tyrosine kinase and the c-Jun NH2-terminal kinase (JNK/stress-activated protein kinase) are activated during the injury response to the DNA-damaging agent cisplatin.	Cisplatin	177-186	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-9
9242457-3	1997	To identify signaling pathways activated by this detector, we investigated the effect of the loss of DNA mismatch repair function on the ability of cisplatin to activate the JNK and c-Abl kinases.	Cisplatin	148-157	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-187
9242457-4	1997	The results demonstrate that cisplatin activates JNK kinase 3.8 +/- 0.2-fold more efficiently in DNA mismatch repair-proficient than repair-deficient cells, and that activation of c-Abl is completely absent in the DNA mismatch repair-deficient cells.	Cisplatin	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	180-185
9242457-6	1997	We conclude that activation of JNK and c-Abl by cisplatin is in part dependent upon the integrity of DNA mismatch repair function, suggesting that these kinases are part of the signal transduction pathway activated when mismatch repair proteins recognize cisplatin adducts in DNA.	Cisplatin	48-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-44
9242457-6	1997	We conclude that activation of JNK and c-Abl by cisplatin is in part dependent upon the integrity of DNA mismatch repair function, suggesting that these kinases are part of the signal transduction pathway activated when mismatch repair proteins recognize cisplatin adducts in DNA.	Cisplatin	255-264	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-44
9211900-0	1997	ArgBP2, a multiple Src homology 3 domain-containing, Arg/Abl-interacting protein, is phosphorylated in v-Abl-transformed cells and localized in stress fibers and cardiocyte Z-disks.	Arginine	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-108
9211900-4	1997	ArgBP2 associates with and is a substrate of Arg and v-Abl, and is phosphorylated on tyrosine in v-Abl-transformed cells.	Arginine	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-58
9211900-4	1997	ArgBP2 associates with and is a substrate of Arg and v-Abl, and is phosphorylated on tyrosine in v-Abl-transformed cells.	Arginine	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-102
9211900-4	1997	ArgBP2 associates with and is a substrate of Arg and v-Abl, and is phosphorylated on tyrosine in v-Abl-transformed cells.	Tyrosine	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-102
9180290-9	1997	RT-PCR analysis of the colonies resulting from the action of the combination IFN alpha plus ATRA showed the presence of an increased number of BCR-ABL-negative colonies relatively to what was observed with IFN alpha alone.	Tretinoin	92-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-150
9299869-15	1997	The fact that BCR-ABL contains tyrosine residues, an SH2 domain, an SH3 domain, and proline-rich sequences raises the possibility of multiple protein-protein interactions.	Tyrosine	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
9299869-15	1997	The fact that BCR-ABL contains tyrosine residues, an SH2 domain, an SH3 domain, and proline-rich sequences raises the possibility of multiple protein-protein interactions.	Proline	84-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
9195915-7	1997	Since CRKL, an SH2, SH3 domain-containing adapter protein is known to bind directly to BCR-ABL and also binds to tyrosine-phosphorylated c-CBL, the ability of CRKL to mediate a complex between c-CBL and BCR-ABL was examined.	Tyrosine	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
9195915-7	1997	Since CRKL, an SH2, SH3 domain-containing adapter protein is known to bind directly to BCR-ABL and also binds to tyrosine-phosphorylated c-CBL, the ability of CRKL to mediate a complex between c-CBL and BCR-ABL was examined.	Tyrosine	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	203-210
9376661-3	1997	BCR-ABL contains tyrosine residues, an SH2 domain, an SH3 domain, and proline-rich sequences.	Tyrosine	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
9376661-3	1997	BCR-ABL contains tyrosine residues, an SH2 domain, an SH3 domain, and proline-rich sequences.	Proline	70-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
9154822-0	1997	Inhibition of the Raf-1 kinase by cyclic AMP agonists causes apoptosis of v-abl-transformed cells.	Cyclic AMP	34-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-79
9154822-3	1997	In v-abl-transformed cells the endogenous Raf-1 protein was phosphorylated on tyrosine and displayed high constitutive kinase activity.	Tyrosine	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	3-8
9154822-14	1997	In conclusion, these results suggest (i) that Raf-1 participates in v-abl transformation via an Erk-independent pathway by providing a survival signal which complements c-myc in transformation, and (ii) that cAMP agonists might become useful for the treatment of malignancies where abl oncogenes are involved, such as chronic myeloid leukemias.	Cyclic AMP	208-212	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-73
9154822-14	1997	In conclusion, these results suggest (i) that Raf-1 participates in v-abl transformation via an Erk-independent pathway by providing a survival signal which complements c-myc in transformation, and (ii) that cAMP agonists might become useful for the treatment of malignancies where abl oncogenes are involved, such as chronic myeloid leukemias.	Cyclic AMP	208-212	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-73
9168116-7	1997	Ectopic expression of a functional ATM kinase domain corrects this defect, as it phosphorylates the c-Abl tyrosine kinase in vitro at Ser 465, leading to the activation of c-Abl.	Serine	134-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-105
9168116-7	1997	Ectopic expression of a functional ATM kinase domain corrects this defect, as it phosphorylates the c-Abl tyrosine kinase in vitro at Ser 465, leading to the activation of c-Abl.	Serine	134-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-177
9144171-8	1997	Moreover, the amino-terminal domain of RIN1 directly associates with, and is tyrosine phosphorylated by, c-ABL.	Tyrosine	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-110
9060613-2	1997	Using the yeast two-hybrid system, we identified the SH3 domain of c-Abl as interacting with the proline-rich p12 domain of Pr60gag.	Proline	97-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-72
9209375-4	1997	In viral forms of abl, gag sequences are fused to Abl portions resulting in a deletion of N-terminal sequences.	Glycosaminoglycans	23-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-21
9067577-3	1997	In cell lines transformed by BCR/ABL, CRKL was tyrosine phosphorylated, while CRK was not.	Tyrosine	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
8912843-3	1996	We report here that a deleted form of Bcr [Bcr(64-413)], encompassing the Abl SH2 binding domains of Bcr, reduced the phosphotyrosine content of c-Abl and Bcr-Abl within cells and inhibited Bcr-Abl autophosphorylation activity in vitro.	Phosphotyrosine	118-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-77
9029029-0	1997	An antisense Bcr-Abl phosphodiester-tailed methylphosphonate oligonucleotide reduces the growth of chronic myeloid leukaemia patient cells by a non-antisense mechanism.	methylphosphonate oligonucleotide	43-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
9029029-1	1997	The specificity of antisense oligonucleotides targeted to the mRNA breakpoint region of the Bcr-Abl oncogene, found in leukaemic cells from patients with chronic myeloid leukaemia, remains controversial due to non-specific effects.	Oligonucleotides	29-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
9029029-3	1997	Growth of chronic myeloid leukaemia (CML) cell lines BV173, KCL-22 and cells of CML patients tested was inhibited by the b2a2 type antisense Bcr-Abl oligonucleotide and not with controls.	Potassium Chloride	60-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-148
9029029-3	1997	Growth of chronic myeloid leukaemia (CML) cell lines BV173, KCL-22 and cells of CML patients tested was inhibited by the b2a2 type antisense Bcr-Abl oligonucleotide and not with controls.	Oligonucleotides	149-164	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-148
9029029-5	1997	Bcr-Abl protein studies in combination with growth-determination experiments indicated that the antisense methylphosphonate Bcr-Abl oligonucleotide tested is a potent inhibitor of the growth of CML cells but works in a non-antisense manner.	Oligonucleotides	132-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
9029029-5	1997	Bcr-Abl protein studies in combination with growth-determination experiments indicated that the antisense methylphosphonate Bcr-Abl oligonucleotide tested is a potent inhibitor of the growth of CML cells but works in a non-antisense manner.	Oligonucleotides	132-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
8978305-1	1997	CRKL has previously been shown to be a major tyrosine phosphorylated protein in neutrophils of patients with BCR-ABL+ chronic myelogenous leukemia and in cell lines expressing BCR-ABL CRKL and BCR-ABL form a complex as demonstrated by coimmunoprecipitation and are capable of a direct interaction in a yeast two-hybrid assay.	Tyrosine	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
8978305-2	1997	We have mapped the site of interaction of CRKL and BCR-ABL to the amino terminal SH3 domain of CRKL with a proline rich region in the C-terminus of ABL.	Proline	107-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
8978305-2	1997	We have mapped the site of interaction of CRKL and BCR-ABL to the amino terminal SH3 domain of CRKL with a proline rich region in the C-terminus of ABL.	Proline	107-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-58
8978305-3	1997	The proline-rich region was mutated and the effect of this deletion on BCR-ABL transforming function was assayed.	Proline	4-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
8978305-5	1997	In cells expressing the proline deletion mutation of BCR-ABL, CRKL is still tyrosine phosphorylated and forms a complex with BCR-ABL as demonstrated by coimmunoprecipitation.	Proline	24-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
8978305-5	1997	In cells expressing the proline deletion mutation of BCR-ABL, CRKL is still tyrosine phosphorylated and forms a complex with BCR-ABL as demonstrated by coimmunoprecipitation.	Proline	24-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
8978305-5	1997	In cells expressing the proline deletion mutation of BCR-ABL, CRKL is still tyrosine phosphorylated and forms a complex with BCR-ABL as demonstrated by coimmunoprecipitation.	Tyrosine	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
9007460-6	1997	O2 values were determined by three methods: (1) a polarographic electrode, ABL-300 (ABL); (2) a spectrophotometric method, Co-Oximeter (COOX); and (3) a galvanic cell, Lex-O2-Con (LEX).	Oxygen	0-2	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
9007460-6	1997	O2 values were determined by three methods: (1) a polarographic electrode, ABL-300 (ABL); (2) a spectrophotometric method, Co-Oximeter (COOX); and (3) a galvanic cell, Lex-O2-Con (LEX).	Oxygen	0-2	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-78
9000132-3	1996	One mechanism by which BCR-ABL signals in cells is by activating the small guanine nucleotide binding protein Ras.	Guanine Nucleotides	75-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
9000132-4	1996	BCR-ABL-transformed cells have constitutively high levels of active, GTP-bound Ras.	Guanosine Triphosphate	69-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
8998181-2	1997	Selective eradication of these cells in vitro can be achieved by combined treatment with antisense phosphorothioate oligodeoxynucleotides ([S]ODNs) specifically targeted to this oncogene (bcr/abl [S]ODNs) and a suboptimal (for use as a single agent) dose of mafosfamide (the in vitro active form of cyclophosphamide).	phosphorothioate oligodeoxynucleotides	99-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	192-195
8998181-12	1997	In addition, cellular uptake of bcr/abl antisense [S]ODNs appeared to be increased twofold to sixfold by prior treatment with mafosfamide.	mafosfamide	126-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-39
8995449-9	1997	SHP-2 was co-immunoprecipitated with phosphatidylinositol 3-kinase in BCR/ABL p210-transformed cells; however, this interaction was not observed in the tetramerization domain-deleted BCR-ABL mutant.	Phosphatidylinositols	37-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-77
9381983-3	1997	Aristeromycin isolated as an Abl function inhibitor induced erythroid differentiation in human CML K562 cells.	aristeromycin	0-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-32
8978305-6	1997	Our data suggest that the interaction between CRKL and the proline deletion mutant of BCR-ABL is an indirect interaction as CRKL does not interact directly with the proline deletion mutant of BCR-ABL in a gel overlay assay or in a yeast two-hybrid assay.	Proline	59-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
8978305-6	1997	Our data suggest that the interaction between CRKL and the proline deletion mutant of BCR-ABL is an indirect interaction as CRKL does not interact directly with the proline deletion mutant of BCR-ABL in a gel overlay assay or in a yeast two-hybrid assay.	Proline	165-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
8912843-3	1996	We report here that a deleted form of Bcr [Bcr(64-413)], encompassing the Abl SH2 binding domains of Bcr, reduced the phosphotyrosine content of c-Abl and Bcr-Abl within cells and inhibited Bcr-Abl autophosphorylation activity in vitro.	Phosphotyrosine	118-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-150
8912843-4	1996	Similarly, a Bcr peptide phosphorylated on Ser-354 blocked the c-Abl and Bcr-Abl kinases in vitro, whereas the same peptide phosphorylated on Tyr-360 was not inhibitory.	Serine	43-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-68
8912843-4	1996	Similarly, a Bcr peptide phosphorylated on Ser-354 blocked the c-Abl and Bcr-Abl kinases in vitro, whereas the same peptide phosphorylated on Tyr-360 was not inhibitory.	Serine	43-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
8912843-5	1996	Bcr(64-413) was also resistant to tyrosine phosphorylation by either activated c-Abl or Bcr-Abl.	Tyrosine	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-84
8912843-5	1996	Bcr(64-413) was also resistant to tyrosine phosphorylation by either activated c-Abl or Bcr-Abl.	Tyrosine	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
8912843-7	1996	Our findings indicate that the Abl SH2 binding domain of Bcr in the phosphoserine form inhibits the Bcr-Abl oncoprotein but that tyrosine phosphorylation of this domain of Bcr reverses its inhibitory effects on Bcr-Abl.	Phosphoserine	68-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-34
8912843-7	1996	Our findings indicate that the Abl SH2 binding domain of Bcr in the phosphoserine form inhibits the Bcr-Abl oncoprotein but that tyrosine phosphorylation of this domain of Bcr reverses its inhibitory effects on Bcr-Abl.	Phosphoserine	68-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
8900110-2	1996	The present studies demonstrate that the antimetabolite 1-beta-D-arabinofuranosylcytosine (ara-C) induces binding of c-Abl and p53.	antimetabolite 1-beta-d-arabinofuranosylcytosine	41-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-122
8900110-2	1996	The present studies demonstrate that the antimetabolite 1-beta-D-arabinofuranosylcytosine (ara-C) induces binding of c-Abl and p53.	Cytarabine	91-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-122
8900110-3	1996	Ara-C treatment of cells that express wild type or a dominant negative, kinase-inactive c-Abl(K-R) was associated with formation of c-Abl-p53 complexes and increased expression of the cyclin-dependent kinase (Cdk) inhibitor p21.	Cytarabine	0-5	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-93
8900110-3	1996	Ara-C treatment of cells that express wild type or a dominant negative, kinase-inactive c-Abl(K-R) was associated with formation of c-Abl-p53 complexes and increased expression of the cyclin-dependent kinase (Cdk) inhibitor p21.	Cytarabine	0-5	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-137
8900110-3	1996	Ara-C treatment of cells that express wild type or a dominant negative, kinase-inactive c-Abl(K-R) was associated with formation of c-Abl-p53 complexes and increased expression of the cyclin-dependent kinase (Cdk) inhibitor p21.	Krypton	94-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-93
8900110-3	1996	Ara-C treatment of cells that express wild type or a dominant negative, kinase-inactive c-Abl(K-R) was associated with formation of c-Abl-p53 complexes and increased expression of the cyclin-dependent kinase (Cdk) inhibitor p21.	Krypton	94-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-137
8900110-4	1996	However, down-regulation of Cdk2 by ara-C was found in cells expressing wild type c-Abl and not in cells expressing c-Abl(K-R) or those deficient in p53.	Cytarabine	36-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-87
8900110-6	1996	Cells that express the c-Abl dominant negative or are null for c-Abl exhibited partial abrogation of Cdk2 down-regulation and G1 arrest in response to MMS exposure.	Methyl Methanesulfonate	151-154	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-28
8900110-6	1996	Cells that express the c-Abl dominant negative or are null for c-Abl exhibited partial abrogation of Cdk2 down-regulation and G1 arrest in response to MMS exposure.	Methyl Methanesulfonate	151-154	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-68
8900110-7	1996	Cells lacking the c-abl gene also responded to ara-C and MMS with increases in p53 levels and induction of p21.	Cytarabine	47-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-23
8900110-7	1996	Cells lacking the c-abl gene also responded to ara-C and MMS with increases in p53 levels and induction of p21.	Methyl Methanesulfonate	57-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-23
8874208-0	1996	Selection of myeloid progenitors lacking BCR/ABL mRNA in chronic myelogenous leukemia patients after in vitro treatment with the tyrosine kinase inhibitor genistein.	Genistein	155-164	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
8810278-2	1996	In primary samples from virtually all patients with CML or Ph+ALL, the CRKL adapter protein is tyrosine phosphorylated and physically associated with p210(BCR/ABL).	Tyrosine	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-162
8810278-4	1996	We have previously shown that CRKL, but not the related adapter protein c-CRK, is tyrosine phosphorylated in cell lines transformed by BCR/ABL, and that CRKL binds to BCR/ABL through the CRKL-SH3 domains.	Tyrosine	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
8810278-4	1996	We have previously shown that CRKL, but not the related adapter protein c-CRK, is tyrosine phosphorylated in cell lines transformed by BCR/ABL, and that CRKL binds to BCR/ABL through the CRKL-SH3 domains.	Tyrosine	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-174
8810278-11	1996	These results suggest that the BCR/ABL oncogene could alter the function of p130(CAS) in at least three ways: tyrosine phosphorylation, inducing constitutive binding of CRKL to a domain in p130(CAS) containing Tyr-X-X-Pro motifs (substrate domain), and disrupting the normal interaction of p130(CAS) with the focal adhesion protein tensin.	Tyrosine	110-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
8810278-11	1996	These results suggest that the BCR/ABL oncogene could alter the function of p130(CAS) in at least three ways: tyrosine phosphorylation, inducing constitutive binding of CRKL to a domain in p130(CAS) containing Tyr-X-X-Pro motifs (substrate domain), and disrupting the normal interaction of p130(CAS) with the focal adhesion protein tensin.	tyr-x-x-pro	210-221	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
8875988-6	1996	RB and v-Abl were found to physically associate in vivo and in vitro via v-Abl"s ATP binding region.	Adenosine Triphosphate	81-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	7-12
8875988-6	1996	RB and v-Abl were found to physically associate in vivo and in vitro via v-Abl"s ATP binding region.	Adenosine Triphosphate	81-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-78
8798604-4	1996	We also demonstrate that cells deficient in c-Abl fail to activate p38 MAP kinase after treatment with cisplatinum and 1-beta-D-arabinofuranosylcytosine but not after exposure to UV and methyl methanesulfonate.	Cisplatin	103-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-49
8798604-4	1996	We also demonstrate that cells deficient in c-Abl fail to activate p38 MAP kinase after treatment with cisplatinum and 1-beta-D-arabinofuranosylcytosine but not after exposure to UV and methyl methanesulfonate.	Cytarabine	119-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-49
8667652-13	1996	We analyzed the response to the prednisone pretreatment and found a higher incidence of poor responders among the BCR/ABL-positive children.	Prednisone	32-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-121
8798460-3	1996	Instead, oligonucleotides with runs of A/T sequences were isolated, and purified c-Abl was shown to bind A/T-containing oligonucleotides better than those without A/T sequences.	Oligonucleotides	9-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-86
8798460-3	1996	Instead, oligonucleotides with runs of A/T sequences were isolated, and purified c-Abl was shown to bind A/T-containing oligonucleotides better than those without A/T sequences.	Oligonucleotides	120-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-86
8798460-4	1996	DNA binding of c-Abl was dependent on three high mobility group 1-like boxes (HLBs), which bound cooperatively to the A/T-rich oligonucleotides.	Oligonucleotides	127-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-20
8798460-9	1996	Interestingly, the HLBs of c-Abl bound better to the oligonucleotide containing the bubble, suggesting a higher affinity for bent DNA rather than A/T sequences per se.	Oligonucleotides	53-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-32
8805596-5	1996	In general, the individual domains are very similar to those of previously solved structures, although the Abl SH2 domain contains a loop which is extended so that one side of the resulting phosphotyrosine-binding pocket is open.	Phosphotyrosine	190-205	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-110
8702917-3	1996	Furthermore, this proline-rich insert was found to modify the efficiency with which Crk-II was phosphorylated by the p140(c-abl) tyrosine kinase.	Proline	18-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-127
8692915-3	1996	Treatment with ionizing radiation is associated with c-Abl-dependent tyrosine phosphorylation of SHPTP1.	Tyrosine	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-58
8700546-8	1996	In addition, Arg, like c-Abl, is expressed as myristoylated and nonmyristoylated isoforms, suggesting that it may have dual cytoplasmic subcellular localizations, and possibly participate in diverse signaling pathways.	Arginine	13-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-28
8757502-8	1996	32Dkit cells transfected with bcr/abl containing an inactivating point mutation (Lys-->Arg271) in the Abl kinase domain (32Dp210(Arg271)kit) retained their responsiveness to the effects of rhSF.	Lysine	81-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
8757502-8	1996	32Dkit cells transfected with bcr/abl containing an inactivating point mutation (Lys-->Arg271) in the Abl kinase domain (32Dp210(Arg271)kit) retained their responsiveness to the effects of rhSF.	Lysine	81-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-108
8974789-9	1996	The resistance of malignant cells to apoptosis, in Chronic Myeloid Leukemia, due to bcr-abl oncogene, has been partially explained by conformational changes in p53 expression and is reversed by retinoic acid.	Tretinoin	194-207	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
8668148-7	1996	Finally, we demonstrate that as with p130cas, transformation with the oncogene v-abl results in an increase in tyrosine phosphorylation on HEF1, mediated by a direct association between HEF1 and v-Abl.	Tyrosine	111-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-84
8668148-7	1996	Finally, we demonstrate that as with p130cas, transformation with the oncogene v-abl results in an increase in tyrosine phosphorylation on HEF1, mediated by a direct association between HEF1 and v-Abl.	Tyrosine	111-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	195-200
8668151-8	1996	Transient overexpression of c-Abl also led to a four- to fivefold increase in the phosphotyrosine content of the RNAP II large subunit.	Phosphotyrosine	82-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-33
8668151-10	1996	Tyrosine phosphorylation of the coprecipitated RNAP II was again dependent on the presence of the CTD-ID in Abl.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-111
8663064-6	1996	In Rat1 cells expressing GST/Bcr-Abl-(Delta1-160), phosphotyrosine contents of p62 and Shc were 70% decreased.	Phosphotyrosine	51-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
8709619-3	1996	We have studied the mechanism of action of bcr-abl in chronic myeloid leukemia (CML) by inhibiting its expression using antisense oligonucleotides.	Oligonucleotides	130-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
8640770-1	1996	ABL 364 is a murine monoclonal IgG3 antibody directed against the Lewis Y carbohydrate antigen (Le(y)) expressed on the surface of many epithelial cell tumors.	Carbohydrates	74-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
8649049-4	1996	The role and contribution of apoptosis in the progression of CML and the possible role of antisense oligonucleotides to the bcr-abl gene as therapeutic agents is discussed.	Oligonucleotides	100-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
8702216-0	1996	BCR/ABL modulates the cytokine and retinoic acid response of c-Rel in human myeloid cells.	retinoic	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
8683981-1	1996	Acyclovir (ACV), a nucleoside analog, has been demonstrated previously to suppress selectively the proliferation of NIH3T3 fibroblastic cells transformed by either v-abl or bcr-abl gene transfection.	Acyclovir	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	173-180
8683981-1	1996	Acyclovir (ACV), a nucleoside analog, has been demonstrated previously to suppress selectively the proliferation of NIH3T3 fibroblastic cells transformed by either v-abl or bcr-abl gene transfection.	Acyclovir	11-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	173-180
8626527-10	1996	In contrast, Ser-807/811 phosphorylation is required to disrupt c-Abl binding.	Serine	13-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-69
8612582-5	1996	Nuclear localization of Abl can be directed by a pentalysine nuclear localization signal in the Abl C-terminus.	pentalysine	49-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-27
8612582-5	1996	Nuclear localization of Abl can be directed by a pentalysine nuclear localization signal in the Abl C-terminus.	pentalysine	49-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-99
8612582-6	1996	Here, we have identified two additional basic motifs in the Abl C-terminus, either of which can function independently of the pentalysine signal to localize Abl to the nucleus.	pentalysine	126-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-63
8612582-6	1996	Here, we have identified two additional basic motifs in the Abl C-terminus, either of which can function independently of the pentalysine signal to localize Abl to the nucleus.	pentalysine	126-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-160
8612582-9	1996	These results indicate that Abl inhibits cell proliferation by interacting with central elements of the cell cycle control apparatus in the nucleus, and suggest a direct connection between p53 and Rb in this growth-inhibitory pathway.	Rubidium	197-199	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-31
8637883-0	1996	p140/c-Abl that binds DNA is preferentially phosphorylated at tyrosine residues.	Tyrosine	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	5-10
8637883-4	1996	Furthermore, by 32P labeling of cells and protein purification, we demonstrate that in vivo the EP-DNA-associated p140/c-Abl is a tyrosine phosphoprotein.	Phosphorus-32	16-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-124
8637883-6	1996	p140/c-Abl is quantitatively the minor population, is heavily phosphorylated at both serine and tyrosine residues, and is active in autophosphorylation reactions.	Serine	85-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	5-10
8637883-6	1996	p140/c-Abl is quantitatively the minor population, is heavily phosphorylated at both serine and tyrosine residues, and is active in autophosphorylation reactions.	Tyrosine	96-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	5-10
8617726-0	1996	In vivo association of v-Abl with Shc mediated by a non-phosphotyrosine-dependent SH2 interaction.	Phosphotyrosine	56-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-28
8617726-4	1996	Surprisingly, a kinase-defective mutant of P120 also binds Shc, demonstrating that Shc/v-Abl association is a phosphotyrosine-independent interaction.	Phosphotyrosine	110-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-92
8617726-6	1996	Consistent with these data, a v-Abl mutant encoding only the Gag and SH2 regions was able to bind Shc in vivo.	Glycosaminoglycans	61-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-35
8617726-7	1996	The unique non-phosphotyrosine-mediated binding of Shc may allow direct tyrosine phosphorylation of Shc by v-Abl and subsequent activation of the Ras pathway through assembly of a signaling complex with Grb2-mSos.	Phosphotyrosine	15-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-112
8617726-7	1996	The unique non-phosphotyrosine-mediated binding of Shc may allow direct tyrosine phosphorylation of Shc by v-Abl and subsequent activation of the Ras pathway through assembly of a signaling complex with Grb2-mSos.	Tyrosine	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-112
8604027-3	1996	Aggregation of Fc epsilon RI by IgE and anti-IgE, IgE and antigen, or anti-Fc epsilon RI monoclonal antibodies on ABL cells or on HBMB, led to increased tyrosine phosphorylation of 120-, 100-, 80-, 72-, 50- to 65-, and 38-kDa substrates.	Tyrosine	153-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-117
8642285-0	1996	Tyrosyl phosphorylation and DNA binding activity of signal transducers and activators of transcription (STAT) proteins in hematopoietic cell lines transformed by Bcr/Abl.	cyclo(tyrosyl-tyrosyl)	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-169
8604027-6	1996	Stimulation of ABL cells for 1 min resulted in extracellular calcium-independent tyrosine phosphorylation and activation of p72syk.	Calcium	61-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-18
8604027-6	1996	Stimulation of ABL cells for 1 min resulted in extracellular calcium-independent tyrosine phosphorylation and activation of p72syk.	Tyrosine	81-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-18
8622703-3	1996	We have previously demonstrated that the Bcr protein is tyrosine phosphorylated within first-exon sequences by the Bcr-Abl oncoprotein.	Tyrosine	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
8907275-1	1996	We have previously demonstrated that liposome-incorporated methylphosphonate antisense oligodeoxynucleotides (oligos) specific for BCR-ABL can selectively inhibit the expression of p210Bcr-Abl protein and the proliferation of chronic myelogenous leukemia cells in vitro.	methylphosphonic acid	59-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
8907275-1	1996	We have previously demonstrated that liposome-incorporated methylphosphonate antisense oligodeoxynucleotides (oligos) specific for BCR-ABL can selectively inhibit the expression of p210Bcr-Abl protein and the proliferation of chronic myelogenous leukemia cells in vitro.	Oligodeoxyribonucleotides	87-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
8907275-2	1996	Here, we show that liposome-entrapment of phosphodiester and phosphorothioate oligos specific for BCR-ABL can also selectively inhibit the proliferation of chronic myelogenous leukemia cells.	Parathion	61-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
8622703-4	1996	Here we report that in addition to tyrose 177 (Y-177), Y-360 and Y283 are phosphorylated in Bcr-Abl proteins in vitro.	tyrose	35-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
8622703-5	1996	Moreover, Bcr tyrosine 360 is phosphorylated in vivo within both Bcr-Abl and Bcr.	Tyrosine	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
8622703-8	1996	Tyrosine-phosphorylated Bcr, phosphorylated in vitro by Bcr-Abl, was greatly inhibited in its serine/threonine kinase activity, impairing both auto- and transkinase activities of Bcr.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
8622703-9	1996	Similarly, the isolation of Bcr from cells expressing Bcr-Abl under conditions that preserve phosphotyrosine residues also reduced Bcr"s kinase activity.	Phosphotyrosine	93-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-61
8632906-2	1996	When introduced into factor dependent hematopoietic cell lines, BCR/ABL induces the tyrosine phosphorylation of many cellular proteins.	Tyrosine	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
8597610-1	1996	Uptake and biochemical and biological effects of antisense oligodeoxynucleotides (ODN) specific for c-abl and bcr genes were studied in normal immature myeloid cells.	Oligodeoxyribonucleotides	59-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-105
8597610-1	1996	Uptake and biochemical and biological effects of antisense oligodeoxynucleotides (ODN) specific for c-abl and bcr genes were studied in normal immature myeloid cells.	Oligodeoxyribonucleotides	82-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-105
8637720-0	1996	Analysis of chimeric Gag-Arg/Abl molecules indicates a distinct negative regulatory role for the Arg C-terminal domain.	Arginine	97-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-32
8637720-5	1996	(1) The analysis of chimeric Gag-Arg/Abl molecules revealed that the Arg C-terminal domain completely abrogated Gag-Abl transforming activity and that the Abl C-terminus conferred transforming activity to Gag-Arg.	Arginine	69-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-40
8637720-5	1996	(1) The analysis of chimeric Gag-Arg/Abl molecules revealed that the Arg C-terminal domain completely abrogated Gag-Abl transforming activity and that the Abl C-terminus conferred transforming activity to Gag-Arg.	Arginine	69-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-119
8637720-5	1996	(1) The analysis of chimeric Gag-Arg/Abl molecules revealed that the Arg C-terminal domain completely abrogated Gag-Abl transforming activity and that the Abl C-terminus conferred transforming activity to Gag-Arg.	Arginine	69-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-119
8637720-5	1996	(1) The analysis of chimeric Gag-Arg/Abl molecules revealed that the Arg C-terminal domain completely abrogated Gag-Abl transforming activity and that the Abl C-terminus conferred transforming activity to Gag-Arg.	Arginine	69-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-40
8637720-5	1996	(1) The analysis of chimeric Gag-Arg/Abl molecules revealed that the Arg C-terminal domain completely abrogated Gag-Abl transforming activity and that the Abl C-terminus conferred transforming activity to Gag-Arg.	Arginine	69-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-119
8637720-5	1996	(1) The analysis of chimeric Gag-Arg/Abl molecules revealed that the Arg C-terminal domain completely abrogated Gag-Abl transforming activity and that the Abl C-terminus conferred transforming activity to Gag-Arg.	Arginine	69-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-119
8805224-5	1996	RESULTS: A dominant-negative mutant of the small GTP-binding protein Rac (Rac N17, containing an asparagine residue at position 17) was found to block v-Abl-induced activation of two mitogenic enhancer elements.	Guanosine Triphosphate	49-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-156
8805224-5	1996	RESULTS: A dominant-negative mutant of the small GTP-binding protein Rac (Rac N17, containing an asparagine residue at position 17) was found to block v-Abl-induced activation of two mitogenic enhancer elements.	Asparagine	97-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-156
8590842-1	1995	Antisense oligonucleotides were used to determine the role of the BCR-ABL gene in the proliferation of chronic myeloid leukaemia (CML) clonogenic cells.	Oligonucleotides	10-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
8605566-7	1996	We therefore performed triple-colour fluorescence in situ hybridization (FISH) for portions of the bcr and abl genes flanking the breakpoint in CML in paraffin sections of CML cases with normal and with increased numbers of megakaryocytes.	Paraffin	151-159	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-110
8542929-9	1995	The level of BCR/ABL fusion signals detected after exposure of CD34+ cells for 16 hours to Eilatin 10(-7) M, IFN-alpha 500 U/mL, or Ara-C 10(-9) M were 54.5 +/- 5%, 63.6 +/- 5%, and 70 +/- 4%, respectively (mean +/- SE, n = 5).	eilatine	91-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
8542929-9	1995	The level of BCR/ABL fusion signals detected after exposure of CD34+ cells for 16 hours to Eilatin 10(-7) M, IFN-alpha 500 U/mL, or Ara-C 10(-9) M were 54.5 +/- 5%, 63.6 +/- 5%, and 70 +/- 4%, respectively (mean +/- SE, n = 5).	Cytarabine	132-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
8542939-0	1995	5-Fluorouracil-resistant CD34+ cell population from peripheral blood of CML patients contains BCR-ABL-negative progenitor cells.	Fluorouracil	0-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
8542939-8	1995	5-FU pretreatment of CML CD34+ cells markedly reduced their clonogenic potential and growth factor-mediated cell proliferation but favored higher frequency of BCR-ABL-free colonies.	Fluorouracil	0-4	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-166
8542954-0	1995	Inhibition of chronic myelogenous leukemia cells harboring a BCR-ABL B3A2 junction by antisense oligonucleotides targeted at the B2A2 junction.	Oligonucleotides	96-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
8542954-3	1995	As the BCR-ABL rearrangement is specific to leukemic cells, selective inhibition of leukemic cell growth by BCR-ABL antisense oligonucleotides (ASO) has been reported in vitro for CML patients and cell lines.	Oligonucleotides	126-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	7-14
8542954-3	1995	As the BCR-ABL rearrangement is specific to leukemic cells, selective inhibition of leukemic cell growth by BCR-ABL antisense oligonucleotides (ASO) has been reported in vitro for CML patients and cell lines.	Oligonucleotides	126-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
8542954-3	1995	As the BCR-ABL rearrangement is specific to leukemic cells, selective inhibition of leukemic cell growth by BCR-ABL antisense oligonucleotides (ASO) has been reported in vitro for CML patients and cell lines.	Oligonucleotides, Antisense	144-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	7-14
8542954-3	1995	As the BCR-ABL rearrangement is specific to leukemic cells, selective inhibition of leukemic cell growth by BCR-ABL antisense oligonucleotides (ASO) has been reported in vitro for CML patients and cell lines.	Oligonucleotides, Antisense	144-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
8524249-9	1995	This finding suggests that in Abl-transformed cells, more than one class of tyrosine-phosphorylated sites (those that bind the Grb2 SH2 domain and those that bind the Crk SH2 domain) can lead to Ras activation.	Tyrosine	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-33
7579358-0	1995	BCR-ABL antisense oligodeoxyribonucleotides suppress the growth of leukemic and normal hematopoietic cells by a sequence-specific but nonantisense mechanism.	Oligodeoxyribonucleotides	18-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
7592951-4	1995	However, c-Src and v-Abl are extremely inefficient as catalysts for certain structural arrangements, including secondary alcohols and primary alcohols containing large substituents in close proximity to the hydroxyl moiety.	Alcohols	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-24
7592951-4	1995	However, c-Src and v-Abl are extremely inefficient as catalysts for certain structural arrangements, including secondary alcohols and primary alcohols containing large substituents in close proximity to the hydroxyl moiety.	Alcohols	142-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-24
7579442-0	1995	Oligodeoxynucleotides antisense to c-abl specifically inhibit entry into S-phase of CD34+ hematopoietic cells and their differentiation to granulocyte-macrophage progenitors.	Oligodeoxyribonucleotides	0-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-40
7579442-8	1995	Exposure to antisense oligonucleotides specifically inhibited the accumulation of c-abl mRNA in CD34+ cells.	Oligonucleotides	22-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-87
7590236-4	1995	Abi-2 is a novel protein that contains an SH3 domain and proline-rich sequences critical for binding to c-Abl.	Proline	57-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-109
7595224-6	1995	We also report that, under conditions in which the morphological features of apoptosis were prevented (macromolecular synthesis inhibition, overexpression of Bcl-2 or Abl), the appearance of PS on the external leaflet of the PM was similarly prevented.	Phosphatidylserines	191-193	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-170
8524328-8	1996	In NIH 3T3 cells transformed by Bcr-Abl, c-Cbl becomes strongly tyrosine phosphorylated and associates with c-Crk.	Tyrosine	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
8524328-10	1996	These results indicate that Crk binds to c-Cbl in a tyrosine phosphorylation-dependent manner, suggesting a physiological role for the Crk-c-Cbl complex in Bcr-Abl tyrosine phosphorylation-mediated transformation.	Tyrosine	52-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
8524328-10	1996	These results indicate that Crk binds to c-Cbl in a tyrosine phosphorylation-dependent manner, suggesting a physiological role for the Crk-c-Cbl complex in Bcr-Abl tyrosine phosphorylation-mediated transformation.	Tyrosine	164-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
8530447-0	1995	c-Abl activation regulates induction of the SEK1/stress-activated protein kinase pathway in the cellular response to 1-beta-D-arabinofuranosylcytosine.	Cytarabine	117-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
8530447-2	1995	The present studies demonstrate that ara-C activates the c-Abl non-receptor tyrosine kinase.	Cytarabine	37-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-62
8530447-4	1995	Using cells deficient in c-Abl (Abl-/-) and after introduction of the c-abl gene, we show that ara-C-induced c-Abl activity is necessary for the stimulation of SAP kinase.	Cytarabine	95-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-30
8530447-4	1995	Using cells deficient in c-Abl (Abl-/-) and after introduction of the c-abl gene, we show that ara-C-induced c-Abl activity is necessary for the stimulation of SAP kinase.	Cytarabine	95-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-30
8530447-4	1995	Using cells deficient in c-Abl (Abl-/-) and after introduction of the c-abl gene, we show that ara-C-induced c-Abl activity is necessary for the stimulation of SAP kinase.	Cytarabine	95-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-75
8530447-4	1995	Using cells deficient in c-Abl (Abl-/-) and after introduction of the c-abl gene, we show that ara-C-induced c-Abl activity is necessary for the stimulation of SAP kinase.	Cytarabine	95-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-114
7478571-1	1995	The SH2/SH3 adaptor protein Crkl is abnormally phosphorylated on tyrosine by the Bcr/Abl protein in leukemic cells from patients with Philadelphia-chromosome (Ph)positive leukemia.	Tyrosine	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
7565761-0	1995	Nuclear localization of v-Abl leads to complex formation with cyclic AMP response element (CRE)-binding protein and transactivation through CRE motifs.	Cyclic AMP	62-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-29
7565761-2	1995	These studies identify the localization of the oncogenic form of the abl gene product encoded by the Abelson murine leukemia virus in the nuclei of myeloid cells and the association of the v-Abl protein with the transcriptional regulator cyclic AMP response element-binding protein (CREB).	Cyclic AMP	238-248	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-72
7565761-2	1995	These studies identify the localization of the oncogenic form of the abl gene product encoded by the Abelson murine leukemia virus in the nuclei of myeloid cells and the association of the v-Abl protein with the transcriptional regulator cyclic AMP response element-binding protein (CREB).	Cyclic AMP	238-248	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	189-194
8590002-8	1995	The structure of the Abl SH(32) dual domain was characterized by NMR spectroscopy using the 1H and 15N resonance assignment of Abl SH3 and Abl SH2.	Hydrogen	92-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-24
8590002-8	1995	The structure of the Abl SH(32) dual domain was characterized by NMR spectroscopy using the 1H and 15N resonance assignment of Abl SH3 and Abl SH2.	15n	99-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-24
8590002-8	1995	The structure of the Abl SH(32) dual domain was characterized by NMR spectroscopy using the 1H and 15N resonance assignment of Abl SH3 and Abl SH2.	15n	99-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-130
8590002-8	1995	The structure of the Abl SH(32) dual domain was characterized by NMR spectroscopy using the 1H and 15N resonance assignment of Abl SH3 and Abl SH2.	15n	99-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-130
8590002-9	1995	On the basis of the high degree of similarity in chemical shifts and hydrogen/deuterium exchange pattern for the individual domains of SH3 and SH2 compared with those of the SH(32) dual domain, a structural model of the Abl SH(32) regulatory apparatus is suggested.	Deuterium	78-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	220-223
8535209-3	1995	Short oligodeoxynucleotide (ODN) sequences complementary (or antisense) to the bcr-abl junction may have potential as leukaemia-specific therapy.	Oligodeoxyribonucleotides	6-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
7493914-4	1995	In contrast, a biphasic change of p210bcr/abl and the abl-associated kinase activities was observed upon treatment with 5-FU.	Fluorouracil	120-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-45
7493914-4	1995	In contrast, a biphasic change of p210bcr/abl and the abl-associated kinase activities was observed upon treatment with 5-FU.	Fluorouracil	120-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-57
8535209-4	1995	However, the studies on ODN targeting bcr-abl reported so far have used ODN linked by either phosphodiester or phosphorothionate linkages.	phosphorothiolate	111-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
8535209-6	1995	In contrast, ODN linked by a mixture of methylphosphonate and conventional linkages can mediate cleavage of bcr-abl mRNA target in a sequence-specific fashion, unlike conventionally linked ODN.	methylphosphonic acid	40-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
7565714-6	1995	Moreover, substitution of Asp for Thr-98 in Abl SH3 changed the binding specificity of this domain and conferred the ability to recognize Arg-containing ligands.	Arginine	138-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-47
7565706-4	1995	RB binds to the ATP-binding lobe in the kinase domain and inhibits the nuclear pool of c-Abl in quiescent and G1 cells.	Adenosine Triphosphate	16-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-92
7545682-11	1995	Since Abl was also found to block apoptosis mediated by ceramide, a recently proposed downstream effector of the apoptotic pathway initiated by Fas, we propose that Abl exerts its protective effects downstream of the early Fas-initiated signaling events.	Ceramides	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-9
7565706-6	1995	In this report, we describe the construction of a mutant Abl, replacing the ATP-binding lobe of c-Abl with that of c-Src.	Adenosine Triphosphate	76-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-60
7565706-6	1995	In this report, we describe the construction of a mutant Abl, replacing the ATP-binding lobe of c-Abl with that of c-Src.	Adenosine Triphosphate	76-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-101
7545682-7	1995	However, down-regulation of Bcr-Abl protein levels in K562.Fas cells using antisense oligonucleotides targeted to bcr-abl mRNA rendered these cells highly susceptible to Fas-induced death.	Oligonucleotides	85-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
7545682-7	1995	However, down-regulation of Bcr-Abl protein levels in K562.Fas cells using antisense oligonucleotides targeted to bcr-abl mRNA rendered these cells highly susceptible to Fas-induced death.	Oligonucleotides	85-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
7545682-8	1995	In the second approach we utilized a Fas-positive HL-60 cell line, which we transfected with a temperature-sensitive mutant of v-Abl.	ammonium ferrous sulfate	37-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-132
7545682-9	1995	HL-60.v-Ablts transfectants were found to be protected from Fas-induced apoptosis at the permissive but not the restrictive temperature for the Abl kinase.	ammonium ferrous sulfate	60-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-11
7566975-0	1995	Increased tyrosine phosphorylation of focal adhesion proteins in myeloid cell lines expressing p210BCR/ABL.	Tyrosine	10-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-106
7566975-4	1995	In this study we examined tyrosine phosphorylation of focal adhesion proteins in cells expressing p210BCR/ABL.	Tyrosine	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-109
7556524-0	1995	Tyrosine phosphorylation and activation of focal adhesion kinase (p125FAK) by BCR-ABL oncoprotein.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
7556524-7	1995	FAK phosphorylation in BCR-ABL-expressing cells was inhibited in a dose-dependent manner by cytochalasin D, a reagent that disrupts the intracellular network of actin filaments.	Cytochalasin D	92-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
7545163-2	1995	Abnormally tyrosine-phosphorylated substrates of the Bcr/Abl kinase in Ph-positive cells are likely to contribute to leukemogenesis by interfering with normal signal transduction pathways.	Tyrosine	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-60
7545163-4	1995	In the current study, a tyrosine-phosphorylated protein with a molecular mass of approximately 120 kDa was identified which binds only to the Crkl Src homology 2 (SH2) domain in cells, including Ph-positive patient material, containing an active Bcr/Abl protein.	Tyrosine	24-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	246-253
7545682-11	1995	Since Abl was also found to block apoptosis mediated by ceramide, a recently proposed downstream effector of the apoptotic pathway initiated by Fas, we propose that Abl exerts its protective effects downstream of the early Fas-initiated signaling events.	Ceramides	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	165-168
9816051-9	1995	Following exposure of CD34(+) cells to norsegoline, dibezine, or IFN-alpha, BCR/ABL fusion signals could be detected in 73 +/- 11%, 66.5 +/- 4.	norsegoline	39-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
9816051-9	1995	Following exposure of CD34(+) cells to norsegoline, dibezine, or IFN-alpha, BCR/ABL fusion signals could be detected in 73 +/- 11%, 66.5 +/- 4.	dibezine	52-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
7606003-0	1995	Optimization of antisense oligodeoxynucleotide structure for targeting bcr-abl mRNA.	Oligodeoxyribonucleotides	26-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
8572618-1	1995	Anti-"benzo(a)pyrene [B(a)P]-like" IgA [referred as idiotypic antibodies (Abl)] from cancer patients" sera were found to react with conjugated B(a)P and a monoclonal anti-anti-conjugated B(a)P, internal image of conjugated B(a)P called AIB1 (referred to as Ab2 beta).	benzo	6-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-77
8572618-1	1995	Anti-"benzo(a)pyrene [B(a)P]-like" IgA [referred as idiotypic antibodies (Abl)] from cancer patients" sera were found to react with conjugated B(a)P and a monoclonal anti-anti-conjugated B(a)P, internal image of conjugated B(a)P called AIB1 (referred to as Ab2 beta).	(a)pyrene	11-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-77
7606003-1	1995	Antisense oligodeoxynucleotides targeted to bcr-abl are potential ex vivo purging agents for use with autologous bone marrow transplantation in the treatment of chronic myeloid leukemia (CML).	Oligodeoxyribonucleotides	10-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
7601569-0	1995	Sequence specificity on the growth suppression and induction of apoptosis of chronic myeloid leukemia cells by BCR-ABL anti-sense oligodeoxynucleoside phosphorothioates.	oligodeoxynucleoside phosphorothioates	130-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
7534303-3	1995	Both IL-3 and v-Abl stimulated the tyrosine phosphorylation of SHC and GTPase-activating protein.	Tyrosine	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
7593300-2	1995	Cellular signalling events associated with the activation of v-ABL included increased levels of sn-1,2-diacylglycerol, an activator of protein kinase C. Calphostin C, a PKC inhibitor, restored apoptosis to interleukin-3-deprived IC.DP cells expressing active v-ABL.	sn-1,2-diacylglycerol	96-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-66
7593300-2	1995	Cellular signalling events associated with the activation of v-ABL included increased levels of sn-1,2-diacylglycerol, an activator of protein kinase C. Calphostin C, a PKC inhibitor, restored apoptosis to interleukin-3-deprived IC.DP cells expressing active v-ABL.	calphostin C	153-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-66
7593300-2	1995	Cellular signalling events associated with the activation of v-ABL included increased levels of sn-1,2-diacylglycerol, an activator of protein kinase C. Calphostin C, a PKC inhibitor, restored apoptosis to interleukin-3-deprived IC.DP cells expressing active v-ABL.	calphostin C	153-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	259-264
7593300-2	1995	Cellular signalling events associated with the activation of v-ABL included increased levels of sn-1,2-diacylglycerol, an activator of protein kinase C. Calphostin C, a PKC inhibitor, restored apoptosis to interleukin-3-deprived IC.DP cells expressing active v-ABL.	dp	232-234	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-66
8535187-5	1995	This resistance can be overcome with the use of appropriate antisense oligonucleotides to the bcr-abl gene.	Oligonucleotides	70-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
7596151-1	1995	In this paper we describe a patient with bcr/abl positive acute undifferentiated leukemia (AUL) derived from acquired sideroblastic anemia secondary to ifosphamide treatment given for the preceding non-Hodgkin lymphoma of the lung.	Ifosfamide	152-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
7596151-7	1995	These results may be direct evidence for the induction of the bcr/abl fusion gene by treatment with an alkylating agent (ifosphamide).	Ifosfamide	121-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
7857307-2	1995	Aristeromycin also induced erythroid differentiation in abl-expressing human chronic myelogenous leukaemia K562 cells.	aristeromycin	0-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-59
7535279-2	1995	We report that the ena protein contains proline-rich motifs and binds to Abl and Src SH3 domains, ena is also a substrate for the Abl kinase; tyrosine phosphorylation of ena is increased when it is coexpressed in cells with human or Drosophila Abl and endogenous ena tyrosine phosphorylation is reduced in Abl mutant animals.	Proline	40-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-76
7535279-2	1995	We report that the ena protein contains proline-rich motifs and binds to Abl and Src SH3 domains, ena is also a substrate for the Abl kinase; tyrosine phosphorylation of ena is increased when it is coexpressed in cells with human or Drosophila Abl and endogenous ena tyrosine phosphorylation is reduced in Abl mutant animals.	Tyrosine	142-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-76
7535279-2	1995	We report that the ena protein contains proline-rich motifs and binds to Abl and Src SH3 domains, ena is also a substrate for the Abl kinase; tyrosine phosphorylation of ena is increased when it is coexpressed in cells with human or Drosophila Abl and endogenous ena tyrosine phosphorylation is reduced in Abl mutant animals.	Tyrosine	267-275	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-76
7533294-0	1995	Src homology 2 domain as a specificity determinant in the c-Abl-mediated tyrosine phosphorylation of the RNA polymerase II carboxyl-terminal repeated domain.	Tyrosine	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-63
7533294-8	1995	The Abl SH2 domain binds the tyrosine-phosphorylated [Tyr(P)] CTD and is required for the processive and stoichiometric phosphorylation of the 52 tyrosines in the CTD.	Tyrosine	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
7533294-8	1995	The Abl SH2 domain binds the tyrosine-phosphorylated [Tyr(P)] CTD and is required for the processive and stoichiometric phosphorylation of the 52 tyrosines in the CTD.	Tyrosine	54-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
7533294-8	1995	The Abl SH2 domain binds the tyrosine-phosphorylated [Tyr(P)] CTD and is required for the processive and stoichiometric phosphorylation of the 52 tyrosines in the CTD.	Tyrosine	146-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
7533294-9	1995	Mutation of the Abl SH2 or exchanging it with that of Src, which does not bind the Tyr(P)-CTD, abolished processivity and reduced the CTD kinase activity without any effect on autophosphorylation or the phosphorylation of nonspecific substrates.	tyr(p)-ctd	83-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-19
7857307-6	1995	Thus, aristeromycin inhibits abl functions indirectly, possibly by inhibiting biological methylations.	aristeromycin	6-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-32
7530656-0	1995	Tyrosine phosphorylation of p95Vav in myeloid cells is regulated by GM-CSF, IL-3 and steel factor and is constitutively increased by p210BCR/ABL.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-144
7602427-6	1995	When this monoclonal antibody was conjugated with a ligand (e.g., biotin), we furthermore found that the enhancement could be suppressed by an antiligand antibody (AbL).	Biotin	66-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	164-167
7812014-0	1995	Specificity of BCR-ABL antisense oligonucleotides.	Oligonucleotides	33-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
7845006-0	1995	Phosphorothioate BCR-ABL antisense oligonucleotides induce cell death, but fail to reduce cellular bcr-abl protein levels.	Parathion	0-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
7845006-0	1995	Phosphorothioate BCR-ABL antisense oligonucleotides induce cell death, but fail to reduce cellular bcr-abl protein levels.	Oligonucleotides	35-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
7845006-5	1995	Phosphorothioate antisense BCR-ABL oligonucleotides were most stable, showed the highest uptake and induced cell death in BV173 but not in LAMA-84 cells.	Parathion	0-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
7988556-9	1994	We find that although the phage-displayed Abl and Src SH3 ligands are proline rich, they are distinct.	Proline	70-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-45
7923130-1	1994	Cells with a temperature-sensitive mutant of the v-abl oncoprotein (IC.DP) were treated with the anticancer drugs melphalan or hydroxyurea.	Melphalan	114-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-54
7808004-4	1994	The CML cell lines tested showed different sensitivities to inhibition of proliferation by AOs--lines with defective expression of the normal ABL protooncogene (e.g. BV173) were more readily inhibited than lines with a normal ABL message (e.g. K562).	D-(+)-ALLOSE	91-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-145
7808004-4	1994	The CML cell lines tested showed different sensitivities to inhibition of proliferation by AOs--lines with defective expression of the normal ABL protooncogene (e.g. BV173) were more readily inhibited than lines with a normal ABL message (e.g. K562).	D-(+)-ALLOSE	91-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	226-229
7773778-4	1994	The orientation of the bound peptide is opposite to that of proline-rich peptides bound to the SH3 domains of Abl, Fyn and p85.	Proline	60-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-113
7524758-9	1994	Our results suggest that pp39 CRKL in CML neutrophils may be stably tyrosine-phosphorylated by the BCR/ABL kinase at an early stage of myeloid differentiation when the ABL kinase is active.	Tyrosine	68-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-106
7939633-4	1994	Bap-1 is a substrate for the Bcr serine-threonine kinase and is also phosphorylated on tyrosine by Bcr-Abl but not by c-Abl.	Tyrosine	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
7537361-2	1995	P210 BCR/abl tyrosine kinase induces tyrosine phosphorylation of Shc, and activation of p21ras and PI 3-Kinase.	Tyrosine	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	5-12
7524739-11	1994	The direct implication of BCR-ABL was further documented (1) by studies of alpha-interferon-treated patients with a chimerism in which the abnormal growth correlates with the presence of the malignant clone and (2) by the use of antisense oligonucleotide against BCR-ABL transcript, which abrogated this abnormal growth.	Oligonucleotides	239-254	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
7923130-1	1994	Cells with a temperature-sensitive mutant of the v-abl oncoprotein (IC.DP) were treated with the anticancer drugs melphalan or hydroxyurea.	Hydroxyurea	127-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-54
8083188-5	1994	This same protein, as assessed by two-dimensional anti-phosphotyrosine immunoblotting, was also present in cell lines expressing p210bcr-abl, including K562 cells.	Phosphotyrosine	55-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-140
7521685-4	1994	Previous experiments have shown that CRKL is phosphorylated on tyrosine in the chronic myelogenous leukemia (CML) cell line K562 and that CRKL is a substrate for ABL and for BCR/ABL in COS-1 cells.	Tyrosine	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-165
7521685-4	1994	Previous experiments have shown that CRKL is phosphorylated on tyrosine in the chronic myelogenous leukemia (CML) cell line K562 and that CRKL is a substrate for ABL and for BCR/ABL in COS-1 cells.	Tyrosine	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-181
7521685-7	1994	In contrast, all BCR/ABL+ CML and acute lymphoblastic leukemia patient samples examined showed clear tyrosine-phosphorylation of CRKL.	Tyrosine	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
7917467-0	1994	Transformation, growth rate, and the heme biosynthetic pathway in V-abl-transfected fibroblasts.	Heme	37-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-71
8207957-0	1994	Capping of bcr-abl antisense oligonucleotides enhances antiproliferative activity against chronic myeloid leukemia cell lines.	Oligonucleotides	29-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-18
8207957-3	1994	We have found antisense phosphodiester oligonucleotides directed at the bcr-abl junction to be ineffective in inhibiting the growth of CML cell lines.	Oligonucleotides	39-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
8161775-5	1994	We found that BCR-ABL expression inappropriately prolongs the growth factor-independent survival of CML myeloid progenitors and granulocytes by inhibiting apoptosis, a genetically programmed process of active cell death; inhibition of BCR-ABL expression by antisense oligonucleotides reversed the suppression of apoptosis as well as the enhancement of survival.	Oligonucleotides	267-283	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
8153630-3	1994	Single point mutations in the Src-homology 2 (SH2) domain, the major tyrosine autophosphorylation site of the kinase domain, and the Grb-2 binding site in the Bcr region impaired the transformation of fibroblasts by Bcr-Abl.	Tyrosine	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	216-223
7926767-5	1994	When bound to Abl, Crk-I was phosphorylated on tyrosine.	Tyrosine	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-17
7926759-8	1994	Together these data demonstrate that the v-abl protein specifically interferes with light-chain gene rearrangement by suppressing at least two pathways essential for this stage of B-cell differentiation and suggest that tyrosine phosphorylation is important in regulating RAG gene expression.	Tyrosine	220-228	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-46
8125961-6	1994	Additional experiments have been carried out on the nonreceptor tyrosine kinase v-Abl using a peptide library based on the v-Src autophosphorylation site (Arg-Arg-Leu-Ile-Glu-Asp-Ala-Glu-Tyr-Ala-Ala-Arg-Gly).	Arginine	155-158	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-85
7520100-5	1994	The mean inhibitory concentration (IC50) of tiazofurin for cellular proliferation inhibition was 2.3-2.8-fold greater in cells expressing p210 bcr-abl than in their corresponding parent cells proliferating under the influence of growth factors or in growth factor-independent derivative cells not expressing detectable p210 bcr-abl.	tiazofurin	44-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-150
7520100-5	1994	The mean inhibitory concentration (IC50) of tiazofurin for cellular proliferation inhibition was 2.3-2.8-fold greater in cells expressing p210 bcr-abl than in their corresponding parent cells proliferating under the influence of growth factors or in growth factor-independent derivative cells not expressing detectable p210 bcr-abl.	tiazofurin	44-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	324-331
7520100-8	1994	In addition, an increase in the Km value for NAD utilization by IMPDH was observed in p210 bcr-abl transformed cells, but this increase was within the range of resident NAD concentrations observed in the cells.	NAD	45-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
7520100-8	1994	In addition, an increase in the Km value for NAD utilization by IMPDH was observed in p210 bcr-abl transformed cells, but this increase was within the range of resident NAD concentrations observed in the cells.	NAD	169-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
7520100-10	1994	Thus, regulation of IMPDH gene expression is mediated at least in part by the bcr-abl gene product and may therefore be indicative of a specific mechanism of intrinsic resistance to tiazofurin.	tiazofurin	182-192	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
7664083-2	1994	We have determined high-resolution crystal structures of the complexes between the SH3 domains of Abl and Fyn tyrosine kinases, and two ten-residue proline-rich peptides derived from the SH3-binding proteins 3BP-1 and 3BP-2.	Proline	148-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-101
8194526-2	1994	We have identified a kinase activity, which binds to the first Crk SH3 domain and phosphorylates c-Crk on tyrosine 221 (Y221), as c-Abl.	Tyrosine	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-135
8164650-7	1994	We demonstrate that SH2 domains from other proteins (Ras-GTPase-activating protein, Src, p85 phosphatidylinositol 3-kinase subunit, and Crk) can complement the absence of the Abl SH2 domain and that mutants with heterologous SH2 domains induce altered patterns of tyrosine-phosphorylated proteins in vivo.	Tyrosine	264-272	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-178
8118022-3	1994	Antisense oligodeoxynucleotides corresponding to the translation start of bcr downregulate bcr-abl protein in these cells and render them susceptible to induction of apoptosis by chemotherapeutic agents or serum deprivation.	Oligodeoxyribonucleotides	10-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
8118022-4	1994	Expression of a temperature sensitive v-Abl protein reverses the effects of the antisense oligonucleotides, such that the cells remain resistant to apoptosis at the permissive temperature.	Oligonucleotides	90-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-43
8139288-6	1994	The sensitivities of the Ph1-positive cell lines to herbimycin A derivatives were different from the data on the rat kidney cell line infected with Rous sarcoma virus (v-src) derived from a previous study, suggesting bcr/abl kinase may differ in sensitivity from other tyrosine kinases.	herbimycin	52-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	217-224
8119916-0	1994	p210Bcr/Abl and p160v-Abl induce an increase in the tyrosine phosphorylation of p93c-Fes.	Tyrosine	52-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-11
8063271-9	1994	Selective inhibition of this proto-oncogene and of the abl-bcr oncogene have been achieved by using of c-abl sequence specific antisense oligonucleotides; this approach sheds new light on the function of this gene in CML.	Oligonucleotides	137-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-58
8063271-9	1994	Selective inhibition of this proto-oncogene and of the abl-bcr oncogene have been achieved by using of c-abl sequence specific antisense oligonucleotides; this approach sheds new light on the function of this gene in CML.	Oligonucleotides	137-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-108
7508932-5	1994	A Shc-associated 140-kDa protein was identified, which was phosphorylated on tyrosine residues transiently after cytokine stimulation and constitutively after expression of p210BCR/ABL.	Tyrosine	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	173-184
8112292-8	1994	In vitro, the Grb2 SH2 domain bound Bcr-Abl through recognition of a tyrosine phosphorylation site within the amino-terminal bcr-encoded sequence (p.Tyr177-Val-Asn-Val), that is common to both Bcr-Abl proteins.	Tyrosine	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
8112292-8	1994	In vitro, the Grb2 SH2 domain bound Bcr-Abl through recognition of a tyrosine phosphorylation site within the amino-terminal bcr-encoded sequence (p.Tyr177-Val-Asn-Val), that is common to both Bcr-Abl proteins.	H-ASN-VAL-OH	160-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
7701917-2	1994	Specific inhibition of the BCR-ABL gene expression with antisense oligodeoxynucleotides has been shown to have profound effects on cell growth in vitro.	Oligodeoxyribonucleotides	66-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
7817711-1	1994	Determination of bcr-abl rearrangement in paraffin-embedded tumors using the polymerase chain reaction.	Paraffin	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
8119916-7	1994	v-abl expression was also found to increase the tyrosine phosphorylation of p93c-Fes.	Tyrosine	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
8026602-1	1994	Synthetic oligodeoxynucleotides (antisenses) complementary to bcr/abl breakpoint junction transcript on Philadelphia chromosome, or c-myb protooncogene inhibit partially the proliferation of Philadelphia positive leukemic cells (antisenses against bcr/abl and c-myb) and other tumor cells (antisenses against c-myb).	Oligodeoxyribonucleotides	10-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
8026602-1	1994	Synthetic oligodeoxynucleotides (antisenses) complementary to bcr/abl breakpoint junction transcript on Philadelphia chromosome, or c-myb protooncogene inhibit partially the proliferation of Philadelphia positive leukemic cells (antisenses against bcr/abl and c-myb) and other tumor cells (antisenses against c-myb).	Oligodeoxyribonucleotides	10-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	248-255
8289478-1	1994	BCR-ABL antisense oligonucleotides can specifically reduce colony formation of early hematopoietic progenitor cells from chronic myeloid leukemia (CML) patients.	Oligonucleotides	18-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
8289478-3	1994	We studied the inhibition of the bcr-abl oncogene using fluorescein-labeled phosphorothioate oligonucleotides in the Philadelphia chromosome-positive cell line BV173.	Fluorescein	56-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
8289478-3	1994	We studied the inhibition of the bcr-abl oncogene using fluorescein-labeled phosphorothioate oligonucleotides in the Philadelphia chromosome-positive cell line BV173.	Phosphorothioate Oligonucleotides	76-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
8289478-7	1994	We detected a decrease in bcr-abl mRNA after 3 days of treatment with antisense oligonucleotides, but much less in controls.	Oligonucleotides	80-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
8289486-3	1994	Different size products are generated from ela2 (p190) and b3a2 or b2a2 (p210) BCR-ABL transcripts which are readily and unambiguously distinguishable after agarose gel electrophoresis without the need for either nested PCR or hybridization.	Sepharose	157-164	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
8249463-2	1993	Individual character of co-tuning of Al, Hl, and Abl as well as the emotional state connected with adaptation of an animal were found to be reflected in the correlation of evoked activity of the structures.	Aluminum	37-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-52
8408645-9	1993	Similarly, a decrease in Bcr and Abl levels occurs in HL-60 cells induced by DMSO to undergo granulocytic differentiation.	Dimethyl Sulfoxide	77-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-36
8379683-2	1993	ErbB-1, erbB-2 and abl oncogenes encoding tyrosine kinases, ras oncogenes encoding GTP binding proteins and myc oncogenes whose functions are not well understood are some examples.	Guanosine Triphosphate	83-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-22
8243571-7	1993	Ethidium bromide fluorescence with NASBA indicated in repeated experiments that similar quantities of total RNA from patient material contained different amounts of BCR-ABL mRNA.	Ethidium	0-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	165-172
8145772-5	1993	This inhibitory activity copurifies with the IR on insulin-Sepharose affinity chromatography and is also effective against the tyrosine kinase activity of the IR-related insulin-like growth factor-I receptor and the oncoprotein v-abl but is ineffective against c-src tyrosine kinase activity.	Sepharose	59-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	228-233
8227078-10	1993	The synthetic YMXM-containing peptides had among the highest apparent affinities described to date for either tyrosine kinase, with Km values as low as 97 microM for v-Src and v-Abl.	Peptides	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	176-181
8227078-13	1993	For v-Abl, the presence of threonine at any position in the YMXM motif caused a reduction in catalytic efficiency.	Threonine	27-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-9
8242749-4	1993	A domain in the C-terminus of RB, outside of the A/B pocket, binds to the ATP-binding lobe of the c-Abl tyrosine kinase, resulting in kinase inhibition.	Adenosine Triphosphate	74-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-103
8285639-0	1993	Selective repression of v-abl-encoded protein by N-methylisatin-beta-4",4"-diethylthiosemicarbazone and N-allylisatin-beta-4",4"-diallylthiosemicarbazone.	N-methylisatin beta-4',4'-diethylthiosemicarbazone	49-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-29
8285639-0	1993	Selective repression of v-abl-encoded protein by N-methylisatin-beta-4",4"-diethylthiosemicarbazone and N-allylisatin-beta-4",4"-diallylthiosemicarbazone.	N-allylisatin-beta-4',4'-diallylthiosemicarbazone	104-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-29
8285639-1	1993	N-Methylisatin-beta-4",4"-diethylthiosemicarbazone (M-IBDET) and N-allylisatin-beta-4",4"-diallylthiosemicarbazone (A-IBDAT) selectively inhibited v-abl protein (P120), an oncogene product associated with tyrosine kinase activity.	N-methylisatin beta-4',4'-diethylthiosemicarbazone	0-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-152
8285639-1	1993	N-Methylisatin-beta-4",4"-diethylthiosemicarbazone (M-IBDET) and N-allylisatin-beta-4",4"-diallylthiosemicarbazone (A-IBDAT) selectively inhibited v-abl protein (P120), an oncogene product associated with tyrosine kinase activity.	N-allylisatin-beta-4',4'-diallylthiosemicarbazone	65-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-152
8402896-5	1993	Binding of GRB-2 to BCR-ABL is mediated by the direct interaction of the GRB-2 SH2 domain with a phosphorylated tyrosine, Y177, within the BCR first exon.	Tyrosine	112-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
8402898-3	1993	Selective binding to a subset of 15 different recombinant SH3 domains occurs through proline-rich sequence motifs similar to those that mediate the interaction of the SH3 domains of Grb2 and Abl proteins to the guanine nucleotide exchange protein, Sos, and to the 3BP1 protein, respectively.	Proline	85-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	191-194
8402898-3	1993	Selective binding to a subset of 15 different recombinant SH3 domains occurs through proline-rich sequence motifs similar to those that mediate the interaction of the SH3 domains of Grb2 and Abl proteins to the guanine nucleotide exchange protein, Sos, and to the 3BP1 protein, respectively.	Guanine Nucleotides	211-229	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	191-194
8402898-3	1993	Selective binding to a subset of 15 different recombinant SH3 domains occurs through proline-rich sequence motifs similar to those that mediate the interaction of the SH3 domains of Grb2 and Abl proteins to the guanine nucleotide exchange protein, Sos, and to the 3BP1 protein, respectively.	sulfur monoxide	248-251	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	191-194
8340987-4	1993	Furthermore, studies in patients with ABL have established the critical role of hepatic secretion of VLDL in the delivery of vitamin E to peripheral tissues and the essential role of vitamin E in the maintenance of normal physiological function of multiple tissues.	Vitamin E	125-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-41
8340987-4	1993	Furthermore, studies in patients with ABL have established the critical role of hepatic secretion of VLDL in the delivery of vitamin E to peripheral tissues and the essential role of vitamin E in the maintenance of normal physiological function of multiple tissues.	Vitamin E	183-192	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-41
8393452-5	1993	Down-regulation of protein kinase C inhibited v-abl-stimulated DNA synthesis in IC.DP cells cultured at 32 degrees C. IC.DP cells cultured at 32 degrees C were found to have a constitutively activated Na+/H+ antiport, although this activation was inhibited by the down-modulation of protein kinase C. These data indicate a role for phospholipid hydrolysis and protein kinase C activation in V-ABL-mediated abrogation of IL-3 dependence.	dp	83-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-51
8393452-5	1993	Down-regulation of protein kinase C inhibited v-abl-stimulated DNA synthesis in IC.DP cells cultured at 32 degrees C. IC.DP cells cultured at 32 degrees C were found to have a constitutively activated Na+/H+ antiport, although this activation was inhibited by the down-modulation of protein kinase C. These data indicate a role for phospholipid hydrolysis and protein kinase C activation in V-ABL-mediated abrogation of IL-3 dependence.	dp	83-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	391-396
8393452-5	1993	Down-regulation of protein kinase C inhibited v-abl-stimulated DNA synthesis in IC.DP cells cultured at 32 degrees C. IC.DP cells cultured at 32 degrees C were found to have a constitutively activated Na+/H+ antiport, although this activation was inhibited by the down-modulation of protein kinase C. These data indicate a role for phospholipid hydrolysis and protein kinase C activation in V-ABL-mediated abrogation of IL-3 dependence.	dp	121-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-51
8393452-5	1993	Down-regulation of protein kinase C inhibited v-abl-stimulated DNA synthesis in IC.DP cells cultured at 32 degrees C. IC.DP cells cultured at 32 degrees C were found to have a constitutively activated Na+/H+ antiport, although this activation was inhibited by the down-modulation of protein kinase C. These data indicate a role for phospholipid hydrolysis and protein kinase C activation in V-ABL-mediated abrogation of IL-3 dependence.	dp	121-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	391-396
8393452-5	1993	Down-regulation of protein kinase C inhibited v-abl-stimulated DNA synthesis in IC.DP cells cultured at 32 degrees C. IC.DP cells cultured at 32 degrees C were found to have a constitutively activated Na+/H+ antiport, although this activation was inhibited by the down-modulation of protein kinase C. These data indicate a role for phospholipid hydrolysis and protein kinase C activation in V-ABL-mediated abrogation of IL-3 dependence.	Phospholipids	332-344	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-51
8336729-5	1993	This class of ABL mutants shows increased tyrosine phosphorylation of cellular proteins in vivo but low levels of autophosphorylation.	Tyrosine	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-17
8329715-2	1993	Inhibition of bcr-abl gene expression may have profound effects on the cell biology of Ph1+ cells, as recent experiments with antisense oligonucleotides have shown.	Oligonucleotides	136-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
8398898-0	1993	Inhibition of phosphorylation of p160 BCR within p210 BCR-ABL complexes during early stages of phorbol ester-induced differentiation of K562 cells.	Phorbol Esters	95-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
8398898-1	1993	The kinase activity of the BCR-ABL gene product is known to be down-regulated in K562 cells treated with low concentrations of the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA).	Phorbol Esters	131-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
8398898-1	1993	The kinase activity of the BCR-ABL gene product is known to be down-regulated in K562 cells treated with low concentrations of the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA).	Tetradecanoylphorbol Acetate	145-181	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
8398898-1	1993	The kinase activity of the BCR-ABL gene product is known to be down-regulated in K562 cells treated with low concentrations of the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA).	Tetradecanoylphorbol Acetate	183-186	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
8398898-5	1993	Our results indicate that BCR-ABL/BCR complexes disappeared at precisely the same time after TPA treatment as the loss of autophosphorylation activity exhibited by total p210 BCR-ABL, which occurred 16-19 h after TPA treatment.	Tetradecanoylphorbol Acetate	93-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
8398898-5	1993	Our results indicate that BCR-ABL/BCR complexes disappeared at precisely the same time after TPA treatment as the loss of autophosphorylation activity exhibited by total p210 BCR-ABL, which occurred 16-19 h after TPA treatment.	Tetradecanoylphorbol Acetate	213-216	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
8398898-5	1993	Our results indicate that BCR-ABL/BCR complexes disappeared at precisely the same time after TPA treatment as the loss of autophosphorylation activity exhibited by total p210 BCR-ABL, which occurred 16-19 h after TPA treatment.	Tetradecanoylphorbol Acetate	213-216	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-182
8398898-6	1993	The loss of kinase activity preceded the loss of p210 BCR by more than 24 h. A degraded form of p210 BCR-ABL (about 175 kilodaltons) accounted for the residual autophosphorylation activity seen during the later phases of kinase inactivation following TPA treatment, and this form was preferentially sequestered within BCR-ABL/BCR complexes.	Tetradecanoylphorbol Acetate	251-254	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-108
8334997-4	1993	In the presence of hormone, the c-Abl:ER fusion protein was transforming, cytoplasmic and tyrosine phosphorylated, whereas it was non-transforming, nuclear and hypophosphorylated without hormone.	Tyrosine	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-37
8510937-0	1993	Mutation of a phenylalanine conserved in SH3-containing tyrosine kinases activates the transforming ability of c-Abl.	Phenylalanine	14-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-116
8510937-4	1993	Phenylalanine 420 is perfectly conserved among tyrosine kinases with N-terminal SH3 domains (the Src and Abl families).	Phenylalanine	0-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-108
8510937-6	1993	Mutation of phenylalanine 420 to other hydrophobic residues activates c-Abl.	Phenylalanine	12-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-75
8343210-4	1993	For testing we used an exogenous substrate kinase assay based on the phosphorylation of (Val5)-angiotensin II with radiolabelled ATP by the catalytic domain of the PTK encoded by the v-abl oncogene (p45 v-abl).	Adenosine Triphosphate	129-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	183-188
8500581-7	1993	Experiments are underway to use this in vivo model to assess the antileukemic activity of BCR/ABL antisense oligonucleotides.	Oligonucleotides	108-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
8398898-8	1993	We conclude that 15 nM TPA treatment of K562 cells initiates effects that simultaneously interfere with the phosphorylation of p160 BCR in BCR-ABL complexes and inactivates the autophosphorylation activity of the full length BCR-ABL protein.	Tetradecanoylphorbol Acetate	23-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-146
8398898-8	1993	We conclude that 15 nM TPA treatment of K562 cells initiates effects that simultaneously interfere with the phosphorylation of p160 BCR in BCR-ABL complexes and inactivates the autophosphorylation activity of the full length BCR-ABL protein.	Tetradecanoylphorbol Acetate	23-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	225-232
8441409-3	1993	In this work, we show that two other structural requirements for full transforming activity of P210 BCR/ABL include a functional tyrosine kinase and the presence of tyrosine 1294, a site of autophosphorylation within the tyrosine kinase domain.	Tyrosine	129-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
8479075-12	1993	Lastly, the use of antisense oligonucleotides for the BCR-ABL junctions should result in the inhibition of growth of CML clone.	Oligonucleotides	29-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
1383690-3	1992	A novel, phosphotyrosine-independent binding interaction between BCR, the Philadelphia chromosome breakpoint cluster region gene product, and the SH2 domain of its translocation partner c-ABL has recently been reported.	Phosphotyrosine	9-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-191
8460498-0	1993	A novel mutation within the kinase domain of v-abl gene responsible for temperature-sensitive colony-forming ability in soft agar.	Agar	125-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-50
8460498-5	1993	Thus, a novel mutation within the kinase domain of the abl gene critical for the ts phenotype in colony-forming ability in soft agar was determined here.	Agar	128-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-58
8237276-0	1993	Analysis of BCR/ABL abnormalities in mRNA from 20-year-old paraffin-embedded tissue for BCR/ABL rearrangement by polymerase chain reaction.	Paraffin	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
8013266-1	1993	The authors examined the effect of a tyrosine kinase inhibitor, erbstatin, and its analogues on abl oncogene functions.	erbstatin	64-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-99
8013266-6	1993	Ethyl 2,5-dihydroxycinnamate also inhibited bcr-abl tyrosine kinase.	ethyl 2,5-dihydroxycinnamate	0-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-51
8013266-7	1993	These results indicate that the stable analogues of erbstatin suppress oncogene functions of Abl by inhibiting its tyrosine kinase.	erbstatin	52-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-96
7504543-8	1993	Most recently, we have treated SCID mice engrafted with bcr-abl expressing human K562 cell leukemia with phosphorothioate modified AS ODN.	Parathion	105-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
8423987-0	1993	BCR-ABL tyrosine kinase is autophosphorylated or transphosphorylates P160 BCR on tyrosine predominantly within the first BCR exon.	Tyrosine	8-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
8423987-3	1993	We now report that tryptic peptides shared by both P160 BCR and P210 BCR-ABL are phosphorylated on tyrosine in vitro either when using immune complexes containing P160 BCR complexed to BCR-ABL or when P160 BCR is phosphorylated in trans by P210 BCR-ABL immune complexes from cells lacking functional P160 BCR.	Peptides	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
8423987-3	1993	We now report that tryptic peptides shared by both P160 BCR and P210 BCR-ABL are phosphorylated on tyrosine in vitro either when using immune complexes containing P160 BCR complexed to BCR-ABL or when P160 BCR is phosphorylated in trans by P210 BCR-ABL immune complexes from cells lacking functional P160 BCR.	Peptides	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	185-192
8423987-3	1993	We now report that tryptic peptides shared by both P160 BCR and P210 BCR-ABL are phosphorylated on tyrosine in vitro either when using immune complexes containing P160 BCR complexed to BCR-ABL or when P160 BCR is phosphorylated in trans by P210 BCR-ABL immune complexes from cells lacking functional P160 BCR.	Peptides	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	185-192
8423987-3	1993	We now report that tryptic peptides shared by both P160 BCR and P210 BCR-ABL are phosphorylated on tyrosine in vitro either when using immune complexes containing P160 BCR complexed to BCR-ABL or when P160 BCR is phosphorylated in trans by P210 BCR-ABL immune complexes from cells lacking functional P160 BCR.	Tyrosine	99-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
8423987-3	1993	We now report that tryptic peptides shared by both P160 BCR and P210 BCR-ABL are phosphorylated on tyrosine in vitro either when using immune complexes containing P160 BCR complexed to BCR-ABL or when P160 BCR is phosphorylated in trans by P210 BCR-ABL immune complexes from cells lacking functional P160 BCR.	Tyrosine	99-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	185-192
8423987-3	1993	We now report that tryptic peptides shared by both P160 BCR and P210 BCR-ABL are phosphorylated on tyrosine in vitro either when using immune complexes containing P160 BCR complexed to BCR-ABL or when P160 BCR is phosphorylated in trans by P210 BCR-ABL immune complexes from cells lacking functional P160 BCR.	Tyrosine	99-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	185-192
8423987-5	1993	As with P210 BCR-ABL, P160 BCR tyrosine phosphopeptides were shared with P185 BCR-ABL, indicating that the major sites of tyrosine phosphorylation in vitro are contained within the first exon of P160 BCR.	Tyrosine	122-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
8423987-6	1993	Similarly, BCR-ABL autophosphorylation was found to occur predominantly at tyrosines within BCR exon 1 sequences.	Tyrosine	75-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-18
8423987-7	1993	These results raise the possibility that the activated ABL protein kinase of BCR-ABL proteins modulates the putative signal transduction activities of P160 BCR by tyrosine phosphorylation of exon 1 sequences.	Tyrosine	163-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-58
8423987-7	1993	These results raise the possibility that the activated ABL protein kinase of BCR-ABL proteins modulates the putative signal transduction activities of P160 BCR by tyrosine phosphorylation of exon 1 sequences.	Tyrosine	163-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
1281542-2	1992	Assignments of nearly all 1H and 15N resonances of the SH2 domain from the c-Abl protein-tyrosine kinase have been obtained from homonuclear and heteronuclear NMR experiments.	Hydrogen	26-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-80
1281542-2	1992	Assignments of nearly all 1H and 15N resonances of the SH2 domain from the c-Abl protein-tyrosine kinase have been obtained from homonuclear and heteronuclear NMR experiments.	15n	33-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-80
1383690-6	1992	Binding of tyrosine-phosphorylated c-ABL 1b by the relatively high-affinity ABL and ARG SH2 domains was quantitatively analyzed, and equilibrium dissociation constants for both interactions were estimated to be in the range of 5 x 10(-7) M. The ABL SH2 domain exhibited relatively high affinity for phosphotyrosine-free BCR as well; however, this interaction appears to be about two orders of magnitude weaker than binding of tyrosine-phosphorylated c-ABL 1b.	Tyrosine	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-40
1383690-6	1992	Binding of tyrosine-phosphorylated c-ABL 1b by the relatively high-affinity ABL and ARG SH2 domains was quantitatively analyzed, and equilibrium dissociation constants for both interactions were estimated to be in the range of 5 x 10(-7) M. The ABL SH2 domain exhibited relatively high affinity for phosphotyrosine-free BCR as well; however, this interaction appears to be about two orders of magnitude weaker than binding of tyrosine-phosphorylated c-ABL 1b.	Tyrosine	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-40
1383690-6	1992	Binding of tyrosine-phosphorylated c-ABL 1b by the relatively high-affinity ABL and ARG SH2 domains was quantitatively analyzed, and equilibrium dissociation constants for both interactions were estimated to be in the range of 5 x 10(-7) M. The ABL SH2 domain exhibited relatively high affinity for phosphotyrosine-free BCR as well; however, this interaction appears to be about two orders of magnitude weaker than binding of tyrosine-phosphorylated c-ABL 1b.	Tyrosine	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-79
1383690-6	1992	Binding of tyrosine-phosphorylated c-ABL 1b by the relatively high-affinity ABL and ARG SH2 domains was quantitatively analyzed, and equilibrium dissociation constants for both interactions were estimated to be in the range of 5 x 10(-7) M. The ABL SH2 domain exhibited relatively high affinity for phosphotyrosine-free BCR as well; however, this interaction appears to be about two orders of magnitude weaker than binding of tyrosine-phosphorylated c-ABL 1b.	Tyrosine	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	450-455
1383690-6	1992	Binding of tyrosine-phosphorylated c-ABL 1b by the relatively high-affinity ABL and ARG SH2 domains was quantitatively analyzed, and equilibrium dissociation constants for both interactions were estimated to be in the range of 5 x 10(-7) M. The ABL SH2 domain exhibited relatively high affinity for phosphotyrosine-free BCR as well; however, this interaction appears to be about two orders of magnitude weaker than binding of tyrosine-phosphorylated c-ABL 1b.	Arginine	84-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-40
1383690-6	1992	Binding of tyrosine-phosphorylated c-ABL 1b by the relatively high-affinity ABL and ARG SH2 domains was quantitatively analyzed, and equilibrium dissociation constants for both interactions were estimated to be in the range of 5 x 10(-7) M. The ABL SH2 domain exhibited relatively high affinity for phosphotyrosine-free BCR as well; however, this interaction appears to be about two orders of magnitude weaker than binding of tyrosine-phosphorylated c-ABL 1b.	Arginine	84-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-40
1383690-6	1992	Binding of tyrosine-phosphorylated c-ABL 1b by the relatively high-affinity ABL and ARG SH2 domains was quantitatively analyzed, and equilibrium dissociation constants for both interactions were estimated to be in the range of 5 x 10(-7) M. The ABL SH2 domain exhibited relatively high affinity for phosphotyrosine-free BCR as well; however, this interaction appears to be about two orders of magnitude weaker than binding of tyrosine-phosphorylated c-ABL 1b.	Phosphotyrosine	299-314	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-40
1383690-6	1992	Binding of tyrosine-phosphorylated c-ABL 1b by the relatively high-affinity ABL and ARG SH2 domains was quantitatively analyzed, and equilibrium dissociation constants for both interactions were estimated to be in the range of 5 x 10(-7) M. The ABL SH2 domain exhibited relatively high affinity for phosphotyrosine-free BCR as well; however, this interaction appears to be about two orders of magnitude weaker than binding of tyrosine-phosphorylated c-ABL 1b.	Phosphotyrosine	299-314	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-79
1383690-6	1992	Binding of tyrosine-phosphorylated c-ABL 1b by the relatively high-affinity ABL and ARG SH2 domains was quantitatively analyzed, and equilibrium dissociation constants for both interactions were estimated to be in the range of 5 x 10(-7) M. The ABL SH2 domain exhibited relatively high affinity for phosphotyrosine-free BCR as well; however, this interaction appears to be about two orders of magnitude weaker than binding of tyrosine-phosphorylated c-ABL 1b.	Tyrosine	306-314	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-40
1383690-6	1992	Binding of tyrosine-phosphorylated c-ABL 1b by the relatively high-affinity ABL and ARG SH2 domains was quantitatively analyzed, and equilibrium dissociation constants for both interactions were estimated to be in the range of 5 x 10(-7) M. The ABL SH2 domain exhibited relatively high affinity for phosphotyrosine-free BCR as well; however, this interaction appears to be about two orders of magnitude weaker than binding of tyrosine-phosphorylated c-ABL 1b.	Tyrosine	306-314	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-79
1383690-8	1992	The ABL and ARG SH2 domains differ by only 10 of 91 amino acids, and the substitution of ABL-specific amino acids into either the amino- or carboxy-terminal half of the ARG SH2 domain was found to increase its affinity for BCR.	Arginine	12-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-92
1383690-8	1992	The ABL and ARG SH2 domains differ by only 10 of 91 amino acids, and the substitution of ABL-specific amino acids into either the amino- or carboxy-terminal half of the ARG SH2 domain was found to increase its affinity for BCR.	Arginine	169-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
1383690-8	1992	The ABL and ARG SH2 domains differ by only 10 of 91 amino acids, and the substitution of ABL-specific amino acids into either the amino- or carboxy-terminal half of the ARG SH2 domain was found to increase its affinity for BCR.	Arginine	169-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-92
1379843-3	1992	Tyrosine phosphorylated proteins with a molecular mass of 150 kDa (p150) and 115 kDa (p110) were found in both K-562 and MR-87.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-71
1643641-0	1992	Benzopyranones and benzothiopyranones: a class of tyrosine protein kinase inhibitors with selectivity for the v-abl kinase.	benzopyranones	0-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-115
1643641-0	1992	Benzopyranones and benzothiopyranones: a class of tyrosine protein kinase inhibitors with selectivity for the v-abl kinase.	benzothiopyranones	19-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-115
1643641-2	1992	A variety of benzopyranone and benzothiopyranone derivatives have been identified which selectively inhibit the v-abl tyrosine protein kinase with 50% inhibitory concentrations ranging from 1 to 30 microM.	coumarin	13-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-117
1643641-2	1992	A variety of benzopyranone and benzothiopyranone derivatives have been identified which selectively inhibit the v-abl tyrosine protein kinase with 50% inhibitory concentrations ranging from 1 to 30 microM.	benzothiopyranone	31-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-117
1643641-8	1992	When tested in Abelson murine leukemia virus-transformed BALB/c cell, active benzopyranone and benzothiopyranone derivatives inhibited tyrosine phosphorylation of cellular proteins by the v-abl tyrosine protein kinase.	coumarin	77-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	188-193
1643641-8	1992	When tested in Abelson murine leukemia virus-transformed BALB/c cell, active benzopyranone and benzothiopyranone derivatives inhibited tyrosine phosphorylation of cellular proteins by the v-abl tyrosine protein kinase.	benzothiopyranone	95-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	188-193
1643641-8	1992	When tested in Abelson murine leukemia virus-transformed BALB/c cell, active benzopyranone and benzothiopyranone derivatives inhibited tyrosine phosphorylation of cellular proteins by the v-abl tyrosine protein kinase.	Tyrosine	135-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	188-193
1564963-0	1992	Induction of differentiation of human leukemia cells with a structurally altered c-abl (bcr/abl) gene by herbimycin A, an inhibitor of tyrosine kinase activity.	herbimycin	105-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-86
1423209-6	1992	FUrd also decreased the levels of several mRNAs, including those for the proto-oncogenes c-myc and c-abl, and for gamma-globin, by 40 to 70%.	5-fluorouridine	0-4	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-104
1564963-0	1992	Induction of differentiation of human leukemia cells with a structurally altered c-abl (bcr/abl) gene by herbimycin A, an inhibitor of tyrosine kinase activity.	herbimycin	105-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
1370482-3	1992	The fidelity of this mimicry by okadaic acid extends to the phosphorylation of the 27 hsp complex, stathmin, eIF-4E, myosin light chain, nucleolin, epidermal growth factor receptor, and other cdc2-kinase substrates (c-abl, RB, and p53).	Okadaic Acid	32-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	216-221
1737071-8	1992	Phosphoamino acid analysis of immunoprecipitated, autophosphorylated baculovirus derived c-Abl protein indicates that the majority of label incorporated is on the tyrosine residues.	Phosphoamino Acids	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-94
1737071-8	1992	Phosphoamino acid analysis of immunoprecipitated, autophosphorylated baculovirus derived c-Abl protein indicates that the majority of label incorporated is on the tyrosine residues.	Tyrosine	163-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-94
1456503-0	1992	[Pertinence of simultaneous measurements of pO2 and sO2 on ABL 510].	PO-2	44-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-62
1456503-0	1992	[Pertinence of simultaneous measurements of pO2 and sO2 on ABL 510].	Sulfur Dioxide	52-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-62
1456503-2	1992	ABL instruments by Radiometer were tested by two types of tonometry (film and bubble tonometry) and the validity of the algorithm for pO2 correction was analysed with these results.	PO-2	134-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
1456503-7	1992	ABL 510 measures simultaneously oxygen saturation by spectrophotometry.	Oxygen	32-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
1923513-1	1991	Arg encodes a protein highly related to the c-abl gene product with regard to overall structural architecture as well as the amino acid sequences of their tyrosine kinase, and src-homologous 2 and 3 domains.	Arginine	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-49
1651810-5	1991	The inhibition of v-abl tyrosine kinase activity preceded induction of differentiation of the cells treated with tyrosine kinase inhibitors such as genistein, herbimycin A, and erbstatin.	Genistein	148-157	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-23
1651810-5	1991	The inhibition of v-abl tyrosine kinase activity preceded induction of differentiation of the cells treated with tyrosine kinase inhibitors such as genistein, herbimycin A, and erbstatin.	herbimycin	159-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-23
1651810-5	1991	The inhibition of v-abl tyrosine kinase activity preceded induction of differentiation of the cells treated with tyrosine kinase inhibitors such as genistein, herbimycin A, and erbstatin.	erbstatin	177-186	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-23
1712671-0	1991	BCR sequences essential for transformation by the BCR-ABL oncogene bind to the ABL SH2 regulatory domain in a non-phosphotyrosine-dependent manner.	Phosphotyrosine	114-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-57
1857987-0	1991	Selective inhibition of leukemia cell proliferation by BCR-ABL antisense oligodeoxynucleotides.	Oligodeoxyribonucleotides	73-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
1712671-0	1991	BCR sequences essential for transformation by the BCR-ABL oncogene bind to the ABL SH2 regulatory domain in a non-phosphotyrosine-dependent manner.	Phosphotyrosine	114-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
1712671-7	1991	Phosphoserine/phosphothreonine but not phosphotyrosine residues on BCR are required for interaction with the ABL SH2 domain.	Phosphoserine	0-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-112
1712671-7	1991	Phosphoserine/phosphothreonine but not phosphotyrosine residues on BCR are required for interaction with the ABL SH2 domain.	Phosphothreonine	14-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-112
1794439-5	1991	If CML-BC cells were mixed with NMBC and incubated with specific BCR/ABL antisense oligomer, leukemic colonies were selectively inhibited, as was shown by reverse, transcriptase-polymerase chain reaction (RT-PCR) performed to detect BCR/ABL mRNA in single colonies.	nmbc	32-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
1712111-1	1991	Phosphotyrosine cannot be detected on normal human ABL protein-tyrosine kinases, but activated oncogenic forms of the human ABL protein are phosphorylated on tyrosine in vivo.	Phosphotyrosine	0-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-127
1712111-1	1991	Phosphotyrosine cannot be detected on normal human ABL protein-tyrosine kinases, but activated oncogenic forms of the human ABL protein are phosphorylated on tyrosine in vivo.	Tyrosine	7-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-127
1712111-5	1991	ABL proteins translated in vitro lack phosphotyrosine, but tyrosine kinase activity is uncovered after immunoprecipitation and removal of lysate components.	Phosphotyrosine	38-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
2017387-0	1991	Dinucleotide repeat polymorphism at the ABL locus (9q34).	Dinucleoside Phosphates	0-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-43
1985690-5	1991	We describe here the clinical application of a new method, the hybridization protection assay (HPA), which uses chemiluminescent acridinium-ester-labeled probes in conjunction with PCR for detection of the amplified BCR-ABL sequences.	acridinium-ester	129-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	216-223
1794439-5	1991	If CML-BC cells were mixed with NMBC and incubated with specific BCR/ABL antisense oligomer, leukemic colonies were selectively inhibited, as was shown by reverse, transcriptase-polymerase chain reaction (RT-PCR) performed to detect BCR/ABL mRNA in single colonies.	nmbc	32-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	233-240
1719348-1	1991	Polyclonal antibodies for phosphotyrosine can be obtained by immunization with a t/abl fusion protein.	Phosphotyrosine	26-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-86
2183353-3	1990	Inhibition of phosphatases with okadaic acid in interphase cells leads to the phosphorylation of c-Abl mitotic sites, indicating that those sites are preferentially dephosphorylated during interphase.	Okadaic Acid	32-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-102
2209769-1	1990	In order to study which hemopoietic precursor cells express the hybrid BCR/ABL fusion mRNA we have developed a technique based on the polymerase chain reaction (PCR) for the examination of single hemopoietic colonies grown on semi-solid agar.	Agar	237-241	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
2198571-1	1990	We have previously described partial genomic sequences of arg, a human gene related to c-abl, and shown that it is expressed as a 12-kilobase transcript and is located at chromosome position 1q24-25.	Arginine	58-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-92
2198571-3	1990	Analysis of the predicted amino acid sequence of arg revealed that it is indeed closely related to that of c-abl.	Arginine	49-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-112
2198571-5	1990	In addition, arg, like c-abl, is expressed as two transcripts that result from a process of alternative splicing and encode alternative protein forms that differ only in their amino termini.	Arginine	13-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-28
12743277-8	2003	The SH2 domain of the v-Abl protein encoded by this mutant contains a substitution that affects the phosphotyrosine-binding pocket, and this mutant is compromised in its ability to transform NIH 3T3 and pre-B cells, especially at 39.5 degrees C. Our data reveal that loss of p53 or Ink4a/Arf locus products complements the transforming defect of the P120/R273K mutant, but it does not completely restore wild-type function.	Phosphotyrosine	100-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-27
33814500-0	2021	BCR/ABL1-positive B-lymphoblastic Lymphoma Successfully Treated with Dasatinib-combined Chemotherapy.	Dasatinib	69-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-8
33814500-6	2021	She was diagnosed with BCR-ABL1-positive B-LBL and administered dasatinib and prednisolone.	Dasatinib	64-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-31
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 Mesylate	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.	Dasatinib	281-290	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.	bosutinib	292-301	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.	nilotinib	303-312	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.	ibrutinib	318-327	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	189-196
33774681-0	2021	The role of ponatinib in adult BCR-ABL1 positive acute lymphoblastic leukemia after allogeneic transplantation: a real-life retrospective multicenter study.	ponatinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-39
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 Mesylate	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
10403766-2	1999	We have previously shown that P210 BCR-ABL binds to the xeroderma pigmentosum group B protein (XPB) through the portion of BCR that is homologous to the catalytic domain of GDP-GTP exchangers such as yeast CDC24 and Dbl.	gdp-gtp	173-180	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
27457438-0	1990	Inhibition of P210BCR/ABL Expression in K562 Cells by Electroporation with an Antisense Oligonucleotide.	Oligonucleotides	88-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-25
27457438-1	1990	We designed experiments to study the effects on P210BCR/ABL expression of introducing antisense oligonucleotides into K562 cells.	Oligonucleotides	96-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-59
2157186-1	1990	A bacterial expression vector containing a segment of the v-abl gene from Abelson murine leukemia virus (A-MuLV) was constructed such that the gag region of v-abl was replaced by a sequence encoding the IgG-binding domain of the S. aureus protein A. pabl HP, a fusion protein encoded by this vector was rapidly purified to near homogeneity by affinity chromatography on IgG-Affigel and Mono Q FPLC.	Glycosaminoglycans	143-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-162
33971041-0	2021	Overcoming TKI resistance in a patient with chronic myeloid leukemia using combination BCR-ABL inhibition with asciminib and bosutinib.	asciminib	111-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
33768841-8	2021	Moreover, BCR-ABL1 transcript copies remained undetectable by RT-PCR, 8 months after stopping bosutinib.	bosutinib	94-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-18
19891780-0	2009	Cbl-associated protein is tyrosine phosphorylated by c-Abl and c-Src kinases.	Tyrosine	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-58
19891780-5	2009	RESULTS: We here show that CAP is Tyr phosphorylated by and interacts with both c-Abl and c-Src.	Tyrosine	34-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-85
19891780-9	2009	Our findings suggest that coordinated action of Src and Abl might regulate the function of CAP and reveal a functional role especially for the Src-mediated Tyr phosphorylation of CAP in cell spreading.	Tyrosine	156-159	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-59
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 Mesylate	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-8
10822173-4	2000	Expression of Bcr-Abl induced tyrosine phosphorylation of both Dok1 and SHIP1 and the formation of a Dok1/SHIP1 complex.	Tyrosine	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
10822173-5	2000	Tyr(P) SHIP1 was also bound to Shc in Bcr-Abl expressing cells.	Tyrosine	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
34953803-0	2022	A bis-pyridinium fullerene derivative induces apoptosis through the generation of ROS in BCR-ABL-positive leukemia cells.	bis-pyridinium fullerene	2-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
34953803-0	2022	A bis-pyridinium fullerene derivative induces apoptosis through the generation of ROS in BCR-ABL-positive leukemia cells.	Reactive Oxygen Species	82-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
34953803-4	2022	BPF reduced the expression of Bcr-Abl mRNA by inhibiting expression of c-Myc through ROS production.	Reactive Oxygen Species	85-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
34953803-5	2022	BPF also accelerated protein degradation of BCR-ABL through ROS production.	Reactive Oxygen Species	60-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
34953803-6	2022	Furthermore, BPF down-regulated the expression of not only BCR-ABL but also T315I-mutated BCR-ABL in ROS-dependent manner.	Reactive Oxygen Species	101-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
34953803-6	2022	Furthermore, BPF down-regulated the expression of not only BCR-ABL but also T315I-mutated BCR-ABL in ROS-dependent manner.	Reactive Oxygen Species	101-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
34774565-1	2022	Imatinib is an ATP-competitive inhibitor of Bcr-Abl kinase and the first drug approved for chronic myelogenous leukemia (CML) treatment.	Adenosine Triphosphate	15-18	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 Mesylate	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
34614211-8	2022	The estimated 5-year survival rate for patients with Philadelphia chromosome-positive acute lymphoblastic leukemia (ALL) exceeds 70% with intensive chemotherapy and ponatinib, a third-generation BCR-ABL1 TKI, and more recent nonchemotherapy regimens using dasatinib or ponatinib with blinatumomab are producing outstanding results.	ponatinib	165-174	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	199-203
34496035-3	2022	Monthly DT was calculated as x = ln(2)/K, where x is the DT and K is the fold BCR-ABL1 change from the previous value divided by the number of days between each measurement.	Thymidine	8-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-86
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 Mesylate	201-209	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-133
34816484-7	2022	Post-mortem studies of PD patients demonstrate increased levels of tyrosine phosphorylated alpha-synuclein, consistent with the activation of c-Abl in human disease.	Tyrosine	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-147
17317816-3	2007	RESULTS: Imatinib, which targets the ABL kinase activity of BCR-ABL, has prolonged survival in CML.	Imatinib Mesylate	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	117-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-143
17317816-6	2007	The IC(50) values of nilotinib and dasatinib are at least 10- to 100-fold lower for BCR-ABL compared with imatinib.	nilotinib	21-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
17317816-6	2007	The IC(50) values of nilotinib and dasatinib are at least 10- to 100-fold lower for BCR-ABL compared with imatinib.	Dasatinib	35-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
34837846-9	2022	MEK inhibitor showed synergy with multikinase inhibitor ponatinib, ABL inhibitor nilotinib, PI3K/mTOR inhibitor pictilisib, and pan-RAF inhibitor LY3009120.	nilotinib	81-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-70
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.	pristimerin	15-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	173-180
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 Mesylate	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	173-180
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 Mesylate	52-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-121
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.	nilotinib	73-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-121
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.	bosutinib	84-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-121
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.	ponatinib	99-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-121
34923994-2	2021	BACKGROUND: Aquagenic pruritus (AP), an intense sensation of scratching induced after water contact, is the most troublesome aspect of BCR-ABL1-negative myeloproliferative neoplasms (MPNs).	Water	86-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-143
34921014-5	2022	Sensitivity to bosutinib did not correlate with ABL dependency; instead, bosutinib likely induces these effects by acting as a SRC tyrosine kinase inhibitor.	bosutinib	73-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-51
34816484-8	2022	Although the c-Abl inhibitor nilotinib failed to demonstrate clinical benefit in two double-blind trials, novel c-Abl inhibitors have been developed that accumulate in the brain and may inhibit c-Abl at saturating levels.	nilotinib	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-18
34673444-2	2021	We used this approach to prospectively examine mutations in the BCR/ABL1 tyrosine kinase from patients with newly diagnosed, chronic-phase chronic myeloid leukemia (CML) treated with the tyrosine kinase inhibitor nilotinib.	nilotinib	213-222	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-72
34100929-1	2021	BACKGROUND: Bosutinib is a small molecule BCR-ABL, and src tyrosine kinase inhibitor used for the treatment of chronic myelogenous leukaemia.	bosutinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
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 Mesylate	135-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-52
34884309-4	2021	We, therefore, investigated if BCL2 inhibition, alone or combined with Nilotinib, a BCR-ABL1 inhibitor, affects the primitive and committed Ph+ cells survival.	nilotinib	71-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-92
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-53
34984204-1	2021	Context Nilotinib is a second-generation BCR-ABL1 tyrosine kinase inhibitor used in the treatment of chronic myeloid leukemia (CML).	nilotinib	8-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-49
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.	Adenosine Triphosphate	35-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-53
34115385-1	2021	Asciminib is an investigational, first-in-class, Specifically Targeting the ABL Myristoyl Pocket (STAMP), inhibitor of BCR-ABL1 with a new mechanism of action compared with approved ATP-competitive tyrosine kinase inhibitors.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-127
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.	Dasatinib	241-250	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	284-291
34938856-1	2021	Resistance to the BCR-ABL inhibitor imatinib mesylate poses a major problem for the treatment of chronic myeloid leukemia.	Imatinib Mesylate	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 Mesylate	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 Mesylate	94-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
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 Mesylate	81-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-24
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	188-192
34967577-0	2021	Thymoquinone Induces Downregulation of BCR-ABL/JAK/STAT Pathway and Apoptosis in K562 Leukemia Cells.	thymoquinone	0-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-46
34563945-15	2021	CONCLUSION: Entinostat plus clofarabine appears to be tolerable and active in older adults with ND ALL/ABL, but less active in R/R patients.	entinostat	12-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-106
34776962-0	2021	SC75741, A Novel c-Abl Inhibitor, Promotes the Clearance of TDP25 Aggregates via ATG5-Dependent Autophagy Pathway.	SC75741	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-22
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.	Tretinoin	20-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
34706244-4	2021	To identify metabolic vulnerabilities that enhance this phenotype, we utilized a CRISPR/Cas9 loss-of-function screen and identified HMG-CoA reductase, the rate-limiting enzyme of the mevalonate pathway and target of statin therapies, as a top-scoring sensitizer to ABL inhibition.	Mevalonic Acid	183-193	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	265-268
34699069-1	2022	The BCR-ABL1 inhibitor ponatinib is approved for the treatment of adults with chronic myeloid leukemia or Philadelphia chromosome-positive acute lymphoblastic leukemia, including those with the T315I mutation.	ponatinib	23-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-12
34697383-7	2021	In addition, knockdown of c-Abl kinase prevented Riluzole-induced apoptosis in LM7 cells.	Riluzole	49-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-31
34697383-10	2021	Our data supports a novel mechanism in which Riluzole activates c-Abl kinase to regulate pro-apoptotic activity of YAP in osteosarcoma.	Riluzole	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-69
34547714-1	2021	Despite the success of imatinib in CML therapy through Bcr-Abl inhibition, acquired drug resistance occurs over time in patients.	Imatinib Mesylate	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
34547714-3	2021	Herein, we embarked on a structural optimization campaign aiming at discovery of novel Bcr-Abl inhibitors toward T315I mutant based on previously reported dibenzoylpiperazin derivatives.	dibenzoylpiperazin	155-173	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
34508625-3	2021	Further experiments revealed that ABL1 inhibitor Nilotinib inhibited leukemia cell migration induced by CXCL12, indicating the possible application of Nilotinib in T-ALL leukemia treatment.	nilotinib	49-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-38
34508625-11	2021	Molecular docking analysis shows that ABL1 interacts with Cofilin1 mainly through hydrogen bonds and ionic interaction between amino acid residues.	Hydrogen	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-42
34599372-0	2021	Investigation on the interaction behavior of afatinib, dasatinib, and imatinib docked to the BCR-ABL protein.	Afatinib	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
34599372-0	2021	Investigation on the interaction behavior of afatinib, dasatinib, and imatinib docked to the BCR-ABL protein.	Dasatinib	55-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
34599372-0	2021	Investigation on the interaction behavior of afatinib, dasatinib, and imatinib docked to the BCR-ABL protein.	Imatinib Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-143
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 Mesylate	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-89
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 Mesylate	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 Mesylate	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-46
34636293-7	2022	In this review, two new BCR-ABL inhibitors (flumatinib, radotinib) and five new BCR-ABL inhibitors have been introduced into the clinical market in recent years, and we reviewed their research status, synthesis methods and clinical applications.	HH-GV-678	44-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
34636293-7	2022	In this review, two new BCR-ABL inhibitors (flumatinib, radotinib) and five new BCR-ABL inhibitors have been introduced into the clinical market in recent years, and we reviewed their research status, synthesis methods and clinical applications.	4-methyl-N-(3-(4-methylimidazol-1-yl)-5-trifluoromethylphenyl)-3-(4-pyrazin-2-ylpyrimidin-2-ylamino)benzamide	56-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
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 Mesylate	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 Mesylate	133-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-116
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 Mesylate	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-140
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 Mesylate	117-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-106
34431498-6	2021	We identified tyrosines in the juxtamembrane region of EphB6 as EphB4 substrates, which can bind the SH2 domains of signalling effectors, including Abl, Src and Vav3, consistent with cellular roles in recruiting these proteins for downstream signaling.	Tyrosine	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	148-151
34659899-0	2021	Asciminib and ponatinib exert synergistic anti-neoplastic effects on CML cells expressing BCR-ABL1 T315I-compound mutations.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-98
34659899-0	2021	Asciminib and ponatinib exert synergistic anti-neoplastic effects on CML cells expressing BCR-ABL1 T315I-compound mutations.	ponatinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-98
34659899-1	2021	Ponatinib is a tyrosine kinase inhibitor (TKI) directed against BCR-ABL1 which is successfully used in patients with BCR-ABL1 T315I+ chronic myeloid leukemia (CML).	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-72
34659899-1	2021	Ponatinib is a tyrosine kinase inhibitor (TKI) directed against BCR-ABL1 which is successfully used in patients with BCR-ABL1 T315I+ chronic myeloid leukemia (CML).	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-125
34659899-3	2021	Asciminib is a novel drug capable of targeting most BCR-ABL1 mutant-forms, including BCR-ABL1T315I, but remains ineffective against most BCR-ABL1T315I+ compound mutation-bearing sub-clones.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-60
34659899-8	2021	Most importantly, we were able to show that the combinations "asciminib+ponatinib" and "asciminib+ponatinib+HU" produce synergistic apoptosis-inducing effects in CD34+/CD38- CML stem cells obtained from patients with chronic phase CML or BCR-ABL1 T315I+ CML blast phase.	asciminib	62-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	242-246
34659899-8	2021	Most importantly, we were able to show that the combinations "asciminib+ponatinib" and "asciminib+ponatinib+HU" produce synergistic apoptosis-inducing effects in CD34+/CD38- CML stem cells obtained from patients with chronic phase CML or BCR-ABL1 T315I+ CML blast phase.	ponatinib	72-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	242-246
34659899-8	2021	Most importantly, we were able to show that the combinations "asciminib+ponatinib" and "asciminib+ponatinib+HU" produce synergistic apoptosis-inducing effects in CD34+/CD38- CML stem cells obtained from patients with chronic phase CML or BCR-ABL1 T315I+ CML blast phase.	asciminib	88-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	242-246
34659899-9	2021	Together, asciminib, ponatinib and HU synergize in producing anti-leukemic effects in multi-resistant CML cells, including cells harboring T315I+ BCR-ABL1 compound mutations and CML stem cells.	asciminib	10-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-154
34659899-9	2021	Together, asciminib, ponatinib and HU synergize in producing anti-leukemic effects in multi-resistant CML cells, including cells harboring T315I+ BCR-ABL1 compound mutations and CML stem cells.	ponatinib	21-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-154
34301758-5	2021	Novel deletions in BCR-ABL1 conferred resistance to imatinib.	Imatinib Mesylate	52-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-27
34292655-3	2021	Here, we determine whether there is synergy or antagonism between ATP-competitive inhibitors and allosteric inhibitors of Abl.	Adenosine Triphosphate	66-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-125
34292655-4	2021	We observe that clinical ATP-competitive inhibitors are not synergistic with allosteric ABL inhibitors, however, "conformation-selective" ATP-site inhibitors that modulate the global conformation of Abl can afford synergy.	Adenosine Triphosphate	25-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	199-202
34292655-4	2021	We observe that clinical ATP-competitive inhibitors are not synergistic with allosteric ABL inhibitors, however, "conformation-selective" ATP-site inhibitors that modulate the global conformation of Abl can afford synergy.	Adenosine Triphosphate	138-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-91
34292655-4	2021	We observe that clinical ATP-competitive inhibitors are not synergistic with allosteric ABL inhibitors, however, "conformation-selective" ATP-site inhibitors that modulate the global conformation of Abl can afford synergy.	Adenosine Triphosphate	138-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	199-202
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 Mesylate	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
34410954-3	2021	MATERIALS AND METHODS: K562 cells were treated with IM and with the combined therapy of ATRA together with IM for 48 and 72 h. The expression of BCR-ABL gene and multidrug resistance gene ABCB1 were evaluated using RT-qPCR.	Tretinoin	88-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-152
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.	Tretinoin	21-25	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 Mesylate	30-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-88
34503182-0	2021	Glutamine Availability Controls BCR/Abl Protein Expression and Functional Phenotype of Chronic Myeloid Leukemia Cells Endowed with Stem/Progenitor Cell Potential.	Glutamine	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-39
34503182-3	2021	The absence of glutamine markedly delayed glucose consumption, which had previously been shown to drive the suppression of BCR/Abl oncoprotein (but not of the fusion oncogene BCR/abl) in low oxygen.	Glutamine	15-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-130
34503182-3	2021	The absence of glutamine markedly delayed glucose consumption, which had previously been shown to drive the suppression of BCR/Abl oncoprotein (but not of the fusion oncogene BCR/abl) in low oxygen.	Glucose	42-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-130
34503182-4	2021	Glutamine availability thus emerged as a key regulator of the balance between the pools of BCR/Abl protein-expressing and -negative CML cells endowed with stem/progenitor cell potential and capable to stand extremely low oxygen.	Glutamine	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-98
34503182-7	2021	Therefore, the treatments capable of interfering with glutamine action may result in the reduction in the BCR/Abl-negative cell subset sustaining MRD and in the concomitant rescue of the TKi sensitivity of CML stem cell potential.	Glutamine	54-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-113
34484330-5	2021	Functional network analysis revealed that ABL1 plays an important role in mitochondrial activity, ATP metabolism, protein translation and metabolism, various neurological diseases, nonalcoholic fatty liver disease, and notch signaling pathway.	Adenosine Triphosphate	98-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-46
34433624-9	2021	Dasatinib also enhanced NK cell cytotoxicity against K562 bearing the BCR-ABL1 T315I TKI resistance-conferring mutation, depending on KIR3DL1/HLA-Bw4 allotypes.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-78
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 Mesylate	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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
34298678-8	2021	Accordingly, the ABL inhibitor imatinib and the FLT3 inhibitor quizartinib sensitize leukemic cells to pro-apoptotic effects of hydroxyurea.	Imatinib Mesylate	31-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-20
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 Mesylate	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 Mesylate	238-246	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	267-271
34422550-11	2021	Out of twenty-two patients, only 6 CML patients who were shifted from imatinib mesylate to nilotinib showed BCR-ABL-positive amplification.	nilotinib	91-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
34408976-6	2021	Here we report the activity of the mTORC1-selective bi-steric inhibitor, RMC-4627, in BCR-ABL-driven models of B-cell acute lymphoblastic leukemia (B-ALL).	RMC-4627	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
34110462-0	2021	Crizotinib acts as ABL1 inhibitor combining ATP-binding with allosteric inhibition and is active against native BCR-ABL1 and its resistance and compound mutants BCR-ABL1T315I and BCR-ABL1T315I-E255K.	Crizotinib	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-23
34110462-0	2021	Crizotinib acts as ABL1 inhibitor combining ATP-binding with allosteric inhibition and is active against native BCR-ABL1 and its resistance and compound mutants BCR-ABL1T315I and BCR-ABL1T315I-E255K.	Crizotinib	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-120
34110462-0	2021	Crizotinib acts as ABL1 inhibitor combining ATP-binding with allosteric inhibition and is active against native BCR-ABL1 and its resistance and compound mutants BCR-ABL1T315I and BCR-ABL1T315I-E255K.	Crizotinib	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	183-187
34110462-3	2021	Here we investigated the therapeutic potential of crizotinib, a TKI approved for targeting ALK and ROS1 in non-small cell lung cancer patients, which inhibited also the ABL1 kinase in cell-free systems, for the treatment of advanced and therapy-resistant Ph+ leukemia.	Crizotinib	50-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	169-173
34156283-2	2021	The BCR-ABL protein leads to an increased level of reactive oxygen species, which is a major cause of endogenous DNA double-strand breaks (DSBs).	Reactive Oxygen Species	51-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-11
34399819-12	2021	Using cell lines derived from conditional MYC, RAS, and BCR-ABL transgenic murine models, we demonstrate shared responses to inhibition of lipogenesis by the acetyl-coA carboxylase inhibitor 5-(tetradecloxy)-2-furic acid (TOFA), and other lipogenesis inhibitors.	5-(tetradecloxy)-2-furic acid	191-220	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
34399819-12	2021	Using cell lines derived from conditional MYC, RAS, and BCR-ABL transgenic murine models, we demonstrate shared responses to inhibition of lipogenesis by the acetyl-coA carboxylase inhibitor 5-(tetradecloxy)-2-furic acid (TOFA), and other lipogenesis inhibitors.	5-(tetradecyloxy)-2-furancarboxylic acid	222-226	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
34399819-16	2021	In a panel of human cell lines, we demonstrate sensitivity to TOFA treatment as a metabolic liability due to the general convergence on de novo lipogenesis in lymphoid malignancies driven by MYC, RAS, or BCR-ABL.	5-(tetradecyloxy)-2-furancarboxylic acid	62-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	204-211
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 Mesylate	141-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-18
34298678-8	2021	Accordingly, the ABL inhibitor imatinib and the FLT3 inhibitor quizartinib sensitize leukemic cells to pro-apoptotic effects of hydroxyurea.	Hydroxyurea	128-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-20
34195988-1	2021	Dasatinib is a second-generation BCR-ABL1 tyrosine kinase inhibitor approved for patients with chronic myeloid leukaemia (CML).	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-41
34238254-11	2021	We observed correct detection of expected direct (ABL, KIT, SRC) and indirect (MAPK) targets of Nilotinib in K562 as well as indirect (PRKC, MAPK, AKT, RPS6K) targets of Midostaurin in MOLM13/MV4-11, respectively.	nilotinib	96-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-53
34452901-3	2021	Glycolic acid concentrations as low as 0.12mM resulted in a >=20% positive bias in lactate assay on the ABL 800 and a concentration of approximately 0.23mM resulted in >20% on the Roche Cobas c502 and Abbott i-STAT.	glycolic acid	0-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-107
34452901-3	2021	Glycolic acid concentrations as low as 0.12mM resulted in a >=20% positive bias in lactate assay on the ABL 800 and a concentration of approximately 0.23mM resulted in >20% on the Roche Cobas c502 and Abbott i-STAT.	Lactic Acid	83-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-107
34452901-4	2021	A significant lactate gap is found at concentrations >0.06mM between the Radiometer ABL 800 and Roche Cobas c502/Abbott i-STAT.	Lactic Acid	14-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-87
34292760-4	2021	We here report the types of BCR-ABL mutations in Ethiopian imatinib-resistant patients with CML and their outcome.	Imatinib Mesylate	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-35
34114373-4	2021	Herein, we report that GZD824, athird generation ABL inhibitor (Phase II, China), overcomes FGFR1-V561F/M mutant resistance in vitro and in vivo.	olverembatinib	23-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-52
34292760-0	2021	Spectrum of BCR-ABL Mutations and Treatment Outcomes in Ethiopian Imatinib-Resistant Patients With Chronic Myeloid Leukemia.	Imatinib Mesylate	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
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 Mesylate	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	267-274
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 Mesylate	163-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-147
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.	Dasatinib	173-182	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-147
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.	ponatinib	187-196	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 Mesylate	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-26
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.	nilotinib	113-122	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.	ruxolitinib	108-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-148
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 Mesylate	123-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-148
34168229-0	2021	The c-Abl inhibitor, radotinib induces apoptosis in multiple myeloma cells via mitochondrial-dependent pathway.	4-methyl-N-(3-(4-methylimidazol-1-yl)-5-trifluoromethylphenyl)-3-(4-pyrazin-2-ylpyrimidin-2-ylamino)benzamide	21-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-9
34157051-8	2021	In both BCR-ABL positive and negative groups, three of five patients demonstrated marked cell growth inhibition in both MTT and trypan blue exclusion assays using 1.2PEI-Lau8/siRNA complexes in comparison with their control siRNA groups.	monooxyethylene trimethylolpropane tristearate	120-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-15
34157051-8	2021	In both BCR-ABL positive and negative groups, three of five patients demonstrated marked cell growth inhibition in both MTT and trypan blue exclusion assays using 1.2PEI-Lau8/siRNA complexes in comparison with their control siRNA groups.	Trypan Blue	128-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-15
34121617-0	2021	Electronic and structural study of T315I mutated form in DFG-out conformation of BCR-ABL inhibitors.	1,3-Diphenylguanidine	57-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-88
34117218-5	2021	Apoptosis of IM-resistant Ph+ALL cells with T315I mutation of BCR-ABL was also upregulated by LEN in the presence of the newly developed TKI ponatinib.	ponatinib	141-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
34117374-8	2021	Levels of phosphorylated BCR-ABL, AKT, STAT5, ERK, and p38 also decreased following cabozantinib treatment.	cabozantinib	84-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
34117374-11	2021	Second, cabozantinib inhibits K562 cell proliferation by inhibiting the phosphorylation of BCR-ABL and the downstream MAPK, PI3K-AKT, and JAK-STAT signaling pathways.	cabozantinib	8-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
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 Mesylate	115-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-146
34361750-7	2021	The interaction of betulin and ABL1 was studied by molecular docking, revealing an interaction of the inhibitor with the ABL1 ATP binding pocket.	betulin	19-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-35
34361750-7	2021	The interaction of betulin and ABL1 was studied by molecular docking, revealing an interaction of the inhibitor with the ABL1 ATP binding pocket.	betulin	19-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-125
34361750-7	2021	The interaction of betulin and ABL1 was studied by molecular docking, revealing an interaction of the inhibitor with the ABL1 ATP binding pocket.	Adenosine Triphosphate	126-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-35
34361750-7	2021	The interaction of betulin and ABL1 was studied by molecular docking, revealing an interaction of the inhibitor with the ABL1 ATP binding pocket.	Adenosine Triphosphate	126-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-125
34102989-0	2022	Brefeldin A Induces Apoptosis, Inhibits BCR-ABL Activation, and Triggers BCR-ABL Degradation in Chronic Myeloid Leukemia K562 Cells.	Brefeldin A	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
34102989-0	2022	Brefeldin A Induces Apoptosis, Inhibits BCR-ABL Activation, and Triggers BCR-ABL Degradation in Chronic Myeloid Leukemia K562 Cells.	Brefeldin A	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
34102989-6	2022	OBJECTIVE: This study was aimed to determine the cytotoxic activity of BFA and the effect on the activation and expression of BCR-ABL in K562 cells.	Brefeldin A	71-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
34102989-10	2022	Importantly, for the first time, we revealed that BFA inhibited the activation of BCR-ABL and consequently inhibited the activation of its downstream signaling molecules in K562 cells.	Brefeldin A	50-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
34102989-12	2022	CONCLUSION: Our present results indicate that BFA acts as a dual functional inhibitor and degrader of BCR-ABL, and BFA is a potential compound for chemotherapeutics to overcome CML.	Brefeldin A	46-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
34205064-4	2021	Among them, Src and Abl target CagA and stimulate tyrosine phosphorylation of the latter at its EPIYA-motifs.	Tyrosine	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-23
34136397-4	2021	Additionally, we show that the RUNX2 transcriptional activity is dependent on the number of its tyrosine residues that are phosphorylated by ABL.	Tyrosine	96-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-144
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 Mesylate	141-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
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 Mesylate	57-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
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 Mesylate	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-64
35500311-7	2022	Ultimately, the quenching labels of streptavidin modified Pt nanoparticles functionalized polydopamine composites (SA-Pt@PDA) were introduced via biotin and streptavidin recognition, realizing ECL emission quenching of S2O82-/O2 system for "on-off" detection of BCR-ABL fusion gene.	Platinum	58-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	262-269
35500311-7	2022	Ultimately, the quenching labels of streptavidin modified Pt nanoparticles functionalized polydopamine composites (SA-Pt@PDA) were introduced via biotin and streptavidin recognition, realizing ECL emission quenching of S2O82-/O2 system for "on-off" detection of BCR-ABL fusion gene.	polydopamine	90-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	262-269
35500311-7	2022	Ultimately, the quenching labels of streptavidin modified Pt nanoparticles functionalized polydopamine composites (SA-Pt@PDA) were introduced via biotin and streptavidin recognition, realizing ECL emission quenching of S2O82-/O2 system for "on-off" detection of BCR-ABL fusion gene.	2-chloro-10-(4'(N-beta-hydroxyethyl)piperazinyl-1')acetylphenothiazine	115-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	262-269
35500311-7	2022	Ultimately, the quenching labels of streptavidin modified Pt nanoparticles functionalized polydopamine composites (SA-Pt@PDA) were introduced via biotin and streptavidin recognition, realizing ECL emission quenching of S2O82-/O2 system for "on-off" detection of BCR-ABL fusion gene.	Platinum	118-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	262-269
35500311-7	2022	Ultimately, the quenching labels of streptavidin modified Pt nanoparticles functionalized polydopamine composites (SA-Pt@PDA) were introduced via biotin and streptavidin recognition, realizing ECL emission quenching of S2O82-/O2 system for "on-off" detection of BCR-ABL fusion gene.	Biotin	146-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	262-269
35500311-7	2022	Ultimately, the quenching labels of streptavidin modified Pt nanoparticles functionalized polydopamine composites (SA-Pt@PDA) were introduced via biotin and streptavidin recognition, realizing ECL emission quenching of S2O82-/O2 system for "on-off" detection of BCR-ABL fusion gene.	s2o82	219-224	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	262-269
35500311-7	2022	Ultimately, the quenching labels of streptavidin modified Pt nanoparticles functionalized polydopamine composites (SA-Pt@PDA) were introduced via biotin and streptavidin recognition, realizing ECL emission quenching of S2O82-/O2 system for "on-off" detection of BCR-ABL fusion gene.	Oxygen	226-228	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	262-269
35597499-15	2022	This strategy identified the toxic target, ABL1, and the potential toxic mechanism of psoralen.	Ficusin	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-47
35570245-2	2022	Through glucose metabolism, glycolysis, and the translocation of the high-affinity glucose transporter to the cell surface, BCR-ABL modulates various signaling pathways in CML cells and maintains ATP turnover in tumor cells.	Glucose	83-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
35597499-9	2022	Based on the above experimental results, ABL1 is a potential direct target of psoralen-induced hepatotoxicity.	Ficusin	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-45
35597499-11	2022	The direct target ABL1 is located upstream of Nrf2 and mTOR, Nrf2 can influence the expression of mTOR by affecting the level of reactive oxygen species.	Oxygen	138-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-22
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 Mesylate	174-182	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-163
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.	Phenytoin	200-203	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-163
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.	Phenytoin	200-203	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	187-191
35597499-13	2022	In summary, we speculated that when psoralen causes hepatotoxicity, it acts on the direct target ABL1, resulting in a decrease in Nrf2 expression, an increase in ROS levels and a reduction in mTOR expression, which may cause cell death.	Ficusin	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-101
35597499-13	2022	In summary, we speculated that when psoralen causes hepatotoxicity, it acts on the direct target ABL1, resulting in a decrease in Nrf2 expression, an increase in ROS levels and a reduction in mTOR expression, which may cause cell death.	ros	162-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-101
35583386-4	2022	Asciminib, a first-in-class BCR::ABL1 inhibitor Specifically Targeting the ABL Myristoyl Pocket (STAMP), has the potential to overcome resistance/intolerance to prior TKI treatment.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-37
35624462-0	2022	The HSP90 inhibitor KW-2478 depletes the malignancy of BCR/ABL and overcomes the imatinib-resistance caused by BCR/ABL amplification.	KW-2478	20-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-62
35624462-0	2022	The HSP90 inhibitor KW-2478 depletes the malignancy of BCR/ABL and overcomes the imatinib-resistance caused by BCR/ABL amplification.	KW-2478	20-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-118
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 Mesylate	81-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-118
35616006-1	2022	Asciminib is a first-in-class inhibitor of BCR::ABL1, specifically targeting the ABL myristoyl pocket.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-52
35616006-1	2022	Asciminib is a first-in-class inhibitor of BCR::ABL1, specifically targeting the ABL myristoyl pocket.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-84
35570245-2	2022	Through glucose metabolism, glycolysis, and the translocation of the high-affinity glucose transporter to the cell surface, BCR-ABL modulates various signaling pathways in CML cells and maintains ATP turnover in tumor cells.	Adenosine Triphosphate	196-199	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
35550008-6	2022	These in situ abnormalities were also replicated in vitro, with cultured PAH-ECs displaying lower cAbl expression and activity and an altered DNA damage response and capacity of tube formation.	pah-ecs	73-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-102
35550008-7	2022	Downregulation of cAbl by RNA-interference in Control-ECs or its inhibition with dasatinib resulted in genomic instability and the failure to form tubes, whereas upregulation of cAbl with DPH reduced DNA damage and apoptosis in PAH-ECs.	Dasatinib	81-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-22
35550008-7	2022	Downregulation of cAbl by RNA-interference in Control-ECs or its inhibition with dasatinib resulted in genomic instability and the failure to form tubes, whereas upregulation of cAbl with DPH reduced DNA damage and apoptosis in PAH-ECs.	Phenytoin	188-191	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-182
35570519-4	2022	METHODS: Cell viability of K562 and R/K562 cells, antiproliferative and antioxidant effects, and inhibition profiles of Bcr-Abl kinase of indole derivatives were determined in comparison to dasatinib and imatinib.	indole	138-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-127
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 Mesylate	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-25
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).	Dasatinib	77-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-25
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).	nilotinib	88-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-25
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).	ponatinib	102-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-25
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 Mesylate	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 Mesylate	129-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
35561654-0	2022	Design, synthesis, and biological evaluation of trizole-based heteroaromatic derivatives as Bcr-Abl kinase inhibitors.	tricyclazole	48-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
35561654-3	2022	As a continuation to our research, a series of compounds with heteroaromatics-trizole scaffold as hinge binding moiety (HBM) were developed as Bcr-Abl inhibitors based on in silico modeling analysis.	tricyclazole	78-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-150
35561654-10	2022	Therefore, aromatic heterocycles incorporated with trizole could serve as a promising HBM for Bcr-Abl inhibitors with proline as fexibile linker, and compounds 9f, 28c, especially 44c could be served as a starting point for further optimization.	tricyclazole	51-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
35561654-10	2022	Therefore, aromatic heterocycles incorporated with trizole could serve as a promising HBM for Bcr-Abl inhibitors with proline as fexibile linker, and compounds 9f, 28c, especially 44c could be served as a starting point for further optimization.	Proline	118-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
35131002-0	2022	Lactate maintainsBCR/Abl expression and signalinginChronic Myeloid Leukemia cells under nutrient restriction.	Lactic Acid	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-24
35131002-4	2022	The results obtained indicated that lactate is a powerful surrogate of glucose to prevent the suppression of BCR/Abl signaling and is therefore capable to maintain BCR/Abl-dependent CML stem/progenitor cell potential.	Lactic Acid	36-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-116
35131002-4	2022	The results obtained indicated that lactate is a powerful surrogate of glucose to prevent the suppression of BCR/Abl signaling and is therefore capable to maintain BCR/Abl-dependent CML stem/progenitor cell potential.	Lactic Acid	36-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	168-171
35131002-4	2022	The results obtained indicated that lactate is a powerful surrogate of glucose to prevent the suppression of BCR/Abl signaling and is therefore capable to maintain BCR/Abl-dependent CML stem/progenitor cell potential.	Glucose	71-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-116
35131002-4	2022	The results obtained indicated that lactate is a powerful surrogate of glucose to prevent the suppression of BCR/Abl signaling and is therefore capable to maintain BCR/Abl-dependent CML stem/progenitor cell potential.	Glucose	71-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	168-171
35412404-2	2022	AREAS COVERED: In this review, the authors discuss the role of ponatinib, an oral pan-inhibitor of BCR-ABL1, with potent activity in heavily pretreated patients, including T315I mutation.	ponatinib	63-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-107
35544670-6	2022	EXPERT OPINION: Ponatinib is a potent pan-BCR-ABL1 TKI with substantial activity in patients with more resistant or advanced CML.	ponatinib	16-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-50
35571170-1	2022	Background: The long-term outcomes of ablation with vein of Marshall ethanol infusion (VOM-ABL) compared with ablation alone in patients with atrial fibrillation (AF) remains elusive.	Ethanol	69-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-94
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 Mesylate	165-173	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-152
35470777-4	2022	According to the data obtained, these compounds exhibit close modes of binding to the Abl kinase active site that are mainly provided by hydrogen bonds and multiple van der Waals contacts.	Hydrogen	137-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-89
35402127-1	2022	The BCR-ABL1 tyrosine kinase inhibitor dasatinib is effective in chronic myeloid leukemia (CML) treatment.	Dasatinib	39-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-12
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 Mesylate	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-99
35468180-1	2022	Asciminib, a first-in-class allosteric inhibitor of BCR::ABL1 kinase activity, is now approved for the treatment of chronic phase CML patients who failed 2 lines of therapy or in patients with the T315I mutation.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-61
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 Mesylate	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-162
35443725-4	2022	2-deoxy-d-glucose (2-DG) was used to modulate the glucose metabolism in CML cells sensitive to IM (KBM5 cell line) and resistant to imatinib with BCR-ABL T315I mutation (KBM5-T315I cell line).	Glucose	10-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-153
35443725-4	2022	2-deoxy-d-glucose (2-DG) was used to modulate the glucose metabolism in CML cells sensitive to IM (KBM5 cell line) and resistant to imatinib with BCR-ABL T315I mutation (KBM5-T315I cell line).	Deoxyglucose	19-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-153
35438229-5	2022	Among them, the salicylaldehyde-containing A5 is the first-ever reversible covalent ABL inhibitor that possessed time-dependent ABL inhibition with prolonged residence time and few cellular off-targets in K562 cells.	salicylaldehyde	16-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-87
35438229-5	2022	Among them, the salicylaldehyde-containing A5 is the first-ever reversible covalent ABL inhibitor that possessed time-dependent ABL inhibition with prolonged residence time and few cellular off-targets in K562 cells.	salicylaldehyde	16-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-131
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 Mesylate	110-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-8
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 Mesylate	168-176	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	205-209
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 Mesylate	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
35129779-2	2022	Asciminib has been recently (2021) approved for patients resistant to former TKIs, and because the binding site of this drug (the myristoyl pocket in the ABL1 kinase) is different from that of other TKIs (ATP-binding sites), it is, therefore, effective against T315I mutation of BCR-ABL oncoprotein.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-158
35129779-2	2022	Asciminib has been recently (2021) approved for patients resistant to former TKIs, and because the binding site of this drug (the myristoyl pocket in the ABL1 kinase) is different from that of other TKIs (ATP-binding sites), it is, therefore, effective against T315I mutation of BCR-ABL oncoprotein.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	279-286
35129779-2	2022	Asciminib has been recently (2021) approved for patients resistant to former TKIs, and because the binding site of this drug (the myristoyl pocket in the ABL1 kinase) is different from that of other TKIs (ATP-binding sites), it is, therefore, effective against T315I mutation of BCR-ABL oncoprotein.	Adenosine Triphosphate	205-208	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-158
35531147-7	2022	The target profile of the dual SRC/ABL inhibitor bosutinib was studied in this study as a first kinase inhibitor to target K562 cells, which has recently been linked to the proliferation of myelogenous leukaemia cells, these results suggest the effectiveness of inhibitory activity on cell viability/proliferation, alone generated a potent value of 250 nM (39.27 +- 1.17) for 48 h as optimal dose.	bosutinib	49-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
35407383-0	2022	In BCR-ABL1 Positive B-Cell Acute Lymphoblastic Leukemia, Steroid Therapy Induces Hypofibrinogenemia.	Steroids	58-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	7-11
35407383-5	2022	In univariate analysis, such a steroid-related HF was significantly associated with BCR-ABL1 rearrangement (p = 0.00158).	Steroids	31-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-92
35407383-7	2022	Our retrospective study suggests that in B-ALL, steroid therapy can also induce HF and that such an event is preferentially observed in patients carrying BCR-ABL1 rearrangements.	Steroids	48-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-162
35337107-1	2022	Imatinib (IMT) is the first-in-class BCR-ABL commercial tyrosine kinase inhibitor (TKI).	Imatinib Mesylate	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 Mesylate	10-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
35337107-7	2022	Molecular docking results suggest that the interaction between the most active inhibitor 2g and the BCR-ABL1 enzyme occurs at the bosutinib binding site through a competitive inhibition mechanism.	bosutinib	130-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-108
35021069-5	2022	It binds to the ABL1 myristoyl-binding pocket and is effective against most ABL1 kinase domain mutations that confer resistance to ATP-competitive TKIs, including the T315I mutation.	Adenosine Triphosphate	131-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-20
35021069-5	2022	It binds to the ABL1 myristoyl-binding pocket and is effective against most ABL1 kinase domain mutations that confer resistance to ATP-competitive TKIs, including the T315I mutation.	Adenosine Triphosphate	131-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-80
35172577-2	2022	Here, we report the design of unique hybrid molecules by combining the two pharmacophores of clinically approved BCR-ABL inhibitor (ponatinib) and HDAC inhibitor (vorinostat) and results of in vitro studies in drug-resistant CML cells.	ponatinib	132-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-120
35172577-4	2022	The developed 2D-QSAR model showed five information rich molecular descriptors while the 3D-pharmacophore model of BCR-ABL showed five different chemical features (hydrogen bond acceptor, donor, hydrophobic group, positive ion group, and aromatic rings) and the HDAC model showed four different chemical features (hydrogen bond acceptor, donor, positive ion group, and aromatic rings) for potent BCR-ABL and HDAC inhibition.	Hydrogen	164-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-122
35172577-4	2022	The developed 2D-QSAR model showed five information rich molecular descriptors while the 3D-pharmacophore model of BCR-ABL showed five different chemical features (hydrogen bond acceptor, donor, hydrophobic group, positive ion group, and aromatic rings) and the HDAC model showed four different chemical features (hydrogen bond acceptor, donor, positive ion group, and aromatic rings) for potent BCR-ABL and HDAC inhibition.	Hydrogen	314-322	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-122
35080463-3	2022	Here, we show that apoptotic body like liposomes loaded with phosphatidylinositol 5-phosphate (ABL/PI5P) enhance the antimycobacterial response, both in macrophages from healthy donors exposed to pharmacological inhibition of cystic fibrosis transmembrane conductance regulator (CFTR) and in macrophages from CF patients, by enhancing phagosome acidification and reactive oxygen species (ROS) production.	phosphatidylinositol 5-phosphate	61-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-103
35080463-3	2022	Here, we show that apoptotic body like liposomes loaded with phosphatidylinositol 5-phosphate (ABL/PI5P) enhance the antimycobacterial response, both in macrophages from healthy donors exposed to pharmacological inhibition of cystic fibrosis transmembrane conductance regulator (CFTR) and in macrophages from CF patients, by enhancing phagosome acidification and reactive oxygen species (ROS) production.	Reactive Oxygen Species	363-386	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-103
35080463-3	2022	Here, we show that apoptotic body like liposomes loaded with phosphatidylinositol 5-phosphate (ABL/PI5P) enhance the antimycobacterial response, both in macrophages from healthy donors exposed to pharmacological inhibition of cystic fibrosis transmembrane conductance regulator (CFTR) and in macrophages from CF patients, by enhancing phagosome acidification and reactive oxygen species (ROS) production.	Reactive Oxygen Species	388-391	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-103
35193953-5	2022	We identified that RtcB, the tRNA ligase responsible for XBP1 mRNA splicing, is tyrosine-phosphorylated by c-Abl and dephosphorylated by PTP1B.	Tyrosine	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-112
35256549-0	2022	Dasatinib-induced reversible pulmonary arterial hypertension in a pediatric patient with BCR/ABL1+ lymphoblastic lymphoma from chronic myeloid leukemia.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-97
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 Mesylate	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 Mesylate	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 Mesylate	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	353-358
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.	nilotinib	323-332	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.	neurotinib	337-347	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-35
35449618-1	2022	Bosutinib is a breakpoint cluster region-Abelson gene (BCR-ABL) tyrosine kinase inhibitor (TKI) used for the treatment of chronic myeloid leukemia (CML).	bosutinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
35021069-0	2022	Development of Asciminib, a Novel Allosteric Inhibitor of BCR-ABL1.	asciminib	15-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-66
35021069-2	2022	Approved tyrosine kinase inhibitors (TKIs) for CML inhibit BCR-ABL1 by competitively targeting its adenosine triphosphate (ATP)-binding site, which significantly improves patient outcomes.	Adenosine	99-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-67
35021069-2	2022	Approved tyrosine kinase inhibitors (TKIs) for CML inhibit BCR-ABL1 by competitively targeting its adenosine triphosphate (ATP)-binding site, which significantly improves patient outcomes.	Adenosine Triphosphate	123-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-67
35021069-4	2022	Asciminib is a promising investigational agent in development that allosterically targets BCR-ABL1 in a non-ATP-competitive manner.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-98
35195876-1	2022	Olverembatinib (HQP1351) is an oral, third-generation BCR-ABL1 tyrosine kinase inhibitor (TKI) developed by Ascentage Pharma for the treatment of chronic myeloid leukaemia (CML), acute myeloid leukaemia, acute lymphoblastic leukaemia (ALL) and solid tumours, including gastrointestinal stromal tumours (GIST).	olverembatinib	0-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-62
35195876-2	2022	Olverembatinib is an ATP binding-site inhibitor of wild type BCR-ABL1 kinase and a broad spectrum of BCR-ABL1 mutants, including mutant T315I, which confers resistance against all first- and second-generation TKIs.	olverembatinib	0-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-69
35195876-2	2022	Olverembatinib is an ATP binding-site inhibitor of wild type BCR-ABL1 kinase and a broad spectrum of BCR-ABL1 mutants, including mutant T315I, which confers resistance against all first- and second-generation TKIs.	olverembatinib	0-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-109
35195876-2	2022	Olverembatinib is an ATP binding-site inhibitor of wild type BCR-ABL1 kinase and a broad spectrum of BCR-ABL1 mutants, including mutant T315I, which confers resistance against all first- and second-generation TKIs.	Adenosine Triphosphate	21-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-69
35072462-4	2022	CABL photocatalysts are based on fluorescein or silarhodamine dyes with activation at 470 or 660 nm.	Fluorescein	33-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-4
35237274-4	2022	In this study, we have evaluated, in an in vitro model of human macrophages, the efficacy of a combined treatment consisting of apoptotic body-like liposomes loaded with phosphatidylinositol 5-phosphate (ABL/PI5P) and phiBO1E, a lytic phage specific for the major high-risk clone of KPC-positive MDR-KP.	phosphatidylinositol 5-phosphate	170-202	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	204-212
35072462-4	2022	CABL photocatalysts are based on fluorescein or silarhodamine dyes with activation at 470 or 660 nm.	silarhodamine	48-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-4
35072462-8	2022	CABL was also applied to spatially resolved live-cell labeling of an endogenous protein target by using TIRF microscopy to selectively activate intracellular monoacylglycerol lipase tagged with DHTz-labeled small molecule covalent inhibitor.	Monoglycerides	158-174	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-4
35072462-8	2022	CABL was also applied to spatially resolved live-cell labeling of an endogenous protein target by using TIRF microscopy to selectively activate intracellular monoacylglycerol lipase tagged with DHTz-labeled small molecule covalent inhibitor.	dhtz	194-198	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-4
35072462-9	2022	Beyond spatiotemporally controlled labeling, CABL also improves the efficiency of "ordinary" tetrazine ligations by rescuing the reactivity of commonly used 3-aryl-6-methyltetrazine reporters that become partially reduced to DHTzs inside cells.	1,2,3,4-tetrazine	93-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-49
35072462-9	2022	Beyond spatiotemporally controlled labeling, CABL also improves the efficiency of "ordinary" tetrazine ligations by rescuing the reactivity of commonly used 3-aryl-6-methyltetrazine reporters that become partially reduced to DHTzs inside cells.	3-aryl-6-methyltetrazine	157-181	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-49
35072462-9	2022	Beyond spatiotemporally controlled labeling, CABL also improves the efficiency of "ordinary" tetrazine ligations by rescuing the reactivity of commonly used 3-aryl-6-methyltetrazine reporters that become partially reduced to DHTzs inside cells.	dhtzs	225-230	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-49
35041175-1	2022	Asciminib (Scemblix ) is an orally administered, small molecule, selective allosteric inhibitor that targets the myristoyl pocket of the BCR-ABL1 tyrosine kinase and is being developed by Novartis for the treatment of haematological malignancies, including Philadelphia chromosome-positive (Ph+) chronic myeloid leukaemia (CML).	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-145
35041175-1	2022	Asciminib (Scemblix ) is an orally administered, small molecule, selective allosteric inhibitor that targets the myristoyl pocket of the BCR-ABL1 tyrosine kinase and is being developed by Novartis for the treatment of haematological malignancies, including Philadelphia chromosome-positive (Ph+) chronic myeloid leukaemia (CML).	asciminib	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-145
35041175-2	2022	The drug is active against a number of the single catalytic-site mutations, such as T315I, that confer resistance to conventional tyrosine kinase inhibitors (TKIs) that bind to the ATP-binding site of BCR-ABL1.	Adenosine Triphosphate	181-184	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	205-209
3477472-0	1987	The bcr-c-abl tyrosine kinase activity is extinguished by TPA in K562 leukemia cells.	Tetradecanoylphorbol Acetate	58-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-13
35205374-2	2022	The first-line treatment for CML is imatinib, a tyrosine kinase inhibitor that acts on the BCR-ABL protein.	Imatinib Mesylate	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
35085070-4	2022	RESULTS: The ROS concentration was increased respectively about 10-12 times in C. albicans and about 3-6 times in human epithelial cells by the ABL treatment with the same fluence of 90J/cm2.	Reactive Oxygen Species	13-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-147
2910452-4	1989	In order to understand the relationship between induction of differentiation and reduction of tyrosine phosphorylation by the c-abl gene product, the effect that herbimycin A, a selective inhibitor of intracellular tyrosine kinase activity, exerts on the differentiation of K562 cells was examined.	Tyrosine	94-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-131
2910452-4	1989	In order to understand the relationship between induction of differentiation and reduction of tyrosine phosphorylation by the c-abl gene product, the effect that herbimycin A, a selective inhibitor of intracellular tyrosine kinase activity, exerts on the differentiation of K562 cells was examined.	herbimycin	162-174	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-131
35092492-2	2022	For this purpose, dasatinib is the second-generation tyrosine kinase inhibitor that is used for inhibition of BCR-ABL.	Dasatinib	18-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
35164068-6	2022	Our results showed that 2-hydroxyestradiol (2HE2), a metabolite of estradiol, and dasatinib, an Abl/Src kinase inhibitor, were significantly effective in overcoming MSC-mediated platinum drug resistance.	Dasatinib	82-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-99
35164068-6	2022	Our results showed that 2-hydroxyestradiol (2HE2), a metabolite of estradiol, and dasatinib, an Abl/Src kinase inhibitor, were significantly effective in overcoming MSC-mediated platinum drug resistance.	Platinum	178-186	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-99
34994556-5	2022	We further establish that EN106 can be used as a covalent recruiter for FEM1B in TPD applications by demonstrating that a PROTAC linking EN106 to the BET bromodomain inhibitor JQ1 or the kinase inhibitor dasatinib leads to the degradation of BRD4 and BCR-ABL, respectively.	EN106	26-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	251-258
34994556-5	2022	We further establish that EN106 can be used as a covalent recruiter for FEM1B in TPD applications by demonstrating that a PROTAC linking EN106 to the BET bromodomain inhibitor JQ1 or the kinase inhibitor dasatinib leads to the degradation of BRD4 and BCR-ABL, respectively.	EN106	137-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	251-258
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 Mesylate	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-174
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).	nilotinib	92-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-174
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).	bosutinib	103-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-174
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).	ponatinib	118-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-174
34980123-10	2022	Interestingly, it was significantly induced in Abl-positive leukemic cells treated by imatinib.	Imatinib Mesylate	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
2600041-8	1989	The ABL method appeared to combine two linear trends: for SO2 greater than 75%, ABL = 0.84 CO-OX +14.4, SEE = 1.77, r = 0.97, n = 369; less than 75%, ABL = 0.98 CO-OX +5.9, SEE = 4.44, r = 0.97, n = 486.	Sulfur Dioxide	58-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
2600041-8	1989	The ABL method appeared to combine two linear trends: for SO2 greater than 75%, ABL = 0.84 CO-OX +14.4, SEE = 1.77, r = 0.97, n = 369; less than 75%, ABL = 0.98 CO-OX +5.9, SEE = 4.44, r = 0.97, n = 486.	Sulfur Dioxide	58-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
2600041-8	1989	The ABL method appeared to combine two linear trends: for SO2 greater than 75%, ABL = 0.84 CO-OX +14.4, SEE = 1.77, r = 0.97, n = 369; less than 75%, ABL = 0.98 CO-OX +5.9, SEE = 4.44, r = 0.97, n = 486.	Sulfur Dioxide	58-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
2600041-8	1989	The ABL method appeared to combine two linear trends: for SO2 greater than 75%, ABL = 0.84 CO-OX +14.4, SEE = 1.77, r = 0.97, n = 369; less than 75%, ABL = 0.98 CO-OX +5.9, SEE = 4.44, r = 0.97, n = 486.	Carbon Monoxide	91-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
2600041-8	1989	The ABL method appeared to combine two linear trends: for SO2 greater than 75%, ABL = 0.84 CO-OX +14.4, SEE = 1.77, r = 0.97, n = 369; less than 75%, ABL = 0.98 CO-OX +5.9, SEE = 4.44, r = 0.97, n = 486.	Carbon Monoxide	91-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
2600041-8	1989	The ABL method appeared to combine two linear trends: for SO2 greater than 75%, ABL = 0.84 CO-OX +14.4, SEE = 1.77, r = 0.97, n = 369; less than 75%, ABL = 0.98 CO-OX +5.9, SEE = 4.44, r = 0.97, n = 486.	Carbon Monoxide	91-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
2672339-4	1989	The c-abl antisense oligodeoxynucleotides inhibited myeloid, but not erythroid, colony formation.	Oligodeoxyribonucleotides	20-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-9
3477472-3	1987	In the present work the activity of the c-abl and c-src oncogene-encoded tyrosine kinase was investigated during phorbol diester (TPA) induced differentiation of the K562 CML cells.	Phorbol Esters	113-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-45
3477472-3	1987	In the present work the activity of the c-abl and c-src oncogene-encoded tyrosine kinase was investigated during phorbol diester (TPA) induced differentiation of the K562 CML cells.	Tetradecanoylphorbol Acetate	130-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-45
3477472-4	1987	The high tyrosine kinase activity of p210bcr-c-abl is strongly reduced during the initial 24 h of TPA treatment.	Tetradecanoylphorbol Acetate	98-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-50
3477472-8	1987	Sodium butyrate caused a slight decrease in growth rate and of bcr-c-abl kinase activity during erythroid differentiation whereas no changes in c-src or c-abl tyrosine kinase activities were seen in DMSO-treated control cells.	Butyric Acid	0-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-72
2440557-6	1987	The bcr/c-abl protein synthesis was reduced in hemin-treated K-562 cells.	Hemin	47-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-13
2440107-6	1987	During the course of these experiments, a transforming recombinant of bcr/abl was isolated which fuses gag determinants derived from helper virus to the NH2-terminus of the bcr/abl protein.	Glycosaminoglycans	103-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
2440107-6	1987	During the course of these experiments, a transforming recombinant of bcr/abl was isolated which fuses gag determinants derived from helper virus to the NH2-terminus of the bcr/abl protein.	Glycosaminoglycans	103-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	173-180
2440107-7	1987	This suggests that a property of viral gag sequences, probably myristylation-dependent membrane localization, must be provided to bcr/abl for it to transform fibroblasts.	Glycosaminoglycans	39-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
2431286-3	1986	The p210 protein was also recognized by antisera against v-abl-encoded polypeptides and displayed kinase activity, phosphorylating itself on tyrosine, in an immunocomplex kinase assay.	Tyrosine	141-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-62
2894000-7	1987	With respect to allele A, allele B contains a deletion of about 1 kb lying in a intronic region in close proximity to highly repetitive Alu sequences and the sequence coding for phosphotyrosine of the c-abl protein.	Phosphotyrosine	178-193	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	201-206
2431286-9	1986	Enhanced tyrosine phosphorylation of cellular proteins is thus a feature shared by cells transformed by v-abl and cells expressing a rearranged bcr-abl gene.	Tyrosine	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-109
2431286-9	1986	Enhanced tyrosine phosphorylation of cellular proteins is thus a feature shared by cells transformed by v-abl and cells expressing a rearranged bcr-abl gene.	Tyrosine	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
3010299-1	1986	A restriction fragment length polymorphism at the human c-abl locus (ABL) has been detected in 67 unrelated individuals by agarose gel electrophoresis and Southern blot hybridization using 32P-labeled v-abl probes.	Sepharose	123-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-61
3010299-1	1986	A restriction fragment length polymorphism at the human c-abl locus (ABL) has been detected in 67 unrelated individuals by agarose gel electrophoresis and Southern blot hybridization using 32P-labeled v-abl probes.	Sepharose	123-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-72
3010299-1	1986	A restriction fragment length polymorphism at the human c-abl locus (ABL) has been detected in 67 unrelated individuals by agarose gel electrophoresis and Southern blot hybridization using 32P-labeled v-abl probes.	Phosphorus-32	189-192	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-61
3010299-1	1986	A restriction fragment length polymorphism at the human c-abl locus (ABL) has been detected in 67 unrelated individuals by agarose gel electrophoresis and Southern blot hybridization using 32P-labeled v-abl probes.	Phosphorus-32	189-192	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-72
3010299-1	1986	A restriction fragment length polymorphism at the human c-abl locus (ABL) has been detected in 67 unrelated individuals by agarose gel electrophoresis and Southern blot hybridization using 32P-labeled v-abl probes.	Phosphorus-32	189-192	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	201-206
3010299-3	1986	The minor allele, b, is due to a deletion of about 500 base pairs in an intron located downstream of the codon for the phosphate-acceptor tyrosine residue of the c-abl gene product.	Phosphates	119-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-167
3010299-3	1986	The minor allele, b, is due to a deletion of about 500 base pairs in an intron located downstream of the codon for the phosphate-acceptor tyrosine residue of the c-abl gene product.	Tyrosine	138-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-167
2420727-0	1986	Protein phosphorylation at tyrosine residues in v-abl transformed mouse lymphocytes and fibroblasts.	Tyrosine	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-53
2420727-2	1986	In pre-B and pre-T lymphoma cells transformed by A-MuLV, the major phosphotyrosine-containing protein has an MW of 160 kDa and shares immunologically detectable sequences with the v-abl oncogene product.	Phosphotyrosine	67-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	180-185
2420727-10	1986	These data show that, upon v-abl-induced transformation, phosphorylation at tyrosine takes place also on proteins other than the 160 or 120-kDa oncogene products.	Tyrosine	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-32
2420727-11	1986	In lymphocytes and fibroblasts these proteins are different, suggesting that the cascade of events triggered by the v-abl gene in different cell types involves tyrosine phosphorylation of different specific proteins.	Tyrosine	160-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-121
6306446-2	1983	The probe detected two cytoplasmic polyadenylic acid-containing c-abl RNAs of about 6.5 and 5.5 kilobases in a variety of rodent cells, and slightly larger RNAs were detected in human cells.	Poly A	35-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-69
2425967-0	1986	Methylation and expression of c-myc and c-abl oncogenes in human leukemic K562 cells before and after treatment with 5-azacytidine.	Azacitidine	117-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-45
6088787-0	1984	A membrane-associated, carbohydrate-modified form of the v-abl protein that cannot be phosphorylated in vivo or in vitro.	Carbohydrates	23-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-62
6191223-0	1983	Homology between phosphotyrosine acceptor site of human c-abl and viral oncogene products.	Phosphotyrosine	17-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-61
6191223-3	1983	In the present study, sequences encoding the tyrosine phosphorylation acceptor sites of the Abelson murine leukaemia virus oncogene, v-abl, and its human cellular homologue, c-abl, have been identified and their nucleic acid sequences determined.	Tyrosine	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-179
3879812-4	1985	It was found that the Formalin-fixed Staphylococcus aureus formerly used for immunoprecipitation inhibits in vitro abl kinase activity.	Formaldehyde	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-118
3879812-5	1985	In addition, the sodium dodecyl sulfate and deoxycholate detergents formerly used in the cell lysis buffer were found to decrease recovered abl kinase activity.	Sodium Dodecyl Sulfate	17-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-143
3879812-5	1985	In addition, the sodium dodecyl sulfate and deoxycholate detergents formerly used in the cell lysis buffer were found to decrease recovered abl kinase activity.	Deoxycholic Acid	44-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-143
3879812-8	1985	Comparison of in vitro and in vivo tyrosine phosphorylation sites of the abl proteins suggests that they function differently in vivo.	Tyrosine	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-76
2982232-3	1985	One antiserum was made against a polypeptide overlapping the in vivo tyrosine phosphorylation site of murine P120gag-abl and what is believed to be a homologous tyrosine phosphorylation site of the predicted normal human c-abl gene product (v-abl 263-280).	Tyrosine	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-120
2982232-7	1985	Immune complex kinase assays using conditions that allow the tyrosine phosphorylation of P120gag-abl showed that in vitro phosphorylation of P190 and P240 occurs primarily at tyrosine residues.	Tyrosine	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-100
33907977-4	2021	Ponatinib is a third generation TKI that demonstrates higher binding affinity for ABL1 than first/second generation TKIs.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-86
1261088-1	1976	Lymphocytes that could bind 125I-labelled thyroid microsomal membranes (ABL) were present in the peripheral blood of patients with various types of thyroid disease as well as in normal healthy subjects.	Iodine-125	28-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-75
34011155-0	2021	Discovery of a Candidate Containing an (S)-3,3-Difluoro-1-(4-methylpiperazin-1-yl)-2,3-dihydro-1H-inden Scaffold as a Highly Potent Pan-Inhibitor of the BCR-ABL Kinase Including the T315I-Resistant Mutant for the Treatment of Chronic Myeloid Leukemia.	(s)-3,3-difluoro-1-(4-methylpiperazin-1-yl)-2,3-dihydro-1h-inden	39-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-160
34011155-2	2021	Herein, we report compound 3a-P1, bearing a difluoro-indene scaffold, as a novel potent pan-inhibitor against BCR-ABL mutants, including the most refractory T315I mutant.	3a-p1	27-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-117
34015503-1	2021	The anti-chronic myeloid leukemia activity of thiazole aminobenzamide derivatives in vitro was tested by a methanethiosulfonate (MTS)-based viability assay method, and the result showed that some compounds exhibited good inhibitory activities against human chronic myeloid leukemia cell line K562, imatinib-resistant strain K562/R and T135I mutant cell line BaF3-ABL-BCR-T315I.	thiazole aminobenzamide	46-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	363-366
33963175-6	2021	Furthermore, we find the antimalarial artesunate (ART) significantly inhibits USP7/BCR-ABL interaction, thereby promoting BCR-ABL degradation and inducing CML cell death.	Artesunate	38-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
33963175-6	2021	Furthermore, we find the antimalarial artesunate (ART) significantly inhibits USP7/BCR-ABL interaction, thereby promoting BCR-ABL degradation and inducing CML cell death.	Artesunate	38-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
33963175-6	2021	Furthermore, we find the antimalarial artesunate (ART) significantly inhibits USP7/BCR-ABL interaction, thereby promoting BCR-ABL degradation and inducing CML cell death.	Artesunate	50-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
33963175-6	2021	Furthermore, we find the antimalarial artesunate (ART) significantly inhibits USP7/BCR-ABL interaction, thereby promoting BCR-ABL degradation and inducing CML cell death.	Artesunate	50-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
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.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	212-219
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 Mesylate	157-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	212-219
33848469-8	2021	Treatment with the Abl inhibitor imatinib increased NSC activation without impairing NSC maintenance in the middle-aged brain.	Imatinib Mesylate	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-22
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 Mesylate	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-131
6270355-5	1981	Specific phosphorylation pattern differences for wild-type and mutant proteins probably represented deletions of specific phosphate acceptor sites in the abl region.	Phosphates	122-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-86
834154-1	1977	The bone calcium status of 39 patients with chronic renal failure on hemodialysis has been measured by in vivo neutron activation analysis (IVNAA) and reported in terms of a calcium bone index (CaBl) which relates the calcium in a patient to that in a normal person of the same height.	Calcium	9-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	194-198
834154-1	1977	The bone calcium status of 39 patients with chronic renal failure on hemodialysis has been measured by in vivo neutron activation analysis (IVNAA) and reported in terms of a calcium bone index (CaBl) which relates the calcium in a patient to that in a normal person of the same height.	Calcium	174-181	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	194-198
834154-1	1977	The bone calcium status of 39 patients with chronic renal failure on hemodialysis has been measured by in vivo neutron activation analysis (IVNAA) and reported in terms of a calcium bone index (CaBl) which relates the calcium in a patient to that in a normal person of the same height.	Calcium	174-181	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	194-198
34036393-0	2021	ND-09 inhibits chronic myeloid leukemia K562 cell growth by regulating BCR-ABL signaling.	nd-09	0-5	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
34036393-4	2021	The results showed that ND-09 demonstrated a high level of inhibitory action toward CML cells overexpressing BCR-ABL and induced K562 cell apoptosis through the mitochondrial pathway.	nd-09	24-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
34036393-7	2021	ND-09 exhibited a good fit within BCR-ABL and occupied its ATP-binding pocket, thus altering BCR-ABL kinase activity.	nd-09	0-5	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
34036393-7	2021	ND-09 exhibited a good fit within BCR-ABL and occupied its ATP-binding pocket, thus altering BCR-ABL kinase activity.	nd-09	0-5	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
34036393-7	2021	ND-09 exhibited a good fit within BCR-ABL and occupied its ATP-binding pocket, thus altering BCR-ABL kinase activity.	Adenosine Triphosphate	59-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
34036393-8	2021	Therefore, ND-09 downregulated the phosphorylation of BCR-ABL and ABL, ultimately inhibiting the downstream signaling pathways in K562 cells.	nd-09	11-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
34036393-8	2021	Therefore, ND-09 downregulated the phosphorylation of BCR-ABL and ABL, ultimately inhibiting the downstream signaling pathways in K562 cells.	nd-09	11-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-61
34036393-9	2021	These findings suggest that ND-09 induces growth arrest in CML cells by targeting BCR-ABL.	nd-09	28-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
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 Mesylate	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 Mesylate	10-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-174
33932144-3	2021	In this study, we demonstrate that c-Abl highly phosphorylates FHL2 at Y97, Y176, Y217 and Y236 through mass spectrometry and tyrosine-to-phenylalanine (Y F) mutant analysis.	Tyrosine	126-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-40
33932144-3	2021	In this study, we demonstrate that c-Abl highly phosphorylates FHL2 at Y97, Y176, Y217 and Y236 through mass spectrometry and tyrosine-to-phenylalanine (Y F) mutant analysis.	Phenylalanine	138-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-40
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 Mesylate	161-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-43
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.	Dasatinib	173-182	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-43
33618586-1	2021	Introduction: Nilotinib is a second-generation tyrosine kinase inhibitor (TKI) targeting BCR/ABL, which is used for the first-line treatment of newly diagnosed chronic myeloid leukemia (CML) patients and the second-line treatment of most CML patients who are resistant or intolerant to prior therapy that includes imatinib.	nilotinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-96
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 Mesylate	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 Mesylate	150-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-75
33924068-6	2021	We observed increase in ROS accumulation in BCR-ABL1 positive cells and distinct levels of ROS accumulation in IM-susceptible cells when compared to IM-resistant ones, as well as increased DNA damage caused by IM action in sensitive cells.	Reactive Oxygen Species	24-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-52
33924068-9	2021	BCR-ABL1 kinase alters ROS metabolism, and IM resistance is accompanied by the changes in activity of GPx, catalase, and alterations in MMP.	Reactive Oxygen Species	23-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-8
34054462-10	2021	Patients with JAK2-positive BCR-ABL-positive CML had a good hematological and cytogenetic response to dasatinib.	Dasatinib	102-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
34054462-11	2021	In such rare coexistence of JAK and BCR-ABL, dasatinib is a good option due to multi-kinase activity.	Dasatinib	45-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
33618586-2	2021	In addition to common adverse reactions, long-term use of nilotinib shows some toxicities that are different from those of occurring during other BCR/ABL TKI treatments, such as cardiovascular toxicity.	nilotinib	58-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-153
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 Mesylate	109-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-36
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).	nilotinib	122-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-36
33903307-10	2021	Mutation analysis which was done 70 months after commencement of nilotinib showed the presence of BCRABL1 kinase domain mutation with nucleotide substitution at position 1187 from Histidine(H) to Proline(P) (H396P).	nilotinib	65-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
33903307-10	2021	Mutation analysis which was done 70 months after commencement of nilotinib showed the presence of BCRABL1 kinase domain mutation with nucleotide substitution at position 1187 from Histidine(H) to Proline(P) (H396P).	Histidine	180-189	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
33903307-10	2021	Mutation analysis which was done 70 months after commencement of nilotinib showed the presence of BCRABL1 kinase domain mutation with nucleotide substitution at position 1187 from Histidine(H) to Proline(P) (H396P).	Proline	196-203	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
33389727-6	2021	Molecular docking and molecular dynamics simulation of Papaverine against the target Bcr-Abl were also carried out.	Papaverine	55-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
33389727-9	2021	Papaverine induces ROS generation, promotes apoptosis, and inhibits Bcr-Abl downstream signaling.	Papaverine	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
34046181-7	2021	Hypoxia-dependent release of the ligand from the cobalt(iii) complexes was proven by changed fluorescence properties, enhanced downstream signaling inhibition and increased in vitro anticancer activity in BCR-ABL- and FGFR-driven cancer models.	cobalt(iii)	49-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-212
34046181-8	2021	Respective tumor-inhibiting in vivo effects in the BCR-ABL-driven K-562 leukemia model were restricted to the cobalt(iii) complex with the higher reduction potential and confirmed in a FGFR-driven urothelial carcinoma xenograft model.	cobalt(iii)	110-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-58
33786723-8	2021	LY294002 abrogated the beneficial effects of targeting c-Abl and exacerbated neuronal apoptosis after SAH.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-60
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 Mesylate	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	205-209
33736651-2	2021	The BCR-ABL1 fusion protein is an optimal target for tyrosine kinase inhibitors (TKIs) that aim for the adenosine triphosphate (ATP) binding site of ABL1.	Adenosine	104-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-12
33736651-2	2021	The BCR-ABL1 fusion protein is an optimal target for tyrosine kinase inhibitors (TKIs) that aim for the adenosine triphosphate (ATP) binding site of ABL1.	Adenosine	104-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-153
33736651-2	2021	The BCR-ABL1 fusion protein is an optimal target for tyrosine kinase inhibitors (TKIs) that aim for the adenosine triphosphate (ATP) binding site of ABL1.	Adenosine Triphosphate	128-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-12
33736651-2	2021	The BCR-ABL1 fusion protein is an optimal target for tyrosine kinase inhibitors (TKIs) that aim for the adenosine triphosphate (ATP) binding site of ABL1.	Adenosine Triphosphate	128-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-153
33736651-4	2021	Mutations can occur in the ATP binding site of ABL1, causing resistance by preventing the binding of many of these drugs and leaving patients with limited treatment options.	Adenosine Triphosphate	27-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-51
33389727-11	2021	Furthermore, the docking and molecular dynamic simulation studies supported that Papaverine binds to the allosteric site of Bcr-Abl.	Papaverine	81-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
33568399-8	2021	The cABL knockout not only significantly inhibited inflammasome function but also decreased release of phosphorylated ASC after LPS/ATP stimulation.	Adenosine Triphosphate	132-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-8
33910311-9	2021	After the knockout of miR-21, the activation of PI3K/Akt signaling molecules was inhibited, while the expression of P210(B)CR-ABL and p-P210(BCR-ABL) was downregulated; however, the expression of PTEN was not affected.	Chromium	123-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-129
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 Mesylate	94-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	193-200
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 Mesylate	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
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.	nilotinib	85-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
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.	Dasatinib	96-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
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.	bosutinib	107-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
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.	ponatinib	122-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
33748144-10	2021	Our results suggest that ZINC21710815 may be a potential BCR-ABL inhibitor that should undergo in vivo evaluation.	ZINC21710815	25-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
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.	Sulfasalazine	0-13	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 Mesylate	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-149
33075386-6	2021	Western blotting confirmed that tyrosine phosphorylation in STAT5, a substrate of ABL1, was enhanced, and the novel mutation was proved to be a gain-of-function mutation.	Tyrosine	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-86
33796468-2	2021	Ponatinib is a 3rd generation TKI that binds BCR-ABL1 with high affinity and inhibits most BCR-ABL1 mutants, including the T315I mutation.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-53
33796468-2	2021	Ponatinib is a 3rd generation TKI that binds BCR-ABL1 with high affinity and inhibits most BCR-ABL1 mutants, including the T315I mutation.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-99
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
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 Mesylate	10-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
33379130-0	2021	Highly sensitive fluorescence biosensing of BCR-ABL1 fusion gene based on exponential transcription-triggered hemin catalysis.	Hemin	110-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-52
33379130-2	2021	In this study, an innovative fluorescence biosensing methodology has been developed for sensitive and specific detection of BCR-ABL1 mRNA by integrating high-efficiency of exponential transcription and superior catalytic performance of DNA-grafted hemin.	Hemin	248-253	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-132
33379130-5	2021	This exponential transcription-triggered hemin catalysis (ET-HC) strategy showed highly sensitive and specific for BCR-ABL1 detection with a limit of detection at 0.5 aM and a good linear range from 2 aM to 200 fM.	Hemin	41-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-123
33644712-3	2021	c-Abl/Arg could mediate STAT1 phosphorylation independent of Janus kinases in the absence of IFNgamma and potentiate IFNgamma-mediated STAT1 phosphorylation.	Arginine	6-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
33618649-10	2021	The correlation coefficient value of uric acid (r = 0.295, p < 0.008) with BCR-ABL showed that weak correlation which exists between the two test parameter.	Uric Acid	37-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
33618649-14	2021	CONCLUSION AND RECOMMENDATION: The CML LDH value strongly correlated with BCR-ABL transcript level, whereas uric acid was weakly correlated with BCR-ABL.	Uric Acid	108-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-152
33098492-4	2021	Furthermore, TPEN induced oxidation of hydrogen peroxide (H2O2) sensor protein DJ-1, induced up-regulation of BH3-only pro-apoptotic protein PUMA, transcription factor p53 and activated the executor protease CASPASE-3 as apoptosis markers, and reduced the reactivity of the cellular proliferating marker Ki-67 in all acute leukemic groups, and reduced the phosphorylation of c-ABL protein signal in an AML case.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	13-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	375-380
33107354-5	2021	In this study, we sought to determine ponatinib"s potential utility, a clinically approved and potent cAbl inhibitor, in MPM treatment.	ponatinib	38-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-106
33107354-12	2021	Western blot analysis showed that the activation of Abl signaling was blocked in the ponatinib-treated MMP lines.	ponatinib	85-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-55
33107354-16	2021	CONCLUSION: Ponatinib may offer a new therapeutic strategy for MPM patients based on cAbl signaling pathway inhibition.	ponatinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-89
33172871-3	2021	BCR-ABL was assessed by quantitative rt-PCR at days 0 and 90 of imatinib therapy.	Imatinib Mesylate	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
33527482-0	2021	Expression of inducible NOS is indispensable for the antiproliferative and proapoptotic effect of imatinib in BCR-ABL positive cells.	Imatinib Mesylate	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 Mesylate	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 Mesylate	178-186	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
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 Mesylate	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.	NG-Nitroarginine Methyl Ester	213-219	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
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 Mesylate	106-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-47
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 Mesylate	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-26
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 Mesylate	166-174	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-8
33181128-13	2021	Indeed, AS1949490 mediated SHIP2 inhibition promotes protein complex formation of SHIP2 together with non-receptor tyrosine kinase SRC and ABL which in turn enhances PI3K/Akt and MAP kinase pathways activation.	3-((4-chlorobenzyl)oxy)-N-((1S)-1-phenylethyl)-2-thiophenecarboxamide	8-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-142
33181128-14	2021	Dual inhibition of SRC/ABL blocked activation of both pathways upon SHIP2 inhibition and H2O2 treatment.	Hydrogen Peroxide	89-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-26
33070465-4	2021	The BCR-ABL protein activates AMP-activated protein kinase (AMPK) for ATP production and the mechanistic target of rapamycin (mTOR) pathway to suppress autophagy.	Adenosine Triphosphate	70-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
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 Mesylate	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
33407162-2	2021	The drug has been shown to act as a potent multikinase inhibitor by blocking not only the BCR-ABL1 gene sequence but also the SRC kinase family, though unexpected adverse events such as pleural effusion have recently been reported in patients undergoing treatment with dasatinib.	Dasatinib	269-278	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-98
32838725-0	2021	A New Series of Antileukemic Agents: Design, Synthesis, In Vitro and In Silico Evaluation of Thiazole-Based ABL1 Kinase Inhibitors.	Thiazoles	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-112
32838725-2	2021	<P> Objectives: Due to the importance of thiazole scaffold in targeted anticancer drug discovery, the goal of this work is the design of new thiazolyl hydrazones as potent ABL1 kinase inhibitors for the management of chronic myeloid leukemia (CML).	Thiazoles	41-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-176
32838725-2	2021	<P> Objectives: Due to the importance of thiazole scaffold in targeted anticancer drug discovery, the goal of this work is the design of new thiazolyl hydrazones as potent ABL1 kinase inhibitors for the management of chronic myeloid leukemia (CML).	thiazolyl hydrazones	141-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-176
32838725-8	2021	In order to investigate the binding mode of compound 2j into the ATP binding site of ABL1 kinase (PDB: 1IEP), molecular docking study was conducted using MOE 2018.01 program.	Adenosine Triphosphate	65-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-89
32838725-15	2021	According to molecular docking studies, compound 2j exhibited high affinity to the ATP binding site of ABL1 kinase forming significant intermolecular interactions.	Adenosine Triphosphate	83-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-107
33191645-6	2021	Nevertheless, the src/abl inhibitor bosutinib and mutations of cortactin phosphorylation site could inhibit the promotion effect of CX3 CL1 on invasion and migration of A549 and H520.	bosutinib	36-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-25
33361165-14	2020	Age, BUN (blood urea nitrogen) and lactate (ABL) were the independent risk factors determined by multivariate analysis.	Lactic Acid	35-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-47
33419251-3	2020	Axitinib has shown in vitro and ex vivo activity in blocking ABL1; however, clinical trials exploring its efficacy in ALL are missing.	Axitinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-65
33419251-4	2020	Here, we presented a 77-year-old male with a diagnosis of Ph positive ALL resistant to ponatinib and carrying a rare threonine to leucine (T315L) mutation on BCR-ABL1 gene.	ponatinib	87-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-166
33419251-4	2020	Here, we presented a 77-year-old male with a diagnosis of Ph positive ALL resistant to ponatinib and carrying a rare threonine to leucine (T315L) mutation on BCR-ABL1 gene.	Threonine	117-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-166
33419251-4	2020	Here, we presented a 77-year-old male with a diagnosis of Ph positive ALL resistant to ponatinib and carrying a rare threonine to leucine (T315L) mutation on BCR-ABL1 gene.	Leucine	130-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-166
32430093-4	2020	This study describes the mechanistic analyses of the novel anthracycline, pivarubicin, and its in vivo efficacy against human primary TNBC.</P><P>Pivarubicin directly activates PKC-delta, triggers rapid mitochondrial-dependent apoptosis and circumvents resistance conferred by overexpression of P-glycoprotein, Bcl-2, Bcl-XL and Bcr-Abl.	Anthracyclines	59-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	329-336
32430093-4	2020	This study describes the mechanistic analyses of the novel anthracycline, pivarubicin, and its in vivo efficacy against human primary TNBC.</P><P>Pivarubicin directly activates PKC-delta, triggers rapid mitochondrial-dependent apoptosis and circumvents resistance conferred by overexpression of P-glycoprotein, Bcl-2, Bcl-XL and Bcr-Abl.	pivarubicin	74-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	329-336
32430093-4	2020	This study describes the mechanistic analyses of the novel anthracycline, pivarubicin, and its in vivo efficacy against human primary TNBC.</P><P>Pivarubicin directly activates PKC-delta, triggers rapid mitochondrial-dependent apoptosis and circumvents resistance conferred by overexpression of P-glycoprotein, Bcl-2, Bcl-XL and Bcr-Abl.	pivarubicin	146-157	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	329-336
33328764-6	2020	Increased tyrosine phosphorylation in multiple receptor/protein tyrosine kinases (EPHA2, EGFR, IGF1R, ABL1 and LYN) was identified in CNE2-IR vs CNE2 cells.	Tyrosine	10-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-106
33291786-1	2020	Dasatinib is a multi-target kinase inhibitor, whose targets include BCR-ABL, SRC family kinases, and various cancer kinases.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
32928796-1	2021	PURPOSE: Flumatinib has been shown to be a more potent inhibitor of BCR-ABL1 tyrosine kinase than imatinib.	HH-GV-678	9-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-76
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.	Dasatinib	82-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-39
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 Mesylate	188-196	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-39
33306831-8	2020	Three mutations, including p.Tyr253Phe, p.Thr315Ile and p.Gly250Glu, were identified in the tyrosine kinase domain of the ABL1 gene during the course of disease.	tyr253phe	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-126
33306831-8	2020	Three mutations, including p.Tyr253Phe, p.Thr315Ile and p.Gly250Glu, were identified in the tyrosine kinase domain of the ABL1 gene during the course of disease.	thr315ile	42-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-126
33306831-8	2020	Three mutations, including p.Tyr253Phe, p.Thr315Ile and p.Gly250Glu, were identified in the tyrosine kinase domain of the ABL1 gene during the course of disease.	gly250glu	58-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-126
33369447-11	2020	Protein modelling studies indicated changes in BCR-ABL mutant protein which may have negatively impacted its binding with nilotinib leading to drug resistance.	nilotinib	122-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
33369447-12	2020	CONCLUSION: We report a novel nilotinib resistant BCR-ABL compound mutation (K245N along with G250W mutation) which impacts structural modification in BCR-ABL mutant protein leading to drug resistance.	nilotinib	30-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
33369447-12	2020	CONCLUSION: We report a novel nilotinib resistant BCR-ABL compound mutation (K245N along with G250W mutation) which impacts structural modification in BCR-ABL mutant protein leading to drug resistance.	nilotinib	30-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-57
33070465-5	2021	BCR-ABL is detected in the nuclei of advanced-stage CML cells, in which ATP is sufficiently supplied via enhanced glucose metabolism.	Adenosine Triphosphate	72-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
33070465-8	2021	Cytoplasmic BCR-ABL protein undergoes autophagic degradation when intracellular ATP is exhausted by disruption of the energy balance or forced autophagy flux with AMP mimetics, mTOR inhibitors or arsenic trioxide, leading to apoptotic cell death.	Adenosine Triphosphate	80-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
33070465-8	2021	Cytoplasmic BCR-ABL protein undergoes autophagic degradation when intracellular ATP is exhausted by disruption of the energy balance or forced autophagy flux with AMP mimetics, mTOR inhibitors or arsenic trioxide, leading to apoptotic cell death.	Adenosine Monophosphate	163-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
33070465-8	2021	Cytoplasmic BCR-ABL protein undergoes autophagic degradation when intracellular ATP is exhausted by disruption of the energy balance or forced autophagy flux with AMP mimetics, mTOR inhibitors or arsenic trioxide, leading to apoptotic cell death.	Arsenic Trioxide	196-212	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
33460055-0	2020	Dynamic evolution of ponatinib-resistant mutations in BCR-ABL1-positive leukaemias revealed by next-generation sequencing.	ponatinib	21-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-62
33074527-5	2020	Patients with Philadelphia chromosome (Ph)-positive or Ph-like ALL with ABL-class fusion should be treated with dasatinib.	Dasatinib	112-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-75
32961435-0	2020	Design, synthesis, and biological evaluations of novel 3-amino-4-ethynyl indazole derivatives as Bcr-Abl kinase inhibitors with potent cellular antileukemic activity.	3-amino-4-ethynyl indazole	55-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
32961435-3	2020	In this respect, a new series of ethynyl bearing 3-aminoindazole based Bcr-Abl inhibitors has been designed, synthesized, and biologically evaluated.	1H-Indazol-3-amine	49-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
32961435-4	2020	The target compounds were designed based on introducing the key structural features of ponatinib, alkyne spacer and diarylamide, into the previously reported indazole II to improve its Bcr-Abl inhibitory activity and overcome its poor cellular potency.	indazole ii	158-169	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	185-192
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-34
33207739-0	2020	8-Hydroxydaidzein, an Isoflavone from Fermented Soybean, Induces Autophagy, Apoptosis, Differentiation, and Degradation of Oncoprotein BCR-ABL in K562 Cells.	8-hydroxydaidzein	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
33244143-9	2020	GNP-HCIm reduced cAbl-p (0.41 GNP-HCIm, 0.24 Imatinib vs. to control; p < 0.001).	Imatinib Mesylate	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-21
33240747-0	2020	Molecular docking and pharmacophoric modelling of 1,5-disubstituted tetrazoles as inhibitors of two proteins present in cancer, the ABL and the mutated T315I kinase.	1,5-disubstituted tetrazoles	50-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-135
33207739-0	2020	8-Hydroxydaidzein, an Isoflavone from Fermented Soybean, Induces Autophagy, Apoptosis, Differentiation, and Degradation of Oncoprotein BCR-ABL in K562 Cells.	Isoflavones	22-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
33078787-4	2020	The ROS fluctuation triggered cellular autophagy and enhanced the level of autophagic protein Beclin-1, which caused the degradation of fusion protein BCR-ABL, the key factor of retarded differentiation and led to the downregulation of phosphorylation of PI3K and AKT.	Reactive Oxygen Species	4-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-158
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 Mesylate	123-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-73
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.	Dasatinib	133-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-73
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.	nilotinib	148-157	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-73
32711219-0	2020	p19INK4d inhibits proliferation and enhances imatinib efficacy through BCR-ABL signaling pathway in chronic myeloid leukemia.	Imatinib Mesylate	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
32869521-4	2020	This study aimed to explore the effect of propofol on apoptosis and neurocognition through its regulation of c-Abl expression in vivo and in vitro.	Propofol	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-114
32869521-10	2020	RESULTS: The in vitro experiment showed that propofol significantly decreased c-Abl expression and ROS levels.	Propofol	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-83
32869521-12	2020	Moreover, in the animal experiment, intraperitoneal injection of 50 mg/kg propofol for 5 days obviously decreased the expression of c-Abl in the neonatal rat brain (p < .05) but did not significantly increase the number of caspase-3-positive cells.	Propofol	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-137
33284894-0	2020	Increased sensitivity of BCR-ABL-induced B-ALL to imatinib by releasing leukemia B cell differentiation blockage.	Imatinib Mesylate	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 Mesylate	130-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	222-229
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.	Tyrosine	184-192	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 Mesylate	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
32606017-2	2020	The non-receptor tyrosine kinases FYN and ABL are known to drive phosphorylation of tyrosine residues in YXXP motifs within the intracellular domains of DCBLD family members, which leads to the recruitment of the Src homology 2 (SH2) domain of the adaptors CT10 regulator of kinase (CRK) and CRK-like (CRKL).	Tyrosine	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-45
33168949-5	2021	p190Bcr-Abl CML patients demonstrated poor response to imatinib and frequent mutations in epigenetic modifiers genes.	Imatinib Mesylate	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-11
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 Mesylate	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-153
33117337-4	2020	Our results show that the in vitro treatment with ABL carrying PI5P (ABL/PI5P) enhances bacterial uptake, ROS production, phagosome acidification, and intracellular bacterial killing in human monocyte-derived macrophages (MDMs) with pharmacologically inhibited cystic fibrosis transmembrane conductance regulator channel (CFTR), and improve uptake and intracellular killing of MDR P. aeruginosa in CF macrophages with impaired bactericidal activity.	phosphatidylinositol 5-phosphate	63-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-77
33117337-4	2020	Our results show that the in vitro treatment with ABL carrying PI5P (ABL/PI5P) enhances bacterial uptake, ROS production, phagosome acidification, and intracellular bacterial killing in human monocyte-derived macrophages (MDMs) with pharmacologically inhibited cystic fibrosis transmembrane conductance regulator channel (CFTR), and improve uptake and intracellular killing of MDR P. aeruginosa in CF macrophages with impaired bactericidal activity.	ros	106-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-77
33019757-5	2020	Upon irradiation and synemin inhibition, c-Abl hyperphosphorylation on tyrosine (Y) 412 and threonine (T) 735 was significantly reduced, prompting us to hypothesize that c-Abl tyrosine kinase is an important signaling component of the synemin-mediated radioresistance pathway.	Tyrosine	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-46
32248338-1	2020	Dasatinib is a tyrosine kinase inhibitor for the treatment of BCR-ABL-positive chronic myeloid leukaemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leukaemia (ALL).	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
31688632-1	2020	Dasatinib is a second-generation potent and efficacious oral tyrosine kinase inhibitor frequently used for imatinib-resistant or intolerant BCR-ABL-positive chronic myeloid leukemia and for Philadelphia chromosome-positive acute lymphocytic leukemia.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
33096322-0	2020	The specificity of asciminib, a potential treatment for chronic myeloid leukemia, as a myristate-pocket binding ABL inhibitor and analysis of its interactions with mutant forms of BCR-ABL1 kinase.	asciminib	19-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-115
33096322-0	2020	The specificity of asciminib, a potential treatment for chronic myeloid leukemia, as a myristate-pocket binding ABL inhibitor and analysis of its interactions with mutant forms of BCR-ABL1 kinase.	asciminib	19-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	184-188
33096322-1	2020	Asciminib is a potent, orally bioavailable, investigational drug that specifically and potently inhibits the tyrosine kinase activity of native ABL1, together with that of the chimeric BCR-ABL1 oncoprotein which causes chronic myeloid leukemia (CML).	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-148
33096322-2	2020	In contrast to ATP-competitive BCR-ABL1 kinase inhibitors employed to treat CML that target multiple kinases, asciminib binds to the myristate binding pocket on the kinase domains of ABL1 and BCR-ABL1.	asciminib	110-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	183-187
33096322-2	2020	In contrast to ATP-competitive BCR-ABL1 kinase inhibitors employed to treat CML that target multiple kinases, asciminib binds to the myristate binding pocket on the kinase domains of ABL1 and BCR-ABL1.	asciminib	110-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	183-187
33096322-6	2020	However, in vitro studies in cells have identified BCR-ABL1 mutations that reduce the anti-proliferative activity of asciminib, some of which are associated with clinical resistance towards the drug in patients.	asciminib	117-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-59
33096322-7	2020	Here we review effects of asciminib on mutant forms of BCR-ABL1, analyse their sensitivity towards the drug from a structural perspective and affirm support for employing combinations with ATP-competitive inhibitors to impede the reactivation of BCR-ABL1 kinase activity in patients receiving monotherapy.	asciminib	26-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-63
31659695-9	2020	Furthermore, results of the molecular docking study revealed that hesperetin is a promising inhibitor that targets ABL1, DNMT3B, and MLH1 due to the similarity of binding properties with its native ligand.	hesperetin	66-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-119
31659695-11	2020	A combinatorial therapy with hesperetin targeting ABL1, DNMT3B, and MLH1 may be effective in circumventing chemoresistance in breast cancer.	hesperetin	29-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-54
33000229-6	2020	AT9283 is a multi-targeted kinase inhibitor with potent activity against Janus kinase (JAK), Aurora kinases, and Abl.	1-cyclopropyl-3-(3-(5-morpholin-4-ylmethyl-1H-benzoimidazol-2-yl)-1H-pyrazol-4-yl)urea	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-116
33122628-5	2020	Significantly, nilotinib (2nd generation ABL1/2 inhibitor) reverses resistance, in vivo, causing prolonged regression of resistant tumors, and also, prevents BRAFi/MEKi resistance from developing in the first place.	nilotinib	15-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-47
33163944-5	2020	Active c-Abl induces TFEB phosphorylation on tyrosine and the inhibition of this kinase promotes lysosomal biogenesis, autophagy, and exocytosis.	Tyrosine	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	7-12
33163944-6	2020	c-Abl inhibition in Niemann-Pick type C (NPC) models, a neurodegenerative disease characterized by cholesterol accumulation in lysosomes, promotes a cholesterol-lowering effect in a TFEB-dependent manner.	Cholesterol	99-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
33163944-6	2020	c-Abl inhibition in Niemann-Pick type C (NPC) models, a neurodegenerative disease characterized by cholesterol accumulation in lysosomes, promotes a cholesterol-lowering effect in a TFEB-dependent manner.	Cholesterol	149-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
33163944-7	2020	Thus, c-Abl is a TFEB regulator that mediates its tyrosine phosphorylation, and the inhibition of c-Abl activates TFEB promoting cholesterol clearance in NPC models.	Tyrosine	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-11
33163944-7	2020	Thus, c-Abl is a TFEB regulator that mediates its tyrosine phosphorylation, and the inhibition of c-Abl activates TFEB promoting cholesterol clearance in NPC models.	Cholesterol	129-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-11
33163944-7	2020	Thus, c-Abl is a TFEB regulator that mediates its tyrosine phosphorylation, and the inhibition of c-Abl activates TFEB promoting cholesterol clearance in NPC models.	Cholesterol	129-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-103
32894673-7	2020	The excellent pTyr sensing capacity make the nanochannels available for real-time monitoring of pTyr process by c-Abl kinase on a peptide substrate, even in a complicated condition, and the proof-of-concept study of monitoring kinase activity demonstrates its potential in kinase inhibitor screening.	Phosphotyrosine	14-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-117
32894673-7	2020	The excellent pTyr sensing capacity make the nanochannels available for real-time monitoring of pTyr process by c-Abl kinase on a peptide substrate, even in a complicated condition, and the proof-of-concept study of monitoring kinase activity demonstrates its potential in kinase inhibitor screening.	Phosphotyrosine	96-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-117
32679184-0	2020	Targeting SKP2/Bcr-Abl pathway with Diosmetin suppresses chronic myeloid leukemia proliferation.	diosmetin	36-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
32679184-5	2020	We demonstrate that Diosmetin, a kind of phytoestrogens, notably downregulates the expression of SKP2, Bcr-Abl phosphorylation, and moderately downregulates the Bcr-Abl level.	diosmetin	20-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-168
32439698-8	2020	RPPA analysis revealed that such resistance emanates from signaling of tyrosine 821 of AXL via the tyrosine kinase c-ABL.	Tyrosine	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-120
32439698-10	2020	CONCLUSIONS: Collectively, the studies presented herein suggest that tyrosine 821 of AXL mediates resistance to cetuximab by activation of c-ABL kinase in HNSCC and that targeting of both EGFR and c-ABL leads to a robust anti-tumor response.	Tyrosine	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-144
32439698-10	2020	CONCLUSIONS: Collectively, the studies presented herein suggest that tyrosine 821 of AXL mediates resistance to cetuximab by activation of c-ABL kinase in HNSCC and that targeting of both EGFR and c-ABL leads to a robust anti-tumor response.	Tyrosine	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	197-202
32792487-8	2020	Subsequently, Pyk2 acted as a scaffold for c-Abl phosphorylating the catalytic domain of NOX5 Tyr476/478 sites, which in turn upregulated hydrogen peroxide (H2O2) inside the Pyk2/NOX5 complex to oxidize and activate local Src.	Hydrogen Peroxide	138-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-48
32792487-8	2020	Subsequently, Pyk2 acted as a scaffold for c-Abl phosphorylating the catalytic domain of NOX5 Tyr476/478 sites, which in turn upregulated hydrogen peroxide (H2O2) inside the Pyk2/NOX5 complex to oxidize and activate local Src.	Hydrogen Peroxide	157-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-48
32684632-7	2020	Subsequently, we identified BTK as a main downstream mediator and targeting the Bcr-Abl-FcgammaRIIb-BTK axis in primary CML CD34+ cells using ibrutinib, in combination with standard TKI therapy, significantly increased apoptosis in quiescent CML stem cells thereby contributing to the eradication of LSCs.. As a potential curative therapeutic approach, we therefore suggest combining Bcr-Abl TKI therapy along with BTK inhibition.	ibrutinib	142-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
32536651-1	2020	We report the case of a 56-year-old man with chronic myeloid leukemia (CML) who developed dasatinib-induced interstitial lung disease (ILD) 7 years after starting dasatinib, a BCR-ABL1 inhibitor.	Dasatinib	90-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	180-184
32536651-6	2020	Bosutinib, another BCR-ABL1 inhibitor, was successfully re-instituted.	bosutinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-27
32536651-7	2020	The present case and relevant literature suggest that dasatinib-induced ILD can present as NSIP after an extended period, responds to corticosteroids, and is amenable to re-challenge at a lower-dose or with alternative BCR-ABL1 inhibitors.	Dasatinib	54-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	223-227
32927433-4	2020	The present study shows that shikonin, an herbal compound used in traditional Chinese medicine, overcomes TKI resistance in BCR/ABL-positive CML cells by inducing necroptosis via activation of RIPK1/RIPK3/MLKL signaling.	shikonin	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-131
32913188-0	2020	A small molecular compound CC1007 induces cross-lineage differentiation by inhibiting HDAC7 expression and HDAC7/MEF2C interaction in BCR-ABL1- pre-B-ALL.	cc1007	27-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-142
32899072-1	2020	INTRODUCTION: Nilotinib is a selective inhibitor of the BCR-ABL tyrosine kinase receptor and is used in the management of chronic myelogenous leukemia (CML).	nilotinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
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.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	183-190
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 Mesylate	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.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	48-57	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 Mesylate	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	169-176
32364815-1	2020	Imatinib-induced tyrosine kinase inhibition extends beyond the BCR-ABL mutation, resulting in adverse effects.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-70
32498906-0	2020	Dual-modal label-free genosensor based on hemoglobin@gold nanocluster stabilized graphene nanosheets for the electrochemical detection of BCR/ABL fusion gene.	Graphite	81-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	142-145
32814537-3	2021	OBJECTIVE: To probe the activity of a recently published series of N1-(anthraquinon-2-yl) amidrazone piperazine derivatives employing computational strategies[1], identify their structural basis of binding to BCR/ABL kinase domain, and explain their anticancer activities in human breast adenocarcinoma (MCF-7) and chronic myelogenous leukemia (K562) cell lines.	n1-(anthraquinon-2-yl) amidrazone piperazine	67-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	213-216
32657579-4	2020	Herein, we systematically designed a set of unique PROTACs by globally targeting all the three binding sites of BCR-ABL, including dasatinib-, ponatinib-, and asciminib-based PROTACs.	asciminib	159-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
32679184-5	2020	We demonstrate that Diosmetin, a kind of phytoestrogens, notably downregulates the expression of SKP2, Bcr-Abl phosphorylation, and moderately downregulates the Bcr-Abl level.	diosmetin	20-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
32685125-1	2020	Imatinib mesylate is a small tyrosine kinase inhibitor that targets BCR-ABL, ckit and platelet-derived growth factor receptor.	Imatinib Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
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 Mesylate	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 Mesylate	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 Mesylate	193-201	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-47
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 Mesylate	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
32764164-14	2020	C m i n     ${C}_{min}\hat{\infty }$ imatinib was found to be significantly associated with BCR-ABL ratio.	Imatinib Mesylate	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 Mesylate	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-104
32764164-16	2020	Conclusions There were high interindividual variations of imatinib and nilotinib correlated with BCR-ABL ratio, but no correlation in nilotinib.	nilotinib	71-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-104
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 Mesylate	88-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
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.	venetoclax	277-287	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
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.	midostaurin	348-359	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.	Berberine	13-22	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.	Berberine	13-22	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 Mesylate	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 Mesylate	144-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
32098768-4	2020	Berberine (BBR) is a potent BCR-ABL inhibitor for imatinib-sensitive and -resistant CML.	Berberine	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
32098768-4	2020	Berberine (BBR) is a potent BCR-ABL inhibitor for imatinib-sensitive and -resistant CML.	Berberine	11-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
32098768-4	2020	Berberine (BBR) is a potent BCR-ABL inhibitor for imatinib-sensitive and -resistant CML.	Imatinib Mesylate	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
31650445-5	2020	Further, naked BCR-ABL-targeting ADO suppressed BCR-ABL protein levels in a dose-dependent manner, inhibited CML cell proliferation, and augmented the inhibitory effects of imatinib mesylate.	imatinib	173-190	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
31650445-5	2020	Further, naked BCR-ABL-targeting ADO suppressed BCR-ABL protein levels in a dose-dependent manner, inhibited CML cell proliferation, and augmented the inhibitory effects of imatinib mesylate.	imatinib	173-190	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
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 Mesylate	49-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-117
32468042-0	2020	c-Abl-mediated tyrosine phosphorylation of DNA damage response proteins and implications in important cellular functions (Review).	Tyrosine	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
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 Mesylate	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 Mesylate	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 Mesylate	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-117
32879093-0	2020	Combination of axitinib with dasatinib improves the outcome of a chronic myeloid leukemia patient with BCR-ABL1 T315I mutation.	Axitinib	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-111
32879093-0	2020	Combination of axitinib with dasatinib improves the outcome of a chronic myeloid leukemia patient with BCR-ABL1 T315I mutation.	Dasatinib	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-111
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 Mesylate	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-51
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.	Dasatinib	132-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-51
32879093-11	2020	It provided a successful example in treating CML patients carrying BCR-ABL1 T315I mutation via combination of axitinib with conditional TKI.	Axitinib	110-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-75
32568522-0	2020	A Nimbolide-Based Kinase Degrader Preferentially Degrades Oncogenic BCR-ABL.	nimbolide	2-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
32568522-5	2020	We demonstrate that a PROTAC linking nimbolide to the kinase and BCR-ABL fusion oncogene inhibitor dasatinib, BT1, selectively degrades BCR-ABL over c-ABL in leukemia cancer cells, compared to previously reported cereblon or VHL-recruiting BCR-ABL degraders that show opposite selectivity or in some cases inactivity.	nimbolide	37-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
32568522-5	2020	We demonstrate that a PROTAC linking nimbolide to the kinase and BCR-ABL fusion oncogene inhibitor dasatinib, BT1, selectively degrades BCR-ABL over c-ABL in leukemia cancer cells, compared to previously reported cereblon or VHL-recruiting BCR-ABL degraders that show opposite selectivity or in some cases inactivity.	nimbolide	37-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-143
32568522-5	2020	We demonstrate that a PROTAC linking nimbolide to the kinase and BCR-ABL fusion oncogene inhibitor dasatinib, BT1, selectively degrades BCR-ABL over c-ABL in leukemia cancer cells, compared to previously reported cereblon or VHL-recruiting BCR-ABL degraders that show opposite selectivity or in some cases inactivity.	nimbolide	37-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-154
32568522-5	2020	We demonstrate that a PROTAC linking nimbolide to the kinase and BCR-ABL fusion oncogene inhibitor dasatinib, BT1, selectively degrades BCR-ABL over c-ABL in leukemia cancer cells, compared to previously reported cereblon or VHL-recruiting BCR-ABL degraders that show opposite selectivity or in some cases inactivity.	nimbolide	37-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-143
32568522-5	2020	We demonstrate that a PROTAC linking nimbolide to the kinase and BCR-ABL fusion oncogene inhibitor dasatinib, BT1, selectively degrades BCR-ABL over c-ABL in leukemia cancer cells, compared to previously reported cereblon or VHL-recruiting BCR-ABL degraders that show opposite selectivity or in some cases inactivity.	Dasatinib	99-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-72
32568522-5	2020	We demonstrate that a PROTAC linking nimbolide to the kinase and BCR-ABL fusion oncogene inhibitor dasatinib, BT1, selectively degrades BCR-ABL over c-ABL in leukemia cancer cells, compared to previously reported cereblon or VHL-recruiting BCR-ABL degraders that show opposite selectivity or in some cases inactivity.	Dasatinib	99-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-143
32568522-5	2020	We demonstrate that a PROTAC linking nimbolide to the kinase and BCR-ABL fusion oncogene inhibitor dasatinib, BT1, selectively degrades BCR-ABL over c-ABL in leukemia cancer cells, compared to previously reported cereblon or VHL-recruiting BCR-ABL degraders that show opposite selectivity or in some cases inactivity.	Dasatinib	99-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-154
32568522-5	2020	We demonstrate that a PROTAC linking nimbolide to the kinase and BCR-ABL fusion oncogene inhibitor dasatinib, BT1, selectively degrades BCR-ABL over c-ABL in leukemia cancer cells, compared to previously reported cereblon or VHL-recruiting BCR-ABL degraders that show opposite selectivity or in some cases inactivity.	Dasatinib	99-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-143
32667912-6	2020	ABL1 tyrosine kinase inhibitors (TKIs), including imatinib, nilotinib, and dasatinib, are used clinically for treating CML.	Imatinib Mesylate	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-4
32667912-6	2020	ABL1 tyrosine kinase inhibitors (TKIs), including imatinib, nilotinib, and dasatinib, are used clinically for treating CML.	nilotinib	60-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-4
32667912-6	2020	ABL1 tyrosine kinase inhibitors (TKIs), including imatinib, nilotinib, and dasatinib, are used clinically for treating CML.	Dasatinib	75-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-4
32439806-4	2020	Using protein degradation, cell proliferation, 5-ethynyl-2-deoxyuridine (EdU), and apoptosis assays, along with xenograft tumor analysis, we found that the N-terminal segment of ABL, which is lost in the BCR-ABL fusion, confers degradation capacity that is promoted by SMAD-specific E3 ubiquitin protein ligase 1 (SMURF1).	5-ethynyl-2'-deoxyuridine	47-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-181
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).	Dasatinib	105-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-12
32439806-4	2020	Using protein degradation, cell proliferation, 5-ethynyl-2-deoxyuridine (EdU), and apoptosis assays, along with xenograft tumor analysis, we found that the N-terminal segment of ABL, which is lost in the BCR-ABL fusion, confers degradation capacity that is promoted by SMAD-specific E3 ubiquitin protein ligase 1 (SMURF1).	5-ethynyl-2'-deoxyuridine	73-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-181
32655840-0	2020	Influence of major BCR-ABL1 transcript subtype on outcome in patients with chronic myeloid leukemia in chronic phase treated frontline with nilotinib.	nilotinib	140-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-27
32291831-4	2020	The c-Abl inhibitor nilotinib used for the treatment of chronic myeloid leukemia based on data collected in preclinical models of PD might interfere with pathogenic mechanisms that are relevant to PD and dementia with Lewy bodies, which motivated its assessment in an open-label clinical trial in PD and dementia with Lewy bodies patients.	nilotinib	20-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-9
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 Mesylate	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-12
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).	nilotinib	90-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-12
32655840-14	2020	In conclusion, even treated with nilotinib first line, patients with chronic phase CML expressing BCR-ABL1 e13a2 transcript have a lower rate of deep molecular responses.	nilotinib	33-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-106
32424388-3	2020	As an example, the crystal structure of the kinase inhibitor dasatinib bound to the Abl1 kinase shows a hydrogen bond between the drug and residue Thr315 and very few contacts between the drug and residues Val299 and Phe317, yet mutations in those residues lead to drug resistance.	Dasatinib	61-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-88
32424388-3	2020	As an example, the crystal structure of the kinase inhibitor dasatinib bound to the Abl1 kinase shows a hydrogen bond between the drug and residue Thr315 and very few contacts between the drug and residues Val299 and Phe317, yet mutations in those residues lead to drug resistance.	Hydrogen	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-88
32655803-1	2020	BACKGROUND: Imatinib resistance is commonly associated with the activation of BCR-ABL signaling in chronic myeloid leukaemia (CML).	Imatinib Mesylate	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
32655803-2	2020	The activation of Lyn can result in imatinib resistance by regulating the formation of BCR-ABL protein complexes.	Imatinib Mesylate	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
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 Mesylate	55-63	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 Mesylate	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	200-203
32655803-4	2020	This study aimed to investigate whether the signaling pathway of Lyn/BCR-ABL/SIRT1 could mediate imatinib resistance in CML.	Imatinib Mesylate	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 Mesylate	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	200-203
32655803-12	2020	Imatinib suppressed BCR-ABL phosphorylation in both K562 and K562R cells.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
32654459-2	2020	Methods: Imatinib-, nilotinib-, and/or dasatinib-resistant patients with CML who screened BCR-ABL mutation (s) in Peking University People"s Hospital between June 2001 and September 2019 were retrospectively reviewed.	Dasatinib	39-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-97
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 Mesylate	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-116
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) .	Dasatinib	73-82	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 Mesylate	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
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.	nilotinib	78-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
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.	Dasatinib	93-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
32671189-0	2020	A Small Molecule Inhibitor, OGP46, Is Effective against Imatinib-Resistant BCR-ABL Mutations via the BCR-ABL/JAK-STAT Pathway.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
32671189-4	2020	Here, we investigate a novel small molecule inhibitor, OGP46, for its inhibitory activity against K562, a panel of murine BaF3 cell lines stably expressing either wild-type BCR-ABL or its mutant forms, including T315I.	ogp46	55-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	173-180
32393599-12	2020	Thus, Src/Hck-mediated Abl1 Tyr488 phosphorylation triggers PIK3CB-dependent PI(3,4,5)P3 production and orchestrates the assembly and function of macrophage podosome.	phosphoinositide-3,4,5-triphosphate	77-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-27
32671189-5	2020	OGP46 exhibits potent activity against imatinib-resistant BCR-ABL mutations, including T315I.	ogp46	0-5	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-65
32671189-5	2020	OGP46 exhibits potent activity against imatinib-resistant BCR-ABL mutations, including T315I.	Imatinib Mesylate	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-65
32671189-7	2020	Treatment with OGP46 significantly decreased the mRNA and protein expression of BCR-ABL in K562 and BaF3-p210-T315I cells.	ogp46	15-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
32671189-10	2020	Thus, OGP46 may be a novel strategy for overcoming imatinib-resistance BCR-ABL mutations, including T315I.	Imatinib Mesylate	51-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
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 Mesylate	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 Mesylate	142-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
32179085-6	2020	In the current study, by performing both in vitro and in vivo experiments in CML cells, we showed that PAB blocked the cell cycle at G2/M phase and subsequently activated the caspase pathway, cleaved the BCR-ABL protein and inhibited the BCR-ABL downstream pathways, ultimately leading to cell proliferation inhibition, cytotoxicity and apoptosis.	pseudolaric acid B	103-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	204-211
32179085-6	2020	In the current study, by performing both in vitro and in vivo experiments in CML cells, we showed that PAB blocked the cell cycle at G2/M phase and subsequently activated the caspase pathway, cleaved the BCR-ABL protein and inhibited the BCR-ABL downstream pathways, ultimately leading to cell proliferation inhibition, cytotoxicity and apoptosis.	pseudolaric acid B	103-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	238-245
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
32247263-1	2020	GZD824 is a novel third-generation BCR-ABL inhibitor.	olverembatinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
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.	makv-8	21-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
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 Mesylate	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
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 Mesylate	129-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-13
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 Mesylate	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
32153174-6	2020	Using the stable form with the best degradation ability against the BCR-ABL fusion and ABL proteins in myelogenous leukemia K562 cells, we showed that Azo-PROTAC combines the potent protein knockdown and facile cell uptake properties of the small-molecule PROTAC with a reversible photoswitchability, offering a promising chemical knockdown strategy based on the light-induced reversible on/off properties.	azo-protac	151-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
32153174-6	2020	Using the stable form with the best degradation ability against the BCR-ABL fusion and ABL proteins in myelogenous leukemia K562 cells, we showed that Azo-PROTAC combines the potent protein knockdown and facile cell uptake properties of the small-molecule PROTAC with a reversible photoswitchability, offering a promising chemical knockdown strategy based on the light-induced reversible on/off properties.	azo-protac	151-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-75
32380976-3	2020	Two of these are (I) Axitinib, which inhibits the T315I mutation of BCR-ABL1, a main source of drug resistance, and (II) Asciminib, which has been developed as an allosteric BCR-ABL1 inhibitor, targeting an entirely different binding site, and as such does not compete for binding with other drugs.	Axitinib	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-76
32380976-3	2020	Two of these are (I) Axitinib, which inhibits the T315I mutation of BCR-ABL1, a main source of drug resistance, and (II) Asciminib, which has been developed as an allosteric BCR-ABL1 inhibitor, targeting an entirely different binding site, and as such does not compete for binding with other drugs.	asciminib	121-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-182
31399521-4	2020	Further analyses of murine cell lines and primary patient material indicate that active BCR-ABL directly interacts with Beclin-1 and phosphorylates its tyrosine residues 233 and 352, resulting in autophagy suppression.	Tyrosine	152-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
32354950-0	2020	Optimal Response in a Patient With CML Expressing BCR-ABL1 E6A2 Fusion Transcript With Nilotinib Therapy: A Case Report.	nilotinib	87-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-58
32354950-6	2020	Treatment with second-generation tyrosine kinase inhibitor nilotinib was effective in this patient expressing the atypical e6a2 BCR-ABL1 fusion transcript.	nilotinib	59-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-136
31686527-7	2020	Over the entire 24-hour period, the rates of moderate to severe glucose clinical outliers are 3.5/1000 (GEM) and 0.6/1000 glucoses (ABL), respectively, using the 15-minute interval (P &lt; .0001).	Glucose	64-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-135
32142251-0	2020	Identification of Phosphate-Containing Compounds as New Inhibitors of 14-3-3/c-Abl Protein-Protein Interaction.	Phosphates	18-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-82
32142251-5	2020	A 37-compound library of PLP and IMP analogues was investigated using a FP assay, leading to the identification of three further molecules acting as weak inhibitors of the 14-3-3/c-Abl complex formation.	Inosine Monophosphate	33-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	179-184
31999850-1	2020	BACKGROUND: Nilotinib is a potent, second-generation inhibitor of BCR-ABL1 tyrosine kinase and has been approved as frontline and salvage therapy for patients with chronic-phase chronic myeloid leukemia (CP-CML).	nilotinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-74
32175644-0	2020	Renovascular hypertension from the BCR-ABL tyrosine kinase inhibitor ponatinib.	ponatinib	69-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
32602291-5	2020	The inhibition of USP1 protein activity by ML323 reduced the level of Bcr-Abl oncoprotein in K562 cells.	ML323	43-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
32269321-0	2020	Retraction Note: Disruption of the Bcr-Abl/Hsp90 protein complex: a possible mechanism to inhibit Bcr-Abl-positive human leukemic blasts by novobiocin.	Novobiocin	140-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
32269321-0	2020	Retraction Note: Disruption of the Bcr-Abl/Hsp90 protein complex: a possible mechanism to inhibit Bcr-Abl-positive human leukemic blasts by novobiocin.	Novobiocin	140-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
32485885-11	2020	ABL gene editing-based therapy might provide a potential strategy for imatinib-insensitive or resistant CML patients.	Imatinib Mesylate	70-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
32340449-4	2020	In this study, we used ABL kinase (target) as a model, and synthesized a fluorescent probe (Cy3-dasatinib) with an affinity to the target using ABL inhibitor dasatinib as a precursor.	cy3-dasatinib	92-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-26
32340449-4	2020	In this study, we used ABL kinase (target) as a model, and synthesized a fluorescent probe (Cy3-dasatinib) with an affinity to the target using ABL inhibitor dasatinib as a precursor.	Dasatinib	96-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-26
32305283-0	2020	Arsenic trioxide-induced p38 MAPK and Akt mediated MCL1 downregulation causes apoptosis of BCR-ABL1-positive leukemia cells.	Arsenic Trioxide	0-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-99
32305283-1	2020	In this study, we investigated the mechanisms underlying arsenic trioxide (ATO)-induced death of human BCR-ABL1-positive K562 and MEG-01 cells.	Arsenic Trioxide	57-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-111
32305283-1	2020	In this study, we investigated the mechanisms underlying arsenic trioxide (ATO)-induced death of human BCR-ABL1-positive K562 and MEG-01 cells.	Arsenic Trioxide	75-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-111
32305283-3	2020	ATO-induced BCR-ABL1 downregulation caused Akt inactivation but not p38 MAPK activation.	Arsenic Trioxide	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-20
32305283-9	2020	Collectively, our data indicate that ATO-induced p38 MAPK- and Akt-mediated MCL1 downregulation triggers apoptosis in K562 and MEG-01 cells, and that p38 MAPK activation is independent of ATO-induced BCR-ABL1 suppression.	Arsenic Trioxide	37-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	204-208
32299471-16	2020	Moreover, inhibition of either c-Abl, using nilotinib, or p53, using pifithrin-alpha, was sufficient to increase autophagic flux in neuronal cells by inducing phosphorylation of AMP-activated kinase (AMPK), ULK1 activation, and down-regulation of mTORC1 signaling.	nilotinib	44-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-36
32266142-6	2020	He was then treated with the ABL1 tyrosine kinase inhibitor dasatinib and achieved complete remission within 2 weeks.	Dasatinib	60-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-33
31891685-0	2020	Excessive arachidonic acid induced actin bunching remodeling and podocyte injury via a PKA-c-Abl dependent pathway.	Arachidonic Acids	10-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-96
31891685-6	2020	H89 (PKA inhibitor) provided protection against AA-induced F-actin bunching remodeling, down-regulated nephrin phosphorylation, and suppressed the c-Abl translocation and activation.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-152
32292555-2	2020	New insights implicating c-Abl activation as a driving force in PD have opened a new drug development avenue for PD treatment beyond the symptomatic relief by L-DOPA.	Levodopa	159-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-30
31785034-7	2020	Molecular docking of ABQ11 into ABL1 kinase ATP binding pocket revealed the formation of some key interactions.	Adenosine Triphosphate	44-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-36
31714657-5	2020	Chol grafting with as little as ~1.0 Chol/PEI on 0.6 and 1.2 kDa PEIs enabled silencing of the reporter Green Fluorescent Protein (GFP) gene as well as the endogenous BCR-Abl oncogene in K562 cells.	Cholesterol	0-4	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-174
31714657-5	2020	Chol grafting with as little as ~1.0 Chol/PEI on 0.6 and 1.2 kDa PEIs enabled silencing of the reporter Green Fluorescent Protein (GFP) gene as well as the endogenous BCR-Abl oncogene in K562 cells.	Cholesterol	37-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-174
31714657-5	2020	Chol grafting with as little as ~1.0 Chol/PEI on 0.6 and 1.2 kDa PEIs enabled silencing of the reporter Green Fluorescent Protein (GFP) gene as well as the endogenous BCR-Abl oncogene in K562 cells.	Polyethyleneimine	65-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-174
31714657-6	2020	The PEI-Chol mediated delivery of siRNAs specific for BCR-Abl and KSP genes significantly arrested the growth the cells which was significantly reflected in colony formation potency of K562 cells.	poly(ethylene imine)	4-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
31985099-7	2020	Amiodarone was continued 40% (14 out of 35) and 40% (20 out of 70) in ABL and CNT groups, respectively (P = 1.000).	Amiodarone	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-73
31714657-6	2020	The PEI-Chol mediated delivery of siRNAs specific for BCR-Abl and KSP genes significantly arrested the growth the cells which was significantly reflected in colony formation potency of K562 cells.	Cholesterol	8-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
31944221-1	2020	Importance: A randomized clinical trial is needed to determine whether the second-generation Abl-tyrosine kinase inhibitor dasatinib is more effective than the first-generation inhibitor imatinib mesylate for childhood Philadelphia chromosome-positive acute lymphoblastic leukemia (ALL).	Tyrosine	97-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-96
31955347-2	2020	First-line therapy for CML consists of treatment with imatinib mesylate, which selectively inhibits the BCR-ABL protein by competing for its ATP-binding site.	imatinib	54-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
31955347-2	2020	First-line therapy for CML consists of treatment with imatinib mesylate, which selectively inhibits the BCR-ABL protein by competing for its ATP-binding site.	Adenosine Triphosphate	141-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
32094501-6	2020	Lastly, in patients administered with dasatinib for the treatment of BCR-ABL-positive leukemias, we provided the proof of concept that the kinase inhibitor also influences the two innate T-cell subsets in humans, as attested by their increased frequency in the peripheral blood.	Dasatinib	38-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
31767149-1	2020	Tyrosine kinase inhibitors (TKIs) that target BCR-ABL are the standard first-line therapy for patients with chronic-phase CML.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
32095692-1	2020	Ponatinib is a multikinase inhibitor that is used to treat chronic myeloid leukemia patients harboring mutated ABL1(T315I) kinase.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-115
32095692-6	2020	A nicotinamide analogue of ponatinib, HSN748, retains activity against FLT3, ABL1, RET, and PDGFRalpha/beta but loses activity against c-Src and P38alpha.	Niacinamide	2-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-81
32095692-6	2020	A nicotinamide analogue of ponatinib, HSN748, retains activity against FLT3, ABL1, RET, and PDGFRalpha/beta but loses activity against c-Src and P38alpha.	ponatinib	27-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-81
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
31901955-1	2020	PURPOSE: ABL tyrosine kinase inhibitors (TKIs) have demonstrated potency in the treatment of chronic myeloid leukemia (CML) patients.	Tyrosine	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-12
31901955-4	2020	METHODS: In this study, we evaluated the effect of combination therapy of CUDC-907 and ABL TKIs, using BCR-ABL-positive cell lines and primary samples.	CUDC-907	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
31901955-10	2020	CONCLUSION: Taken together, our results indicate that administration of CUDC-907, a dual PI3K and HDAC inhibitor, may be an effective strategy against ABL TKI-resistant cells, including cells harboring the T315I mutation.	CUDC-907	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-154
31901955-11	2020	Moreover, CUDC-907 may enhance the cytotoxic effects of ABL TKI when a combined treatment strategy is used against Philadelphia chromosome-positive leukemia cells.	CUDC-907	10-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-59
30621530-0	2020	Oxidative stress-induced activation of Abl and Src kinases rapidly induces P-glycoprotein internalization via phosphorylation of caveolin-1 on tyrosine-14, decreasing cortisol efflux at the blood-brain barrier.	Tyrosine	143-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-42
30621530-7	2020	A brain perfusion study in rats showed that cortisol efflux at the BBB was markedly decreased by H2O2 administration, and inhibitors of Abl kinase and Src kinase, which phosphorylate tyrosine-14 in caveolin-1, suppressed this decrease.	Hydrocortisone	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-139
30621530-7	2020	A brain perfusion study in rats showed that cortisol efflux at the BBB was markedly decreased by H2O2 administration, and inhibitors of Abl kinase and Src kinase, which phosphorylate tyrosine-14 in caveolin-1, suppressed this decrease.	Tyrosine	183-191	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-139
30621530-8	2020	Overall, these findings support the idea that oxidative stress-induced activation of Abl kinase and Src kinase induces internalization of P-gp via the phosphorylation of tyrosine-14 in caveolin-1, leading to a rapid decrease of P-gp-mediated cortisol efflux at the BBB.	Tyrosine	170-178	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-88
31810012-0	2020	Acetylshikonin induces apoptosis of human leukemia cell line K562 by inducing S phase cell cycle arrest, modulating ROS accumulation, depleting Bcr-Abl and blocking NF-kappaB signaling.	acetylshikonin	0-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-151
31810012-12	2020	In addition, acetylshikonin decreased Bcr-Abl expression and inhibited its downstream signaling.	acetylshikonin	13-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
31831854-0	2020	The role of phosphorylation of MLF2 at serine 24 in BCR-ABL leukemogenesis.	cholecystokinin C-terminal flanking peptide	39-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
32078113-0	2020	Mechanisms of Cardiovascular Toxicity of BCR-ABL1 Tyrosine Kinase Inhibitors in Chronic Myelogenous Leukemia.	Tyrosine	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
31944221-1	2020	Importance: A randomized clinical trial is needed to determine whether the second-generation Abl-tyrosine kinase inhibitor dasatinib is more effective than the first-generation inhibitor imatinib mesylate for childhood Philadelphia chromosome-positive acute lymphoblastic leukemia (ALL).	dasatinib	123-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-96
31952182-2	2020	Although tyrosine kinase inhibitors (TKIs) against BCR-ABL represent the standard therapeutic option for CML, resistances to TKIs can be a serious problem.	Tyrosine	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
31952182-7	2020	Here, we show for the first time the therapeutic potential of allopurinol against BCR-ABL-positive CML cells.	Allopurinol	62-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
31988993-0	2020	Successful treatment of T315I BCR-ABL mutated lymphoid blast phase chronic myeloid leukemia with chimeric antigen receptor T cell therapy followed by dasatinib.	dasatinib	150-159	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
32999163-0	2020	Emodin Inhibits Resistance to Imatinib by Downregulation of Bcr-Abl and STAT5 and Allosteric Inhibition in Chronic Myeloid Leukemia Cells.	Emodin	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
31925328-3	2020	Using BCR-ABL as a case study, we successfully recaptured the clinically observed mutations that confer resistance imatinib, nilotinib, dasatinib, bosutinib, and ponatinib.	imatinib	115-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-13
31925328-3	2020	Using BCR-ABL as a case study, we successfully recaptured the clinically observed mutations that confer resistance imatinib, nilotinib, dasatinib, bosutinib, and ponatinib.	nilotinib	125-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-13
31925328-3	2020	Using BCR-ABL as a case study, we successfully recaptured the clinically observed mutations that confer resistance imatinib, nilotinib, dasatinib, bosutinib, and ponatinib.	dasatinib	136-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-13
31925328-3	2020	Using BCR-ABL as a case study, we successfully recaptured the clinically observed mutations that confer resistance imatinib, nilotinib, dasatinib, bosutinib, and ponatinib.	bosutinib	147-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-13
31925328-3	2020	Using BCR-ABL as a case study, we successfully recaptured the clinically observed mutations that confer resistance imatinib, nilotinib, dasatinib, bosutinib, and ponatinib.	ponatinib	162-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-13
32999163-1	2020	Imatinib-resistance is a significant concern for Bcr-Abl-positive chronic myelogenous leukemia (CML) treatment.	Imatinib Mesylate	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.	Emodin	19-25	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.	Emodin	19-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
32999163-5	2020	After treatment of emodin and imatinib together, the levels of p-Bcr-Abl and Bcr-Abl were significantly downregulated.	Imatinib Mesylate	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 Mesylate	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
32999163-9	2020	More importantly, emodin simultaneously targeted both the ATP-binding and allosteric sites on Bcr-Abl by molecular docking, with higher affinity with the myristoyl-binding site for enhanced Bcr-Abl kinase inhibition.	Emodin	18-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
32999163-9	2020	More importantly, emodin simultaneously targeted both the ATP-binding and allosteric sites on Bcr-Abl by molecular docking, with higher affinity with the myristoyl-binding site for enhanced Bcr-Abl kinase inhibition.	Emodin	18-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	190-197
31699386-0	2020	New 2,6,9-trisubstituted purine derivatives as Bcr-Abl and Btk inhibitors and as promising agents against leukemia.	Purines	4-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
32829325-1	2020	INTRODUCTION: Ponatinib (PNT) is a tyrosine kinase inhibitor approved for treating patients with Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph + ALL), or chronic myeloid leukemia, resistant or intolerant to other tyrosine kinase inhibitor or showing T315I mutation of BCR-ABL.	ponatinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	288-295
31563145-2	2020	There have been successful examples of targeted therapy improving the outcome of some childhood cancers, such as the addition of an ABL class tyrosine kinase inhibitor to conventional chemotherapy substantially improving the cure rate for patients with BCR-ABL1 positive acute lymphoblastic leukemia.	Tyrosine	142-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-135
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 Mesylate	96-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-131
31833784-1	2020	The availability of several BCR-ABL1 tyrosine kinase inhibitor (TKI) options means physicians and patients can select the most appropriate treatment for a patient with chronic myeloid leukemia (CML).	Tyrosine	37-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
30661457-0	2020	How does the novel T315L mutation of breakpoint cluster region-abelson (BCR-ABL) kinase confer resistance to ponatinib: a comparative molecular dynamics simulation study.	ponatinib	109-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-70
30661457-0	2020	How does the novel T315L mutation of breakpoint cluster region-abelson (BCR-ABL) kinase confer resistance to ponatinib: a comparative molecular dynamics simulation study.	ponatinib	109-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
30661457-5	2020	The latest third-generation TKIs, ponatinib, can tackle most abnormal BCR-ABL kinases, including the T315I mutant that is resistant to first- and second-generations TKIs such as imatinib.	ponatinib	34-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
30661457-7	2020	Here, using molecular dynamics (MD) simulations, we explored into the detailed interactions between ponatinib and BCR-ABL in the wild-type (WT), T315I, and T315L systems.	ponatinib	100-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
30661457-9	2020	Binding free energy analysis unveiled that the affinity of ponatinib to BCR-ABL decreased upon T315L mutation, which resulted in its unfavorable binding and drug resistance.	ponatinib	59-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
31699386-2	2020	Therefore, several strategies have focused on the use of inhibitors as chemotherapeutic tools to treat these types of leukemia, such as imatinib (for Bcr-Abl) or ibrutinib (for Btk).	imatinib	136-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
31699386-4	2020	In this study, we designed, synthesized and evaluated 2,6,9-trisubstituted purine derivatives as novel Bcr-Abl and Btk inhibitors.	Purines	56-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
31765938-1	2020	Chronic myelogenous leukemia (CML) is caused by the BCR-ABL chimeric tyrosine kinase, which is derived from the reciprocal translocation, t(9;22)(q34;q11).	Tyrosine	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
31765938-2	2020	BCR-ABL tyrosine kinase inhibitors (TKIs) can provide prolonged overall survival in CML patients, resulting in life expectancy nearly to general population, and now approximately half of patients who achieved deep molecular response (DMR) can sustain durable molecular remission after discontinuation TKIs.	Tyrosine	8-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
31789418-0	2020	Homoharringtonine promotes BCR-ABL degradation through the p62-mediated autophagy pathway.	Homoharringtonine	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
31777258-0	2020	Second-generation Src/Abl inhibitor bosutinib effectively induces apoptosis in human esophageal squamous cell carcinoma (ESCC) cells via inhibiting Src/Abl signaling.	bosutinib	36-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-25
31777258-0	2020	Second-generation Src/Abl inhibitor bosutinib effectively induces apoptosis in human esophageal squamous cell carcinoma (ESCC) cells via inhibiting Src/Abl signaling.	bosutinib	36-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-155
31777258-4	2020	In this paper, we report that the potent dual Src/Abl inhibitor bosutinib exerts anti-tumor effects on ESCC.	bosutinib	64-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-53
31777258-7	2020	Mechanistically, bosutinib effectively inhibits c-Abl and Src and its downstream signaling pathways, PI3K/AKT/mTOR and JAK/STAT3.	bosutinib	17-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-53
31777258-9	2020	In summary, our results reveal that Src and Abl are potential therapeutic targets in ESCC and that the novel Src/Abl inhibitor bosutinib alone or in combination with other chemotherapeutic agents may be a viable option for treating ESCC patients.	bosutinib	127-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-116
31789418-3	2020	In the present study, HHT treatment demonstrated induction of apoptosis in imatinib-resistant K562G cells by using MTS assay and western blotting, and BCR-ABL protein was reduced.	Homoharringtonine	22-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-158
32507808-0	2020	[BCR-ABL1-positive myelodysplastic syndrome with neutropenia and anemia treated successfully with imatinib mesylate].	Imatinib Mesylate	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 Mesylate	70-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-129
31890203-11	2019	In contrast, inhibition of BCR-ABL did impact on glucose consumption and lactate production regardless of the presence of HIFs.	Lactic Acid	73-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
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 Mesylate	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 Mesylate	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-122
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.	Arginine	127-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-108
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 Mesylate	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-140
32240815-7	2020	In addition, direct activation of Abl family kinases with the small molecule activator DPH resulted in endothelial barrier disruption that was attenuated by Arg siRNA.	Phenytoin	87-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-37
32240815-7	2020	In addition, direct activation of Abl family kinases with the small molecule activator DPH resulted in endothelial barrier disruption that was attenuated by Arg siRNA.	Arginine	157-160	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-37
31862885-3	2019	Here, we show that PM mechanoadaptation is controlled by a tension-sensing pathway composed of c-Abl tyrosine kinase and membrane curvature regulator FBP17.	Tyrosine	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-100
31439580-0	2019	Purinostat Mesylate is a uniquely potent and selective inhibitor of HDACs for the treatment of BCR-ABL-induced B-cell acute lymphoblastic leukemia.	UNII-FTV8V4AYQ8	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
31861239-1	2019	Signal transducers and activators of transcription 5A and 5B (STAT5A and STAT5B) are crucial downstream effectors of tyrosine kinase oncogenes (TKO) such as BCR-ABL in chronic myeloid leukemia (CML) and FLT3-ITD in acute myeloid leukemia (AML).	Tyrosine	117-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-164
31699612-0	2019	Structure-based analysis and biological characterization of imatinib derivatives reveal insights towards the inhibition of wild-type BCR-ABL and its mutants.	imatinib	60-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
32570264-0	2020	Sustained Complete Remission with Incomplete Hematologic Recovery (CRi) in a Patient with Relapsed AML and Concurrent BCR-ABL1 and CBFB Rearrangement Treated with a Combination of Venetoclax and 5-Azacytidine.	venetoclax	180-190	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-126
31699612-1	2019	To reveal insights into the inhibition of BCR-ABL and its mutants, structure-based computing methods, such as docking, molecular dynamics (MD) simulation, the molecular mechanics generalized born surface area (MMGBSA), and biological characterizations, were employed to analyze two main pharmacophore zones and two related regions of imatinib derivatives.	imatinib	334-342	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
31699612-4	2019	To reveal insights into the inhibition of BCR-ABL mutants, the bioactivities of imatinib, nilotinib and flumatinib against BCR-ABL mutants were evaluated, and a point mutant (Y253F) of BCR-ABL was simulated.	HH-GV-678	104-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-130
31699612-4	2019	To reveal insights into the inhibition of BCR-ABL mutants, the bioactivities of imatinib, nilotinib and flumatinib against BCR-ABL mutants were evaluated, and a point mutant (Y253F) of BCR-ABL was simulated.	HH-GV-678	104-114	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-130
31699612-5	2019	The results of our structure-based analysis and biological characterization of imatinib derivatives towards the inhibition of wild-type BCR-ABL and its mutants may provide new ideas for the design of imatinib analogs with potent activity.	imatinib	79-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-143
31699612-5	2019	The results of our structure-based analysis and biological characterization of imatinib derivatives towards the inhibition of wild-type BCR-ABL and its mutants may provide new ideas for the design of imatinib analogs with potent activity.	imatinib	200-208	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-143
31615652-4	2019	In addition, morphine alleviated the anti-proliferative and pro-apoptotic effects of BCR-ABL tyrosine kinase inhibitor (TKI) in BP-CML cells.	Morphine	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
31615652-4	2019	In addition, morphine alleviated the anti-proliferative and pro-apoptotic effects of BCR-ABL tyrosine kinase inhibitor (TKI) in BP-CML cells.	Tyrosine	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
31615652-6	2019	In addition, morphine alleviated the inhibitory effects of BCR-ABL TKIs in cell survival, colony formation and replating capacity in BP-CML CD34 + stem/progenitor cells.	Morphine	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-66
31615652-8	2019	The effects of morphine in BP-CML were abolished by Wnt inhibitor LGK-974 or XAV939, which further confirmed that morphine protected BP-CML cells from BCR-ABL TKIs-induced toxicity via activating Wnt/beta-catenin signaling.	Morphine	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-158
31615652-8	2019	The effects of morphine in BP-CML were abolished by Wnt inhibitor LGK-974 or XAV939, which further confirmed that morphine protected BP-CML cells from BCR-ABL TKIs-induced toxicity via activating Wnt/beta-catenin signaling.	Morphine	114-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-158
31808889-1	2019	Subsequent to the development and global availability of BCR/ABL-targeted tyrosine kinase inhibitors (TKIs), the prognosis of patients with chronic myeloid leukemia (CML), at least those in the chronic phase, has markedly improved, and in the developed world, the average lifespan of these patients is now close to that of age- and sex-matched subjects without the disease.	Tyrosine	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
31998490-0	2020	An Imatinib-non-responsive patient with an ABL Leu387Trp mutation achieves cytogenetic and molecular response under bosutinib: Case report and biological characterization.	imatinib	3-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-46
31998490-0	2020	An Imatinib-non-responsive patient with an ABL Leu387Trp mutation achieves cytogenetic and molecular response under bosutinib: Case report and biological characterization.	tryptophan-leucine	47-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-46
31998490-0	2020	An Imatinib-non-responsive patient with an ABL Leu387Trp mutation achieves cytogenetic and molecular response under bosutinib: Case report and biological characterization.	bosutinib	116-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-46
31796494-3	2019	Induced pluripotent stem cell (iPSC)-based drug repurposing identified an Src/c-Abl inhibitor, bosutinib, as a candidate molecular targeted therapy for ALS.	bosutinib	95-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-83
31915450-10	2019	Either ASFE alone or in combined treatment with IM on K-562 CML cells resulted in a significant reduction of the Bcr-Abl levels.	imatinib	48-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
31760572-4	2019	Management and outcomes of patients with chronic myeloid leukemia have been revolutionized by the discovery, development, and approval of BCR-ABL tyrosine kinase inhibitors (TKIs).	Tyrosine	146-154	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
31602720-7	2019	The binding mode of AQ15 into the ATP binding pocket of ABL1 kinase was predicted in silico, showing the formation of some key interactions.	Adenosine Triphosphate	34-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-60
30929559-1	2019	Imatinib is the first molecularly targeted compound for chronic myeloid leukemia (CML) capable to inhibit BCR-ABL kinase activity.	Imatinib Mesylate	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 Mesylate	145-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-105
32699984-2	2019	Imatinib, the first BCR-ABL1 TKI, was introduced into clinical practice in the early 2000s.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-28
31759365-3	2019	Our aim is to explore regions outside the BCR-ABL oncoprotein to identify potential therapeutic targets to curb drug resistance by targeting growth factor receptor-bound protein-2 (Grb-2) which binds to BCR-ABL at the phosphorylated tyrosine (Y177) thereby activating the Ras and PI3K/AKT signaling pathway.	Tyrosine	233-241	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
31756944-3	2019	Here, we show that, in contrast to BCR/ABL causing Ph-positive leukemias, FLT3-ITD distinctively activates the serine/threonine kinases RSK1/2 through activation of the MEK/ERK pathway and PDK1 to transduce signals required for FLT3-ITD-dependent, but not BCR/ABL-dependent, proliferation and survival of various cells, including MV4-11.	cholecystokinin C-terminal flanking peptide	111-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	256-263
31717629-1	2019	Chronic Myeloid Leukemia (CML) is a disease arising in stem cells expressing the BCR-ABL oncogenic tyrosine kinase that transforms one Hematopoietic stem/progenitor Cell into a Leukemic Stem Cell (LSC) at the origin of differentiated and proliferating leukemic cells in the bone marrow (BM).	Tyrosine	99-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
31717629-2	2019	CML-LSCs are recognized as being responsible for resistances and relapses that occur despite the advent of BCR-ABL-targeting therapies with Tyrosine Kinase Inhibitors (TKIs).	Tyrosine	140-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
31759365-3	2019	Our aim is to explore regions outside the BCR-ABL oncoprotein to identify potential therapeutic targets to curb drug resistance by targeting growth factor receptor-bound protein-2 (Grb-2) which binds to BCR-ABL at the phosphorylated tyrosine (Y177) thereby activating the Ras and PI3K/AKT signaling pathway.	Tyrosine	233-241	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	203-210
31542717-6	2019	PQ2 showed anti-Abelson kinase 1 (Abl1) activity with different inhibitory profile than Imatinib in the panel of eight kinases.	Plastoquinone	0-2	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-32
31542717-6	2019	PQ2 showed anti-Abelson kinase 1 (Abl1) activity with different inhibitory profile than Imatinib in the panel of eight kinases.	Plastoquinone	0-2	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-38
31542717-8	2019	In addition, PQ2 induced Bcr-Abl1 mediated ERK pathway in human chronic myelogenous leukemia (CML) cells.	Plastoquinone	13-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-33
31542717-11	2019	These results indicated that PQ2 has multiple mechanism of action and two of them are anti-Bcr-Abl1 and DNA-cleaving activity.	Plastoquinone	29-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-99
31374292-4	2019	We found that histone H3 lysine 4 (H3K4) demethylase RBP2 expression is negatively correlated with BCR-ABL expression, which suggests a regulatory link between these two genes.	Lysine	25-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
31428968-0	2019	BCR-ABL induces tyrosine phosphorylation of YAP leading to expression of Survivin and Cyclin D1 in chronic myeloid leukemia cells.	Tyrosine	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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 Mesylate	129-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	275-282
31428968-7	2019	These results suggest that BCR-ABL induces tyrosine phosphorylation of YAP presumably through Src family kinases, which results in expression of Survivin and Cyclin D leading to leukemogenesis in CML cells.	Tyrosine	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
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.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
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 Mesylate	88-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
30580670-3	2019	In this study, 44 BCR-ABL kinase inhibitors, which are derivatives of ponatinib, were used to develop a robust two-dimensional quantitative structure-activity relationship (2D-QSAR) and 3D-Pharmacophore models by dividing dataset into 32 training sets and 12 test set molecules.	ponatinib	70-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
31014138-0	2019	Response to single agent dasatinib post allogeneic transplant in B-cell acute lymphoblastic leukemia with NUP214-ABL1.	Dasatinib	25-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-117
31807112-3	2019	Since the development of the tyrosine kinase inhibitor of the BCR-ABL kinase, the clinical approach to CML has dramatically changed, with a stunning improvement in the quality of life and response rates of patients.	Tyrosine	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
31698436-0	2019	En-Abl-ing treatment of "Ph-like" ALL?	N-(4'-bromophenyl)-2,2-diphenylacetanilide	25-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	3-6
31578349-5	2019	Miniaturization of the procedure enabled determining the target selectivity of the clinical BCR-ABL inhibitor dasatinib in peripheral blood mononuclear cell (PBMC) lysates from individual donors.	dasatinib	110-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
31422076-1	2019	Epidemiological studies of 1,3-butadiene (BD) exposures have reported a possible association with chronic myelogenous leukemia (CML), which is defined by the presence of the t(9;22) translocation (Philadelphia chromosome) creating an oncogenic BCR-ABL fusion gene.	1,3-butadiene	27-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	244-251
31569304-6	2019	We found that bosutinib, as a potent dual Src/Abl inhibitor, could exert anti-tumor effects on cervical cancer.	bosutinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-49
31510844-0	2019	Ponatinib use in two pediatric patients with relapsed Ph + ALL with ABL1 kinase domain mutations.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-72
31683623-1	2019	Tyrosine kinase inhibitors (TKI) such as the BCR-ABL inhibitor dasatinib and nilotinib are highly effective therapies for chronic myeloid leukemia (CML).	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
31683623-1	2019	Tyrosine kinase inhibitors (TKI) such as the BCR-ABL inhibitor dasatinib and nilotinib are highly effective therapies for chronic myeloid leukemia (CML).	dasatinib	63-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
31539241-0	2019	Discovery of SIAIS178 as an effective BCR-ABL degrader by recruiting von Hippel-Lindau (VHL) E3 Ubiquitin Ligase.	SIAIS178	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
31539241-3	2019	Herein, we described the design, synthesis, and evaluation of novel proteolysis-targeting chimeric (PROTAC) small molecules targeting BCR-ABL which connect dasatinib and VHL E3 ubiquitin ligase ligand by extensive optimization of linkers.	Dasatinib	156-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
31607295-8	2019	The study results also revealed that dehydrocostus lactone significantly inhibited the expression of BCR/ABL STAT3, STAT5, CyclinB1, CDK1 and BCL-2, and up-regulated the expression level of BAX and p21.	dehydrocostus lactone	37-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-108
30045148-0	2019	Acute Lymphoblastic Leukemia With INPP5D-ABL1 Fusion Responds to Imatinib Treatment.	Imatinib Mesylate	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-45
31859798-4	2019	MATERIAL AND METHODS: Prospective HBsAg screening cohort of immigrant and Chilean pregnant women with RB, between July 1, 2017 and June 30, 2018 in CABL.	Hepatitis B Surface Antigens	34-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	148-152
31468670-0	2019	An ent-Kaurane Diterpenoid Isolated from Rabdosia excisa Suppresses Bcr-Abl Protein Expression in Vitro and in Vivo and Induces Apoptosis of CML Cells.	Diterpenes, Kaurane	7-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
31468670-0	2019	An ent-Kaurane Diterpenoid Isolated from Rabdosia excisa Suppresses Bcr-Abl Protein Expression in Vitro and in Vivo and Induces Apoptosis of CML Cells.	Diterpenes	15-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
31468670-6	2019	We conducted in vitro and in vivo biological experiments and found that kamebakaurin potently inhibits cell proliferation, mainly by enhancing cell apoptosis and down-regulating Bcr-Abl protein levels.	kamebakaurin	72-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185
31607295-9	2019	CONCLUSION: Dehydrocostus lactone can suppress the proliferation of K562 cells and induce the apoptosis of K562 cells through BCR/ABL-STAT signaling pathways.	dehydrocostus lactone	12-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-133
31574962-7	2019	The molecular modeling results for analogue 10 showed that the use of the 4-(aminomethyl)benzamide as a flexible linker leads to a favorable overall geometry of the molecule, which allows one to bypass the bulk isoleucine residue and provides the necessary binding to the active center of the T315I-mutant Abl (PDB: 3QRJ).	4-(aminomethyl)benzamide	74-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	306-309
31574962-7	2019	The molecular modeling results for analogue 10 showed that the use of the 4-(aminomethyl)benzamide as a flexible linker leads to a favorable overall geometry of the molecule, which allows one to bypass the bulk isoleucine residue and provides the necessary binding to the active center of the T315I-mutant Abl (PDB: 3QRJ).	Isoleucine	211-221	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	306-309
31572674-9	2019	Additionally, the dMLPA assay could reliably identify ploidy status and copy number-based gene fusions (SIL-TAL1, NUP214-ABL, EBF1-PDGFRB).	dmlpa	18-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-124
31574910-1	2019	Imatinib, an Abelson (ABL) tyrosine kinase inhibitor, is a lead molecular-targeted drug against chronic myelogenous leukemia (CML).	Imatinib Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-25
31430499-0	2019	siRNA-mediated BCR-ABL silencing in primary chronic myeloid leukemia cells using lipopolymers.	lipopolymers	81-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
31430499-8	2019	These results showed that a low dose of BCR-ABL siRNA could be used with lipopolymers to reduce BCR-ABL mRNA expression, CML cell survival and colony formation.	lipopolymers	73-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
31430499-8	2019	These results showed that a low dose of BCR-ABL siRNA could be used with lipopolymers to reduce BCR-ABL mRNA expression, CML cell survival and colony formation.	lipopolymers	73-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
31527518-0	2019	Xanthohumol, a Prenylated Flavonoid from Hops, Induces Caspase-Dependent Degradation of Oncoprotein BCR-ABL in K562 Cells.	xanthohumol	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
31527518-0	2019	Xanthohumol, a Prenylated Flavonoid from Hops, Induces Caspase-Dependent Degradation of Oncoprotein BCR-ABL in K562 Cells.	Flavonoids	26-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
31620229-1	2019	Compound 3a, DV2-103, is a kinase inactive analogue of a potent Abl1/Src kinase inhibitor, PD173955, 2.	PD 173955	91-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-68
31399520-0	2019	c-Abl-Mediated Tyrosine Phosphorylation of PARP1 Is Crucial for Expression of Proinflammatory Genes.	Tyrosine	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
31700719-12	2019	It also discusses the successful utilization of tyrosine kinase inhibitors (TKIs) in the treatment of BCR-ABL-positive AML, as there are no established guidelines.	Tyrosine	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
31737104-0	2019	Overexpression of miR-4433 by suberoylanilide hydroxamic acid suppresses growth of CML cells and induces apoptosis through targeting Bcr-Abl.	vorinostat	30-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
31737104-3	2019	In present study, a histone deacetylase inhibitor, suberoylanilide hydroxamic acid (SAHA), was used to screen for microRNA that can target Bcr-Abl.	vorinostat	51-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-146
31737104-3	2019	In present study, a histone deacetylase inhibitor, suberoylanilide hydroxamic acid (SAHA), was used to screen for microRNA that can target Bcr-Abl.	vorinostat	84-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-146
31737104-9	2019	Results: SAHA up-regulated the acetylation level of histone 3, and effectively inhibited Bcr-Abl mRNA level and its downstream signal transduction pathway, while inhibiting the growth of CML cells and inducing apoptosis.	vorinostat	9-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
31737104-10	2019	Furthermore, bioinformatics tools predicted that miR-4433 is a putative microRNA targeting Bcr-Abl and that the expression level of miR-4433 was significantly increased after SAHA treatment in K562 cells.	vorinostat	175-179	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
31737104-14	2019	Conclusion: miR-4433 was identified as a microRNA targeting Bcr-Abl, which may be subject to epigenetic regulation of SAHA, a histone deacetylase inhibitor that has been approved by the US FDA for the treatment of cutaneous T-cell lymphoma.	vorinostat	118-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
31296381-5	2019	Structural and sequence comparison showed that hGas7-SH3 shares high similarity with Abl SH3 domain, which binds to a high-affinity proline-rich peptide P41 in a canonical SH3-ligand binding mode through two hydrophobic pockets and a specificity site in the RT-loop.	Proline	132-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-88
31349760-0	2019	The NEDD8-activating enzyme inhibitor MLN4924 induces DNA damage in Ph+ leukemia and sensitizes for ABL kinase inhibitors.	pevonedistat	38-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-103
31220669-13	2019	Docking simulation was performed to position active synthesized compounds 6-32, 6-33, and 6-34 over the ABL1 active site in two different wild-type (DFG-in and DFG-out motif conformer) and T315I mutant to determine the probable binding orientation, conformation and mode of interaction.	1,3-Diphenylguanidine	149-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-108
31220669-13	2019	Docking simulation was performed to position active synthesized compounds 6-32, 6-33, and 6-34 over the ABL1 active site in two different wild-type (DFG-in and DFG-out motif conformer) and T315I mutant to determine the probable binding orientation, conformation and mode of interaction.	1,3-Diphenylguanidine	160-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-108
31100317-4	2019	Here, we show that the interaction between PLEKHG2 and ABL1 attenuated the PLEKHG2-induced serum response element-dependent gene transcription in a tyrosine phosphorylation-independent manner.	Tyrosine	148-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-59
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 Mesylate	88-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-71
31493432-0	2019	BCR-ABL1 tyrosine kinase inhibitor K0706 exhibits preclinical activity in Philadelphia chromosome-positive leukemia.	Vodobatinib	35-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-8
31493432-3	2019	K0706 is a novel BCR-ABL1 TKI currently under clinical investigation with structural elements similar to those of ponatinib and dasatinib.	Vodobatinib	0-5	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-25
31448223-5	2019	This includes the use asciminib as first in class inhibitor targeting the myristoyl pocket of BCR-ABL, combination treatments with established non-TKI drugs such as interferon and drugs with novel targets relevant to CML biology such as gliptins and thiazolidinediones.	asciminib	22-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-162
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-27
31233186-2	2019	Imatinib resistance can be ascribed to Bcr-Abl-dependent and independent resistance.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
31396300-0	2019	Reactive Oxygen Species Are Involved in the Development of Gastric Cancer and Gastric Cancer-Related Depression through ABL1-Mediated Inflammation Signaling Pathway.	Reactive Oxygen Species	0-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-124
31358779-4	2019	It is mainly treated with BCR-ABL inhibitors, such as imatinib.	Imatinib Mesylate	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
31413564-0	2019	Arsenic sulfide nanoformulation induces erythroid differentiation in chronic myeloid leukemia cells through degradation of BCR-ABL.	arsenic trisulfide	0-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-130
31413564-5	2019	Results: Results showed that instead of inhibiting the activity of BCR-ABL, ee-As4S4 induced direct degradation of BCR-ABL in K562 cells within 6 hr incubation, followed by the occurrence of erythroid differentiation in K562 after 72 hr incubation, evidenced by the significantly upregulated CD235a and benzidine staining, which was not detectable with r-As4S4.	as4s4	79-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-122
31413564-7	2019	Mechanistic studies indicated that ee-As4S4 induced autophagy by downregulating the level of intracellular ROS and hypoxia-inducible factor-1alpha significantly, which led to the subsequent degradation of BCR-ABL.	ee-as4s4	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	205-212
31396300-8	2019	The effect of ABL1 on inflammation was detected with Imatinib/Nilotinib-treated GC cell lines.	Imatinib Mesylate	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-18
31396300-8	2019	The effect of ABL1 on inflammation was detected with Imatinib/Nilotinib-treated GC cell lines.	nilotinib	62-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-18
31396300-14	2019	With the treatment of ROS, the activities of ABL1 and inflammatory signaling were enhanced both in vitro and in vivo, and blocking the activities of ABL1 inhibited inflammatory signaling.	Reactive Oxygen Species	22-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-49
31396300-14	2019	With the treatment of ROS, the activities of ABL1 and inflammatory signaling were enhanced both in vitro and in vivo, and blocking the activities of ABL1 inhibited inflammatory signaling.	Reactive Oxygen Species	22-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-153
31396300-15	2019	Conclusions: ROS-activated ABL1 mediates inflammation through regulating NF-kappaB1 and STAT3, which subsequently leads to the development of GC and GC-related depression.	Reactive Oxygen Species	13-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-31
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 Mesylate	154-162	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-51
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
31217480-0	2019	Correction: AMN107 (nilotinib): a novel and selective inhibitor of BCR-ABL.	nilotinib	12-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
31217480-0	2019	Correction: AMN107 (nilotinib): a novel and selective inhibitor of BCR-ABL.	nilotinib	20-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
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 Mesylate	32-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-157
31115499-0	2019	PF-114, a novel selective inhibitor of BCR-ABL tyrosine kinase, is a potent inducer of apoptosis in chronic myelogenous leukemia cells.	PF-114	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
30879266-4	2019	However, CML relapsed 4 months after starting dasatinib due to increased BCR-ABL fusion signals in the peripheral blood.	Dasatinib	46-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
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 Mesylate	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 Mesylate	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-37
31115499-3	2019	PF-114, a derivative of the third generation BCR-ABL inhibitor ponatinib, demonstrated a high inhibitory activity against wild-type and mutant BCR-ABL forms, such as the clinically important T315I.	PF-114	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
31115499-3	2019	PF-114, a derivative of the third generation BCR-ABL inhibitor ponatinib, demonstrated a high inhibitory activity against wild-type and mutant BCR-ABL forms, such as the clinically important T315I.	PF-114	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-150
31115499-3	2019	PF-114, a derivative of the third generation BCR-ABL inhibitor ponatinib, demonstrated a high inhibitory activity against wild-type and mutant BCR-ABL forms, such as the clinically important T315I.	ponatinib	63-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
31115499-3	2019	PF-114, a derivative of the third generation BCR-ABL inhibitor ponatinib, demonstrated a high inhibitory activity against wild-type and mutant BCR-ABL forms, such as the clinically important T315I.	ponatinib	63-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-150
31115499-10	2019	Collectively, the targeted killing of BCR-ABL-positive cells, along with other beneficial properties, such as in vivo characteristics, suggests PF-114 as a potential candidate for analysis in clinical trials with CML patients.	PF-114	144-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
30568173-5	2019	Furthermore, NUP98-NSD1+/FLT3-ITD+ patient cells were also very sensitive to BCL2-inhibitor navitoclax, although the highest select sensitivity was found to SRC/ABL-inhibitor dasatinib (mean IC50 = 2.2 nM).	Dasatinib	175-184	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-164
30052122-4	2019	MD simulations revealed that the conformation of the phosphate-binding loop (P-loop) was altered significantly in the AS Abl system.	Phosphates	53-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-124
30052122-5	2019	DCCM results unraveled that mutations increased anticorrelated motions in the AS Abl system.	dccm	0-4	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-84
30919310-6	2019	However, similar doses of multi-kinase Abl/DDR inhibitor Nilotinib, DDR/Src inhibitor LCB-03-0110 and Abl/Src inhibitor Bosutinib were much more effective than the more selective Abl inhibitors Radotinib and Bafetinib.	bosutinib	120-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-105
30919310-6	2019	However, similar doses of multi-kinase Abl/DDR inhibitor Nilotinib, DDR/Src inhibitor LCB-03-0110 and Abl/Src inhibitor Bosutinib were much more effective than the more selective Abl inhibitors Radotinib and Bafetinib.	bosutinib	120-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-105
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
31252559-0	2019	Coordinate Modulation of Glycolytic Enzymes and OXPHOS by Imatinib in BCR-ABL Driven Chronic Myelogenous Leukemia Cells.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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 Mesylate	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 Mesylate	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	177-184
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-161
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 Mesylate	67-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-126
30861422-5	2019	To antagonize intracellular MDM2/MDMX for p53 activation, we extended this protein, PMIBcr/Abl, by a C-terminal Arg-repeating hexapeptide to facilitate its cellular uptake.	Arginine	112-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-94
30546081-2	2019	We here characterize the curative potential of BH3-mimetics differentially targeting mitochondrial BCL2-family members using a combination therapy approach with dexamethasone and tyrosine kinase inhibitors targeting BCR-ABL.	BH 3	47-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	216-223
30546081-3	2019	In BCR-ABL + ALL BH3-mimetics act by redistribution of mitochondrial activator BIM, which is strongly required for cytotoxicity of the BCL2-specific BH3-mimetic ABT-199, tyrosine kinase inhibitors (TKIs) and dexamethasone.	BH 3	17-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	3-10
30546081-3	2019	In BCR-ABL + ALL BH3-mimetics act by redistribution of mitochondrial activator BIM, which is strongly required for cytotoxicity of the BCL2-specific BH3-mimetic ABT-199, tyrosine kinase inhibitors (TKIs) and dexamethasone.	BH 3	149-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	3-10
30546081-3	2019	In BCR-ABL + ALL BH3-mimetics act by redistribution of mitochondrial activator BIM, which is strongly required for cytotoxicity of the BCL2-specific BH3-mimetic ABT-199, tyrosine kinase inhibitors (TKIs) and dexamethasone.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	161-164	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	3-10
30546081-3	2019	In BCR-ABL + ALL BH3-mimetics act by redistribution of mitochondrial activator BIM, which is strongly required for cytotoxicity of the BCL2-specific BH3-mimetic ABT-199, tyrosine kinase inhibitors (TKIs) and dexamethasone.	Dexamethasone	208-221	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	3-10
30546081-4	2019	BIM expression is enhanced by dexamethasone and TKIs and both synergize with ABT-199 in BCR-ABL + ALL.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	77-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
30546081-6	2019	Notably, the dasatinib-containing combination led to treatment- and leukemia-free long-term survival in a BCR-ABL + mouse model.	Dasatinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
30568173-8	2019	We found that SRC/ABL-inhibitor dasatinib is highly synergistic with BCL2-inhibitor navitoclax in NUP98-NSD1+/FLT3-ITD+ cells.	Dasatinib	32-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-21
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 Mesylate	166-174	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-37
30585758-2	2019	In this study, we explored the feasibility of BCR-Abl siRNA therapy in CML K562 cells in vitro by employing a cationic polymer derived from cholesterol (Chol) grafted low-molecular weight polyethyleneimine (PEI).	Cholesterol	140-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
30585758-2	2019	In this study, we explored the feasibility of BCR-Abl siRNA therapy in CML K562 cells in vitro by employing a cationic polymer derived from cholesterol (Chol) grafted low-molecular weight polyethyleneimine (PEI).	Cholesterol	153-157	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
30585758-2	2019	In this study, we explored the feasibility of BCR-Abl siRNA therapy in CML K562 cells in vitro by employing a cationic polymer derived from cholesterol (Chol) grafted low-molecular weight polyethyleneimine (PEI).	aziridine	188-205	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
30585758-3	2019	The first generation TKI imatinib upregulated the expression of BCR-Abl in K562 cells as expected.	Imatinib Mesylate	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
30927708-0	2019	Molecular dynamics investigation on the Asciminib resistance mechanism of I502L and V468F mutations in BCR-ABL.	asciminib	40-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
30927708-1	2019	Asciminib, a highly selective non-ATP competitive inhibitor of BCR-ABL, has demonstrated to be a promising drug for patients with chronic myeloid leukemia.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
30927708-4	2019	The obtained results indicate that the mutations have adversely influence on the binding of Asciminib to BCR-ABL, as the nonpolar contributions decline in the two mutants.	asciminib	92-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-112
30927708-7	2019	Our results provide the molecular insights of Asciminib resistance mechanism in BCR-ABL mutants, which may help the design of novel inhibitors.	asciminib	46-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
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 Mesylate	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-164
31164822-6	2019	Our results show that GNF-2 reduced lipopolysaccharide (LPS)-induced nitric oxide and pro-inflammatory cytokine production in cultured glial cells in a c-Abl-dependent manner.	Nitric Oxide	69-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-157
30822403-0	2019	Andrographolide and its potent derivative exhibit anticancer effects against imatinib-resistant chronic myeloid leukemia cells by downregulating the Bcr-Abl oncoprotein.	andrographolide	0-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
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 Mesylate	6-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
31017783-4	2019	While the inhibitor binding can strengthen the closed ABL state and induce allosteric communications directed from the allosteric pocket to the ATP binding site, the DPH activator may induce a more dynamic open form and activate allosteric couplings between the ATP and substrate binding sites.	Adenosine Triphosphate	144-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-57
31017783-4	2019	While the inhibitor binding can strengthen the closed ABL state and induce allosteric communications directed from the allosteric pocket to the ATP binding site, the DPH activator may induce a more dynamic open form and activate allosteric couplings between the ATP and substrate binding sites.	Adenosine Triphosphate	262-265	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-57
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 Mesylate	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
30822403-1	2019	Chronic myelogenous leukemia (CML) is clinically treated with imatinib, which inhibits the kinase activity of the Bcr-Abl oncoprotein.	Imatinib Mesylate	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.	andrographolide	5-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
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.	nctu-322	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
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 Mesylate	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
30822403-6	2019	In addition, NCTU-322 had stronger effects than andrographolide on downregulation of Bcr-Abl oncoprotein, induction of Hsp90 cleavage and cytotoxicity of CML cells.	nctu-322	13-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
30822403-6	2019	In addition, NCTU-322 had stronger effects than andrographolide on downregulation of Bcr-Abl oncoprotein, induction of Hsp90 cleavage and cytotoxicity of CML cells.	andrographolide	48-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
30822403-9	2019	In summary, our data demonstrated that andrographolide and NCTU-322 inhibit Bcr-abl function via a mechanism different from that of imatinib, and they induced multiple anticancer effects in both imatinib-sensitive and resistant CML cells.	andrographolide	39-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
30822403-9	2019	In summary, our data demonstrated that andrographolide and NCTU-322 inhibit Bcr-abl function via a mechanism different from that of imatinib, and they induced multiple anticancer effects in both imatinib-sensitive and resistant CML cells.	nctu-322	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
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 Mesylate	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	169-176
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 Mesylate	117-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-79
30864683-8	2019	TOPK inhibitor OTS514 suppressed proliferation of BCR/ABL-positive cell lines and colony formation of CD34-positive cells from patients with CML compared with lymphoma patients without bone marrow involvement.	OTS514	15-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
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 Mesylate	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-89
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 Mesylate	218-226	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	169-176
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 Mesylate	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-22
30668775-5	2019	Here we show that the Abelson tyrosine kinase c-Abl/ABL1 causes formation of RNA polymerase II (RNAPII) foci, predominantly phosphorylated at carboxy-terminal domain (CTD) residue Tyr1, at DSBs.	dsbs	189-193	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-51
30668775-5	2019	Here we show that the Abelson tyrosine kinase c-Abl/ABL1 causes formation of RNA polymerase II (RNAPII) foci, predominantly phosphorylated at carboxy-terminal domain (CTD) residue Tyr1, at DSBs.	dsbs	189-193	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-56
30684523-14	2019	The simulations highlight modifications in two structurally important regions of Abl1, the activation and phosphate binding loops, upon mutations.	Phosphates	106-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-85
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
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.	neferine	15-23	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 Mesylate	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
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 Mesylate	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
30985724-9	2019	Also, a higher percentage of patients on nilotinib therapy achieved EMR compared with patients on imatinib therapy (93.3% vs 63.6% on 3-month nilotinib therapy, P = .001; 88.9% vs 59.9% on 6-month nilotinib therapy, P = .004).This study demonstrates that EMR, especially a 3-month BCR-ABL &lt;=1% and 6-month BCR-ABL &lt;=0.1%, have predictive value for DMR achievement.	nilotinib	41-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	281-288
30985724-9	2019	Also, a higher percentage of patients on nilotinib therapy achieved EMR compared with patients on imatinib therapy (93.3% vs 63.6% on 3-month nilotinib therapy, P = .001; 88.9% vs 59.9% on 6-month nilotinib therapy, P = .004).This study demonstrates that EMR, especially a 3-month BCR-ABL &lt;=1% and 6-month BCR-ABL &lt;=0.1%, have predictive value for DMR achievement.	nilotinib	41-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	309-316
30659095-6	2019	Here, we present the first crystal structures of tyrosine-phosphorylated human SH3 domains derived from the Abelson-family kinases ABL1 and ABL2 at 1.6 and 1.4 A resolutions, respectively.	Tyrosine	49-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-135
30906562-1	2019	Nilotinib is a broad-based tyrosine kinase inhibitor with the highest affinity to inhibit Abelson (c-Abl) and discoidin domain receptors (DDR1/2).	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-104
30956968-0	2019	Coexistence of BCR/ABL1-positive chronic myeloid leukemia and JAK2 V617F-mutated myelofibrosis successfully treated with dasatinib and ruxolitinib.	Dasatinib	121-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-23
30956968-0	2019	Coexistence of BCR/ABL1-positive chronic myeloid leukemia and JAK2 V617F-mutated myelofibrosis successfully treated with dasatinib and ruxolitinib.	ruxolitinib	135-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-23
30692753-5	2019	We give a short account of the potential of c-Abl inhibitors, the currently used anticancer drugs such as nilotinib in preventing the neurodegenerative process in PD.	nilotinib	106-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-49
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.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
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 Mesylate	132-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
30689376-4	2019	This paper describes the discovery and optimization of a thiazole series of novel small molecule c-Abl activators, initially identified by a high throughput screening.	Thiazoles	57-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-102
30689376-5	2019	Subsequently, a scaffold-hop, which exploited the improved physicochemical properties of a dihydropyrazole analogue, identified through fragment screening, delivered potent, soluble, cell-active c-Abl activators, which demonstrated the intracellular activation of c-Abl in vivo.	dihydropyrazole	91-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	195-200
30689376-5	2019	Subsequently, a scaffold-hop, which exploited the improved physicochemical properties of a dihydropyrazole analogue, identified through fragment screening, delivered potent, soluble, cell-active c-Abl activators, which demonstrated the intracellular activation of c-Abl in vivo.	dihydropyrazole	91-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	264-269
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 Mesylate	199-207	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
30548479-0	2019	Potent antiproliferative effect of fatty-acid derivative AIC-47 on leukemic mice harboring BCR-ABL mutation.	Fatty Acids	35-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
30548479-3	2019	We previously reported that a medium-chain fatty-acid derivative AIC-47 induced transcriptional suppression of BCR-ABL and perturbation of the Warburg effect, leading to growth inhibition in Ph-positive leukemia cells.	chain fatty-acid	37-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
30251267-0	2019	(-)-Epigallocatechin-3-gallate induces cell apoptosis in chronic myeloid leukaemia by regulating Bcr/Abl-mediated p38-MAPK/JNK and JAK2/STAT3/AKT signalling pathways.	epigallocatechin gallate	0-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-104
30251267-3	2019	In the present study, we investigated the effect of EGCG on the growth of Bcr/Abl+ CML cell lines, including imatinib-resistant cell lines and primary CML cells.	epigallocatechin gallate	52-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	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.	epigallocatechin gallate	53-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-110
30705592-3	2019	Iclusig  (ponatinib, previously known as AP24534) is an orally active multi-tyrosine kinase inhibitor and is currently approved by the US Food and Drug Administration for patients with chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia, specifically targeting the BCR-ABL gene mutation, T315I.	ponatinib	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	304-311
30705592-3	2019	Iclusig  (ponatinib, previously known as AP24534) is an orally active multi-tyrosine kinase inhibitor and is currently approved by the US Food and Drug Administration for patients with chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia, specifically targeting the BCR-ABL gene mutation, T315I.	ponatinib	10-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	304-311
30705592-3	2019	Iclusig  (ponatinib, previously known as AP24534) is an orally active multi-tyrosine kinase inhibitor and is currently approved by the US Food and Drug Administration for patients with chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia, specifically targeting the BCR-ABL gene mutation, T315I.	ponatinib	41-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	304-311
30705677-2	2018	ABL tyrosine kinase inhibitors (TKIs), such as imatinib, nilotinib, and dasatinib, are currently the front-line treatment options for CML.	Imatinib Mesylate	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
30705677-2	2018	ABL tyrosine kinase inhibitors (TKIs), such as imatinib, nilotinib, and dasatinib, are currently the front-line treatment options for CML.	nilotinib	57-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
30705677-2	2018	ABL tyrosine kinase inhibitors (TKIs), such as imatinib, nilotinib, and dasatinib, are currently the front-line treatment options for CML.	Dasatinib	72-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
30705677-13	2018	Our results highlight the dual effects of dasatinib in direct inhibition of ABL kinase and in immunomodulation through NKG2A down-regulation, contributing to accelerated molecular responses (MR) in CML.	Dasatinib	42-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-79
30478172-8	2019	RAD51 Cys-319 resides within the SH3-binding site of ABL proto-oncogene 1, nonreceptor tyrosine kinase (ABL1), so we investigated the effect of OA-NO2-mediated Cys-319 alkylation on ABL1 binding and found that OA-NO2 inhibits RAD51-ABL1 complex formation both in vitro and in cell-based immunoprecipitation assays.	Cysteine	6-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-102
30478172-8	2019	RAD51 Cys-319 resides within the SH3-binding site of ABL proto-oncogene 1, nonreceptor tyrosine kinase (ABL1), so we investigated the effect of OA-NO2-mediated Cys-319 alkylation on ABL1 binding and found that OA-NO2 inhibits RAD51-ABL1 complex formation both in vitro and in cell-based immunoprecipitation assays.	Cysteine	6-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-108
30478172-8	2019	RAD51 Cys-319 resides within the SH3-binding site of ABL proto-oncogene 1, nonreceptor tyrosine kinase (ABL1), so we investigated the effect of OA-NO2-mediated Cys-319 alkylation on ABL1 binding and found that OA-NO2 inhibits RAD51-ABL1 complex formation both in vitro and in cell-based immunoprecipitation assays.	Cysteine	160-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-102
30478172-9	2019	The inhibition of the RAD51-ABL1 complex also suppressed downstream RAD51 Tyr-315 phosphorylation.	Tyrosine	74-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-32
30713559-2	2019	Imatinib inhibits BCR-ABL tyrosine kinase produced due to reciprocal translocation t(9;22) in neoplastic CML cells.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
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 Mesylate	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
30813433-16	2019	EGCG, an abundant catechin in tea, was found to suppress the neurotoxicity induced by Abeta as it activates glycogen synthase kinase-3beta (GSK-3beta), along with inhibiting c-Abl/FE65-the cytoplasmic nonreceptor tyrosine kinase which is involved in the development of the nervous system and in nuclear translocation.	epigallocatechin gallate	0-4	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-179
30813433-16	2019	EGCG, an abundant catechin in tea, was found to suppress the neurotoxicity induced by Abeta as it activates glycogen synthase kinase-3beta (GSK-3beta), along with inhibiting c-Abl/FE65-the cytoplasmic nonreceptor tyrosine kinase which is involved in the development of the nervous system and in nuclear translocation.	UNII-042A8N37WH	86-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-179
30787317-0	2019	Novel mutations in the kinase domain of BCR-ABL gene causing imatinib resistance in chronic myeloid leukemia patients.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	93-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
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 Mesylate	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 Mesylate	136-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-125
30704478-10	2019	We report a novel mechanism and identified strong c-Abl threonine 735 phosphorylation (pAblT735) mediated by the type-IV secretion system (T4SS) effector D-glycero-beta-D-manno-heptose-1,7-bisphosphate (betaHBP) and protein kinase C (PKC) as a new c-Abl kinase.	Threonine	56-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-55
30704478-10	2019	We report a novel mechanism and identified strong c-Abl threonine 735 phosphorylation (pAblT735) mediated by the type-IV secretion system (T4SS) effector D-glycero-beta-D-manno-heptose-1,7-bisphosphate (betaHBP) and protein kinase C (PKC) as a new c-Abl kinase.	Threonine	56-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	248-253
30704478-10	2019	We report a novel mechanism and identified strong c-Abl threonine 735 phosphorylation (pAblT735) mediated by the type-IV secretion system (T4SS) effector D-glycero-beta-D-manno-heptose-1,7-bisphosphate (betaHBP) and protein kinase C (PKC) as a new c-Abl kinase.	D-glycero-beta-D-manno-heptose 1,7-bisphosphate	154-201	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-55
30704478-10	2019	We report a novel mechanism and identified strong c-Abl threonine 735 phosphorylation (pAblT735) mediated by the type-IV secretion system (T4SS) effector D-glycero-beta-D-manno-heptose-1,7-bisphosphate (betaHBP) and protein kinase C (PKC) as a new c-Abl kinase.	D-glycero-beta-D-manno-heptose 1,7-bisphosphate	154-201	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	248-253
30704478-10	2019	We report a novel mechanism and identified strong c-Abl threonine 735 phosphorylation (pAblT735) mediated by the type-IV secretion system (T4SS) effector D-glycero-beta-D-manno-heptose-1,7-bisphosphate (betaHBP) and protein kinase C (PKC) as a new c-Abl kinase.	betahbp	203-210	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-55
30703161-6	2019	Our biosensor could detect the ZIKV in a wide concentration range from 10-107 RNA copies/mL, and we found that the limit of detection (LOD) for the ZIKV followed the order Ab-L-cysteine-AuNPs (LOD = 8.2 copies/mL) > Ab-3-mercaptopropionic acid-AuNPs (LOD = 35.0 copies/mL).	ab-3-mercaptopropionic acid-aunps	216-249	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-176
31296070-0	2019	Quinacrine Depletes BCR-ABL and Suppresses Ph-Positive Leukemia Cells.	Quinacrine	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
31250767-4	2019	OBJECTIVE: In recent studies, the dual inhibition of BCR-ABL by Nilotinib and Asciminib has been shown to overcome drug resistance.	nilotinib	64-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
31250767-4	2019	OBJECTIVE: In recent studies, the dual inhibition of BCR-ABL by Nilotinib and Asciminib has been shown to overcome drug resistance.	asciminib	78-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
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 Mesylate	297-305	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
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 Mesylate	297-305	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
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 Mesylate	297-305	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-66
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 Mesylate	297-305	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-66
30561126-10	2019	Although FAERS- and JADER-based signal detection analyses cannot determine causality perfectly, our study suggests the effects on glucose metabolism are different between BCR-ABL inhibitors and provides useful information for the selection of appropriate BCR-ABL inhibitors.	Glucose	130-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-178
30561126-10	2019	Although FAERS- and JADER-based signal detection analyses cannot determine causality perfectly, our study suggests the effects on glucose metabolism are different between BCR-ABL inhibitors and provides useful information for the selection of appropriate BCR-ABL inhibitors.	Glucose	130-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	255-262
31296070-2	2019	In this study, we demonstrate that quinacrine (QC) induces apoptosis in BCR-ABL positive CML and acute lymphoblastic leukemia (ALL) cells.	Quinacrine	35-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
30093398-1	2019	Dasatinib, a second-generation BCR-ABL1 tyrosine kinase inhibitor, is approved for the treatment of chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia, both as first-line therapy and after imatinib intolerance or resistance.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-39
30311036-1	2018	Background Imatinib mesylate is a potent inhibitor of the Abl, KIT and platelet derived growth factor (PDGF) receptor tyrosine kinases.	Imatinib Mesylate	11-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-61
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 Mesylate	190-198	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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.	Dasatinib	200-209	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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.	nilotinib	215-224	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
30332954-8	2019	This review outlines the Bcr-Abl dependent and independent mechanism of TKIs resistance development and the strategies used to overcome drug resistance, such as the development of ATP site and allosteric site inhibitors.	Adenosine Triphosphate	180-183	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
30971653-9	2019	In addition, taxodione significantly induced apoptosis in transformed Ba/F3 cells by not only BCR-ABL but also T315I-mutated BCR-ABL through the generation of ROS, suggesting that taxodione has potential as anti-tumor drug with high efficacy to overcome BCR-ABL T315I mutation-mediated resistance in leukemia cells.	taxodione	180-189	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
30971653-9	2019	In addition, taxodione significantly induced apoptosis in transformed Ba/F3 cells by not only BCR-ABL but also T315I-mutated BCR-ABL through the generation of ROS, suggesting that taxodione has potential as anti-tumor drug with high efficacy to overcome BCR-ABL T315I mutation-mediated resistance in leukemia cells.	taxodione	180-189	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
30971653-9	2019	In addition, taxodione significantly induced apoptosis in transformed Ba/F3 cells by not only BCR-ABL but also T315I-mutated BCR-ABL through the generation of ROS, suggesting that taxodione has potential as anti-tumor drug with high efficacy to overcome BCR-ABL T315I mutation-mediated resistance in leukemia cells.	taxodione	180-189	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
31586504-2	2019	Dasatinib, a representative of those drugs, acts by inhibiting key proteins included in CML development, predominantly Bcr-Abl and Src.	dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-126
31994517-5	2019	Specific inhibition of kinases ABL1, PINK1, CDK5 and arginine N-methyltransferase PRMT5 by the peptides of cerebrolysin has a multidirectional effect on the dopaminergic system, also helping to stabilize mood.	Arginine Vasopressin	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-35
30687767-1	2018	Radotinib (Supect ) was developed to treat chronic myeloid leukemia (CML) as a BCR-ABL1 tyrosine kinase inhibitor (TKI).	4-methyl-N-(3-(4-methylimidazol-1-yl)-5-trifluoromethylphenyl)-3-(4-pyrazin-2-ylpyrimidin-2-ylamino)benzamide	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
30587121-1	2018	BACKGROUND: Dasatinib (Sprycel) was developed as a tyrosine kinase inhibitor targeting Bcr-Abl and the family of Src kinases.	Dasatinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
30587215-1	2018	Bosutinib, a BCR-ABL1 tyrosine kinase inhibitor (TKI), has been available for several years as a treatment for chronic-, accelerated-, and blast-phase chronic myeloid leukemia (CML), for patients with resistance or intolerance to prior therapy.	bosutinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
30971653-0	2019	[The mechanisms of taxodione-induced apoptosis in BCR-ABL-positive leukemia cells].	taxodione	19-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
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 Mesylate	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
30971653-2	2019	The specific BCR-ABL inhibitors including imatinib, nilotinib, and dasatinib, are clinically utilized in the treatment with CML and ALL patients.	nilotinib	52-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
30971653-2	2019	The specific BCR-ABL inhibitors including imatinib, nilotinib, and dasatinib, are clinically utilized in the treatment with CML and ALL patients.	Dasatinib	67-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
30971653-4	2019	Recently, we found that taxodione, a quinone methide diterpene isolated from a conifer, Taxodium distichum, significantly induced apoptosis in human myelogenous leukemia-derived K562 cells, which is positive for the bcr-abl gene.	taxodione	24-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	216-223
30971653-7	2019	Furthermore, in K562 cells treated with taxodione, BCR-ABL, STAT5 and Akt were sequestered in mitochondrial fraction, and their localization changes decrease their abilities to stimulate cell proliferation.	taxodione	40-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
30971653-8	2019	Strikingly, NAC canceled these taxodione-caused inhibition of BCR-ABL, STAT5 and Akt.	Acetylcysteine	12-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
30971653-8	2019	Strikingly, NAC canceled these taxodione-caused inhibition of BCR-ABL, STAT5 and Akt.	taxodione	31-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
30971653-9	2019	In addition, taxodione significantly induced apoptosis in transformed Ba/F3 cells by not only BCR-ABL but also T315I-mutated BCR-ABL through the generation of ROS, suggesting that taxodione has potential as anti-tumor drug with high efficacy to overcome BCR-ABL T315I mutation-mediated resistance in leukemia cells.	taxodione	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
30971653-9	2019	In addition, taxodione significantly induced apoptosis in transformed Ba/F3 cells by not only BCR-ABL but also T315I-mutated BCR-ABL through the generation of ROS, suggesting that taxodione has potential as anti-tumor drug with high efficacy to overcome BCR-ABL T315I mutation-mediated resistance in leukemia cells.	taxodione	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
30971653-9	2019	In addition, taxodione significantly induced apoptosis in transformed Ba/F3 cells by not only BCR-ABL but also T315I-mutated BCR-ABL through the generation of ROS, suggesting that taxodione has potential as anti-tumor drug with high efficacy to overcome BCR-ABL T315I mutation-mediated resistance in leukemia cells.	taxodione	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
30177833-0	2019	Desuppression of TGF-beta signaling via nuclear c-Abl-mediated phosphorylation of TIF1gamma/TRIM33 at Tyr-524, -610, and -1048.	Tyrosine	102-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-53
30177833-5	2019	Replacement of the three tyrosine residues Tyr-524, -610, and -1048 with phenylalanine (3YF) inhibits c-Abl-mediated phosphorylation of TIF1gamma and enhances TIF1gamma"s association with Smad3.	Tyrosine	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-107
30177833-5	2019	Replacement of the three tyrosine residues Tyr-524, -610, and -1048 with phenylalanine (3YF) inhibits c-Abl-mediated phosphorylation of TIF1gamma and enhances TIF1gamma"s association with Smad3.	Tyrosine	43-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-107
30177833-5	2019	Replacement of the three tyrosine residues Tyr-524, -610, and -1048 with phenylalanine (3YF) inhibits c-Abl-mediated phosphorylation of TIF1gamma and enhances TIF1gamma"s association with Smad3.	Phenylalanine	73-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-107
30177833-7	2019	Intriguingly, activation of c-Abl by epidermal growth factor (EGF) induces desuppression of TGF-beta signaling via enhancing the tyrosine phosphorylation level of TIF1gamma.	Tyrosine	129-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-33
30177833-9	2019	These results suggest that nuclear c-Abl-mediated tyrosine phosphorylation of TIF1gamma has a desuppressive role in TGF-beta-Smad2/3 signaling.	Tyrosine	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-40
30594176-0	2018	MLH1 enhances the sensitivity of human endometrial carcinoma cells to cisplatin by activating the MLH1/c-Abl apoptosis signaling pathway.	Cisplatin	70-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-108
30594176-10	2018	Mechanistically, cisplatin induced the MLH1/c-Abl apoptosis signaling pathway in ADV-MLH1-infected endometrial carcinoma cells, and these effects involved c-Abl, caspase-9, caspase-3 and PARP.	Cisplatin	17-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-49
30594176-10	2018	Mechanistically, cisplatin induced the MLH1/c-Abl apoptosis signaling pathway in ADV-MLH1-infected endometrial carcinoma cells, and these effects involved c-Abl, caspase-9, caspase-3 and PARP.	Cisplatin	17-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	155-160
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 Mesylate	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-21
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 Mesylate	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	259-266
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 Mesylate	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.	Axitinib	33-41	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.	Axitinib	33-41	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.	Axitinib	33-41	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.	Axitinib	33-41	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	396-404	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	233-236
30174304-2	2018	Here, we show that oncogenic HER2 tyrosine kinase signaling induces phosphorylation of mitochondrial creatine kinase 1 (MtCK1) on tyrosine 153 (Y153) in an ABL-dependent manner in breast cancer cells.	Tyrosine	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-159
30517893-3	2018	(2018) show that HER2 signaling promotes ABL-mediated phosphorylation of the mitochondrial creatine kinase (MtCK1), providing ATP to support breast tumor growth.	Adenosine Triphosphate	126-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-44
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-148
30297534-4	2018	Given that oxidation can regulate protein-tyrosine phosphatase (PTP) catalytic activity, inactivation of an ABL-directed PTP by ROS might account for ABL1 activation in this malignancy.	Reactive Oxygen Species	128-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-111
30297534-4	2018	Given that oxidation can regulate protein-tyrosine phosphatase (PTP) catalytic activity, inactivation of an ABL-directed PTP by ROS might account for ABL1 activation in this malignancy.	Reactive Oxygen Species	128-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-154
30297534-12	2018	These results show that ROS-induced oxidation of PTPN12 accounts for ABL1 phosphorylation in HLRCC-associated PRCC, revealing a novel mechanism for inactivating a tumor suppressor gene product and establishing a direct link between pathologic PTP oxidation and neoplastic disease.	Reactive Oxygen Species	24-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-73
30297534-13	2018	SIGNIFICANCE: This work identifies a novel mechanism of activation of the oncogenic kinase ABL1 via ROS-induced, oxidation-mediated inactivation of cognate protein tyrosine phosphatases.	Reactive Oxygen Species	100-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-95
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 Mesylate	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
30168245-5	2018	An adapted 3-probe FISH strategy identified two patients with ETV6-ABL1 fusion who received imatinib.	Imatinib Mesylate	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-71
30301525-1	2018	Chronic myeloid leukemia (CML) responds well to BCR-ABL tyrosine kinase inhibitors (TKI), such as imatinib and dasatinib.	Imatinib Mesylate	98-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
30616322-0	2018	[Study on mechanism for dasatinib inhibiting PDGFR/Bcr-Abl signaling pathway in hepatic stellate cells mediated hepatic fibrosis].	Dasatinib	24-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
30400842-1	2018	BACKGROUND: Chronic myeloid leukemia is associated with a BCR/ABL oncoprotein inhibited by imatinib mesylate, the first tyrosine kinase inhibitor.	Imatinib Mesylate	91-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
30301525-12	2018	Our work suggests that anisomycin is a potential drug to overcome resistance to BCR-ABL TKI treatment in blast phase CML.	Anisomycin	23-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
30301525-1	2018	Chronic myeloid leukemia (CML) responds well to BCR-ABL tyrosine kinase inhibitors (TKI), such as imatinib and dasatinib.	Dasatinib	111-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
30301525-3	2018	In this work, we show that anisomycin, a clinically available drug, targets CML cells at all stages of development and enhances BCR-ABL TKIs" efficacy.	Anisomycin	27-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
30324134-7	2018	Furthermore, the muscle contractions were recovered by single treatments and cotreatment with rapamycin (a mechanistic target of rapamycin inhibitor) and bosutinib (an Src/c-Abl inhibitor).	bosutinib	154-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-177
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 Mesylate	177-185	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
30370304-5	2018	Treatment with SM or SB was found to significantly reduce the genotoxicity of MMS, upregulate the expression of PTEN and BCL2, and downregulate the expression of BAX and ABL1.	Silymarin	15-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-174
30370304-5	2018	Treatment with SM or SB was found to significantly reduce the genotoxicity of MMS, upregulate the expression of PTEN and BCL2, and downregulate the expression of BAX and ABL1.	Silybin	21-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-174
30202081-3	2018	Recently, potent degraders against BCR-ABL have been developed by conjugating dasatinib to ligands for E3 ubiquitin ligases.	Dasatinib	78-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
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 Mesylate	109-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-51
29157947-7	2018	IL-4- and histamine-induced ABL1 activation in human VE cells and VE barrier dysfunction was ABL1-dependent.	Histamine	10-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-32
29157947-7	2018	IL-4- and histamine-induced ABL1 activation in human VE cells and VE barrier dysfunction was ABL1-dependent.	Histamine	10-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-97
30137981-4	2018	We describe the discovery of asciminib (ABL001), the first allosteric BCR-ABL1 inhibitor to reach the clinic.	asciminib	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-78
30137981-4	2018	We describe the discovery of asciminib (ABL001), the first allosteric BCR-ABL1 inhibitor to reach the clinic.	asciminib	40-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-78
30137981-5	2018	Asciminib binds to the myristate pocket of BCR-ABL1 and maintains activity against TKI-resistant ATP-site mutations.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-51
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.	Cisplatin	82-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-107
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 Mesylate	158-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-152
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.	Cisplatin	176-185	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-107
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.	Cisplatin	176-185	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-152
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 Mesylate	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.	Dasatinib	97-106	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.	nilotinib	108-117	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.	ponatinib	122-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
30057314-4	2018	The specificity of this spectral signature is confirmed using a Dox-inducible T315I-mutated BCR-ABL-expressing human UT-7 cells as well as in murine embryonic stem cells.	Doxorubicin	64-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
30202081-4	2018	Since the degraders contain the dasatinib moiety, they also inhibit BCR-ABL kinase activity, which complicates our understanding of the impact of BCR-ABL degradation by degraders in CML growth inhibition.	Dasatinib	32-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
29913272-3	2018	The lipopolymer, based on the lipid alpha-linolenic acid (alphaLA) substitution on low molecular weight polyethyleneimine (PEI), was used to deliver siRNA against the BCR-ABL gene and, the resultant therapeutic effect was evaluated in in vitro and in vivo CML models.	lipopolymer	4-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-174
30238007-1	2018	Ponatinib is a multi-targeted third generation tyrosine kinase inhibitor (TKI) used in the treatment of chronic myeloid leukemia (CML) patients harboring the Abelson (Abl)-breakpoint cluster region (Bcr) T315I mutation.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-165
30238007-1	2018	Ponatinib is a multi-targeted third generation tyrosine kinase inhibitor (TKI) used in the treatment of chronic myeloid leukemia (CML) patients harboring the Abelson (Abl)-breakpoint cluster region (Bcr) T315I mutation.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-170
30180406-11	2018	The height of Koch triangle (CSo-His) was (22.3+-5.8) mm and related with the weight of children (Y=0.171X+ 16.660, r(2)=0.224, P&lt;0.001).The distance between the successful ablation target and the lowest point of His zone (ABL-His) was (11.7+-2.6) mm.	cso-his	29-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	226-229
29675611-9	2018	Ponatinib seems a valid second-line treatment option for chronic phase CML, in particular for patients who failed a front-line second-generation TKI due to BCR-ABL-independent mechanisms of resistance.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
29807053-0	2018	c-Abl phosphorylation of Yin Yang 1"s conserved tyrosine 254 in the spacer region modulates its transcriptional activity.	Tyrosine	48-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
29807053-3	2018	Here we report that YY1 is a substrate for c-Abl kinase phosphorylation at conserved residue Y254 in the spacer region.	y254	93-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-48
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 Mesylate	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-35
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.	nilotinib	56-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-35
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.	olverembatinib	70-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-35
29807053-5	2018	Both radioactive and non-radioactive in vitro kinase assays, as well as co-immunoprecipitation in different cell lines, show that the target of c-Abl phosphorylation is tyrosine residue 254.	Tyrosine	169-177	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-149
29913272-3	2018	The lipopolymer, based on the lipid alpha-linolenic acid (alphaLA) substitution on low molecular weight polyethyleneimine (PEI), was used to deliver siRNA against the BCR-ABL gene and, the resultant therapeutic effect was evaluated in in vitro and in vivo CML models.	alpha-Linolenic Acid	36-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-174
29913272-3	2018	The lipopolymer, based on the lipid alpha-linolenic acid (alphaLA) substitution on low molecular weight polyethyleneimine (PEI), was used to deliver siRNA against the BCR-ABL gene and, the resultant therapeutic effect was evaluated in in vitro and in vivo CML models.	alpha-Linolenic Acid	58-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-174
29913272-3	2018	The lipopolymer, based on the lipid alpha-linolenic acid (alphaLA) substitution on low molecular weight polyethyleneimine (PEI), was used to deliver siRNA against the BCR-ABL gene and, the resultant therapeutic effect was evaluated in in vitro and in vivo CML models.	aziridine	104-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-174
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 Mesylate	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 Mesylate	103-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-118
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
30054832-6	2018	We demonstrated that cryptotanshinone, as a dual inhibitor of p-STAT5 and p-STAT3, can effectively block IL-6-mediated STAT3 activation and reverse BCR-ABL kinase-independent drug resistance.	cryptotanshinone	21-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	148-155
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 Mesylate	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
29701267-0	2018	Costunolide promotes imatinib-induced apoptosis in chronic myeloid leukemia cells via the Bcr/Abl-Stat5 pathway.	costunolide	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
29701267-0	2018	Costunolide promotes imatinib-induced apoptosis in chronic myeloid leukemia cells via the Bcr/Abl-Stat5 pathway.	Imatinib Mesylate	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
29701267-5	2018	Costunolide promoted imatinib-induced apoptosis via the Bcr/Abl-signal transducer and activator of transcription 5 pathway.	costunolide	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
29701267-5	2018	Costunolide promoted imatinib-induced apoptosis via the Bcr/Abl-signal transducer and activator of transcription 5 pathway.	Imatinib Mesylate	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
29859988-8	2018	Taxodione induced apoptosis in transformed Ba/F3 cells induced not only by BCR-ABL, but also T315I-mutated BCR-ABL through the generation of ROS.	taxodione	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
30165626-0	2018	Role of c-Abl-GSK3beta Signaling in MPP+-Induced Autophagy-Lysosomal Dysfunction.	mangion-purified polysaccharide (Candida albicans)	36-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-13
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 Mesylate	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.	mangion-purified polysaccharide (Candida albicans)	145-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-31
30165626-8	2018	In addition, c-Abl directly interacted with GSK3beta and catalyzed its phosphorylation at tyrosine 216, and their interaction was enhanced under MPP+ treatment.	Tyrosine	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-18
30165626-8	2018	In addition, c-Abl directly interacted with GSK3beta and catalyzed its phosphorylation at tyrosine 216, and their interaction was enhanced under MPP+ treatment.	mangion-purified polysaccharide (Candida albicans)	145-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-18
30165626-10	2018	Taken together, these results demonstrate that GSK3beta is a novel c-Abl substrate, and c-Abl-GSk3beta pathway mediates MPP+-induced ALP defects and neuronal cell death, which may represent a potential therapeutic target for PD.	mangion-purified polysaccharide (Candida albicans)	120-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-72
30165626-10	2018	Taken together, these results demonstrate that GSK3beta is a novel c-Abl substrate, and c-Abl-GSk3beta pathway mediates MPP+-induced ALP defects and neuronal cell death, which may represent a potential therapeutic target for PD.	mangion-purified polysaccharide (Candida albicans)	120-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-93
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 Mesylate	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
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.	Dasatinib	74-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
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.	ponatinib	89-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
29975106-5	2018	Because nuclear Abl stimulates miR-34c biogenesis, we measured miR-34c in EV and found that its levels correlated with the ROS-inducing activity of EV.	Reactive Oxygen Species	123-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-19
29859988-0	2018	Taxodione induces apoptosis in BCR-ABL-positive cells through ROS generation.	taxodione	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
29859988-0	2018	Taxodione induces apoptosis in BCR-ABL-positive cells through ROS generation.	Reactive Oxygen Species	62-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
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 Mesylate	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
29859988-3	2018	In the present study, we found that taxodione, a quinone methide diterpene isolated from Taxodium distichum, significantly induced apoptosis in human myelogenous leukemia-derived K562 cells, which were transformed by BCR-ABL.	taxodione	36-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	217-224
29859988-6	2018	Furthermore, in K562 cells treated with taxodione, BCR-ABL and its major signaling molecules, such as STAT5 and Akt were sequestered in mitochondrial fraction, and their localization changes decrease their abilities to stimulate cell proliferation, suggesting that these actions seem to be a mechanism how taxodione functions as an anti-tumor drug.	taxodione	40-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
29859988-6	2018	Furthermore, in K562 cells treated with taxodione, BCR-ABL and its major signaling molecules, such as STAT5 and Akt were sequestered in mitochondrial fraction, and their localization changes decrease their abilities to stimulate cell proliferation, suggesting that these actions seem to be a mechanism how taxodione functions as an anti-tumor drug.	taxodione	306-315	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
29859988-8	2018	Taxodione induced apoptosis in transformed Ba/F3 cells induced not only by BCR-ABL, but also T315I-mutated BCR-ABL through the generation of ROS.	taxodione	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
29859988-9	2018	Collectively, the present results suggest that in the treatment of leukemia, taxodione has potential as a compound with high efficacy to overcome BCR-ABL T315I mutation-mediated resistance in leukemia cells.	taxodione	77-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	146-153
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 Mesylate	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 Mesylate	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
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 Mesylate	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	198-205
29733872-6	2018	ETS1 protein expression was also shown to be highly increased in UT-7 cells expressing BCR-ABL either constitutively or under the control of TET-inducible promoters.	tetramethylenedisulfotetramine	141-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
29730354-5	2018	c-Abl-mediated tyrosine phosphorylation in the Runx1 transcription inhibition domain negatively regulated the transcriptional activity of Runx1 and inhibited Runx1-mediated MK maturation.	Tyrosine	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
30045750-2	2018	Imatinib (gleevec, STI-571) is a selective inhibitor of BCR-ABL activity highly effective in the treatment of CML.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
29902613-6	2018	RESULTS: Here, we report the discovery of a synergistic interaction between dasatinib (ABL and SRC family kinase inhibitor) and the mitogen-activated protein kinase kinase (MEK) inhibitor trametinib in KRAS-mutant cancer cells.	Dasatinib	76-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-90
29902613-6	2018	RESULTS: Here, we report the discovery of a synergistic interaction between dasatinib (ABL and SRC family kinase inhibitor) and the mitogen-activated protein kinase kinase (MEK) inhibitor trametinib in KRAS-mutant cancer cells.	trametinib	188-198	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-90
29717260-6	2018	One such compound, bafetinib, a second generation BCR/ABL inhibitor, reduced phosphorylation of ERK and when combined with trametinib, both in vitro and in vivo, reduced growth of vemurafenib resistant melanoma cells.	bafetinib	19-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
29717260-6	2018	One such compound, bafetinib, a second generation BCR/ABL inhibitor, reduced phosphorylation of ERK and when combined with trametinib, both in vitro and in vivo, reduced growth of vemurafenib resistant melanoma cells.	trametinib	123-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
29717260-6	2018	One such compound, bafetinib, a second generation BCR/ABL inhibitor, reduced phosphorylation of ERK and when combined with trametinib, both in vitro and in vivo, reduced growth of vemurafenib resistant melanoma cells.	Vemurafenib	180-191	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
30045750-2	2018	Imatinib (gleevec, STI-571) is a selective inhibitor of BCR-ABL activity highly effective in the treatment of CML.	Imatinib Mesylate	19-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
30038712-0	2018	KLF5 controls glutathione metabolism to suppress p190-BCR-ABL+ B-cell lymphoblastic leukemia.	Glutathione	14-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
30277861-5	2018	RESULTS: Simultaneous inhibition of c-Abl and Src kinases with Bosutinib reduced the expression of numerous fibrosis-associated genes including COL1A1, COL1A3, FN, and TGFbeta and the production of the corresponding proteins by SSc dermal fibroblasts.	bosutinib	63-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-41
30277861-7	2018	CONCLUSIONS: Simultaneous inhibition of c-Abl and Src kinases with Bosutinib abrogates the exaggerated expression of genes encoding fibrillar collagens, fibronectin, and TGF-beta-responsive genes and reduces type I collagen, fibronectin and alpha-SMA production by SSc dermal fibroblasts in vitro.	bosutinib	67-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-45
29897434-2	2018	Nilotinib, a c-Abl inhibitor, has shown improved motor and cognitive symptoms in PD patients.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-18
29897434-4	2018	Radotinib HCl is a selective Bcr-Abl kinase inhibitor that not only effectively access the brain, but also exhibits greater pharmacokinetic properties and safety profiles compared to Nilotinib and other c-Abl inhibitors.	radotinib hcl	0-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	203-208
29897434-5	2018	Here, we show the neuroprotective efficacy of Radotinib HCl, a brain penetrant c-Abl inhibitor, in a pre-clinical model of PD.	radotinib hcl	46-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-84
29897434-6	2018	Importantly, in vitro studies demonstrate that the treatment of Radotinib HCl protects the alpha-synuclein preformed fibrils (PFF)-induced neuronal toxicity, reduces the alpha-synuclein PFF-induced Lewy bodies (LB)/Lewy neurites (LN)-like pathology and inhibits the alpha-synuclein PFF-induced c-Abl activation in primary cortical neurons.	radotinib hcl	64-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	294-299
29897434-7	2018	Furthermore, administration of Radotinib HCl inhibits c-Abl activation and prevents dopaminergic neuron loss, neuroinflammation and behavioral deficits following alpha-synuclein PFF-induced toxicity in vivo.	radotinib hcl	31-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-59
29897434-8	2018	Taken together, our findings indicate that Radotinib HCl has beneficial neuroprotective effects in PD and provides an evidence that selective and brain permeable c-Abl inhibitors can be potential therapeutic agents for the treatment of PD and related alpha-synucleinopathies.	radotinib hcl	43-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-167
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
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 Mesylate	86-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-161
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 Mesylate	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 Mesylate	139-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-41
29933569-3	2018	An analysis of data from large-scale, high-throughput drug screening cell line projects identified Bosutinib, a Src/Abl inhibitor that is currently used for the treatment of chronic myelogenous leukemia, as a candidate drug to treat HNSCC.	bosutinib	99-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-119
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 Mesylate	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 Mesylate	131-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
29925402-6	2018	More recently, preclinical evidence on bafetinib, rebastinib, tozasertib, danusertib, HG-7-85-01, GNF-2, and 1,3,4-thiadiazole derivatives lay promising foundations for better inhibitors to be approved for clinic in the near future.Notably, structural mechanisms of action and drug design exemplified by Bcr-Abl inhibitors have broad relevance to both break through resistances in CML treatment and develop inhibitors against other kinases as targeted chemotherapeutics.	1,3,4-thiadiazole	109-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	304-311
31723781-7	2018	For example, in 1 poor risk subtype, known as Ph-like/BCR-ABL1-like ALL, approximately 10% have rearrangements of ABL-class tyrosine kinases: including ABL1, ABL2, PDGFRB, PDGFRA, and CSF1R.	Tyrosine	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-62
31723781-7	2018	For example, in 1 poor risk subtype, known as Ph-like/BCR-ABL1-like ALL, approximately 10% have rearrangements of ABL-class tyrosine kinases: including ABL1, ABL2, PDGFRB, PDGFRA, and CSF1R.	Tyrosine	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-156
29914565-17	2018	By using inverse polymerase chain reaction (IPCR), we demonstrated that hydrogen peroxide (H2O2)-induced apoptosis in normal nasopharyngeal epithelial and NPC cells led to chromosomal breakages within the ABL BCR that contains a MAR/SAR.	Hydrogen Peroxide	72-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	205-208
29914565-17	2018	By using inverse polymerase chain reaction (IPCR), we demonstrated that hydrogen peroxide (H2O2)-induced apoptosis in normal nasopharyngeal epithelial and NPC cells led to chromosomal breakages within the ABL BCR that contains a MAR/SAR.	Hydrogen Peroxide	91-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	205-208
29675955-7	2018	Consistently, primary cells from BCR/ABL1-like cases responded in vitro to ponatinib.	ponatinib	75-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-41
29608815-0	2018	Alkynylnicotinamide-Based Compounds as ABL1 Inhibitors with Potent Activities against Drug-Resistant CML Harboring ABL1(T315I) Mutant Kinase.	alkynylnicotinamide	0-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-43
29608815-0	2018	Alkynylnicotinamide-Based Compounds as ABL1 Inhibitors with Potent Activities against Drug-Resistant CML Harboring ABL1(T315I) Mutant Kinase.	alkynylnicotinamide	0-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	115-119
29608815-5	2018	Ponatinib (AP24534) is currently the only approved CML drug that is active against the ABL1(T315I) mutation.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-91
29608815-6	2018	However, ponatinib has severe cardiovascular toxicities; hence, there have been efforts to find safer CML drugs that work against ABL1 secondary mutations.	ponatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-134
29608815-7	2018	We reveal that isoquinoline- or naphthyridine-based compounds, such as HSN431, HSN576, HSN459, and HSN608 potently inhibit the enzymatic activities of ABL1, ABL1(T315I), and ABL1(E255K).	isoquinoline	15-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-155
29608815-7	2018	We reveal that isoquinoline- or naphthyridine-based compounds, such as HSN431, HSN576, HSN459, and HSN608 potently inhibit the enzymatic activities of ABL1, ABL1(T315I), and ABL1(E255K).	isoquinoline	15-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-161
29608815-7	2018	We reveal that isoquinoline- or naphthyridine-based compounds, such as HSN431, HSN576, HSN459, and HSN608 potently inhibit the enzymatic activities of ABL1, ABL1(T315I), and ABL1(E255K).	isoquinoline	15-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-161
29608815-7	2018	We reveal that isoquinoline- or naphthyridine-based compounds, such as HSN431, HSN576, HSN459, and HSN608 potently inhibit the enzymatic activities of ABL1, ABL1(T315I), and ABL1(E255K).	Naphthyridines	32-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-155
29608815-7	2018	We reveal that isoquinoline- or naphthyridine-based compounds, such as HSN431, HSN576, HSN459, and HSN608 potently inhibit the enzymatic activities of ABL1, ABL1(T315I), and ABL1(E255K).	Naphthyridines	32-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-161
29608815-7	2018	We reveal that isoquinoline- or naphthyridine-based compounds, such as HSN431, HSN576, HSN459, and HSN608 potently inhibit the enzymatic activities of ABL1, ABL1(T315I), and ABL1(E255K).	Naphthyridines	32-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-161
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 Mesylate	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
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 Mesylate	108-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	224-231
29524554-4	2018	Furthermore, we found that cisplatin resistance of TSCC cells was related to cisplatin inducing lysosome biogenesis in a TFEB-dependent manner, which was regulated by c-Abl.	Cisplatin	27-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-172
31723769-1	2018	Dasatinib is an ABL1 tyrosine kinase inhibitor (TKI) with a short in vivo plasmatic half-life but with good efficiency, which is not fully understood.	dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-20
31723769-1	2018	Dasatinib is an ABL1 tyrosine kinase inhibitor (TKI) with a short in vivo plasmatic half-life but with good efficiency, which is not fully understood.	Tyrosine	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-20
31723769-5	2018	This was verified in total blood where the huge cellular volume of erythrocytes constituted a large reservoir of dasatinib able to induce apoptosis in naive BCR-ABL1 cell lines and primitive chronic myeloid leukemia (CML) CD34+ cells.	dasatinib	113-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-165
29665256-5	2018	We further demonstrated that BCR-ABL enhances the prolyl isomerase activity of Pin 1 by decreasing the phosphorylated level of Pin 1 at Ser 71 and interacting with DAPK1.	Serine	136-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
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 Mesylate	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
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 Mesylate	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-179
29945329-1	2018	BACKGROUND: T315I mutation is the most common BCR-ABL mutation and confers resistance to all the first and second generation BCR-ABL tyrosine kinases, including nilotinib and dasatinib.	nilotinib	161-170	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
29945329-1	2018	BACKGROUND: T315I mutation is the most common BCR-ABL mutation and confers resistance to all the first and second generation BCR-ABL tyrosine kinases, including nilotinib and dasatinib.	nilotinib	161-170	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
29945329-1	2018	BACKGROUND: T315I mutation is the most common BCR-ABL mutation and confers resistance to all the first and second generation BCR-ABL tyrosine kinases, including nilotinib and dasatinib.	Dasatinib	175-184	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
29945329-1	2018	BACKGROUND: T315I mutation is the most common BCR-ABL mutation and confers resistance to all the first and second generation BCR-ABL tyrosine kinases, including nilotinib and dasatinib.	Dasatinib	175-184	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
29660671-0	2018	Computational study of molecular electrostatic potential, docking and dynamics simulations of gallic acid derivatives as ABL inhibitors.	Gallic Acid	94-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-124
29660671-2	2018	Pharmacological activity of Gallic acid and 1,3,4-Oxadiazole as potential inhibitors of ABL kinase has already been reported.	Gallic Acid	28-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-91
29660671-2	2018	Pharmacological activity of Gallic acid and 1,3,4-Oxadiazole as potential inhibitors of ABL kinase has already been reported.	1,3,4-oxadiazole	44-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-91
29660671-3	2018	Objective of this study is to evaluate the ABL kinase inhibitory activity of derivatives of Gallic acid fused with 1,3,4-Oxadiazole moieties.	Gallic Acid	92-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-46
29660671-3	2018	Objective of this study is to evaluate the ABL kinase inhibitory activity of derivatives of Gallic acid fused with 1,3,4-Oxadiazole moieties.	1,3,4-oxadiazole	115-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-46
29660671-5	2018	To investigate the inhibitory activity of Gallic acid derivatives towards the ABL receptor, we have applied molecular docking and molecular dynamics (MD) simulation approaches.	Gallic Acid	42-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-81
29899872-2	2018	Ponatinib blocks a variety of tyrosine kinases including ABL and fibroblast growth factor receptor (FGFR), and the BET bromodomain (BRD) antagonists JQ1 and dBET1 impede MYC oncogene expression.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-60
29684708-8	2018	SAR indicated that 5-deazaalloxazines have a higher selectivity for Abl-1 and FAK kinases than alloxazines.	5-deazaalloxazines	19-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-73
29684708-8	2018	SAR indicated that 5-deazaalloxazines have a higher selectivity for Abl-1 and FAK kinases than alloxazines.	isoalloxazine	26-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-73
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 Mesylate	209-217	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	189-192
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.	Dasatinib	219-228	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	189-192
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.	nilotinib	230-239	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	189-192
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.	ponatinib	245-254	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	189-192
29524554-4	2018	Furthermore, we found that cisplatin resistance of TSCC cells was related to cisplatin inducing lysosome biogenesis in a TFEB-dependent manner, which was regulated by c-Abl.	Cisplatin	77-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-172
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 Mesylate	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
29937990-6	2018	Dasatinib (BMS-354825), a SRC/ABL inhibitor, effectively blocked SFK activation at nanomolar concentrations which correlated with a significant decrease in cell numbers of multiple lung cancer cell lines.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-33
29468363-0	2018	The BCR-ABL inhibitor nilotinib influences phenotype and function of monocyte-derived human dendritic cells.	nilotinib	22-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
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 Mesylate	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 Mesylate	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 Mesylate	273-281	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	249-256
29468363-4	2018	Meanwhile, second generation BCR-ABL inhibitors like nilotinib, which inhibits BCR-ABL with enhanced potency have become standard of treatment, at least in patients with BCR-ABL kinase domain mutations.	nilotinib	53-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
29468363-4	2018	Meanwhile, second generation BCR-ABL inhibitors like nilotinib, which inhibits BCR-ABL with enhanced potency have become standard of treatment, at least in patients with BCR-ABL kinase domain mutations.	nilotinib	53-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
29468363-4	2018	Meanwhile, second generation BCR-ABL inhibitors like nilotinib, which inhibits BCR-ABL with enhanced potency have become standard of treatment, at least in patients with BCR-ABL kinase domain mutations.	nilotinib	53-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
29165716-2	2018	Although ponatinib, a third-generation TKI, improves outcomes for patients with BCR-ABL-dependent mechanisms of resistance, including the T315I mutation, a proportion of patients may have or develop BCR-ABL-independent resistance and fail ponatinib treatment.	ponatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
29577681-1	2018	Radotinib is a second-generation BCR-ABL1 tyrosine kinase inhibitor approved for the treatment of chronic myeloid leukemia in chronic phase (CP-CML).	4-methyl-N-(3-(4-methylimidazol-1-yl)-5-trifluoromethylphenyl)-3-(4-pyrazin-2-ylpyrimidin-2-ylamino)benzamide	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
29625382-4	2018	Moreover, the past two years have witnessed remarkable advances in the development of phthalimide conjugation as a strategy for the degradation instead of inhibition of the targets, including BET family proteins, Sirtuin 2, CDK 9, Smad 3, and BCR-ABL proteins.	phthalimide	86-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	243-250
29165716-2	2018	Although ponatinib, a third-generation TKI, improves outcomes for patients with BCR-ABL-dependent mechanisms of resistance, including the T315I mutation, a proportion of patients may have or develop BCR-ABL-independent resistance and fail ponatinib treatment.	ponatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	199-206
29165716-4	2018	Methods: Two CML cell lines with acquired BCR-ABL-independent resistance were generated following culture in ponatinib.	ponatinib	109-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
29165716-9	2018	Results: We show that ponatinib-resistant CML cells can acquire BCR-ABL-independent resistance mediated through alternative activation of mTOR.	ponatinib	22-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
29544149-1	2018	Through exploration of the non-highly conserved allosteric hydrophobic pocket generated by DFG-out shifting in the inactive conformation, we discovered a highly selective type II PDGFRalpha kinase inhibitor 15i (CHMFL-PDGFRalpha-159), which exhibited strong potency against purified PDGFRalpha (IC50: 132 nM) but not structurally similar PDGFRbeta, ABL, c-KIT and VEGFR2 kinases.	1,3-Diphenylguanidine	91-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	349-352
29522716-5	2018	MTT assay was first performed to detect the effect of inhibitors of c-ABL (imatinib) and EGFR (lapatinib) on FRBC cells.	monooxyethylene trimethylolpropane tristearate	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-73
29636436-7	2018	Furthermore, Abl (HeLa and Caco2) and Lyn (Caco2) were enriched specifically in the EspJ-containing samples.	caco2	27-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
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 Mesylate	75-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-73
29315500-2	2018	Dasatinib is a potent inhibitor of BCR-ABL, KIT, and SRC family kinases as well as imatinib-resistant cells.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
29386476-0	2018	The First Pentacyclic Triterpenoid Gypsogenin Derivative Exhibiting Anti-ABL1 Kinase and Anti-chronic Myelogenous Leukemia Activities.	triterpenoid TP-222	22-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-77
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 Mesylate	118-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
29386476-4	2018	Here we examined whether plant-derived pentacyclic triterpenoid gypsogenin and/or their derivatives show inhibitory activity against BCR-ABL.	triterpenoid TP-222	51-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
29522367-8	2018	Asciminib, an allosteric ABL1 inhibitor, could demonstrate a higher capacity in overcoming common TKIs resistant mutations, including T315I, but clinical findings are needed.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-29
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 Mesylate	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
29501569-9	2018	Further, LY294002 treatment had no effect on decreased expression of Bach2 induced by BCR-ABL, but significantly eliminated BCR-ABL-induced phosphorylation of Bach2 and restored reduced nuclear translocation of Bach2 induced by BCR-ABL in B cells from SLE.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
29501569-9	2018	Further, LY294002 treatment had no effect on decreased expression of Bach2 induced by BCR-ABL, but significantly eliminated BCR-ABL-induced phosphorylation of Bach2 and restored reduced nuclear translocation of Bach2 induced by BCR-ABL in B cells from SLE.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
29501569-10	2018	CONCLUSIONS: Bach2 may play a suppressive role in B cells from SLE, and BCR-ABL may inhibit the nuclear translocation of Bach2 via serine phosphorylation through the PI3K pathway.	Serine	131-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
29541231-6	2018	The present data suggest that BCR-ABL gene amplification may be associated with imatinib resistance, which can be overcome with dasatinib.	Dasatinib	128-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-37
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 Mesylate	70-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-27
29414416-3	2018	This is largely due to the suppression of BCR/Abl protein, driven by the reduction of energy supply due to oxygen or glucose shortage, in stem cell niches of bone marrow.	Oxygen	107-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
29414416-3	2018	This is largely due to the suppression of BCR/Abl protein, driven by the reduction of energy supply due to oxygen or glucose shortage, in stem cell niches of bone marrow.	Glucose	117-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
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 Mesylate	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 Mesylate	144-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-23
29438361-0	2018	A first-in-human phase I study to determine the maximum tolerated dose of the oral Src/ABL inhibitor AZD0424.	AZD-0424	101-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-90
29438361-2	2018	AZD0424, an oral inhibitor of Src and ABL1, has shown evidence of anti-tumour activity in pre-clinical studies.	AZD-0424	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-42
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 Mesylate	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 Mesylate	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 Mesylate	115-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
29487179-4	2018	Vinculin targeting requires its phosphorylation at tyrosine 822 by Abl family kinases (hereafter Abl), but the origin of force-dependent Abl activation had not been identified.	Tyrosine	51-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-70
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.	Ropivacaine	28-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
29487179-4	2018	Vinculin targeting requires its phosphorylation at tyrosine 822 by Abl family kinases (hereafter Abl), but the origin of force-dependent Abl activation had not been identified.	Tyrosine	51-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-100
29487179-4	2018	Vinculin targeting requires its phosphorylation at tyrosine 822 by Abl family kinases (hereafter Abl), but the origin of force-dependent Abl activation had not been identified.	Tyrosine	51-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-100
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.	Dasatinib	57-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
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 Mesylate	207-215	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
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.	Dasatinib	219-228	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
29385394-1	2018	Bosutinib (SKI-606) is an oral, dual Src/Abl tyrosine kinase inhibitor (TKI) approved for treatment of patients with Philadelphia chromosome-positive (Ph+) chronic myeloid leukemia (CML) that is resistant or intolerant to prior TKI therapy or for whom other TKIs are not appropriate choices.	bosutinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-44
29385394-1	2018	Bosutinib (SKI-606) is an oral, dual Src/Abl tyrosine kinase inhibitor (TKI) approved for treatment of patients with Philadelphia chromosome-positive (Ph+) chronic myeloid leukemia (CML) that is resistant or intolerant to prior TKI therapy or for whom other TKIs are not appropriate choices.	bosutinib	11-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-44
29334667-4	2018	Our results demonstrated that the combination of lithium + nilotinib (L + N) induced K562-cell death and cleaved caspase-3 when compared to lithium or nilotinib alone, accompanied by GSK-3beta phosphorylation and Bcr-Abl oncoprotein levels reduction.	Lithium	49-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	213-220
29334667-4	2018	Our results demonstrated that the combination of lithium + nilotinib (L + N) induced K562-cell death and cleaved caspase-3 when compared to lithium or nilotinib alone, accompanied by GSK-3beta phosphorylation and Bcr-Abl oncoprotein levels reduction.	nilotinib	59-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	213-220
29334667-7	2018	This pioneering research has demonstrated that lithium might be of therapeutic value when targeting Bcr-Abl cells with nilotinib because it triggers cell death in addition to exerting classical antiproliferative effects, opening new perspectives for novel target and therapeutic approaches to eradicate CML.	Lithium	47-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
29334667-7	2018	This pioneering research has demonstrated that lithium might be of therapeutic value when targeting Bcr-Abl cells with nilotinib because it triggers cell death in addition to exerting classical antiproliferative effects, opening new perspectives for novel target and therapeutic approaches to eradicate CML.	nilotinib	119-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
29325229-2	2018	Acquired drug resistance in mutant Bcr-Abl has enhanced pathogenesis with the use of single therapy agents such as nilotinib.	nilotinib	115-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
29325229-3	2018	Moreover, allosteric targeting has been identified to consequentially inhibit Bcr-Abl activity, which led to the recent development of ABL-001 (asciminib) that selectively binds the myristoyl pocket.	asciminib	144-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
29325229-4	2018	Experimental studies have revealed that the combination of nilotinib and ABL-001 induced a "bent" conformation in the C-terminal helix of Bcr-Abl; a benchmark of inhibition, thereby exhibiting a greater potency in the treatment of CML, surmounting the setbacks of drug resistance, disease regression and relapse.	nilotinib	59-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
29037704-6	2018	Anthocyanins exhibited tyrosine kinase inhibitory potential in silico and biochemically; cyanidin-3-O-glucoside had one of the highest binding affinities with all kinases, especially ABL1 (-8.5kcal/mol).	Anthocyanins	0-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	183-187
29037704-6	2018	Anthocyanins exhibited tyrosine kinase inhibitory potential in silico and biochemically; cyanidin-3-O-glucoside had one of the highest binding affinities with all kinases, especially ABL1 (-8.5kcal/mol).	cyanidin-3-o-glucoside	89-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	183-187
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.	nilotinib	20-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
29435021-1	2018	Tyrosine kinase inhibitors (TKIs), including imatinib, dasatinib and nilotinib are primarily used in the initial treatment of chronic phase (CP)-chronic myeloid leukemia (CML), as CMLs harbor the BCR-ABL fusion product.	nilotinib	69-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	196-203
29341593-0	2018	Analysis of Cellular Tyrosine Phosphorylation via Chemical Rescue of Conditionally Active Abl Kinase.	Tyrosine	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-93
29463776-0	2018	Abl and Arg mediate cysteine cathepsin secretion to facilitate melanoma invasion and metastasis.	Cysteine	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
29463776-6	2018	We found that the nonreceptor tyrosine kinases Abl and Arg (Abl/Arg) promoted the secretion of cathepsin B and cathepsin L by activating transcription factors (namely, Ets1, Sp1, and NF-kappaB/p65) that have key roles in the epithelial-mesenchymal transition (EMT), invasion, and therapeutic resistance.	Arginine	55-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-63
29463776-6	2018	We found that the nonreceptor tyrosine kinases Abl and Arg (Abl/Arg) promoted the secretion of cathepsin B and cathepsin L by activating transcription factors (namely, Ets1, Sp1, and NF-kappaB/p65) that have key roles in the epithelial-mesenchymal transition (EMT), invasion, and therapeutic resistance.	Arginine	64-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
29463776-6	2018	We found that the nonreceptor tyrosine kinases Abl and Arg (Abl/Arg) promoted the secretion of cathepsin B and cathepsin L by activating transcription factors (namely, Ets1, Sp1, and NF-kappaB/p65) that have key roles in the epithelial-mesenchymal transition (EMT), invasion, and therapeutic resistance.	Arginine	64-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-63
29463776-7	2018	In some melanoma cell lines, Abl/Arg promoted the Ets1/p65-induced secretion of cathepsin B and cathepsin L in a kinase-independent manner, whereas in other melanoma lines, Abl/Arg promoted the kinase-dependent, Sp1/Ets1/p65-mediated induction of cathepsin L secretion and the Sp1/p65-mediated induction of cathepsin B secretion.	Arginine	177-180	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-32
29463776-8	2018	As an indication of clinical relevance, the abundance of mRNAs encoding Abl/Arg, Sp1, Ets1, and cathepsins was positively correlated in primary melanomas, and Abl/Arg-driven invasion in culture and metastasis in vivo required cathepsin secretion.	Arginine	76-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-75
29463776-8	2018	As an indication of clinical relevance, the abundance of mRNAs encoding Abl/Arg, Sp1, Ets1, and cathepsins was positively correlated in primary melanomas, and Abl/Arg-driven invasion in culture and metastasis in vivo required cathepsin secretion.	Arginine	163-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-75
29463776-8	2018	As an indication of clinical relevance, the abundance of mRNAs encoding Abl/Arg, Sp1, Ets1, and cathepsins was positively correlated in primary melanomas, and Abl/Arg-driven invasion in culture and metastasis in vivo required cathepsin secretion.	Arginine	163-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-162
29336809-2	2018	The screening method was established by using 5-carboxyfluorescein labeled peptide substrate of BCR-ABL (F-ABLS), a known BCR-ABL tyrosine kinase inhibitor dasatinib, as well as a small chemical library consisting of 37 natural products.	4-carboxyfluorescein	46-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
29336809-2	2018	The screening method was established by using 5-carboxyfluorescein labeled peptide substrate of BCR-ABL (F-ABLS), a known BCR-ABL tyrosine kinase inhibitor dasatinib, as well as a small chemical library consisting of 37 natural products.	Dasatinib	156-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
29336809-7	2018	By taking the advantage of the screening method, luteolin and epicatechin gallate were discovered as the new BCR-ABL inhibitors.	Luteolin	49-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
29336809-7	2018	By taking the advantage of the screening method, luteolin and epicatechin gallate were discovered as the new BCR-ABL inhibitors.	epicatechin gallate	62-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
29319304-2	2018	We show that this assembly state strictly correlates with the conformation of the kinase activation loop induced by a total of 14 ATP site ligands, comprising all FDA-approved Bcr-Abl inhibiting drugs.	Adenosine Triphosphate	130-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	176-183
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 Mesylate	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
29251010-2	2018	The ABL/ALN sequence resulted in greater bone mineral density gains at all skeletal sites and in a reduction of vertebral, non-vertebral, major and clinical fractures compared to what is observed after 18 months of placebo followed by 6 months of ALN.	Aluminum	247-250	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
29035389-6	2018	The Src/Abl inhibitor dasatinib, a candidate anti-invasive drug, abrogated the invasive properties induced by MCC deficiency.	Dasatinib	22-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-11
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.	bosutinib	35-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
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.	ponatinib	68-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
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 Mesylate	153-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-158
29358661-0	2018	Anthelmintic niclosamide suppresses transcription of BCR-ABL fusion oncogene via disabling Sp1 and induces apoptosis in imatinib-resistant CML cells harboring T315I mutant.	Niclosamide	13-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
29385210-3	2018	Additionally, increased expression of ABCC6 mRNA was observed during in vitro development of nilotinib resistance in BCR-ABL1-expressing cell lines.	nilotinib	93-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-125
29358661-3	2018	The third generation TKI ponatinib is the only effective TKI to treat CML patients harboring T315I-BCR-ABL mutation, but with high rate of major arterial thrombotic events.	ponatinib	25-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
29358661-7	2018	Treatment of WT- and T315I-BCR-ABL-expressing CML cells by niclosamide diminished such an enrichment of Sp1, and decreased WT- and T315I-BCR-ABL transcription and its downstream signaling molecules such as STAT5 and Akt.	Niclosamide	59-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
29358661-7	2018	Treatment of WT- and T315I-BCR-ABL-expressing CML cells by niclosamide diminished such an enrichment of Sp1, and decreased WT- and T315I-BCR-ABL transcription and its downstream signaling molecules such as STAT5 and Akt.	Niclosamide	59-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-144
29358661-9	2018	The in vivo efficacy validation of p-niclosamide, a water soluble derivative of niclosamide, showed that p-niclosamide significantly inhibited the tumor burden of nude mice subcutaneously bearing T315I-BCR-ABL-expressing CML cells, and prolonged the survival of allografted leukemic mice harboring BaF3-T315I-BCR-ABL.	p-niclosamide	35-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	202-209
29358661-9	2018	The in vivo efficacy validation of p-niclosamide, a water soluble derivative of niclosamide, showed that p-niclosamide significantly inhibited the tumor burden of nude mice subcutaneously bearing T315I-BCR-ABL-expressing CML cells, and prolonged the survival of allografted leukemic mice harboring BaF3-T315I-BCR-ABL.	p-niclosamide	35-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	309-316
29358661-9	2018	The in vivo efficacy validation of p-niclosamide, a water soluble derivative of niclosamide, showed that p-niclosamide significantly inhibited the tumor burden of nude mice subcutaneously bearing T315I-BCR-ABL-expressing CML cells, and prolonged the survival of allografted leukemic mice harboring BaF3-T315I-BCR-ABL.	Niclosamide	37-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	202-209
29358661-9	2018	The in vivo efficacy validation of p-niclosamide, a water soluble derivative of niclosamide, showed that p-niclosamide significantly inhibited the tumor burden of nude mice subcutaneously bearing T315I-BCR-ABL-expressing CML cells, and prolonged the survival of allografted leukemic mice harboring BaF3-T315I-BCR-ABL.	Niclosamide	37-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	309-316
29358661-9	2018	The in vivo efficacy validation of p-niclosamide, a water soluble derivative of niclosamide, showed that p-niclosamide significantly inhibited the tumor burden of nude mice subcutaneously bearing T315I-BCR-ABL-expressing CML cells, and prolonged the survival of allografted leukemic mice harboring BaF3-T315I-BCR-ABL.	p-niclosamide	105-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	202-209
29358661-9	2018	The in vivo efficacy validation of p-niclosamide, a water soluble derivative of niclosamide, showed that p-niclosamide significantly inhibited the tumor burden of nude mice subcutaneously bearing T315I-BCR-ABL-expressing CML cells, and prolonged the survival of allografted leukemic mice harboring BaF3-T315I-BCR-ABL.	p-niclosamide	105-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	309-316
29358661-10	2018	We conclude that niclosamide is active against T315I-BCR-ABL-expressing cells, and may be a promising agent for CML patients regardless of T315I mutation status.	Niclosamide	17-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
29343719-5	2018	Reduction in c-Abl expression by siRNA attenuates both thrombin- and sphingosine 1-phosphate (S1P)-mediated structural changes in ECs, specifically spatially-defined changes in elastic modulus and distribution of critical proteins.	sphingosine 1-phosphate	69-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-18
29343719-5	2018	Reduction in c-Abl expression by siRNA attenuates both thrombin- and sphingosine 1-phosphate (S1P)-mediated structural changes in ECs, specifically spatially-defined changes in elastic modulus and distribution of critical proteins.	sphingosine 1-phosphate	94-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-18
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 Mesylate	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
29464092-0	2018	mTOR inhibition enhances efficacy of dasatinib in ABL-rearranged Ph-like B-ALL.	Dasatinib	37-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-53
29464092-5	2018	Here we show that combinations of the ABL-directed TKI dasatinib with mTOR kinase inhibitors (TOR-KIs) are more effective than TKI alone against patient-derived Ph-like B-ALL cells harboring rearrangements of ABL1 or ABL2.	Dasatinib	55-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-41
29464092-5	2018	Here we show that combinations of the ABL-directed TKI dasatinib with mTOR kinase inhibitors (TOR-KIs) are more effective than TKI alone against patient-derived Ph-like B-ALL cells harboring rearrangements of ABL1 or ABL2.	Dasatinib	55-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-213
29343029-1	2018	Objective: microRNA targeted to chronic myeloid leukemia Bcr-Abl oncogene were screened using the deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA).	Vorinostat	120-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
29343029-1	2018	Objective: microRNA targeted to chronic myeloid leukemia Bcr-Abl oncogene were screened using the deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA).	Vorinostat	153-157	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
29343029-4	2018	Effect of SAHA on Bcr-Abl Gene Transcription in K562 Cells was determined by Fluorescence Quantitative PCR.	Vorinostat	10-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
29343029-7	2018	Results: SAHA significantly inhibited the proliferation of K562 cells and induced apoptosis, meanwhile SAHA significantly down-regulated the transcriptional level of Bcr-Abl gene.	Vorinostat	103-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-173
29343029-11	2018	Conclusion: Acetylation inhibitor SAHA promoted the expression of miR-192 and miR-6816 in K562 cells by acetylation regulation, miR-192 and miR-6816 further down-regulated the transcription of Bcr-Abl gene, thereby inhibiting K562 cell proliferation and induced apoptosis.	Vorinostat	34-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	193-200
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 Mesylate	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
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.	Dasatinib	97-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
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.	Sunitinib	112-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
29745343-8	2018	RESULTS: In the recent years, many efforts have been taken to develop indazole derivatives as fibroblast growth factor receptor (FGFR) inhibitors, indoleamine-2,3-dioxygenase1 (IDO1) inhibitors, proviral integration site MuLV (Pim) kinase inhibitors, aurora kinases inhibitors, Bcr-Abl inhibitors, hypoxia inducible factor-1 (HIF-1) inhibitors and carbonic anhydrase (CA) inhibitors.	Indazoles	70-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	278-285
29578162-3	2018	We demonstrated that curcumin inhibited activation of Akt-mTOR, ABL/STAT5 pathways, inhibited cell proliferation, and induced apoptosis in Ph + ALL cells.	Curcumin	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-67
28554234-0	2018	Molecular characterization and therapeutic reaction to dasatinib in a CML patient harboring a novel e8a2 BCR-ABL1 transcript with a somatic mutation in TP53BP2 and cadherin-10 genes.	Dasatinib	55-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-113
30121665-4	2018	RESULTS: We combined a nilotinib-based therapy targeting the overexpressed ABL1 gene with a proteasome inhibitor and Peg-asparaginase, achieving a spectacular response: the percentage of lymphoblasts in the bone marrow was reduced from 70% to 5%, which enabled a second HCT to be performed.	nilotinib	23-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-79
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 Mesylate	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 Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	287-294
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 Mesylate	213-221	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
30069624-3	2018	Dasatinib is a very potent inhibitor of BCR-ABL and an effective treatment for the BCR-ABL-driven diseases chronic myeloid leukemia (CML) and Philadelphia-chromosome-positive acute lymphoblastic leukemia (Ph+ ALL), characterized by the constitutively active tyrosine kinase, BCR-ABL.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
30069624-3	2018	Dasatinib is a very potent inhibitor of BCR-ABL and an effective treatment for the BCR-ABL-driven diseases chronic myeloid leukemia (CML) and Philadelphia-chromosome-positive acute lymphoblastic leukemia (Ph+ ALL), characterized by the constitutively active tyrosine kinase, BCR-ABL.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
30069624-3	2018	Dasatinib is a very potent inhibitor of BCR-ABL and an effective treatment for the BCR-ABL-driven diseases chronic myeloid leukemia (CML) and Philadelphia-chromosome-positive acute lymphoblastic leukemia (Ph+ ALL), characterized by the constitutively active tyrosine kinase, BCR-ABL.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
30069627-10	2018	In conclusion, ponatinib has proved to be a powerful BCR-ABL inhibitor, which exhibits clinical activity both in BCR-ABL wild-type and mutant CML, including the pan-resistant T315I mutation.	ponatinib	15-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
30069627-10	2018	In conclusion, ponatinib has proved to be a powerful BCR-ABL inhibitor, which exhibits clinical activity both in BCR-ABL wild-type and mutant CML, including the pan-resistant T315I mutation.	ponatinib	15-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
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 Mesylate	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
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 Mesylate	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
30618318-0	2018	Low-dose staurosporine selectively reverses BCR-ABL-independent IM resistance through PKC-alpha-mediated G2/M phase arrest in chronic myeloid leukaemia.	Staurosporine	9-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
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 Mesylate	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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 Mesylate	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 Mesylate	38-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	165-172
29205725-5	2018	A subset of wild-type p210 BCR-ABL that was transiently expressed in HEK293 cells was dramatically translocated from the cytosol to mitochondria in response to carbonyl cyanide m-chlorophenylhydrazone (CCCP) treatment, which induces mitochondrial depolarization and subsequent externalization of CL to the organelle"s outer membrane, whereas an R726A mutant of the protein was not translocated.	Carbonyl Cyanide m-Chlorophenyl Hydrazone	160-200	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
29205725-5	2018	A subset of wild-type p210 BCR-ABL that was transiently expressed in HEK293 cells was dramatically translocated from the cytosol to mitochondria in response to carbonyl cyanide m-chlorophenylhydrazone (CCCP) treatment, which induces mitochondrial depolarization and subsequent externalization of CL to the organelle"s outer membrane, whereas an R726A mutant of the protein was not translocated.	Carbonyl Cyanide m-Chlorophenyl Hydrazone	202-206	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
29205725-6	2018	Furthermore, only wild-type p210 BCR-ABL, but not the R726A mutant, suppressed CCCP-induced mitophagy and subsequently enhanced reactive oxygen species production.	Carbonyl Cyanide m-Chlorophenyl Hydrazone	79-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
29205725-6	2018	Furthermore, only wild-type p210 BCR-ABL, but not the R726A mutant, suppressed CCCP-induced mitophagy and subsequently enhanced reactive oxygen species production.	Reactive Oxygen Species	128-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
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 Mesylate	247-264	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-76
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.	IBR2	0-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-168
29066624-0	2017	Active site-adjacent phosphorylation at Tyr-397 by c-Abl kinase inactivates caspase-9.	Tyrosine	40-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-56
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 Mesylate	139-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	255-262
29066624-4	2017	Caspase-9 phosphorylation by the non-receptor tyrosine kinase c-Abl at Tyr-153 reportedly leads to caspase-9 activation.	Tyrosine	71-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-67
29066624-7	2017	Instead, we identified a new site for c-Abl-mediated phosphorylation, Tyr-397.	Tyrosine	70-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-43
29066624-9	2017	Our results further indicate that Tyr-397 is the dominant site of c-Abl phosphorylation both in vitro and upon c-Abl activation in cells.	Tyrosine	34-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-71
29066624-9	2017	Our results further indicate that Tyr-397 is the dominant site of c-Abl phosphorylation both in vitro and upon c-Abl activation in cells.	Tyrosine	34-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-116
29280989-1	2017	In an attempt to develop potent antitumor agents, new 1,3,4-thiadiazole derivatives were synthesized and evaluated for their cytotoxic effects on multiple human cancer cell lines, including the K562 chronic myelogenous leukemia cell line that expresses the Bcr-Abl tyrosine kinase.	1,3,4-thiadiazole	54-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	257-264
29280989-2	2017	N-(5-Nitrothiazol-2-yl)-2-((5-((4-(trifluoromethyl)phenyl)amino)-1,3,4-thiadiazol-2-yl)thio)acetamide (2) inhibited the Abl protein kinase with an IC50 value of 7.4 microM and showed selective activity against the Bcr-Abl positive K562 cell line.	n-(5-nitrothiazol-2-yl)-2-((5-((4-(trifluoromethyl)phenyl)amino	0-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	214-221
29280989-2	2017	N-(5-Nitrothiazol-2-yl)-2-((5-((4-(trifluoromethyl)phenyl)amino)-1,3,4-thiadiazol-2-yl)thio)acetamide (2) inhibited the Abl protein kinase with an IC50 value of 7.4 microM and showed selective activity against the Bcr-Abl positive K562 cell line.	n-(5-nitrothiazol-2-yl)-2-((5-((4-(trifluoromethyl)phenyl)amino	0-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-123
29280989-2	2017	N-(5-Nitrothiazol-2-yl)-2-((5-((4-(trifluoromethyl)phenyl)amino)-1,3,4-thiadiazol-2-yl)thio)acetamide (2) inhibited the Abl protein kinase with an IC50 value of 7.4 microM and showed selective activity against the Bcr-Abl positive K562 cell line.	4-thiadiazol-2-yl)thio)acetamide	69-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-123
28986256-8	2017	Expression level of BCR-ABL and the activity of its downstream PI3K/AKT pathway were significantly reduced in miR-7-transfected cells.	mir-7	110-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
29280989-2	2017	N-(5-Nitrothiazol-2-yl)-2-((5-((4-(trifluoromethyl)phenyl)amino)-1,3,4-thiadiazol-2-yl)thio)acetamide (2) inhibited the Abl protein kinase with an IC50 value of 7.4 microM and showed selective activity against the Bcr-Abl positive K562 cell line.	4-thiadiazol-2-yl)thio)acetamide	69-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	214-221
29280989-3	2017	Furthermore, a Bcr-Abl-compound 2 molecular modelling simulation highlighted the anchoring role of the nitrothiazole moiety in bonding and hydrophobic interaction with the key amino acid residues.	Niridazole	103-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
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.	Tigecycline	115-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
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 Mesylate	131-139	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
28974549-0	2017	Modulation of Navitoclax Sensitivity by Dihydroartemisinin-Mediated MCL-1 Repression in BCR-ABL+ B-Lineage Acute Lymphoblastic Leukemia.	navitoclax	14-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
28974549-0	2017	Modulation of Navitoclax Sensitivity by Dihydroartemisinin-Mediated MCL-1 Repression in BCR-ABL+ B-Lineage Acute Lymphoblastic Leukemia.	artenimol	40-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
28974549-6	2017	The repression of MCL-1 renders leukemic cells highly sensitive to synergistic cell death induced by ABT-263 in a mouse model of BCR-ABL+ B-ALL both in vitro and in vivo Furthermore, DHA synergizes with ABT-263 in human Ph+ ALL cell lines, and primary patient-derived xenografts of Ph+ ALL in culture.Conclusions: Our findings suggest that combining DHA with ABT-263 can improve therapeutic response in BCR-ABL+ B-ALL.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	101-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
29423045-0	2018	Ovatodiolide targets chronic myeloid leukemia stem cells by epigenetically upregulating hsa-miR-155, suppressing the BCR-ABL fusion gene and dysregulating the PI3K/AKT/mTOR pathway.	ovatodiolide	0-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
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.	ovatodiolide	28-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	221-228
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 Mesylate	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	221-228
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 Mesylate	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-51
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 Mesylate	12-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
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 Mesylate	150-158	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-174
28939746-1	2017	Purpose: Radotinib is a second-generation BCR-ABL1 tyrosine kinase inhibitor (TKI) approved in Korea for chronic phase chronic myeloid leukemia (CML-CP) in patients newly diagnosed or with insufficient response to other TKIs.	4-methyl-N-(3-(4-methylimidazol-1-yl)-5-trifluoromethylphenyl)-3-(4-pyrazin-2-ylpyrimidin-2-ylamino)benzamide	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
28260399-4	2017	Thus, GZD856 may serve as a promising lead for the development of Bcr-Abl inhibitors overcoming acquired imatinib resistance.	GZD856	6-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
28928163-0	2017	High BCR-ABL/GUSIS Levels at Diagnosis of Chronic Phase CML Are Associated with Unfavorable Responses to Standard-Dose Imatinib.	Imatinib Mesylate	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 Mesylate	329-337	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	191-198
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 Mesylate	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 Mesylate	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
28260399-4	2017	Thus, GZD856 may serve as a promising lead for the development of Bcr-Abl inhibitors overcoming acquired imatinib resistance.	Imatinib Mesylate	105-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
29152650-0	2017	Semi-random mutagenesis profile of BCR-ABL during imatinib resistance acquirement in K562 cells.	Imatinib Mesylate	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
28386107-2	2017	As with ABL, translocations that fuse ARG to ETV6/TEL have been identified in patients with leukemia.	Arginine	38-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-11
29152650-4	2017	Clone sequencing of the BCR-ABL gene and other control genes was applied in two imatinib-resistant cell models.	Imatinib Mesylate	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 Mesylate	32-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
28990077-0	2017	Inhibitory effect of the anthelmintic drug pyrvinium pamoate on T315I BCR-ABL-positive CML cells.	pyrvinium	43-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
28990077-4	2017	In the present study, it was demonstrated that pyrvinium pamoate, an anthelmintic drug approved by the Food and Drug Administration had potent inhibitory effects on growth and survival in CML cells with T315I BCR-ABL.	pyrvinium	47-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-216
28990077-6	2017	Thus, the clinical efficacy of pyrvinium pamoate in treating patients with CML bearing T315I BCR-ABL should be further investigated.	pyrvinium	31-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
29312576-4	2017	RT-PCR and Western blot assay demonstrated that the expression of BCR/ABL in K562 and HL-60 cells was significantly inhibited by matrine treatment.	matrine	129-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
29256412-1	2017	The protein kinase inhibitor dasatinib, targeting BCR-ABL and Src family kinases, is used in chronic myeloid leukaemia and Philadelphia-chromosome positive acute lymphoblastic leukaemia.	Dasatinib	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
29127384-1	2017	Dasatinib and radotinib are oral BCR-ABL tyrosine kinase inhibitors that were developed as drugs for the treatment of chronic myeloid leukemia.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
29127384-1	2017	Dasatinib and radotinib are oral BCR-ABL tyrosine kinase inhibitors that were developed as drugs for the treatment of chronic myeloid leukemia.	4-methyl-N-(3-(4-methylimidazol-1-yl)-5-trifluoromethylphenyl)-3-(4-pyrazin-2-ylpyrimidin-2-ylamino)benzamide	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
28801986-6	2017	After switching to nilotinib, both BCR-ABL and BCR-ABLIns35bp became undetectable in 3 patients who attained complete molecular response (CMR), whereas in the remaining all 34 patients, BCR-ABLIns35bp was persistently detected, and minimal residual disease (MRD) fluctuated at low but detectable levels.	nilotinib	19-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
29067094-0	2017	Dasatinib and chemotherapy in a patient with early T-cell precursor acute lymphoblastic leukemia and NUP214-ABL1 fusion: A case report.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-112
28821556-1	2017	Purpose: Dasatinib is a short-acting dual ABL/SRC family tyrosine kinase inhibitor (TKI), which is frequently used to treat chronic myeloid leukemia.	Dasatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-45
28822797-0	2017	Influence of BCR-ABL Transcript Type on Outcome in Patients With Chronic-Phase Chronic Myeloid Leukemia Treated With Imatinib.	Imatinib Mesylate	117-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
29067094-1	2017	The present study aimed to evaluate the therapeutic efficacy of dasatinib in a patient with nucleoporin 214-tyrosine protein kinase ABL1 proto-oncogene 1 (NUP214-ABL1)-positive early T-cell precursor-acute lymphoblastic leukemia (ETP-ALL), as well as that of selinexor and dasatinib for NUP214-ABL1-positive ETP-ALL in vitro.	Dasatinib	64-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-136
29067094-1	2017	The present study aimed to evaluate the therapeutic efficacy of dasatinib in a patient with nucleoporin 214-tyrosine protein kinase ABL1 proto-oncogene 1 (NUP214-ABL1)-positive early T-cell precursor-acute lymphoblastic leukemia (ETP-ALL), as well as that of selinexor and dasatinib for NUP214-ABL1-positive ETP-ALL in vitro.	Dasatinib	64-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-166
29067094-1	2017	The present study aimed to evaluate the therapeutic efficacy of dasatinib in a patient with nucleoporin 214-tyrosine protein kinase ABL1 proto-oncogene 1 (NUP214-ABL1)-positive early T-cell precursor-acute lymphoblastic leukemia (ETP-ALL), as well as that of selinexor and dasatinib for NUP214-ABL1-positive ETP-ALL in vitro.	Dasatinib	64-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-166
29067094-1	2017	The present study aimed to evaluate the therapeutic efficacy of dasatinib in a patient with nucleoporin 214-tyrosine protein kinase ABL1 proto-oncogene 1 (NUP214-ABL1)-positive early T-cell precursor-acute lymphoblastic leukemia (ETP-ALL), as well as that of selinexor and dasatinib for NUP214-ABL1-positive ETP-ALL in vitro.	selinexor	259-268	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-136
29067094-1	2017	The present study aimed to evaluate the therapeutic efficacy of dasatinib in a patient with nucleoporin 214-tyrosine protein kinase ABL1 proto-oncogene 1 (NUP214-ABL1)-positive early T-cell precursor-acute lymphoblastic leukemia (ETP-ALL), as well as that of selinexor and dasatinib for NUP214-ABL1-positive ETP-ALL in vitro.	selinexor	259-268	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-166
29067094-1	2017	The present study aimed to evaluate the therapeutic efficacy of dasatinib in a patient with nucleoporin 214-tyrosine protein kinase ABL1 proto-oncogene 1 (NUP214-ABL1)-positive early T-cell precursor-acute lymphoblastic leukemia (ETP-ALL), as well as that of selinexor and dasatinib for NUP214-ABL1-positive ETP-ALL in vitro.	selinexor	259-268	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-166
29067094-1	2017	The present study aimed to evaluate the therapeutic efficacy of dasatinib in a patient with nucleoporin 214-tyrosine protein kinase ABL1 proto-oncogene 1 (NUP214-ABL1)-positive early T-cell precursor-acute lymphoblastic leukemia (ETP-ALL), as well as that of selinexor and dasatinib for NUP214-ABL1-positive ETP-ALL in vitro.	Dasatinib	273-282	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-136
29067094-1	2017	The present study aimed to evaluate the therapeutic efficacy of dasatinib in a patient with nucleoporin 214-tyrosine protein kinase ABL1 proto-oncogene 1 (NUP214-ABL1)-positive early T-cell precursor-acute lymphoblastic leukemia (ETP-ALL), as well as that of selinexor and dasatinib for NUP214-ABL1-positive ETP-ALL in vitro.	Dasatinib	273-282	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-166
29067094-1	2017	The present study aimed to evaluate the therapeutic efficacy of dasatinib in a patient with nucleoporin 214-tyrosine protein kinase ABL1 proto-oncogene 1 (NUP214-ABL1)-positive early T-cell precursor-acute lymphoblastic leukemia (ETP-ALL), as well as that of selinexor and dasatinib for NUP214-ABL1-positive ETP-ALL in vitro.	Dasatinib	273-282	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-166
29067094-3	2017	The NUP214-ABL1 gene is present in ~6% of T-ALL cases, however the prevalence of NUP214-ABL1 gene expression in ETP-ALL in particular has not yet been verified.	Ethionamide	112-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-92
29067094-12	2017	Dasatinib used in combination with traditional induction chemotherapy may reverse the high induction failure of ETP-ALL with NUP214-ABL1 fusion gene; however, further prospective studies are required to confirm this.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-136
29067094-13	2017	Therefore, selinexor with or without dasatinib may serve as a potential salvage therapy in the case of relapse and may be developed as a novel treatment for ETP-ALL with the NUP214-ABL1 fusion gene.	selinexor	11-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	181-185
28757617-1	2017	The BCR/ABL1 inhibitor Nilotinib is increasingly used to treat patients with chronic myeloid leukemia (CML).	nilotinib	23-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-12
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 Mesylate	122-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-63
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 Mesylate	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	9-12
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 Mesylate	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-17
29091939-2	2017	Dasatinib is a potent Src/Abl inhibitor and has demonstrated to have anti-proliferative and anti-invasive activity in many preclinical models.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-29
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 Mesylate	112-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	207-214
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 Mesylate	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 Mesylate	10-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-74
28848440-7	2017	We observed that OAG suppressed Hh pathway and subsequently nuclear translocation of GLI1, followed by downregulation of BCR-ABL and its downstream effectors, thus facilitating IM to induce apoptosis of K562 cells.	1-oleoyl-2-acetylglycerol	17-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
28842136-9	2017	Patients with ABL-class fusions respond clinically to ABL1 tyrosine kinase inhibitors, whereas mutations activating the JAK-STAT pathway are amendable to treatment with JAK inhibitors in vitro or in preclinical models.	lauric acid	14-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-58
28919041-2	2017	We describe the engineering of a split-cAbl kinase (sKin-Abl) that is rapidly activated in cells with rapamycin and allows temporal, dose, and compartmentalization control.	Sirolimus	102-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-43
29022905-4	2017	In this study, we found that c-Abl phosphorylated Drp1 at tyrosine 266, 368 and 449 in vitro and in vivo, which augmented the GTPase activity of Drp1 and promoted Drp1-mediated mitochondrial fragmentation.	Tyrosine	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-34
28891817-7	2017	Accordingly, inhibition of Abl/Src with bosutinib reduced FcgammaRIIA-mediated glomerular neutrophil accumulation and renal injury in experimental, crescentic anti-GBM nephritis.	bosutinib	40-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-30
28338290-4	2017	Two natural inhibitors ZINC08764498 (hit1) and ZINC12891610 (hit2) were selected by considering their high Glide docking score and critical interaction with the hinge region residue Met-318 of Abl kinase.	zinc08764498	23-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	193-196
28338290-4	2017	Two natural inhibitors ZINC08764498 (hit1) and ZINC12891610 (hit2) were selected by considering their high Glide docking score and critical interaction with the hinge region residue Met-318 of Abl kinase.	STL010856	47-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	193-196
28338290-6	2017	Further, the conformational transition, hydrogen bond interactions, and the binding energies were investigated during 10-ns molecular dynamics simulation of the Abl-hit complex.	Hydrogen	40-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-164
28300289-0	2017	Dehydrocostus Lactone Suppresses Proliferation of Human Chronic Myeloid Leukemia Cells Through Bcr/Abl-JAK/STAT Signaling Pathways.	Lactones	14-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
28300289-5	2017	We also found that dehydrocostus lactone significantly inhibits the phosphorylation expression of Bcr/Abl, STAT5, JAK2, and STAT3 and downstream molecules including p-CrkL, Mcl-1, Bcl-XL, and Bcl-2 proteins in K562 cells.	Lactones	33-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
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 Mesylate	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 Mesylate	7-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	160-167
28962554-0	2017	Propofol enhances BCR-ABL TKIs" inhibitory effects in chronic myeloid leukemia through Akt/mTOR suppression.	Propofol	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
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.	Propofol	99-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	207-214
29050692-3	2017	In particular, ponatinib, a potent pan-BCR-ABL TKI capable of overcoming the T315I mutation, holds significant promise in the treatment of Ph+ ALL, although the potential cardiovascular toxicity of this agent remains a concern.	ponatinib	15-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
29050694-5	2017	Compelling preclinical data suggest patients harboring ABL-class rearrangements are candidates for ABL1-inhibitors, whilst alterations activating the JAK-STAT pathway may be amenable to treatment with JAK inhibitors.	lauric acid	55-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-103
28578803-3	2017	Based on our previous findings indicating c-Abl hyperphosphorylation on tyrosine (Y) 412 and threonine (T) 735 upon beta1-integrin inhibition, we hypothesized c-Abl tyrosine kinase as an important mediator of beta1-integrin signaling for radioresistance.	Tyrosine	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-47
28578803-3	2017	Based on our previous findings indicating c-Abl hyperphosphorylation on tyrosine (Y) 412 and threonine (T) 735 upon beta1-integrin inhibition, we hypothesized c-Abl tyrosine kinase as an important mediator of beta1-integrin signaling for radioresistance.	Tyrosine	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-164
28578803-3	2017	Based on our previous findings indicating c-Abl hyperphosphorylation on tyrosine (Y) 412 and threonine (T) 735 upon beta1-integrin inhibition, we hypothesized c-Abl tyrosine kinase as an important mediator of beta1-integrin signaling for radioresistance.	Threonine	93-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	159-164
28578803-7	2017	In this subgroup, we observed a non-statistically significant trend between the radioresponse and phospho-c-Abl Y412.	y412	112-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-111
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 Mesylate	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 Mesylate	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-24
29296813-6	2017	In vitro screening using a panel of tyrosine kinase inhibitors against 14 different kinase alterations identified the ABL1-inhibitor, dasatinib, as a potent inhibitor of ABL-class fusions (ABL1, ABL2, CSF1R, PDGFRB), whereas the JAK1/JAK2 inhibitor ruxolitinib, was most effective against JAK-STAT-activating alterations (JAK1, JAK2, JAK3, IL7R, IL2RB), but not TYK2.	Dasatinib	134-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-122
29296813-6	2017	In vitro screening using a panel of tyrosine kinase inhibitors against 14 different kinase alterations identified the ABL1-inhibitor, dasatinib, as a potent inhibitor of ABL-class fusions (ABL1, ABL2, CSF1R, PDGFRB), whereas the JAK1/JAK2 inhibitor ruxolitinib, was most effective against JAK-STAT-activating alterations (JAK1, JAK2, JAK3, IL7R, IL2RB), but not TYK2.	Dasatinib	134-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-121
29296813-6	2017	In vitro screening using a panel of tyrosine kinase inhibitors against 14 different kinase alterations identified the ABL1-inhibitor, dasatinib, as a potent inhibitor of ABL-class fusions (ABL1, ABL2, CSF1R, PDGFRB), whereas the JAK1/JAK2 inhibitor ruxolitinib, was most effective against JAK-STAT-activating alterations (JAK1, JAK2, JAK3, IL7R, IL2RB), but not TYK2.	Dasatinib	134-143	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	189-193
29296813-6	2017	In vitro screening using a panel of tyrosine kinase inhibitors against 14 different kinase alterations identified the ABL1-inhibitor, dasatinib, as a potent inhibitor of ABL-class fusions (ABL1, ABL2, CSF1R, PDGFRB), whereas the JAK1/JAK2 inhibitor ruxolitinib, was most effective against JAK-STAT-activating alterations (JAK1, JAK2, JAK3, IL7R, IL2RB), but not TYK2.	ruxolitinib	249-260	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-122
29296813-6	2017	In vitro screening using a panel of tyrosine kinase inhibitors against 14 different kinase alterations identified the ABL1-inhibitor, dasatinib, as a potent inhibitor of ABL-class fusions (ABL1, ABL2, CSF1R, PDGFRB), whereas the JAK1/JAK2 inhibitor ruxolitinib, was most effective against JAK-STAT-activating alterations (JAK1, JAK2, JAK3, IL7R, IL2RB), but not TYK2.	ruxolitinib	249-260	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-121
28666867-0	2017	Enhancement of TGF-beta-induced Smad3 activity by c-Abl-mediated tyrosine phosphorylation of its coactivator SKI-interacting protein (SKIP).	Tyrosine	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-55
28666867-4	2017	The c-Abl inhibitor imatinib suppressed TGF-beta-induced expression of Smad3 targets as well as SKIP/Smad3 interaction.	Imatinib Mesylate	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-9
28928866-0	2017	CT-721, a Potent Bcr-Abl Inhibitor, Exhibits Excellent In Vitro and In Vivo Efficacy in the Treatment of Chronic Myeloid Leukemia.	CT-721	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
28928866-4	2017	Herein we have described a newly developed Bcr-Abl inhibitor CT-721, which displayed potent inhibitory effects on wild-type and T315I mutant Bcr-Abl.	CT-721	61-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
28928866-4	2017	Herein we have described a newly developed Bcr-Abl inhibitor CT-721, which displayed potent inhibitory effects on wild-type and T315I mutant Bcr-Abl.	CT-721	61-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-148
28928866-5	2017	It functioned as a typically ATP-competitive inhibitor, superior to other existing Bcr-Abl inhibitors.	Adenosine Triphosphate	29-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
28928866-6	2017	CT-721 also demonstrated time-dependent inhibition of Bcr-Abl activation and the resultant downstream signaling transduction pathways in Bcr-Abl positive cells.	CT-721	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
28928866-6	2017	CT-721 also demonstrated time-dependent inhibition of Bcr-Abl activation and the resultant downstream signaling transduction pathways in Bcr-Abl positive cells.	CT-721	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-144
28928866-7	2017	Furthermore, CT-721 induced cell apoptosis and cell cycle arrest, and efficaciously inhibited tumor growth in Bcr-Abl-expressed K562 and KU812 xenograft models in a mechanism-based manner.	CT-721	13-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
28928866-9	2017	Taken together, CT-721 is a potent and time-dependent Bcr-Abl kinase inhibitor, and has shown strong in vitro and in vivo anti-CML activities with a favorable pharmacokinetic profile, differentiating it from other Bcr-Abl kinase inhibitors already approved and current in development for the treatment of CML.	CT-721	16-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
28928866-9	2017	Taken together, CT-721 is a potent and time-dependent Bcr-Abl kinase inhibitor, and has shown strong in vitro and in vivo anti-CML activities with a favorable pharmacokinetic profile, differentiating it from other Bcr-Abl kinase inhibitors already approved and current in development for the treatment of CML.	CT-721	16-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	214-221
28623130-6	2017	We have here by using multiplex single cell PCR analyzed the expression of the mediators of the leukotriene pathway in bone marrow (BM) BCR-ABL+CD34+CD38- cells at diagnosis, and found low or undetectable expression of ALOX5.	Leukotrienes	96-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-143
28801299-8	2017	Western blotting showed that bortezomib treatment dose-dependently decreased the protein levels of both Mcl-1and Bcr/Abl in K562R cells without affecting bcl-2 protein expression.	Bortezomib	29-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
28801299-9	2017	CONCLUSION: Bortezomib can inhibit the proliferation of K562R cells and induce cell apoptosis possibly by down-regulating Mcl-1 and Bcr/Abl expression and enhancing Mcl-1 cleavage.	Bortezomib	12-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-139
28601294-0	2017	The c-Abl inhibitor, nilotinib, as a potential therapeutic agent for chronic cerebellar ataxia.	nilotinib	21-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-9
28601294-1	2017	Nilotinib is a potent inhibitor of tyrosine kinase BCR-ABL that penetrates the blood-brain barrier.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
28368422-6	2017	Importantly, Abl/Arg activation downstream of BRAFV600E has functional and biological significance, driving proliferation, invasion, as well as switch in epithelial-mesenchymal-transition transcription factor expression, which is known to be critical for melanoma cells to shift between differentiated and invasive states.	Arginine	17-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
28368422-7	2017	Finally, we describe findings of high translational significance by demonstrating that Abl/Arg cooperate with PI3K/Akt/PTEN, a parallel pathway that is associated with intrinsic resistance to BRAFi and immunotherapy, as Abl/Arg and Akt inhibitors cooperate to prevent viability, cell cycle progression and in vivo growth of melanomas harboring mutant BRAF/PTEN.	Arginine	91-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-90
28368422-7	2017	Finally, we describe findings of high translational significance by demonstrating that Abl/Arg cooperate with PI3K/Akt/PTEN, a parallel pathway that is associated with intrinsic resistance to BRAFi and immunotherapy, as Abl/Arg and Akt inhibitors cooperate to prevent viability, cell cycle progression and in vivo growth of melanomas harboring mutant BRAF/PTEN.	Arginine	91-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	220-223
28368422-7	2017	Finally, we describe findings of high translational significance by demonstrating that Abl/Arg cooperate with PI3K/Akt/PTEN, a parallel pathway that is associated with intrinsic resistance to BRAFi and immunotherapy, as Abl/Arg and Akt inhibitors cooperate to prevent viability, cell cycle progression and in vivo growth of melanomas harboring mutant BRAF/PTEN.	Arginine	224-227	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-90
28787438-8	2017	Among 7 kinases with high predicted affinity, we experimentally validated 4 new off-targets of tivozanib, namely the Src-family kinases FRK and FYN A, the non-receptor tyrosine kinase ABL1, and the serine/threonine kinase SLK.	tivozanib	95-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	184-188
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.	Dasatinib	56-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-17
28556300-6	2017	The resulting SNIPER(ABL)-39, in which dasatinib is conjugated to an IAP ligand LCL161 derivative by polyethylene glycol (PEG) x 3 linker, shows a potent activity to degrade the BCR-ABL protein.	Dasatinib	39-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-24
28556300-6	2017	The resulting SNIPER(ABL)-39, in which dasatinib is conjugated to an IAP ligand LCL161 derivative by polyethylene glycol (PEG) x 3 linker, shows a potent activity to degrade the BCR-ABL protein.	Dasatinib	39-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185
28556300-6	2017	The resulting SNIPER(ABL)-39, in which dasatinib is conjugated to an IAP ligand LCL161 derivative by polyethylene glycol (PEG) x 3 linker, shows a potent activity to degrade the BCR-ABL protein.	Polyethylene Glycols	101-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-24
28556300-6	2017	The resulting SNIPER(ABL)-39, in which dasatinib is conjugated to an IAP ligand LCL161 derivative by polyethylene glycol (PEG) x 3 linker, shows a potent activity to degrade the BCR-ABL protein.	Polyethylene Glycols	101-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185
28556300-6	2017	The resulting SNIPER(ABL)-39, in which dasatinib is conjugated to an IAP ligand LCL161 derivative by polyethylene glycol (PEG) x 3 linker, shows a potent activity to degrade the BCR-ABL protein.	Polyethylene Glycols	122-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-24
28556300-6	2017	The resulting SNIPER(ABL)-39, in which dasatinib is conjugated to an IAP ligand LCL161 derivative by polyethylene glycol (PEG) x 3 linker, shows a potent activity to degrade the BCR-ABL protein.	Polyethylene Glycols	122-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185
28456613-5	2017	In addition, ROS disassembles adherens junctions in epithelial cells via posttranslational mechanisms, that is, activation of Src/Abl kinases and degradation of beta-catenin/E-cadherin.	Reactive Oxygen Species	13-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-133
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 Mesylate	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
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.	Dasatinib	94-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
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.	nilotinib	108-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
28456613-6	2017	The key role of tyrosine kinases in this process is further substantiated by the rescue effect of the tyrosine kinase inhibitor genistein, and the more specific Src/Abl kinase inhibitor dasatinib: both reduced ROS-induced degradation of beta-catenin/E-cadherin in vitro and ameliorated skin damage in rodent models.	Dasatinib	186-195	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	165-168
28654842-10	2017	Post-HSCT BCR-ABL transcript positivity was a significant factor for clinical relapse after allo-HSCT in the imatinib era.	Imatinib Mesylate	109-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
27931141-2	2017	This may be due to BCR-ABL-independent, aberrant signaling pathways, one of which leads to leukotriene (LT) formation.	Leukotrienes	91-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
27931141-2	2017	This may be due to BCR-ABL-independent, aberrant signaling pathways, one of which leads to leukotriene (LT) formation.	Leukotrienes	104-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
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 Mesylate	19-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
28725163-11	2016	In all cases, the bivalent inhibitors exhibited enhanced binding affinity and selectivity for ABL1 when compared to the parental compound conjugated to SNAPtag alone.	snaptag	152-159	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-98
28719608-0	2017	Cholesterol esterification inhibition and imatinib treatment synergistically inhibit growth of BCR-ABL mutation-independent resistant chronic myelogenous leukemia.	Cholesterol	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
28719608-0	2017	Cholesterol esterification inhibition and imatinib treatment synergistically inhibit growth of BCR-ABL mutation-independent resistant chronic myelogenous leukemia.	Imatinib Mesylate	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
28719608-5	2017	Using label-free Raman spectromicroscopy, we evaluated a number of leukemia cell lines and discovered an aberrant accumulation of cholesteryl ester (CE) in CML, which was found to be a result of BCR-ABL kinase activity.	Cholesterol Esters	130-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	195-202
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).	Cholesterol	9-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	195-202
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).	avasimibe	41-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	195-202
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 Mesylate	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
28682311-0	2017	Platinum pyrithione induces apoptosis in chronic myeloid leukemia cells resistant to imatinib via DUB inhibition-dependent caspase activation and Bcr-Abl downregulation.	platinum pyrithione	0-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	146-153
28706179-3	2017	Nilotinib is a second-generation TKI, approved in 2007; it inhibits BCR-ABL, PDGFR, and c-KIT, and is 30 times more potent than imatinib.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-75
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 Mesylate	102-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-45
28599273-3	2017	Interestingly, new pre-clinically-validated analogs of Icaritin (SNG162 and SNG1153), which target abnormal ERalpha36 activity, inhibit cell growth and induce apoptosis of BCR-ABL+ leukemic cells, particularly BCR-ABL-T315I mutant cells.	icaritin	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-179
28599273-3	2017	Interestingly, new pre-clinically-validated analogs of Icaritin (SNG162 and SNG1153), which target abnormal ERalpha36 activity, inhibit cell growth and induce apoptosis of BCR-ABL+ leukemic cells, particularly BCR-ABL-T315I mutant cells.	icaritin	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	210-217
28599273-5	2017	Oral TKI dasatinib combined with potent SNG1153 inhibitor effectively eliminates infiltrated BCR-ABL+ blast cells and enhances survival of mice.	Dasatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
28599273-5	2017	Oral TKI dasatinib combined with potent SNG1153 inhibitor effectively eliminates infiltrated BCR-ABL+ blast cells and enhances survival of mice.	SNG1153	40-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
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 Mesylate	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 Mesylate	8-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-132
28682311-2	2017	T315I Bcr-Abl is the most notorious point mutation to elicit acquired resistance to imatinib (IM), leading to poor prognosis.	Imatinib Mesylate	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-13
27696211-1	2017	Five clinically approved BCR-ABL1-targeted tyrosine kinase inhibitors (bosutinib, dasatinib, imatinib, nilotinib, and ponatinib) used for treating chronic myelogenous leukemia have been studied in a neonatal rat myocyte model for their relative ability to induce myocyte damage.	bosutinib	71-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-33
27696211-1	2017	Five clinically approved BCR-ABL1-targeted tyrosine kinase inhibitors (bosutinib, dasatinib, imatinib, nilotinib, and ponatinib) used for treating chronic myelogenous leukemia have been studied in a neonatal rat myocyte model for their relative ability to induce myocyte damage.	ponatinib	118-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-33
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 Mesylate	173-181	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-72
28749919-5	2017	In this review, we outline the age-related and geographic incidence of Ph-like ALL, the association with worse clinical outcomes, and early evidence for the use of ruxolitinib (a Janus kinase 2 inhibitor) and dasatinib (a tyrosine kinase inhibitor targeting ABL1).	ruxolitinib	164-175	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	258-262
28749919-5	2017	In this review, we outline the age-related and geographic incidence of Ph-like ALL, the association with worse clinical outcomes, and early evidence for the use of ruxolitinib (a Janus kinase 2 inhibitor) and dasatinib (a tyrosine kinase inhibitor targeting ABL1).	Dasatinib	209-218	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	258-262
29200684-3	2017	There were few studies reported from India on BCR-ABL kinase mutations in imatinib failure patients.	Imatinib Mesylate	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
28224300-0	2017	Nilotinib first-line therapy in patients with Philadelphia chromosome-negative/BCR-ABL-positive chronic myeloid leukemia in chronic phase: ENEST1st sub-analysis.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
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 Mesylate	82-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	195-202
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.	Adenosine Triphosphate	160-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	195-202
27566554-3	2017	We demonstrate that sustained activation of STAT5 induced by Bcr-Abl in chronic myeloid leukemia (CML) cells promotes ROS production by repressing expression of two antioxidant enzymes, catalase and glutaredoxin-1(Glrx1).	Reactive Oxygen Species	118-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
28544567-3	2017	Herein we report the synthesis and evaluation of dedicated EPHA2 inhibitors based on the clinical BCR-ABL/SRC inhibitor dasatinib as a lead structure.	Dasatinib	120-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
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 Mesylate	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-16
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.	Dasatinib	66-75	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 Mesylate	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-135
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.	Dasatinib	33-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-135
28622336-11	2017	The performance of the proposed T2-statistic is demonstrated using five published experimental datasets: the T-cell activation, the cAMP/PKA signaling, the myoblast differentiation, and the effect of dasatinib on the BCR-ABL pathway are proteomic datasets produced by mass spectrometry; and the protective effect of myocilin via the MAPK signaling pathway is a gene expression dataset of limited sample size.	Dasatinib	200-209	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	217-224
28378189-5	2017	Serine and tyrosine phosphorylation of galectin-3 by c-Abl, CKI, and GSK-3beta could regulate its localization and associated signal transduction.	Serine	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-58
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 Mesylate	148-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-37
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 Mesylate	20-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-90
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 Mesylate	174-182	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
27883218-2	2017	In this study, we analyzed tyrosine phosphorylation of FoxA1 by the non-receptor-type tyrosine kinase c-Abl.	Tyrosine	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-107
27883218-8	2017	In contrast, the c-Abl inhibitor imatinib reduced its activation.	Imatinib Mesylate	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-22
28596663-9	2017	Our Patient detected rare BCR-ABL fusion variant e8a2 was on imatinib 400 mg since last 3 months.	Imatinib Mesylate	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
27353341-6	2017	Detailed investigations of the selected drugs in the allosteric site of Abl kinase, using molecular dynamics and steered molecular dynamics simulation shows that gefitinib, an EGFR inhibitor approved for the treatment of lung cancer, could bind effectively to the allosteric site of Bcr-Abl.	Gefitinib	162-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	283-290
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.	Gefitinib	20-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
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 Mesylate	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
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.	Adenosine Triphosphate	90-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
28458002-6	2017	It was invigorating to identify that chlorohexidine, paromomycin and deferoxamine could inhibit the wild-type ABL1, while chlorohexidine and ritonavir could inhibit the T315I mutant ABL1.	Chlorhexidine	37-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-114
28458002-6	2017	It was invigorating to identify that chlorohexidine, paromomycin and deferoxamine could inhibit the wild-type ABL1, while chlorohexidine and ritonavir could inhibit the T315I mutant ABL1.	Chlorhexidine	37-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-186
28458002-6	2017	It was invigorating to identify that chlorohexidine, paromomycin and deferoxamine could inhibit the wild-type ABL1, while chlorohexidine and ritonavir could inhibit the T315I mutant ABL1.	Paromomycin	53-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-114
28458002-6	2017	It was invigorating to identify that chlorohexidine, paromomycin and deferoxamine could inhibit the wild-type ABL1, while chlorohexidine and ritonavir could inhibit the T315I mutant ABL1.	Deferoxamine	69-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-114
28458002-6	2017	It was invigorating to identify that chlorohexidine, paromomycin and deferoxamine could inhibit the wild-type ABL1, while chlorohexidine and ritonavir could inhibit the T315I mutant ABL1.	Deferoxamine	69-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-186
28458002-6	2017	It was invigorating to identify that chlorohexidine, paromomycin and deferoxamine could inhibit the wild-type ABL1, while chlorohexidine and ritonavir could inhibit the T315I mutant ABL1.	Chlorhexidine	122-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-186
28458002-6	2017	It was invigorating to identify that chlorohexidine, paromomycin and deferoxamine could inhibit the wild-type ABL1, while chlorohexidine and ritonavir could inhibit the T315I mutant ABL1.	Ritonavir	141-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-186
28488190-0	2017	Computational dissection of allosteric inhibition of the SH2 domain of Bcr-Abl kinase by the monobody inhibitor AS25.	as25	112-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
28488190-3	2017	An I164E mutation in the SH2 domain disrupts AS25 binding to the SH2 domain of Bcr-Abl.	as25	45-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
28378189-5	2017	Serine and tyrosine phosphorylation of galectin-3 by c-Abl, CKI, and GSK-3beta could regulate its localization and associated signal transduction.	Tyrosine	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-58
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 Mesylate	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-112
27608133-10	2017	The key disease targets of leukemia namely tyrosine kinase (ABL1), aurora-like kinase (AUKRB), and polo-like kinase (PLK-2) showed that they had the comparable binding affinities of -9.7 k cal/mol, -8.7 k cal/mol, and -8.6 k cal/mol, respectively with curcumin.	Curcumin	252-260	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-64
28555614-3	2017	In this study, differentially expressed genes (DEGs) regulated by c-Abl/Arg were identified, and related cellular functions and associated pathways were investigated.	Arginine	72-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-71
28555614-7	2017	RESULTS A total of 1,034 DEGs were significantly regulated by c-Abl/Arg (399 were up-regulated and 635 were down-regulated after c-Abl/Arg double knockdown).	Arginine	68-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-67
28555614-7	2017	RESULTS A total of 1,034 DEGs were significantly regulated by c-Abl/Arg (399 were up-regulated and 635 were down-regulated after c-Abl/Arg double knockdown).	Arginine	68-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-134
28555614-7	2017	RESULTS A total of 1,034 DEGs were significantly regulated by c-Abl/Arg (399 were up-regulated and 635 were down-regulated after c-Abl/Arg double knockdown).	Arginine	135-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-67
28555614-9	2017	CONCLUSIONS Our data collectively support the hypothesis that c-Abl/Arg regulate differential gene expression, providing new insights into the biological functions of c-Abl and Arg.	Arginine	68-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-172
28555614-9	2017	CONCLUSIONS Our data collectively support the hypothesis that c-Abl/Arg regulate differential gene expression, providing new insights into the biological functions of c-Abl and Arg.	Arginine	177-180	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-67
28365527-0	2017	Imatinib discontinuation in chronic myeloid leukaemia patients with undetectable BCR-ABL transcript level: A systematic review and a meta-analysis.	Imatinib Mesylate	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 Mesylate	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
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 Mesylate	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 Mesylate	113-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
27890928-0	2017	Identification and characterization of activating ABL1 1b kinase mutations: impact on sensitivity to ATP-competitive and allosteric ABL1 inhibitors.	Adenosine Triphosphate	101-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-54
27890928-7	2017	Collectively, our findings support clinical investigation of ATP-competitive TKIs in malignancies harboring ABL1 point mutations, and sequencing of BCR-ABL1 and ABL1 1b in patients with acquired resistance to allosteric ABL1 inhibitors.	Adenosine Triphosphate	61-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-112
28455521-3	2017	Since intracellular effective TKIs must enter the cell to reach their intracellular targets, here we investigated the interaction of the TKI saracatinib, a dual inhibitor of c-Src and c-Abl signaling, with transporters for organic cations as well as the role of these transporters for the biological effect of saracatinib in human RA-synovial fibroblasts (hRASF).	saracatinib	141-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	184-189
28372728-3	2017	In the presence of methylene blue (MB) as an intercalator, the hybridization of QDs-(N)DNA with the target BCR/ABL fusion gene (complementary DNA), brings the MB (acceptor) at close proximity of the QDs (donor), leading to FRET upon photoexcitation of the QDs.	Methylene Blue	19-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
28372728-3	2017	In the presence of methylene blue (MB) as an intercalator, the hybridization of QDs-(N)DNA with the target BCR/ABL fusion gene (complementary DNA), brings the MB (acceptor) at close proximity of the QDs (donor), leading to FRET upon photoexcitation of the QDs.	Methylene Blue	35-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
28427224-4	2017	The goal of this study was to determine whether ponatinib, an FDA-approved ABL/SRC inhibitor, reduced proliferation and/or survival of merlin-deficient human Schwann cells (HSC).	ponatinib	48-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-78
28486134-0	2017	Abl Regulates Planar Polarized Junctional Dynamics through beta-Catenin Tyrosine Phosphorylation.	Tyrosine	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
27856601-0	2017	Axl Blockade by BGB324 Inhibits BCR-ABL Tyrosine Kinase Inhibitor-Sensitive and -Resistant Chronic Myeloid Leukemia.	bemcentinib	16-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
27856601-7	2017	BGB324 also inhibits BCR-ABL TKI-resistant cells, including T315I-mutated and ponatinib-resistant primary cells.	bemcentinib	0-6	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
28475010-1	2017	The ABL kinase inhibitor imatinib has been used as front-line therapy for Philadelphia-positive chronic myeloid leukemia.	Imatinib Mesylate	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 Mesylate	37-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-112
28428613-4	2017	In this report, we identify Abl-mediated phosphorylation of a highly conserved Tyr residue in the P + 1 loop of protein kinase D2 (PKD2) during oxidative stress.	Tyrosine	79-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-31
28323047-11	2017	The biocomponents of CCL were chemical characterized and we identify cynaropicrin and its deacyl derivative having the capability to down-regulate the p210BCR/ABL oncoprotein.	Cefaclor	21-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-162
28323047-11	2017	The biocomponents of CCL were chemical characterized and we identify cynaropicrin and its deacyl derivative having the capability to down-regulate the p210BCR/ABL oncoprotein.	cynaropicrin	69-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-162
28103625-0	2017	Phase II study of imatinib-based chemotherapy for newly diagnosed BCR-ABL-positive acute lymphoblastic leukemia.	Imatinib Mesylate	18-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
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 Mesylate	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
28278078-2	2017	In recent years, compound BCR-ABL mutations have emerged as a new threat to CML patients by causing higher degrees of resistance involving multiple TKIs, including ponatinib.	ponatinib	164-173	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
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 Mesylate	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 Mesylate	165-173	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
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.	3-((3-trifluoromethyl)phenyl)-5-((3-carboxyphenyl)methylene)-2-thioxo-4-thiazolidinone	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
28469513-0	2017	BCR-ABL V280G Mutation, Potential Role in Imatinib Resistance: First Case Report.	Imatinib Mesylate	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
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 Mesylate	151-159	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
28103625-2	2017	We conducted a phase II trial of imatinib-combined chemotherapy for newly diagnosed BCR-ABL-positive ALL in adults.	Imatinib Mesylate	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
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 Mesylate	121-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-4
28283735-2	2017	Dasatinib, a BCR-ABL1 tyrosine kinase inhibitor (TKI) approved for the treatment of chronic myelogenous leukemia, has been associated with PAH.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
28329763-3	2017	Second-generation ABL1 kinase inhibitors induce more potent molecular responses in both previously untreated and imatinib-resistant patients with CML.	Imatinib Mesylate	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-22
28329763-5	2017	Here we characterize ABL001 (asciminib), a potent and selective allosteric ABL1 inhibitor that is undergoing clinical development testing in patients with CML and Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukaemia.	asciminib	21-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-79
28329763-5	2017	Here we characterize ABL001 (asciminib), a potent and selective allosteric ABL1 inhibitor that is undergoing clinical development testing in patients with CML and Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukaemia.	asciminib	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-79
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 Mesylate	8-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
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 Mesylate	18-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
28267803-0	2017	Correction: MicroRNA-1301-Mediated RanGAP1 Downregulation Induces BCR-ABL Nuclear Entrapment to Enhance Imatinib Efficacy in Chronic Myeloid Leukemia Cells.	Imatinib Mesylate	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
28087699-3	2017	Here we report that the c-Abl non-receptor kinase phosphorylates DDB1 at residue Tyr-316 to recruit a small regulatory protein, DDA1, leading to increased substrate ubiquitination.	Tyrosine	81-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-29
28087699-4	2017	Pharmacological inhibition or genetic ablation of the Abl-DDB1-DDA1 axis decreases the ubiquitination of CRL4 substrates, including IKZF1 and IKZF3, in lenalidomide-treated multiple myeloma cells.	crl4	105-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-57
28087699-4	2017	Pharmacological inhibition or genetic ablation of the Abl-DDB1-DDA1 axis decreases the ubiquitination of CRL4 substrates, including IKZF1 and IKZF3, in lenalidomide-treated multiple myeloma cells.	Lenalidomide	152-164	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-57
28087699-5	2017	Importantly, panobinostat, a recently approved anti-myeloma drug, and dexamethasone enhance lenalidomide-induced substrate degradation and cytotoxicity by activating c-Abl, therefore providing a mechanism underlying their combination with lenalidomide to treat multiple myeloma.	Panobinostat	13-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-171
28087699-5	2017	Importantly, panobinostat, a recently approved anti-myeloma drug, and dexamethasone enhance lenalidomide-induced substrate degradation and cytotoxicity by activating c-Abl, therefore providing a mechanism underlying their combination with lenalidomide to treat multiple myeloma.	Dexamethasone	70-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-171
28087699-5	2017	Importantly, panobinostat, a recently approved anti-myeloma drug, and dexamethasone enhance lenalidomide-induced substrate degradation and cytotoxicity by activating c-Abl, therefore providing a mechanism underlying their combination with lenalidomide to treat multiple myeloma.	Lenalidomide	92-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-171
28087699-5	2017	Importantly, panobinostat, a recently approved anti-myeloma drug, and dexamethasone enhance lenalidomide-induced substrate degradation and cytotoxicity by activating c-Abl, therefore providing a mechanism underlying their combination with lenalidomide to treat multiple myeloma.	Lenalidomide	239-251	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-171
28279034-9	2017	Conclusion: ACA often emerged during the disease progress in CML patients, regular and timely detection of chromosomes karyotype and ABL tyrosine point mutations during TKI treatment was important for therapeutic evaluation, progress and prognosis of CML.	Tyrosine	137-145	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-136
28288113-6	2017	We overexpressed the mutant constructs in HEK 293T cells and observed increased tyrosine phosphorylation, suggesting increased ABL1 kinase activities associated with both the p.Tyr245Cys and p.Ala356Thr substitutions.	Tyrosine	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-131
28184964-1	2017	PURPOSE: Ponatinib is a novel tyrosine kinase inhibitor (TKI) specifically designed to inhibit native and mutated BCR-ABL.	ponatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
27848186-0	2017	Dasatinib induces autophagy in mice with Bcr-Abl-positive leukemia.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
27848186-1	2017	Dasatinib, a second-generation tyrosine kinase inhibitor, is a highly effective treatment for Bcr-Abl-positive leukemia.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
27848186-5	2017	Here, we report that dasatinib induces autophagy in Bcr-Abl-positive leukemia cell lines and further show the induction of autophagy in an immunodeficient mouse model of human Bcr-Abl-positive leukemia with central nervous system (CNS) infiltration.	Dasatinib	21-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
27848186-5	2017	Here, we report that dasatinib induces autophagy in Bcr-Abl-positive leukemia cell lines and further show the induction of autophagy in an immunodeficient mouse model of human Bcr-Abl-positive leukemia with central nervous system (CNS) infiltration.	Dasatinib	21-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	176-183
26982633-4	2017	In this work, we employed energy optimized multiple pharmacophore modeling strategy from multiple c-Abl structures bound with ligands in the inactive ATP binding conformation (DFG-out).	Adenosine Triphosphate	150-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-103
26982633-4	2017	In this work, we employed energy optimized multiple pharmacophore modeling strategy from multiple c-Abl structures bound with ligands in the inactive ATP binding conformation (DFG-out).	1,3-Diphenylguanidine	176-179	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-103
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 Mesylate	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
28076826-4	2017	Enzymatic assays against a mini-panel of kinases (Src, Fyn, EGFR, Kit, Flt3, Abl, AblT315I) have been performed, showing an unexpected selectivity of our pyrrolo[2,3-d]pyrimidines for Src.	Pyrrolo(2,3-d)pyrimidine	154-179	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-80
27761606-0	2017	BCR-ABL-positive acute myeloid leukemia: About one case treated with ponatinib.	ponatinib	69-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
27718039-2	2017	The first line treatment for CML consists on BCR-ABL inhibitors such as Imatinib.	Imatinib Mesylate	72-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
27864605-0	2017	Erratum to: BCR-ABL-positive acute myeloid leukemia: About one case treated with ponatinib.	ponatinib	81-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
28141795-8	2017	Importantly, in vivo data showed that the deficiency of MAVS or c-Abl prevented MPTP-induced microglial activation and dopaminergic neuron loss.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	80-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-69
27686674-5	2017	RT-PCR revealed the major BCR-ABL fusion transcript, and CML in the chronic phase was diagnosed, followed by nilotinib treatment.	nilotinib	109-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
26628269-7	2017	Statistical analysis revealed good correlation between PaCO2 by IRMA and ABL (R2 = 0.766; p &lt; 0.01) as well as between PTCCO2 and ABL (R2 = 0.619; p &lt; 0.01), whereas correlation between PETCO2 and ABL was weaker (R2 = 0.405; p &lt; 0.01).	paco2	55-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-76
28213007-3	2017	A recent report suggested that dasatinib (an ABL/Src kinase inhibitor) inhibits EMT induced by transforming growth factor (TGF)-beta in lung cancer cells (Wilson et al., 2014).	Dasatinib	31-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-48
28573218-9	2017	The hexane extract decreased Bcr/Abl protein expression in K562 cells by 74.6% and WT1 protein expressions in Molt4 and K562 cells by 68.4 and 72.1%, respectively.	Hexanes	4-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
28573218-12	2017	CONCLUSION: The hexane fraction from M. siamensis flowers inhibited cell proliferation via the suppression of WT1 expression in Molt4 and K562 cells and Bcr/Abl expression in K562 cells.	Hexanes	16-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
27777238-8	2017	Similarly, superior efficacy of combined gedatolisib and dasatinib was observed in ABL/PDGFR-mutant models (P &lt; .001).	gedatolisib	41-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-86
27777238-8	2017	Similarly, superior efficacy of combined gedatolisib and dasatinib was observed in ABL/PDGFR-mutant models (P &lt; .001).	Dasatinib	57-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-86
27966954-1	2017	The discovery of a novel potent type II ABL/c-KIT dual kinase inhibitor compound 34 (CHMFL-ABL/KIT-155), which utilized a hydrogen bond formed by NH on the kinase backbone and carbonyl oxygen of 34 as a unique hinge binding, is described.	Hydrogen	122-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-43
27966954-1	2017	The discovery of a novel potent type II ABL/c-KIT dual kinase inhibitor compound 34 (CHMFL-ABL/KIT-155), which utilized a hydrogen bond formed by NH on the kinase backbone and carbonyl oxygen of 34 as a unique hinge binding, is described.	Oxygen	185-191	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-43
27875633-2	2017	The dasatinib-l-arginine derivative (Das-R, 7) was found to be the most potent of the inhibitors tested, with IC50 values of 4.4, &lt;0.25, and &lt;0.45 nm against Csk, Src, and Abl kinases, respectively.	dasatinib-l-arginine	4-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-181
27875633-5	2017	Compounds 15 (Das-glutamic acid) and 13 (Das-cysteine) demonstrated the largest gains (10.2 and 10.3 Abl/Src IC50 ratios).	das-glutamic acid	14-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-104
27875633-5	2017	Compounds 15 (Das-glutamic acid) and 13 (Das-cysteine) demonstrated the largest gains (10.2 and 10.3 Abl/Src IC50 ratios).	das-cysteine	41-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-104
27903968-0	2017	Novel Src/Abl tyrosine kinase inhibitor bosutinib suppresses neuroblastoma growth via inhibiting Src/Abl signaling.	bosutinib	40-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-13
27903968-0	2017	Novel Src/Abl tyrosine kinase inhibitor bosutinib suppresses neuroblastoma growth via inhibiting Src/Abl signaling.	bosutinib	40-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-104
27903968-4	2017	In this paper, we report that the potent dual Src/Abl inhibitor bosutinib exerts anti-tumor effects on NB.	bosutinib	64-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-53
27903968-6	2017	Mechanistically, bosutinib effectively decreased the activity of Src/Abl and PI3K/AKT/mTOR, MAPK/ERK, and JAK/STAT3 signaling pathways.	bosutinib	17-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-72
27904889-0	2017	Reactive oxygen species in BCR-ABL1-expressing cells - relevance to chronic myeloid leukemia.	Reactive Oxygen Species	0-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-35
28044939-1	2017	In a series of studies carried out over the last couple of years in various cell types, it was observed that the experimentally used Src family kinase inhibitors PP1 and PP2 and the clinically used Src/Abl inhibitors AZM475271 and dasatinib are potent inhibitors of TGF-beta mediated cellular responses such as Smad and p38 mitogen-activated protein kinase phosphorylation, Smad-dependent transcriptional activation, growth inhibition, epithelial-mesenchymal transition (EMT), and cell motility.	AZM475271	217-226	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	202-205
28044939-1	2017	In a series of studies carried out over the last couple of years in various cell types, it was observed that the experimentally used Src family kinase inhibitors PP1 and PP2 and the clinically used Src/Abl inhibitors AZM475271 and dasatinib are potent inhibitors of TGF-beta mediated cellular responses such as Smad and p38 mitogen-activated protein kinase phosphorylation, Smad-dependent transcriptional activation, growth inhibition, epithelial-mesenchymal transition (EMT), and cell motility.	Dasatinib	231-240	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	202-205
28044939-3	2017	In contrast, the anti-TGF-beta effect of yet another Src/Abl inhibitor, bosutinib, is more variable with respect to the type of the TGF-beta response and the cell type affected, and lacks a clear dose-dependency.	bosutinib	72-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-60
28403779-1	2017	BACKGROUND: Chronic myeloid leukemia (CML) is currently treated with imatinib, a Bcr-Abl inhibitor.	Imatinib Mesylate	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-88
28403779-3	2017	Triptolide, a diterpenoid triepoxide, has been shown active against CML cells resistant to imatinib, acting mainly on the level of Bcr-Abl transcription inhibition.	triptolide	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
28403779-3	2017	Triptolide, a diterpenoid triepoxide, has been shown active against CML cells resistant to imatinib, acting mainly on the level of Bcr-Abl transcription inhibition.	triepoxide	26-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	131-138
27889234-14	2017	Molecular docking studies suggest that ICA may possibly exhibit its anticancer effect by inhibiting EGFR in A549, Bcr-Abl in K562 and GSK-3beta kinase in SW480 cell line.	isocyanic acid	39-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
28160873-8	2017	At 25 months, bone mineral density percentage change from ACTIVE baseline for ABL-SC/ALN vs PBO/ALN was as follows: lumbar spine, 12.8%; total hip, 5.5%; femoral neck, 4.5% vs 3.5%, 1.4%, 0.5%, respectively (group differences at all sites P&lt;.001).	Alendronate	85-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-81
28245378-1	2017	OBJECTIVE: To investigate the effects of Btk inhibitor (PCI-32765) and BCR-ABL tyrosine kinase inhibitor (Dasatinib) on proliferation and apoptosis of acute lymphoblastic leukemia (ALL) cell lines (Sup-B15, RS4;11) and the possible mechanism.	Dasatinib	106-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
28245378-8	2017	PCI-32765 and Dasatinib could decrease the expression and activity of BCR-ABL, Btk, Lyn, Src in Sup-B15 and RS4;11 cells.	Dasatinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
26628269-9	2017	Arterial CO2 partial pressure by IRMA (PaCO2) and PTCCO2 provided greater accuracy compared to the reference measurement (ABL) than the end-tidal CO2 measurements in critically ill in mechanically ventilated patients patients.	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	9-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-125
27845183-6	2017	This change of partners is under the control of a tyrosine phosphorylation of Mtx1 by c-Abl.	Tyrosine	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-91
27965460-0	2017	Opposing roles of KIT and ABL1 in the therapeutic response of gastrointestinal stromal tumor (GIST) cells to imatinib mesylate.	Imatinib Mesylate	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 Mesylate	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 Mesylate	29-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	173-177
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 Mesylate	112-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-93
29375916-0	2017	Late Emergence of an Imatinib-Resistant ABL1 Kinase Domain Mutation in a Patient with Chronic Myeloid Leukemia.	Imatinib Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	113-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-45
28743118-2	2017	Given the loss of major molecular response, we switched treatment to dasatinib 100 mg daily, observing a reduction in BCR-ABL transcript, a significant improvement of anemia, and a gradual disappearance of fibrosis.	Dasatinib	69-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
28828991-12	2017	Nevertheless, owing to the similar pharmacological properties with Rebastinib, Pubchem ID: 67254402 can be expected to form potential BCR-ABL inhibitor.	rebastinib	67-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-141
27718000-1	2017	PURPOSE: Bosutinib is an oral, dual Src and Abl tyrosine kinase inhibitor (TKI) approved for the treatment of Philadelphia chromosome-positive chronic myeloid leukemia resistant or intolerant to prior TKI therapy.	bosutinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-47
27901368-5	2017	Other drugs, such as ABL001, which targets the myristoyl pocket of the ABL1 kinase, are currently in development, to offer therapeutic alternatives for resistant patients to ATP-binders.	Adenosine Triphosphate	174-177	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-75
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.	Dasatinib	122-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
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.	nilotinib	133-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
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.	ponatinib	147-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
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 Mesylate	285-293	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
28143387-4	2017	First and second generation Bcr-Abl inhibitors have focused on targeting the ATP-binding domain of the kinase.	Adenosine Triphosphate	77-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
28143387-11	2017	The possibility of using this model for the design of drugs for the treatment of &amp;#946;-thalassemia and sickle cell disease (SCD), since several Bcr-Abl inhibitors are able to promote erythroid differentiation and &amp;#947;-globin expression in CML cell lines and primary erythroid cells is discussed.	Adenosine Monophosphate	82-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
28143387-11	2017	The possibility of using this model for the design of drugs for the treatment of &amp;#946;-thalassemia and sickle cell disease (SCD), since several Bcr-Abl inhibitors are able to promote erythroid differentiation and &amp;#947;-globin expression in CML cell lines and primary erythroid cells is discussed.	Adenosine Monophosphate	219-222	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
28978850-11	2017	Several proteins, such as BRD4 and BCR-ABL, have been successfully degraded by CRL4CRBN using these technologies.	crl4crbn	79-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
27892697-6	2017	DAE inhibitory effect was associated with the dephosphorylation of the BCR-ABL kinase and interfered with ERK1/2, Akt, and STAT5 pathways.	o,p-dinitrophenyl aminoethyldiphosphate-beryllium trifluoride	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-78
27717999-1	2017	PURPOSE: Bosutinib, a dual Src and Abl tyrosine kinase inhibitor for the treatment of chronic myeloid leukemia, demonstrated concentration-dependent inhibitory effects on P-glycoprotein (P-gp)-mediated digoxin efflux in vitro, suggesting that bosutinib may inhibit P-gp substrates.	bosutinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
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.	Celecoxib	235-244	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	345-352
30167550-2	2016	Imatinib and dasatinib are 2 BCR-ABL tyrosine kinase inhibitors (TKI) used in the treatment of CML.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
30167550-2	2016	Imatinib and dasatinib are 2 BCR-ABL tyrosine kinase inhibitors (TKI) used in the treatment of CML.	Dasatinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
27852045-2	2016	We previously showed that BCR/Abl protein is suppressed in low oxygen, where viable cells retain stem cell potential.	Oxygen	63-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
27852045-3	2016	This study addressed the regulation of BCR/Abl protein expression under oxygen or glucose shortage, characteristic of the in vivo environment where cells resistant to tyrosine kinase inhibitors (TKi) persist.	Oxygen	72-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
27852045-3	2016	This study addressed the regulation of BCR/Abl protein expression under oxygen or glucose shortage, characteristic of the in vivo environment where cells resistant to tyrosine kinase inhibitors (TKi) persist.	Glucose	82-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
27852045-5	2016	BCR/abl mRNA steady-state analysis and ChIP-qPCR on BCR promoter revealed that BCR/abl transcriptional activity is reduced in K562 cells under oxygen shortage.	Oxygen	143-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
27852045-5	2016	BCR/abl mRNA steady-state analysis and ChIP-qPCR on BCR promoter revealed that BCR/abl transcriptional activity is reduced in K562 cells under oxygen shortage.	Oxygen	143-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
27852045-7	2016	However, only low oxygen decreased polysome-associated BCR/abl mRNA significantly in KCL22 cells, suggesting a decreased BCR/Abl translation.	Oxygen	18-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
27852045-7	2016	However, only low oxygen decreased polysome-associated BCR/abl mRNA significantly in KCL22 cells, suggesting a decreased BCR/Abl translation.	Oxygen	18-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
27852045-8	2016	The proteasome inhibitor MG132 or the pan-caspase inhibitor z-VAD-fmk extended BCR/Abl expression under oxygen/glucose shortage in K562 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
27852045-8	2016	The proteasome inhibitor MG132 or the pan-caspase inhibitor z-VAD-fmk extended BCR/Abl expression under oxygen/glucose shortage in K562 cells.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	60-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
27852045-8	2016	The proteasome inhibitor MG132 or the pan-caspase inhibitor z-VAD-fmk extended BCR/Abl expression under oxygen/glucose shortage in K562 cells.	Oxygen	104-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
27852045-8	2016	The proteasome inhibitor MG132 or the pan-caspase inhibitor z-VAD-fmk extended BCR/Abl expression under oxygen/glucose shortage in K562 cells.	Glucose	111-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
27852045-9	2016	Glucose shortage induced autophagy-dependent BCR/Abl protein degradation in KCL22 cells.	Glucose	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
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.	Celecoxib	15-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	345-352
27531525-1	2016	Bosutinib is an Src/Abl tyrosine kinase inhibitor (TKI) indicated for adults with Ph+ chronic myeloid leukemia (CML) resistant/intolerant to prior TKIs.	bosutinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-23
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 Mesylate	111-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-100
27693719-0	2016	Attomolar electrochemical detection of the BCR/ABL fusion gene based on an amplifying self-signal metal nanoparticle-conducting polymer hybrid composite.	Metals	98-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
27693719-0	2016	Attomolar electrochemical detection of the BCR/ABL fusion gene based on an amplifying self-signal metal nanoparticle-conducting polymer hybrid composite.	Polymers	128-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
27693719-2	2016	In the present study, we describe the construction and use of an electrochemical DNA biosensor based on a nanostructured polyaniline-gold composite, specifically developed for the detection of the BCR/ABL chimeric oncogene.	polyaniline	121-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	197-204
28191543-0	2016	The third-time chronic myeloid leukemia in lymphoblastic crisis with ABL1 kinase mutation induced by decitabine, dexamethason combined with nilotinib and dasatinib.	Decitabine	101-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-73
28191543-0	2016	The third-time chronic myeloid leukemia in lymphoblastic crisis with ABL1 kinase mutation induced by decitabine, dexamethason combined with nilotinib and dasatinib.	Dexamethasone	113-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-73
28191543-0	2016	The third-time chronic myeloid leukemia in lymphoblastic crisis with ABL1 kinase mutation induced by decitabine, dexamethason combined with nilotinib and dasatinib.	nilotinib	140-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-73
28191543-0	2016	The third-time chronic myeloid leukemia in lymphoblastic crisis with ABL1 kinase mutation induced by decitabine, dexamethason combined with nilotinib and dasatinib.	Dasatinib	154-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-73
28024479-12	2016	Tetracycline induced its expression for 48 h and 72 h. pTER117, pTER363 decreased the mRNA level of BCR/ABL 90%, 82% and 91.5%, 84%, respectively, P210 protein were almost measured in K562 cells.	Tetracycline	0-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
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 Mesylate	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 Mesylate	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-110
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.	nilotinib	53-62	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.	nilotinib	53-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-110
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.	olverembatinib	67-73	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.	olverembatinib	67-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-110
27884201-0	2016	Nickel pyrithione induces apoptosis in chronic myeloid leukemia cells resistant to imatinib via both Bcr/Abl-dependent and Bcr/Abl-independent mechanisms.	nickel pyrithione	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-108
27884201-0	2016	Nickel pyrithione induces apoptosis in chronic myeloid leukemia cells resistant to imatinib via both Bcr/Abl-dependent and Bcr/Abl-independent mechanisms.	nickel pyrithione	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-130
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 Mesylate	21-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
27884201-5	2016	In this present study, we investigated the effect of NiPT, a novel proteasomal deubiquitinase inhibitor, on cell survival or apoptosis in CML cells bearing Bcr-Abl-T315I or wild-type Bcr-Abl.	dichlorobis(azomycin)platinum II	53-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
27884201-12	2016	RESULTS: NiPT induced apoptosis in CML cells and inhibited the growth of IM-resistant Bcr-Abl-T315I xenografts in nude mice.	dichlorobis(azomycin)platinum II	9-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
27884201-13	2016	Mechanistically, NiPT induced decreases in Bcr-Abl proteins, which were associated with downregulation of Bcr-Abl transcription and with the cleavage of Bcr-Abl protein by activated caspases.	dichlorobis(azomycin)platinum II	17-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
27884201-13	2016	Mechanistically, NiPT induced decreases in Bcr-Abl proteins, which were associated with downregulation of Bcr-Abl transcription and with the cleavage of Bcr-Abl protein by activated caspases.	dichlorobis(azomycin)platinum II	17-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
27884201-13	2016	Mechanistically, NiPT induced decreases in Bcr-Abl proteins, which were associated with downregulation of Bcr-Abl transcription and with the cleavage of Bcr-Abl protein by activated caspases.	dichlorobis(azomycin)platinum II	17-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
27884201-14	2016	NiPT-induced ubiquitin proteasome system inhibition induced caspase activation in both IM-resistant and IM-sensitive CML cells, and the caspase activation was required for NiPT-induced Bcr-Abl downregulation and apoptotic cell death.	dichlorobis(azomycin)platinum II	0-4	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	185-192
27884201-14	2016	NiPT-induced ubiquitin proteasome system inhibition induced caspase activation in both IM-resistant and IM-sensitive CML cells, and the caspase activation was required for NiPT-induced Bcr-Abl downregulation and apoptotic cell death.	dichlorobis(azomycin)platinum II	172-176	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	185-192
27884201-15	2016	CONCLUSIONS: These findings support that NiPT can overcome IM resistance through both Bcr-Abl-dependent and Bcr-Abl-independent mechanisms, providing potentially a new option for CML treatment.	dichlorobis(azomycin)platinum II	41-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
27884201-15	2016	CONCLUSIONS: These findings support that NiPT can overcome IM resistance through both Bcr-Abl-dependent and Bcr-Abl-independent mechanisms, providing potentially a new option for CML treatment.	dichlorobis(azomycin)platinum II	41-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
27699828-7	2017	The effect of the Src-Abl inhibitor PD 180970 was further characterized using cell-proliferation assays, quantitative PCR, and western blot analysis in multiple hormone-sensitive and CRPC cell lines.	PD 180970	36-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-25
27699828-10	2017	The Src-Abl dual kinase inhibitor PD180970 decreased expression of AR-V7 by greater than 46% and decreased ligand-independent transcription of AR target genes in the 22RV1 human prostate carcinoma cell line.	PD 180970	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-11
27989101-0	2016	Cantharidin Overcomes Imatinib Resistance by Depleting BCR-ABL in Chronic Myeloid Leukemia.	Cantharidin	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
27989101-0	2016	Cantharidin Overcomes Imatinib Resistance by Depleting BCR-ABL in Chronic Myeloid Leukemia.	Imatinib Mesylate	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
27989101-10	2016	These findings indicated that CTD overcomes imatinib resistance through depletion of BCR-ABL.	Imatinib Mesylate	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
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 Mesylate	99-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
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 Mesylate	25-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
27864817-1	2016	BACKGROUND: Nilotinib inhibits the tyrosine kinase activities of ABL1/BCR-ABL1, KIT, and platelet-derived growth factor receptors (PDGFRs).	nilotinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-69
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.	Celecoxib	245-254	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	345-352
27806266-0	2016	Kinetic Insights into the Binding between the nSH3 Domain of CrkII and Proline-Rich Motifs in cAbl.	Proline	71-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-98
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 Mesylate	158-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-69
27682200-2	2016	First, only the open conformation of the Abl kinase domain"s activation loop (A-loop) favors ATP binding to the catalytic cleft.	Adenosine Triphosphate	93-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-44
27682200-3	2016	In this regard, the trans-autophosphorylation of the Y412 residue, which is located along the A-loop, favors the stability of the open conformation, in turn enhancing Abl activity.	y412	53-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-170
27682200-4	2016	Another key factor for full Abl activity is the formation of active conformations of the catalytic DFG motif in the Abl kinase domain.	1,3-Diphenylguanidine	99-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-31
27682200-4	2016	Another key factor for full Abl activity is the formation of active conformations of the catalytic DFG motif in the Abl kinase domain.	1,3-Diphenylguanidine	99-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-119
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 Mesylate	145-162	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	219-226
28030911-10	2016	Conclusion: D. pentandra methanol extract exerts potentanti-proliferative effect on BCR/ABL positive K562 cells.	pentandra methanol	15-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
27474918-0	2016	Novel pyrazolo[3,4-d]pyrimidines as dual Src-Abl inhibitors active against mutant form of Abl and the leukemia K-562 cell line.	pyrazolo(3,4-d)pyrimidine	6-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-48
27474918-0	2016	Novel pyrazolo[3,4-d]pyrimidines as dual Src-Abl inhibitors active against mutant form of Abl and the leukemia K-562 cell line.	pyrazolo(3,4-d)pyrimidine	6-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-93
27806266-2	2016	This interaction starts with the binding of the N-terminal Src homology 3 (nSH3) domain of CrkII to the proline-rich motifs of cAbl (PRMscAbl).	Proline	104-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-131
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 Mesylate	261-278	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
27666407-0	2016	Depression accelerates the development of gastric cancer through reactive oxygen species-activated ABL1 (Review).	Reactive Oxygen Species	65-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-103
27666407-4	2016	Recent evidence indicates that ABL1 was dysregulated in both major depressive disorder (MDD) and cancer patients with depression, and high levels of reactive oxygen species (ROS) can lead to the activation of ABL1 in response to OS and that activated ABL1 subsequently contributes to development of GC via interactions with the downstream targets and corresponding signaling pathways.	Reactive Oxygen Species	149-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-35
27666407-4	2016	Recent evidence indicates that ABL1 was dysregulated in both major depressive disorder (MDD) and cancer patients with depression, and high levels of reactive oxygen species (ROS) can lead to the activation of ABL1 in response to OS and that activated ABL1 subsequently contributes to development of GC via interactions with the downstream targets and corresponding signaling pathways.	Reactive Oxygen Species	149-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-213
27666407-4	2016	Recent evidence indicates that ABL1 was dysregulated in both major depressive disorder (MDD) and cancer patients with depression, and high levels of reactive oxygen species (ROS) can lead to the activation of ABL1 in response to OS and that activated ABL1 subsequently contributes to development of GC via interactions with the downstream targets and corresponding signaling pathways.	Reactive Oxygen Species	149-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-213
27666407-4	2016	Recent evidence indicates that ABL1 was dysregulated in both major depressive disorder (MDD) and cancer patients with depression, and high levels of reactive oxygen species (ROS) can lead to the activation of ABL1 in response to OS and that activated ABL1 subsequently contributes to development of GC via interactions with the downstream targets and corresponding signaling pathways.	Reactive Oxygen Species	174-177	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-213
27666407-4	2016	Recent evidence indicates that ABL1 was dysregulated in both major depressive disorder (MDD) and cancer patients with depression, and high levels of reactive oxygen species (ROS) can lead to the activation of ABL1 in response to OS and that activated ABL1 subsequently contributes to development of GC via interactions with the downstream targets and corresponding signaling pathways.	Reactive Oxygen Species	174-177	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	209-213
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 Mesylate	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
27726390-7	2016	Docking calculations suggested that active indirubins might inhibit T315I Abl kinase through an unprecedented binding to both active and Src-like inactive conformations.	indirubin	43-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-77
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 Mesylate	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-136
27666635-0	2016	Development of BCR-ABL degradation inducers via the conjugation of an imatinib derivative and a cIAP1 ligand.	Imatinib Mesylate	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 Mesylate	79-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-120
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 Mesylate	83-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-138
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 Mesylate	95-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-12
27801322-0	2016	[Application of imatinib in BCR- ABL positive acute lymphoblastic leukemia treatment in the real world].	Imatinib Mesylate	16-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-36
27636353-2	2016	Efforts to elucidate the role they play in these malignancies have led to important diagnostic and therapeutic triumphs, including the famous development of the tyrosine kinase inhibitor dasatinib targeting the BCR-ABL fusion.	Dasatinib	187-196	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	211-218
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
27810077-9	2016	It may also contribute to the resistance to imatinib, as imatinib only targets on BCR-ABL fusion.	Imatinib Mesylate	57-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
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 Mesylate	145-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-130
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.	Adenosine Triphosphate	106-109	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 Mesylate	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-131
26479578-6	2016	Baustinib, Nilotinib, Dasatinib, Ponatinib, Bafetinib, etc., which can able to combat against mutated domain of ABL tyrosine kinase protein.	baustinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-115
26479578-6	2016	Baustinib, Nilotinib, Dasatinib, Ponatinib, Bafetinib, etc., which can able to combat against mutated domain of ABL tyrosine kinase protein.	nilotinib	11-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-115
26479578-6	2016	Baustinib, Nilotinib, Dasatinib, Ponatinib, Bafetinib, etc., which can able to combat against mutated domain of ABL tyrosine kinase protein.	Dasatinib	22-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-115
26479578-6	2016	Baustinib, Nilotinib, Dasatinib, Ponatinib, Bafetinib, etc., which can able to combat against mutated domain of ABL tyrosine kinase protein.	ponatinib	33-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-115
26479578-6	2016	Baustinib, Nilotinib, Dasatinib, Ponatinib, Bafetinib, etc., which can able to combat against mutated domain of ABL tyrosine kinase protein.	bafetinib	44-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-115
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 Mesylate	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 Mesylate	62-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-29
27520370-2	2016	Here we show that niclosamide, a FDA-approved anthelmintic drug, enhances the sensitivity of BP-CML cells to dasatinib (2nd generation of BCR-ABL TKI) through inhibiting Erk/Mnk1/eIF4E signaling pathway.	Niclosamide	18-29	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
27803756-1	2016	Dasatinib is a drug for treatment of oncogene fusion protein BCR-ABL-positive chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia resistant/intolerant to imatinib.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
27520370-2	2016	Here we show that niclosamide, a FDA-approved anthelmintic drug, enhances the sensitivity of BP-CML cells to dasatinib (2nd generation of BCR-ABL TKI) through inhibiting Erk/Mnk1/eIF4E signaling pathway.	Dasatinib	109-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
27432881-2	2016	BCR-ABL tyrosine kinase inhibitors (TKIs) imatinib and dasatinib inhibit fludarabine and cytarabine uptake.	fludarabine	73-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
27432881-2	2016	BCR-ABL tyrosine kinase inhibitors (TKIs) imatinib and dasatinib inhibit fludarabine and cytarabine uptake.	Imatinib Mesylate	42-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
27432881-9	2016	In experiments with mutant hENT1, we showed for the first time interaction of Met(33) (involved in dipyridamole binding) with BCR-ABL inhibitors and reduced interaction with M33A mutant hENT1.	Dipyridamole	99-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
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 Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-47
27036136-8	2016	Visfatin-promoted in vitro cell viability and metastatic capability were suppressed by imatinib (c-Abl inhibitor) and Stattic (STAT3 inhibitor).	Imatinib Mesylate	87-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-102
27520370-11	2016	Our work is the first to demonstrate that niclosamide is a potential drug to overcome resistance to BCR-ABL TKI treatment in BP-CML.	Niclosamide	42-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
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 Mesylate	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	191-198
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 Mesylate	118-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
27444277-0	2016	Sensitivity of imatinib-resistant T315I BCR-ABL CML to a synergistic combination of ponatinib and forskolin treatment.	Imatinib Mesylate	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
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 Mesylate	169-177	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
27437766-6	2016	Here we investigated the efficacy of combination therapy of copanlisib with an ABL TKI (imatinib, nilotinib, or ponatinib) using BCR-ABL-positive cells.	copanlisib	60-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-136
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.	Dasatinib	90-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
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.	nilotinib	101-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
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 Mesylate	148-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
27492780-0	2016	miRNA143 Induces K562 Cell Apoptosis Through Downregulating BCR-ABL.	mirna143	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
27492780-10	2016	miRNA143 transfection decreased BCR-ABL expression.	mirna143	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
27492780-11	2016	BCR-ABL overexpression suppressed miRNA143-induced K562 cell apoptosis, while its reduction enhanced miRNA143-induced apoptosis.	mirna143	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
27492780-12	2016	CONCLUSIONS miRNA143 induced K562 cell apoptosis through downregulating BCR-ABL.	mirna143	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
27432881-2	2016	BCR-ABL tyrosine kinase inhibitors (TKIs) imatinib and dasatinib inhibit fludarabine and cytarabine uptake.	Cytarabine	89-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
27432881-6	2016	Studies in yeast with mutants at two amino acid residues of hENT1 (L442I, L442T, M33A, M33A/L442I) previously shown to be involved in uridine and dipyridamole binding, suggested that BCR-ABL TKIs interacted with Met(33) (TM1) and Leu(442) (TM11) residues of hENT1.	Uridine	134-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	183-190
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 Mesylate	30-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
27432881-6	2016	Studies in yeast with mutants at two amino acid residues of hENT1 (L442I, L442T, M33A, M33A/L442I) previously shown to be involved in uridine and dipyridamole binding, suggested that BCR-ABL TKIs interacted with Met(33) (TM1) and Leu(442) (TM11) residues of hENT1.	Dipyridamole	146-158	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	183-190
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.	ros	150-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
27432881-6	2016	Studies in yeast with mutants at two amino acid residues of hENT1 (L442I, L442T, M33A, M33A/L442I) previously shown to be involved in uridine and dipyridamole binding, suggested that BCR-ABL TKIs interacted with Met(33) (TM1) and Leu(442) (TM11) residues of hENT1.	Leucine	230-233	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	183-190
27432881-8	2016	In conclusion, BCR-ABL TKIs variously inhibit five different hNTs, cause a decrease in cell surface hENT1 expression, and decrease uridine accumulation when presented together with uridine or when given before uridine.	Uridine	131-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
27432881-8	2016	In conclusion, BCR-ABL TKIs variously inhibit five different hNTs, cause a decrease in cell surface hENT1 expression, and decrease uridine accumulation when presented together with uridine or when given before uridine.	Uridine	181-188	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
27432881-8	2016	In conclusion, BCR-ABL TKIs variously inhibit five different hNTs, cause a decrease in cell surface hENT1 expression, and decrease uridine accumulation when presented together with uridine or when given before uridine.	Uridine	181-188	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
27521332-5	2016	Dasatinib is a potent second-generation tyrosine kinase inhibitor designed to inhibit ABL and SRC kinases while also interfering with the c-Kit, platelet-derived growth factor receptor, and STAT5 pathways.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-89
27125982-0	2016	Imatinib-induced long-term remission in a relapsed RCSD1-ABL1-positive acute lymphoblastic leukemia.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-61
27348587-8	2016	Furthermore, in vitro studies show that c-Abl phosphorylation of alpha-synuclein at tyrosine 39 enhances alpha-synuclein aggregation.	Tyrosine	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-45
27434297-1	2016	BACKGROUND: We evaluated the effects of low doses of the tyrosine kinase Abelson (Abl) inhibitor Nilotinib, on safety and pharmacokinetics in Parkinson"s disease dementia or dementia with Lewy bodies.	nilotinib	97-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
27244255-0	2016	The sensitivity of chronic myeloid leukemia CD34 cells to Bcr-Abl tyrosine kinase inhibitors is modulated by ceramide levels.	Ceramides	109-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
27244255-5	2016	BP-CML CD34 ceramide(low) were more resistant to BCR-ABL TKIs compared to BP-CML CD34 ceramide(normal).	Ceramides	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
27322145-0	2016	Discovery and characterization of a novel potent type II native and mutant BCR-ABL inhibitor (CHMFL-074) for Chronic Myeloid Leukemia (CML).	chmfl-074	94-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
27322145-2	2016	With a structure-based drug design approach we have discovered a novel inhibitor CHMFL-074, that potently inhibits both the native and a variety of clinically emerged mutants of BCR-ABL kinase.	chmfl-074	81-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185
27322145-3	2016	The X-ray crystal structure of CHMFL-074 in complex with ABL1 kinase (PDB ID: 5HU9) revealed a typical type II binding mode (DFG-out) but relatively rare hinge binding.	chmfl-074	31-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-61
27322145-3	2016	The X-ray crystal structure of CHMFL-074 in complex with ABL1 kinase (PDB ID: 5HU9) revealed a typical type II binding mode (DFG-out) but relatively rare hinge binding.	1,3-Diphenylguanidine	125-128	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-61
27434297-1	2016	BACKGROUND: We evaluated the effects of low doses of the tyrosine kinase Abelson (Abl) inhibitor Nilotinib, on safety and pharmacokinetics in Parkinson"s disease dementia or dementia with Lewy bodies.	nilotinib	97-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-85
27434297-5	2016	Nilotinib is detectable in the cerebrospinal fluid (CSF) and seems to engage the target Abl.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-91
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 Mesylate	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-84
27217448-8	2016	Fifteen dasatinib-treated and 19 imatinib-treated patients had BCR-ABL1 mutations identified at discontinuation.	Imatinib Mesylate	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-71
27007600-2	2016	Constitutively activated Bcr-Abl signaling in CML creates high levels of reactive oxygen species (ROS) that produce 8-oxo-guanine in DNA; this is mutagenic and causes chronic phase (CP) progression to blast phase (BP).	Reactive Oxygen Species	73-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
27007600-2	2016	Constitutively activated Bcr-Abl signaling in CML creates high levels of reactive oxygen species (ROS) that produce 8-oxo-guanine in DNA; this is mutagenic and causes chronic phase (CP) progression to blast phase (BP).	Reactive Oxygen Species	98-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
27007600-2	2016	Constitutively activated Bcr-Abl signaling in CML creates high levels of reactive oxygen species (ROS) that produce 8-oxo-guanine in DNA; this is mutagenic and causes chronic phase (CP) progression to blast phase (BP).	8-hydroxyguanine	116-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
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 Mesylate	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
27166836-10	2016	Ponatinib inhibited phosphorylation not only of BCR-ABL but also of downstream signal transducer and activator of transcription 5, protein kinase B, and ERK1/2 in both K562/IM-R1 and Ba/F3/T315I, and the addition of panobinostat to ponatinib further inhibited these phosphorylations.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
27166836-11	2016	In conclusion, panobinostat enhanced the cytotoxicity of ponatinib towards IM-resistant CML cells including those with T315I-mutated BCR-ABL.	Panobinostat	15-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
27166836-11	2016	In conclusion, panobinostat enhanced the cytotoxicity of ponatinib towards IM-resistant CML cells including those with T315I-mutated BCR-ABL.	ponatinib	57-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
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 Mesylate	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 Mesylate	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
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.	Dasatinib	208-217	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.	Dasatinib	208-217	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.	nilotinib	219-228	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.	nilotinib	219-228	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.	ponatinib	232-241	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.	ponatinib	232-241	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-161
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 Mesylate	159-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-92
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.	Dasatinib	172-181	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-92
27144331-0	2016	Liposomal bortezomib is active against chronic myeloid leukemia by disrupting the Sp1-BCR/ABL axis.	Bortezomib	10-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	86-93
27347777-2	2016	We present here a chronic myeloid leukemia patient harboring the T315I and E255V BCR-ABL1 mutation successfully achieved deep molecular response with a combined treatment of dasatinib and IFN-alpha.	Dasatinib	174-183	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-89
27144331-9	2016	Furthermore, L-BORT exposure significantly blocked BCR/ABL kinase activities and sensitized CML cell lines, tumor cells and doxorubicin (DOX) resistant cells to DOX.	l-bort	13-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-58
27332121-0	2016	Binding Mechanism of the N-Terminal SH3 Domain of CrkII and Proline-Rich Motifs in cAbl.	Proline	60-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-87
27332121-1	2016	The N-terminal Src homology 3 (nSH3) domain of a signaling adaptor protein, CT-10 regulator of kinase II (CrkII), recognizes proline-rich motifs (PRMs) of binding partners, such as cAbl kinase.	Proline	125-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	181-185
27144331-10	2016	This occurred through the more pronounced inhibition of BCR/ABL activity by L-BORT and DOX.	l-bort	76-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
27144331-10	2016	This occurred through the more pronounced inhibition of BCR/ABL activity by L-BORT and DOX.	Doxorubicin	87-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
27144331-11	2016	Collectively, these findings highlight the therapeutic relevance of disrupting BCR/ABL protein expression and strongly support the utilization of L-BORT alone or in combination with DOX to treat CML patients with overexpressing BCR/ABL.	l-bort	146-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
27144331-11	2016	Collectively, these findings highlight the therapeutic relevance of disrupting BCR/ABL protein expression and strongly support the utilization of L-BORT alone or in combination with DOX to treat CML patients with overexpressing BCR/ABL.	l-bort	146-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	228-235
27431076-2	2016	METHODS: Screening ABL(Deltaexon7) and ABL(35INS) in 74 normal people and 76 CML patients (53 patients in remission and 23 patients with TKIs resistance) by using polyacrylamide gel electrophoresis combined with cloning sequencing.	polyacrylamide	163-177	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-22
27161995-5	2016	The analysis suggests that tyrosine phosphorylation of SH3 domains found in Abl kinases act as a switch that can induce both the loss and, unexpectedly, gain of affinity for proline-rich ligands.	Tyrosine	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-79
27161995-5	2016	The analysis suggests that tyrosine phosphorylation of SH3 domains found in Abl kinases act as a switch that can induce both the loss and, unexpectedly, gain of affinity for proline-rich ligands.	Proline	174-181	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-79
27431076-2	2016	METHODS: Screening ABL(Deltaexon7) and ABL(35INS) in 74 normal people and 76 CML patients (53 patients in remission and 23 patients with TKIs resistance) by using polyacrylamide gel electrophoresis combined with cloning sequencing.	polyacrylamide	163-177	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-42
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.	nilotinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	168-171
27293031-0	2016	Imatinib and Nilotinib increase glioblastoma cell invasion via Abl-independent stimulation of p130Cas and FAK signalling.	Imatinib Mesylate	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.	nilotinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-66
27002306-7	2016	Moreover, Y-632 efficiently overcame imatinib resistance mediated by Bcr-Abl point mutations both in vitro and in vivo.	Y-632	10-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
27002306-7	2016	Moreover, Y-632 efficiently overcame imatinib resistance mediated by Bcr-Abl point mutations both in vitro and in vivo.	Imatinib Mesylate	37-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
27133948-2	2016	However, imatinib, the first approved BCR-ABL inhibitor, must be discontinued in many patients because of resistance or intolerance.	Imatinib Mesylate	9-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
27078848-9	2016	Furthermore, CRKL tyrosine phosphorylation was inhibited by dasatinib (an inhibitor of ABL and SRC kinases), which in combination with the ALK inhibitor crizotinib displayed a synergistic inhibitory effect in vitro.	Tyrosine	18-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-90
27078848-9	2016	Furthermore, CRKL tyrosine phosphorylation was inhibited by dasatinib (an inhibitor of ABL and SRC kinases), which in combination with the ALK inhibitor crizotinib displayed a synergistic inhibitory effect in vitro.	Dasatinib	60-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-90
27078848-9	2016	Furthermore, CRKL tyrosine phosphorylation was inhibited by dasatinib (an inhibitor of ABL and SRC kinases), which in combination with the ALK inhibitor crizotinib displayed a synergistic inhibitory effect in vitro.	Crizotinib	153-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-90
27157787-2	2016	Discovered by structure-based virtual screening algorithms, bafetinib, a Bcr-Abl/Lyn tyrosine kinase inhibitor, was found to have inhibitory effects on both ABCB1- and ABCG2-mediated MDR in this in-vitro investigation.	bafetinib	60-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
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 Mesylate	114-122	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	185-192
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 Mesylate	130-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-161
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 Mesylate	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
26812110-0	2016	CR-LAAO antileukemic effect against Bcr-Abl(+) cells is mediated by apoptosis and hydrogen peroxide.	Hydrogen Peroxide	82-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
27748288-6	2016	INTERPRETATION &amp; CONCLUSIONS: Though our data support the previous findings that co-expression of BCR-ABL transcripts is due to the occurrence of exonic and intronic polymorphisms in the BCR gene, it also shows that the intronic polymorphism can arise without the linked exonic polymorphism.	Adenosine Monophosphate	16-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
27010810-1	2016	Efforts were made to improve a series of potent dual ABL/SRC inhibitors based on a 7-azaindole core with the aim of developing compounds that demonstrate a wider activity on selected oncogenic kinases.	7-azaindole dimer	83-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
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 Mesylate	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 Mesylate	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.	ponatinib	141-150	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.	ponatinib	141-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-99
27027438-9	2016	In summary, results clearly demonstrated BCR/ABL-independent Stat5 survival pathway could contribute to resistance of CML LSCs to IM in BM microenvironment and suggested that natural durgs effectively inhibiting Stat5 may be an attractive approach to overcome resistance to BCR/ABL kinase inhibitors.	durgs	183-188	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
27018250-5	2016	The major tyrosine phosphorylation sites on RBM39 that are phosphorylated by c-Abl are Y95 and Y99, as demonstrated by liquid chromatography coupled with tandem mass spectrometry (LC/MS/MS) and mutational analysis.	Tyrosine	10-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-82
27027438-9	2016	In summary, results clearly demonstrated BCR/ABL-independent Stat5 survival pathway could contribute to resistance of CML LSCs to IM in BM microenvironment and suggested that natural durgs effectively inhibiting Stat5 may be an attractive approach to overcome resistance to BCR/ABL kinase inhibitors.	durgs	183-188	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	274-281
26912659-2	2016	We have shown that a tandem fusion of two designed binding proteins, termed monobodies, directed to the interaction interface between the Src homology 2 (SH2) and kinase domains and to the phosphotyrosine-binding site of the SH2 domain, respectively, inhibits the Bcr-Abl kinase activity.	Phosphotyrosine	189-204	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	264-271
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.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
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.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	171-178
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 Mesylate	111-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-40
26607600-9	2016	Moreover, the BCR/ABL1 inhibitors nilotinib and ponatinib were found to decrease STAT5 activity and CD25 expression in KU812 cells and primary CML LSCs.	nilotinib	34-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-22
26607600-9	2016	Moreover, the BCR/ABL1 inhibitors nilotinib and ponatinib were found to decrease STAT5 activity and CD25 expression in KU812 cells and primary CML LSCs.	ponatinib	48-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	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 Mesylate	35-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-13
27228340-0	2016	MicroRNA-1301-Mediated RanGAP1 Downregulation Induces BCR-ABL Nuclear Entrapment to Enhance Imatinib Efficacy in Chronic Myeloid Leukemia Cells.	Imatinib Mesylate	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
27228340-14	2016	Furthermore, immunofluorescence assay demonstrated that Tyr-99 of nuclear P73 was phosphorylated accompanied with nuclear entrapment of BCR-ABL after transfection with RanGAP1 shRNA or miR-1301 in IM-treated K562 cells.	Tyrosine	56-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	136-143
27055152-0	2016	Hypoxia-Like Signatures Induced by BCR-ABL Potentially Alter the Glutamine Uptake for Maintaining Oxidative Phosphorylation.	Glutamine	65-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
26059983-0	2016	Gender and BCR-ABL transcript type are correlated with molecular response to imatinib treatment in patients with chronic myeloid leukemia.	Imatinib Mesylate	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-18
27055152-7	2016	Lactate and pyruvate levels were increased in BCR-ABL-expressing cells even under normoxia, coinciding with enhanced glutaminolysis which occurred in an HIF1/2-dependent manner.	Lactic Acid	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
27055152-7	2016	Lactate and pyruvate levels were increased in BCR-ABL-expressing cells even under normoxia, coinciding with enhanced glutaminolysis which occurred in an HIF1/2-dependent manner.	Pyruvic Acid	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53
27055152-8	2016	Expression of the glutamine importer SLC1A5 was increased in BCR-ABL+ cells, coinciding with an increased susceptibility to the glutaminase inhibitor BPTES.	bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide	150-155	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-68
27055152-10	2016	The current study suggests that BCR-ABL-positive cancer cells make use of enhanced glutamine metabolism to maintain TCA cell cycle activity in glycolytic cells.	Glutamine	83-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
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 Mesylate	46-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
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 Mesylate	3-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
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 Mesylate	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
26582603-3	2016	The first-line treatment consists on BCR-ABL inhibitors such as Imatinib, Nilotinib and Dasatinib.	Imatinib Mesylate	64-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
26582603-3	2016	The first-line treatment consists on BCR-ABL inhibitors such as Imatinib, Nilotinib and Dasatinib.	nilotinib	74-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
26582603-3	2016	The first-line treatment consists on BCR-ABL inhibitors such as Imatinib, Nilotinib and Dasatinib.	Dasatinib	88-97	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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
27150995-11	2016	CONCLUSION: The DCDF-FISH is a sensitive and reliable method for the detection of BCR/ABL rearrangement.	dcdf	16-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
27757426-0	2016	TIE2-mediated tyrosine phosphorylation of H4 regulates DNA damage response by recruiting ABL1.	Tyrosine	14-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-93
27757426-5	2016	Nuclear TIE2 binds to key components of DNA repair and phosphorylates H4 at tyrosine 51, which, in turn, is recognized by the proto-oncogene ABL1, indicating a role for nuclear TIE2 as a sensor for genotoxic stress by action as a histone modifier.	Tyrosine	76-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-145
27757426-6	2016	H4Y51 constitutes the first tyrosine phosphorylation of core histones recognized by ABL1, defining this histone modification as a direct signal to couple genotoxic stress with the DNA repair machinery.	Tyrosine	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-88
25997106-6	2016	There was a trend to better OS in patients with &gt;= 4 log reduction of BCR-ABL transcript prior to HSCT (92% vs. 50%; P = 0.065).	Osmium	28-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
26789553-0	2016	Discovery of 2-((3-Amino-4-methylphenyl)amino)-N-(2-methyl-5-(3-(trifluoromethyl)benzamido)phenyl)-4-(methylamino)pyrimidine-5-carboxamide (CHMFL-ABL-053) as a Potent, Selective, and Orally Available BCR-ABL/SRC/p38 Kinase Inhibitor for Chronic Myeloid Leukemia.	2-((3-amino-4-methylphenyl)amino)-N-(2-methyl-5-(3-(trifluoromethyl)benzamido)phenyl)-4-(methylamino)pyrimidine-5-carboxamide	140-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	200-207
26789553-1	2016	Starting from a dihydropyrimidopyrimidine core scaffold based compound 27 (GNF-7), we discovered a highly potent (ABL1: IC50 of 70 nM) and selective (S score (1) = 0.02) BCR-ABL inhibitor 18a (CHMFL-ABL-053).	dihydropyrimidopyrimidine	16-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-118
26789553-1	2016	Starting from a dihydropyrimidopyrimidine core scaffold based compound 27 (GNF-7), we discovered a highly potent (ABL1: IC50 of 70 nM) and selective (S score (1) = 0.02) BCR-ABL inhibitor 18a (CHMFL-ABL-053).	dihydropyrimidopyrimidine	16-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-177
26789553-1	2016	Starting from a dihydropyrimidopyrimidine core scaffold based compound 27 (GNF-7), we discovered a highly potent (ABL1: IC50 of 70 nM) and selective (S score (1) = 0.02) BCR-ABL inhibitor 18a (CHMFL-ABL-053).	chmfl-abl	193-202	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-118
26789553-1	2016	Starting from a dihydropyrimidopyrimidine core scaffold based compound 27 (GNF-7), we discovered a highly potent (ABL1: IC50 of 70 nM) and selective (S score (1) = 0.02) BCR-ABL inhibitor 18a (CHMFL-ABL-053).	chmfl-abl	193-202	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-177
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 Mesylate	123-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-185
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 Mesylate	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-43
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 Mesylate	248-256	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-125
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.	Deferasirox	47-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-104
26833194-0	2016	GADD45alpha modulates curcumin sensitivity through c-Abl- and JNK-dependent signaling pathways in a mismatch repair-dependent manner.	gadd45alpha	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-65
26833194-0	2016	GADD45alpha modulates curcumin sensitivity through c-Abl- and JNK-dependent signaling pathways in a mismatch repair-dependent manner.	Curcumin	22-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	51-65
26833194-9	2016	Moreover, inhibition of Abl through ST571 treatment and its downstream effector JNK through SP600125 treatment blocked GADD45alpha upregulation and cell death triggered by curcumin.	pyrazolanthrone	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-27
26833194-9	2016	Moreover, inhibition of Abl through ST571 treatment and its downstream effector JNK through SP600125 treatment blocked GADD45alpha upregulation and cell death triggered by curcumin.	Curcumin	172-180	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-27
26833194-10	2016	Collective results lead us to conclude that GADD45alpha modulates curcumin sensitivity through activation of c-Abl &gt; JNK signaling in a mismatch repair-dependent manner.	gadd45alpha	44-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-114
26833194-10	2016	Collective results lead us to conclude that GADD45alpha modulates curcumin sensitivity through activation of c-Abl &gt; JNK signaling in a mismatch repair-dependent manner.	Curcumin	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-114
26847385-0	2016	Complete cytogenetic response to Nilotinib in a chronic myeloid leukemia case with a rare e13a3(b2a3) BCR-ABL fusion transcript: A case report.	nilotinib	33-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
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 Mesylate	63-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-104
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 Mesylate	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-161
26912052-2	2016	Bcr-Abl tyrosine kinase inhibitors (TKIs), such as imatinib mesylate (IM), revolutionized CML therapy.	Imatinib Mesylate	51-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
26607903-0	2016	Perturbation of energy metabolism by fatty-acid derivative AIC-47 and imatinib in BCR-ABL-harboring leukemic cells.	Fatty Acids	37-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
26607903-0	2016	Perturbation of energy metabolism by fatty-acid derivative AIC-47 and imatinib in BCR-ABL-harboring leukemic cells.	Imatinib Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-54
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 Mesylate	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
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 Mesylate	111-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-61
26298727-10	2016	Ruxolitinib is a promising agent in chronic myeloid leukemia treatment by blocking JAK/STAT pathway known as downstream of BCR-ABL and triggering autophagy.	ruxolitinib	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-130
26507546-1	2016	PURPOSE: Dasatinib is a novel, oral, multi-targeted kinase inhibitor of breakpoint cluster region-abelson (BCR-ABL) and Src family kinases.	Dasatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
26831735-0	2016	Secretion of IL-1beta from imatinib-resistant chronic myeloid leukemia cells contributes to BCR-ABL mutation-independent imatinib resistance.	Imatinib Mesylate	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
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 Mesylate	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-62
26815740-2	2016	Clinical resistance to the Bcr-Abl inhibitor imatinib is a critical problem in treating CML.	Imatinib Mesylate	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
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 Mesylate	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 Mesylate	207-215	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-62
26585829-3	2016	The bicyclo[1.1.1]pentane- and cubane-containing analogues were found to possess higher themodynamic solubility, whereas cubane- and cyclohexyl-containing analogues exhibited the highest inhibitory activity against ABL1 kinase and the most potent cytotoxicity values against cancer cell lines K562 and SUP-B15.	Bicyclo[1.1.1]pentane	4-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	215-219
26585829-3	2016	The bicyclo[1.1.1]pentane- and cubane-containing analogues were found to possess higher themodynamic solubility, whereas cubane- and cyclohexyl-containing analogues exhibited the highest inhibitory activity against ABL1 kinase and the most potent cytotoxicity values against cancer cell lines K562 and SUP-B15.	Cubane	31-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	215-219
26585829-3	2016	The bicyclo[1.1.1]pentane- and cubane-containing analogues were found to possess higher themodynamic solubility, whereas cubane- and cyclohexyl-containing analogues exhibited the highest inhibitory activity against ABL1 kinase and the most potent cytotoxicity values against cancer cell lines K562 and SUP-B15.	Cubane	121-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	215-219
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 Mesylate	133-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
27656875-1	2016	Dasatinib is a potent inhibitor of the altered tyrosine kinase activity in disease states associated with BCR/ABL1.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-114
26459144-0	2016	Expansion of a BCR-ABL clone in a JAK2 V617F myeloproliferative neoplasm treated by ruxolitinib.	ruxolitinib	84-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
26656091-4	2016	CrkII Tyr221 phosphorylation by the Abl or EGFR kinases induces an inhibited state of CrkII by means of an intramolecular SH2-pTyr221 interaction, causing signaling interruption.	ptyr221	126-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-39
26537529-1	2016	The dual SRC/ABL1 tyrosine kinase inhibitor bosutinib is indicated for adults with Ph+ chronic myeloid leukaemia (CML) resistant/intolerant to prior therapy.	bosutinib	44-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-17
26494904-8	2016	This was most extensive in SU5402 and AZD1480, which inhibited DDR2, IGF1R, FLT3, TRKA, FLT4, ABL and JAK3 with efficiencies similar to or greater than those for FGFR.	SU 5402	27-33	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-97
26494904-8	2016	This was most extensive in SU5402 and AZD1480, which inhibited DDR2, IGF1R, FLT3, TRKA, FLT4, ABL and JAK3 with efficiencies similar to or greater than those for FGFR.	AZD 1480	38-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-97
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 Mesylate	43-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
27491651-6	2016	The Bcr-Abl inhibitor bosutinib and EGFR inhibitor gefitinib were selected as the representatives of, respectively, sensitization and insusceptibility to perform kinase assay against the GST-tagged, recombinant kinase domains of wild-type HER2(WT) and HER2(YVMA) variant.	bosutinib	22-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	19-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	181-185
26866052-1	2016	This article expands on crystal structure data for human H-RAS with mutations at position Y137, briefly described in a paper on the effects of phosphorylation of Y137 by ABL kinases (Tyrosine phosphorylation of RAS by ABL allosterically enhances effector binding, published in the FASEB Journal [1]).	Tyrosine	183-191	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-173
27268912-3	2016	Omacetaxine mepesuccinate inhibits protein translation through prevention of the initial elongation step of protein synthesis and its use benefits CML patients possessing the BCR-ABL oncogene.	Homoharringtonine	0-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	175-182
26876246-0	2016	[Dasatinib treatment based on BCR- ABL mutation detection in imatinib- resistant patients with chronic myeloid leukemia].	Dasatinib	1-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-38
26876246-0	2016	[Dasatinib treatment based on BCR- ABL mutation detection in imatinib- resistant patients with chronic myeloid leukemia].	Imatinib Mesylate	61-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-38
26876246-1	2016	OBJECTIVE: To evaluate the efficiency of dasatinib as the second- or third-line tyrosine kinase inhibitor (TKI)in imatinib-resistant patients with chronic myeloid leukemia (CML)based on BCR-ABL mutation detection.	Dasatinib	41-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-193
26876246-5	2016	BCR- ABL mutation detection was performed once the patients failed on dasatinib.	Dasatinib	70-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-8
26866052-1	2016	This article expands on crystal structure data for human H-RAS with mutations at position Y137, briefly described in a paper on the effects of phosphorylation of Y137 by ABL kinases (Tyrosine phosphorylation of RAS by ABL allosterically enhances effector binding, published in the FASEB Journal [1]).	Tyrosine	183-191	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	218-221
26562217-0	2015	Development of Alkyne-Containing Pyrazolopyrimidines To Overcome Drug Resistance of Bcr-Abl Kinase.	Alkynes	15-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
26562217-0	2015	Development of Alkyne-Containing Pyrazolopyrimidines To Overcome Drug Resistance of Bcr-Abl Kinase.	pyrazolopyrimidines	33-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
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 Mesylate	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 Mesylate	33-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
26562217-3	2015	Inspired by the successful development of ponatinib to curb drug resistance, we hypothesize that the incorporation of an alkyne linker in other heterocyclic scaffolds can also achieve potent inhibition of Bcr-Abl(T315I) by allowing for simultaneous occupancy of both the active site and the allosteric pocket in the Abl kinase domain.	ponatinib	42-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	205-212
26562217-3	2015	Inspired by the successful development of ponatinib to curb drug resistance, we hypothesize that the incorporation of an alkyne linker in other heterocyclic scaffolds can also achieve potent inhibition of Bcr-Abl(T315I) by allowing for simultaneous occupancy of both the active site and the allosteric pocket in the Abl kinase domain.	Alkynes	121-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	205-212
26562217-4	2015	Herein, we describe the design, synthesis, and characterization of a series of alkyne-containing pyrazolopyrimidines as Bcr-Abl inhibitors.	alkyne-containing pyrazolopyrimidines	79-116	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
26562217-5	2015	Our results demonstrate that some alkyne-containing pyrazolopyrimidines potently inhibit not only Abl(T315I) in vitro but also Bcr-Abl(T315I) in cells.	Alkynes	34-40	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
26562217-5	2015	Our results demonstrate that some alkyne-containing pyrazolopyrimidines potently inhibit not only Abl(T315I) in vitro but also Bcr-Abl(T315I) in cells.	pyrazolopyrimidines	52-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
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 Mesylate	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
26456889-0	2015	Inhibition of crosstalk between Bcr-Abl and PKC signaling by PEITC, augments imatinib sensitivity in chronic myelogenous leukemia cells.	Imatinib Mesylate	77-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39
26779374-5	2015	In recent years, imatinib, a PDGFbetaR, ABL and KIT inhibitor, has revolutionized systemic therapy in DFSP.	Imatinib Mesylate	17-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-43
26542215-6	2015	These isothiocyanates also increased ubiquitination of the oncogenic fusion protein Bcr-Abl, resulting in degradation under low isothiocyanate concentrations and aggregation under high isothiocyanate concentrations.	Isothiocyanates	6-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
26542215-6	2015	These isothiocyanates also increased ubiquitination of the oncogenic fusion protein Bcr-Abl, resulting in degradation under low isothiocyanate concentrations and aggregation under high isothiocyanate concentrations.	isothiocyanic acid	6-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
26542215-6	2015	These isothiocyanates also increased ubiquitination of the oncogenic fusion protein Bcr-Abl, resulting in degradation under low isothiocyanate concentrations and aggregation under high isothiocyanate concentrations.	isothiocyanic acid	128-142	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
26542215-7	2015	USP9x inhibition paralleled the decrease in Bcr-Abl levels induced by isothiocyanate treatment, and USP9x silencing was sufficient to decrease Bcr-Abl levels, further suggesting that Bcr-Abl is a USP9x substrate.	isothiocyanic acid	70-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
26644081-0	2015	Synergistic cytotoxicity from combination of imatinib and platinum-based anticancer drugs specifically in Bcr-Abl positive leukemia cells.	Imatinib Mesylate	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	106-113
26346504-2	2015	DESIGN AND METHODS: The effectiveness of AT9283 was examined in several mouse models engrafted with BCR-ABL(+) leukemic, human multiple myeloma (MM), and human colorectal carcinoma (HCT116) cells.	1-cyclopropyl-3-(3-(5-morpholin-4-ylmethyl-1H-benzoimidazol-2-yl)-1H-pyrazol-4-yl)urea	41-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
26644081-0	2015	Synergistic cytotoxicity from combination of imatinib and platinum-based anticancer drugs specifically in Bcr-Abl positive leukemia cells.	Platinum	58-66	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
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 Mesylate	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 Mesylate	45-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	256-263
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.	Platinum	59-67	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.	Platinum	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	256-263
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.	Platinum	69-71	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.	Platinum	69-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	256-263
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.	Cisplatin	108-117	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.	Cisplatin	108-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	256-263
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.	Oxaliplatin	122-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	190-197
26802644-5	2016	We report two CP-CML patients achieving and maintaining major molecular responses while on very low doses of dasatinib, ultimately achieving undetectable levels of BCR-ABL fusion transcript in their peripheral blood.	Dasatinib	109-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	164-171
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.	Oxaliplatin	122-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	256-263
26423566-0	2015	Characteristics of the TCR Vbeta repertoire in imatinib-resistant chronic myeloid leukemia patients with ABL mutations.	Imatinib Mesylate	47-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-108
26697169-8	2015	Furthermore, exposure of HLMVECs to HGF or S1P stimulated c-Abl-mediated tyrosine phosphorylation of paxillin at Y31 and Y118 in a time-dependent fashion, and down-regulation of c-Abl with siRNA attenuated HGF- or S1P-mediated lamellipodia formation, translocation of p47 (phox) to lamellipodia, and endothelial barrier enhancement.	Tyrosine	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-63
26697169-10	2015	Together, these results suggest that c-Abl-mediated tyrosine phosphorylation of paxillin at Y31 and Y118 regulates HGF- or S1P-mediated lamellipodia formation, ROS generation in lamellipodia, and endothelial permeability.	Tyrosine	52-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-42
26697169-10	2015	Together, these results suggest that c-Abl-mediated tyrosine phosphorylation of paxillin at Y31 and Y118 regulates HGF- or S1P-mediated lamellipodia formation, ROS generation in lamellipodia, and endothelial permeability.	Reactive Oxygen Species	160-163	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-42
26501568-0	2015	Discovery of 2-Acylaminothiophene-3-Carboxamides as Multitarget Inhibitors for BCR-ABL Kinase and Microtubules.	2-acylaminothiophene-3-carboxamides	13-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-86
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 Mesylate	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 Mesylate	101-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-74
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 Mesylate	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 Mesylate	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
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 Mesylate	65-73	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-47
26501568-4	2015	Among them, nine compounds, which share a common thiophene-based scaffold and adopt similar binding poses, were chosen for experimental testing and one of them was shown to have low micromolar inhibition activities against both WT and mutant ABL kinases.	Thiophenes	49-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	242-245
26588899-2	2015	Here, we investigated the ability of the clinically utilised SRC/ABL inhibitor dasatinib to mimic the PP2/PP1 effect.	Dasatinib	79-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-68
26513170-4	2015	Notably, cisplatin treatment increased NOX5-L levels through CREB activation and enhanced NOX5-L activity through augmentation of Ca2+ release and c-Abl expression, ultimately triggering ROS-mediated cancer cell death-a distinct pathway absent in normal cells.	Cisplatin	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-152
26513170-4	2015	Notably, cisplatin treatment increased NOX5-L levels through CREB activation and enhanced NOX5-L activity through augmentation of Ca2+ release and c-Abl expression, ultimately triggering ROS-mediated cancer cell death-a distinct pathway absent in normal cells.	Reactive Oxygen Species	187-190	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	147-152
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 Mesylate	136-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
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.	Pentosephosphates	81-98	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 Mesylate	164-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
26451772-0	2015	Expanding the structural diversity of Bcr-Abl inhibitors: Dibenzoylpiperazin incorporated with 1H-indazol-3-amine.	dibenzoylpiperazin	58-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
26451772-0	2015	Expanding the structural diversity of Bcr-Abl inhibitors: Dibenzoylpiperazin incorporated with 1H-indazol-3-amine.	1H-indazol-3-amine	95-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
26451772-1	2015	A series of N,N"-dibenzoylpiperazine derivatives incorporated with 1H-indazol-3-amine have been designed, synthesized and evaluated as novel Bcr-Abl inhibitors.	N,N'-dibenzoylpiperazine	12-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-148
26451772-1	2015	A series of N,N"-dibenzoylpiperazine derivatives incorporated with 1H-indazol-3-amine have been designed, synthesized and evaluated as novel Bcr-Abl inhibitors.	1H-indazol-3-amine	67-85	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-148
26451772-7	2015	Therefore, it could serve as promising lead compound for further optimization of Bcr-Abl(WT) and Bcr-Abl(T315I) inhibitors.	t315i	105-110	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
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 Mesylate	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	184-187
26284693-2	2015	Few cases of pulmonary arterial hypertension (PAH) have been reported in patients with leukemia treated with dasatinib, a second-generation BCR-ABL TKI.	Dasatinib	109-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
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 Mesylate	45-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35
26722260-0	2015	Proteasome inhibitor MG-132 enhances histone deacetylase inhibitor SAHA-induced cell death of chronic myeloid leukemia cells by an ROS-mediated mechanism and downregulation of the Bcr-Abl fusion protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	180-187
26722260-9	2015	Notably, the ROS scavenger, N-acetyl-L-cysteine, almost fully reversed the cell death and Bcr-Abl downregulation that was induced by the combination of SAHA and MG-132.	Reactive Oxygen Species	13-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
26722260-9	2015	Notably, the ROS scavenger, N-acetyl-L-cysteine, almost fully reversed the cell death and Bcr-Abl downregulation that was induced by the combination of SAHA and MG-132.	Acetylcysteine	28-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
26722260-9	2015	Notably, the ROS scavenger, N-acetyl-L-cysteine, almost fully reversed the cell death and Bcr-Abl downregulation that was induced by the combination of SAHA and MG-132.	Vorinostat	152-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
26722260-9	2015	Notably, the ROS scavenger, N-acetyl-L-cysteine, almost fully reversed the cell death and Bcr-Abl downregulation that was induced by the combination of SAHA and MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	161-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
26722260-11	2015	These results indicated that increased intracellular ROS levels are important in the induction of cell death and the downregulation of Bcr-Abl.	Reactive Oxygen Species	53-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	135-142
26217035-0	2015	c-Abl-mediated tyrosine phosphorylation of JunB is required for Adriamycin-induced expression of p21.	Tyrosine	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
26217035-0	2015	c-Abl-mediated tyrosine phosphorylation of JunB is required for Adriamycin-induced expression of p21.	Doxorubicin	64-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
26217035-5	2015	We first analysed phosphorylation sites of JunB and found that c-Abl majorly phosphorylates JunB at Tyr(173), Tyr(182) and Tyr(188).	Tyrosine	100-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-68
26217035-5	2015	We first analysed phosphorylation sites of JunB and found that c-Abl majorly phosphorylates JunB at Tyr(173), Tyr(182) and Tyr(188).	Tyrosine	110-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-68
26217035-5	2015	We first analysed phosphorylation sites of JunB and found that c-Abl majorly phosphorylates JunB at Tyr(173), Tyr(182) and Tyr(188).	Tyrosine	110-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-68
26217035-6	2015	Because c-Abl promotes expression of the cyclin-dependent kinase inhibitor p21 upon stimulation with the DNA-damaging agent Adriamycin (doxorubicin), we analysed the involvement of JunB in Adriamycin-induced p21 expression.	Doxorubicin	124-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-13
26217035-6	2015	Because c-Abl promotes expression of the cyclin-dependent kinase inhibitor p21 upon stimulation with the DNA-damaging agent Adriamycin (doxorubicin), we analysed the involvement of JunB in Adriamycin-induced p21 expression.	Doxorubicin	136-147	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-13
26217035-6	2015	Because c-Abl promotes expression of the cyclin-dependent kinase inhibitor p21 upon stimulation with the DNA-damaging agent Adriamycin (doxorubicin), we analysed the involvement of JunB in Adriamycin-induced p21 expression.	Doxorubicin	189-199	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-13
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 Mesylate	145-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-134
26217035-11	2015	Taken together, these results suggest that, although JunB represses p21 promoter activity, c-Abl phosphorylates JunB and conversely inhibits its suppressive role on p21 promoter activity upon Adriamycin stimulation.	Doxorubicin	192-202	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-96
26217035-12	2015	Therefore JunB is likely to be a key target of c-Abl in expression of p21 in Adriamycin-induced DDR.	Doxorubicin	77-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-52
26298495-0	2015	Expanding the structural diversity of Bcr-Abl inhibitors: Hybrid molecules based on GNF-2 and Imatinib.	Imatinib Mesylate	94-102	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
26359456-0	2015	Implication of the Autologous Immune System in BCR-ABL Transcript Variations in Chronic Myelogenous Leukemia Patients Treated with Imatinib.	Imatinib Mesylate	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 Mesylate	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 Mesylate	123-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
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 Mesylate	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 Mesylate	57-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-134
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 Mesylate	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	164-171
26622510-0	2015	Nilotinib rapidly reverses breakpoint cluster region-Abelson oncogene fusion gene and M244V mutations in a patient with chronic myelogenous leukemia: A case report.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-69
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.	nilotinib	122-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	164-171
26622510-6	2015	This suggests that nilotinib may be effective for treating CML cases in which the BCR-ABL fusion protein has an M244V mutation.	nilotinib	19-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
26473951-4	2015	We found that KOSR protects CML cells from killing by BCR-ABL inhibitors--imatinib, dasatinib and nilotinib.	Imatinib Mesylate	74-82	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
26473951-4	2015	We found that KOSR protects CML cells from killing by BCR-ABL inhibitors--imatinib, dasatinib and nilotinib.	Dasatinib	84-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
26473951-4	2015	We found that KOSR protects CML cells from killing by BCR-ABL inhibitors--imatinib, dasatinib and nilotinib.	nilotinib	98-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
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 Mesylate	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
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 Mesylate	117-125	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-92
26099262-1	2015	Imatinib has been identified as a tyrosine kinase inhibitor that selectively inhibits the Abl tyrosine kinases, including Bcr-Abl.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
26430722-0	2015	Concomitant JAK2 V617F-positive polycythemia vera and BCR-ABL-positive chronic myelogenous leukemia treated with ruxolitinib and dasatinib.	ruxolitinib	113-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
26430722-0	2015	Concomitant JAK2 V617F-positive polycythemia vera and BCR-ABL-positive chronic myelogenous leukemia treated with ruxolitinib and dasatinib.	Dasatinib	129-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
26225736-8	2015	Concomitantly it was found that PEG-coated lipoplexes improved cellular uptake and transfection efficiency in H1299 cells, and had the ability to silence BCR-ABL, affecting the survival of K562 cells.	Polyethylene Glycols	32-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-161
26458439-1	2015	The ABL tyrosine kinase inhibitor (TKI) imatinib mesylate has dramatically changed the treatment of chronic myeloid leukemia (CML).	Imatinib Mesylate	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 Mesylate	85-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	36-39
26458439-6	2015	Four second-generation ATP competitive ABL TKIs, i.e., dasatinib, nilotinib, bosutinib and bafetinib, have been developed.	Adenosine Triphosphate	23-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-42
26458439-6	2015	Four second-generation ATP competitive ABL TKIs, i.e., dasatinib, nilotinib, bosutinib and bafetinib, have been developed.	bafetinib	91-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-42
26458439-10	2015	Thus, a third-generation ABL TKI, ponatinib, was developed to inhibit all mutated BCR-ABL and showed clinical efficacy in CML cells harboring T315I.	ponatinib	34-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-28
26458439-10	2015	Thus, a third-generation ABL TKI, ponatinib, was developed to inhibit all mutated BCR-ABL and showed clinical efficacy in CML cells harboring T315I.	ponatinib	34-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
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 Mesylate	154-162	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
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 Mesylate	136-144	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-124
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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	97-104
26231079-7	2015	These aromatic-heterocyclic biphenyls could be considered as novel lead compound for optimized as Bcr-Abl(T315I) inhibitors.	diphenyl	28-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
26195136-0	2015	Hybrid pyrimidine alkynyls inhibit the clinically resistance related Bcr-Abl(T315I) mutant.	pyrimidine alkynyls	7-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	69-76
26195136-1	2015	A series of pyrimidine alkynyl derivatives were designed and synthesized as new Bcr-Abl inhibitors by hybriding the structural moieties from GNF-7, ponatinib and nilotinib.	pyrimidine alkynyl	12-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
26195136-1	2015	A series of pyrimidine alkynyl derivatives were designed and synthesized as new Bcr-Abl inhibitors by hybriding the structural moieties from GNF-7, ponatinib and nilotinib.	ponatinib	148-157	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
26195136-1	2015	A series of pyrimidine alkynyl derivatives were designed and synthesized as new Bcr-Abl inhibitors by hybriding the structural moieties from GNF-7, ponatinib and nilotinib.	nilotinib	162-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
25999467-0	2015	Tyrosine phosphorylation of RAS by ABL allosterically enhances effector binding.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
25999467-5	2015	Here we report that ABL phosphorylates tyrosine 137 of H-, K-, and NRAS.	Tyrosine	39-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-23
25999467-6	2015	Increased RIN1 levels enhanced HRAS-Tyr(137) phosphorylation by nearly 5-fold, suggesting that RAS-stimulated RIN1 can drive ABL-mediated RAS modification in a feedback circuit.	Tyrosine	36-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	125-128
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.	Ribavirin	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-152
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 Mesylate	126-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-152
26310847-5	2015	Moreover, ROS1, HCK, ABL1, ABL2, JAK3, LCK and TYR03 were identified as candidate kinases responsible for the phosphorylation of Tyr(136) of LIX1L.	Tyrosine	129-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-25
26008977-4	2015	A 72-h rigosertib treatment was found to inhibit cell growth, induce apoptosis, reduce phosphorylation of the breakpoint cluster region-c (BCR)-ABL and its substrate Crk-L, and increase the activities of caspase 3 and poly (ADP-ribose) polymerase (PARP).	ON 01910	7-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-147
26008977-6	2015	Rigosertib also potently inhibited the growth of ABL TKI-resistant cells, and cotreatment with ABL TKIs and rigosertib induced higher cytotoxicity.	ON 01910	0-10	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-52
26008977-6	2015	Rigosertib also potently inhibited the growth of ABL TKI-resistant cells, and cotreatment with ABL TKIs and rigosertib induced higher cytotoxicity.	ON 01910	108-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-52
26008977-7	2015	These results indicate that rigosertib treatment may be a powerful strategy against ABL TKI-resistant cells and could enhance the cytotoxic effects of ABL TKIs.	ON 01910	28-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-87
26008977-7	2015	These results indicate that rigosertib treatment may be a powerful strategy against ABL TKI-resistant cells and could enhance the cytotoxic effects of ABL TKIs.	ON 01910	28-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	151-154
26346348-3	2015	Among ALL subtypes, BCR-ABL+ ALL cells exhibited the highest sensitivity to 2-DG suggesting BCR-ABL expression may be linked to this increased vulnerability.	Deoxyglucose	76-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
26134485-5	2015	Proximity-driven intramolecular azo coupling was showcased in cyclization of a beta-hairpin peptide, structural features of the azo linked cyclic peptide was elucidated by NMR, and intermolecular azo coupling was achieved between an SH3 protein Abl-SH3 and its polyproline peptide ligands at specific tyrosine residues.	anthrone	32-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	245-248
26134485-5	2015	Proximity-driven intramolecular azo coupling was showcased in cyclization of a beta-hairpin peptide, structural features of the azo linked cyclic peptide was elucidated by NMR, and intermolecular azo coupling was achieved between an SH3 protein Abl-SH3 and its polyproline peptide ligands at specific tyrosine residues.	anthrone	128-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	245-248
26134485-5	2015	Proximity-driven intramolecular azo coupling was showcased in cyclization of a beta-hairpin peptide, structural features of the azo linked cyclic peptide was elucidated by NMR, and intermolecular azo coupling was achieved between an SH3 protein Abl-SH3 and its polyproline peptide ligands at specific tyrosine residues.	Tyrosine	301-309	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	245-248
26290562-11	2015	On evaluation, he was found to be BCR-ABL positive and responded well to imatinib treatment.	Imatinib Mesylate	73-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
26343430-0	2015	Coupling a universal DNA circuit with graphene sheets/polyaniline/AuNPs nanocomposites for the detection of BCR/ABL fusion gene.	Graphite	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
26343430-0	2015	Coupling a universal DNA circuit with graphene sheets/polyaniline/AuNPs nanocomposites for the detection of BCR/ABL fusion gene.	polyaniline	54-65	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-115
26343430-1	2015	This article described a novel method by coupling a universal DNA circuit with graphene sheets/polyaniline/AuNPs nanocomposites (GS/PANI/AuNPs) for highly sensitive and specific detection of BCR/ABL fusion gene (bcr/abl) in chronic myeloid leukemia (CML).	Graphite	79-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	191-198
26343430-1	2015	This article described a novel method by coupling a universal DNA circuit with graphene sheets/polyaniline/AuNPs nanocomposites (GS/PANI/AuNPs) for highly sensitive and specific detection of BCR/ABL fusion gene (bcr/abl) in chronic myeloid leukemia (CML).	Graphite	79-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	212-219
26343430-1	2015	This article described a novel method by coupling a universal DNA circuit with graphene sheets/polyaniline/AuNPs nanocomposites (GS/PANI/AuNPs) for highly sensitive and specific detection of BCR/ABL fusion gene (bcr/abl) in chronic myeloid leukemia (CML).	polyaniline	95-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	191-198
26343430-1	2015	This article described a novel method by coupling a universal DNA circuit with graphene sheets/polyaniline/AuNPs nanocomposites (GS/PANI/AuNPs) for highly sensitive and specific detection of BCR/ABL fusion gene (bcr/abl) in chronic myeloid leukemia (CML).	polyaniline	95-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	212-219
26346348-3	2015	Among ALL subtypes, BCR-ABL+ ALL cells exhibited the highest sensitivity to 2-DG suggesting BCR-ABL expression may be linked to this increased vulnerability.	Deoxyglucose	76-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-99
26346348-4	2015	To confirm the role of BCR-ABL, we constructed a NALM6/BCR-ABL stable cell line and found significant increase in 2-DG-induced apoptosis compared to control.	Deoxyglucose	114-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
26346348-4	2015	To confirm the role of BCR-ABL, we constructed a NALM6/BCR-ABL stable cell line and found significant increase in 2-DG-induced apoptosis compared to control.	Deoxyglucose	114-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
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 Mesylate	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
25842192-2	2015	Dasatinib is a small-molecule inhibitor of the tyrosine kinases SRC and ABL that has been approved for the treatment of chronic myeloid leukemia (CML) and Philadelphia chromosome-positive acute lymphoblastic leukemia.	Dasatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-75
26316776-2	2015	Imatinib mesylate is an oral small molecular tyrosine kinase inhibitor that mainly targets abl, c-KIT, and PDGFRalpha.	Imatinib Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-94
26235616-0	2015	c-Abl Mediated Tyrosine Phosphorylation of Aha1 Activates Its Co-chaperone Function in Cancer Cells.	Tyrosine	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
26235616-4	2015	Here, we show that c-Abl kinase phosphorylates Y223 in human Aha1 (hAha1), promoting its interaction with Hsp90.	y223	47-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-24
26264857-0	2015	Design of substrate-based BCR-ABL kinase inhibitors using the cyclotide scaffold.	Cyclotides	62-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
25900790-0	2015	Long-term efficacy and safety of nilotinib therapy after imatinib failure in eosinophilic myeloproliferative neoplasm and ETV6-ABL rearrangement.	nilotinib	33-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-130
26264857-2	2015	Current CML treatments rely on the long-term use of tyrosine kinase inhibitors (TKIs), which target the ATP binding site of BCR-ABL.	Adenosine Triphosphate	104-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
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 Mesylate	240-248	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-57
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.	Dasatinib	268-277	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-57
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 Mesylate	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	188-195
26239229-0	2015	Anti-leukemic activity of axitinib against cells harboring the BCR-ABL T315I point mutation.	Axitinib	26-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
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.	Curcumin	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-112
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 Mesylate	50-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-112
25979368-6	2015	Here, we reported that curcumin induced apoptosis by inhibition of AKT/mTOR and ABL/STAT5 signaling, down-regulation of BCR/ABL expression, and induction of the BCL2/BAX imbalance.	Curcumin	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-83
25979368-6	2015	Here, we reported that curcumin induced apoptosis by inhibition of AKT/mTOR and ABL/STAT5 signaling, down-regulation of BCR/ABL expression, and induction of the BCL2/BAX imbalance.	Curcumin	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-127
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.	Curcumin	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	163-170
26208715-7	2015	Imatinib treatment was resumed in the patients" posttransplantation following detection of BCR-ABL transcripts.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
26022120-10	2015	Lysosomal inhibitor chloroquine restored Bcl-xL and Bcr/Abl protein levels and inhibited caspase-3 activation.	Chloroquine	20-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-59
26149173-1	2015	BACKGROUND: Bosutinib is a recently approved ABL inhibitor.	bosutinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-48
26266095-2	2015	We report the challenging case of a CML patient who was resistant to multiple TKIs because of different emerging ABL mutations and became pregnant while on Nilotinib therapy despite repeated and clear discouragement to conceive.	nilotinib	156-165	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-116
26052668-0	2015	Discovery of novel Bcr-Abl inhibitors with diacylated piperazine as the flexible linker.	diacylated piperazine	43-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
26052668-1	2015	Forty-two compounds (series 8, 9 and 10) incorporated with diacylated piperazine have been synthesized and evaluated as novel Bcr-Abl inhibitors based on "six-atom linker".	diacylated piperazine	59-80	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
26022079-0	2015	Design, synthesis, and biological activity of phenyl-pyrazole derivatives as BCR-ABL kinase inhibitors.	phenyl-pyrazole	46-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-84
26222440-5	2015	This fluorescence polarization (FP) assay is based on a purified recombinant ABL protein consisting of the N-cap, SH3 and SH2 domains plus the SH2-kinase linker (N32L protein) and a short fluorescein-labeled probe peptide that binds to the SH3 domain.	n-cap	107-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-80
26222440-5	2015	This fluorescence polarization (FP) assay is based on a purified recombinant ABL protein consisting of the N-cap, SH3 and SH2 domains plus the SH2-kinase linker (N32L protein) and a short fluorescein-labeled probe peptide that binds to the SH3 domain.	Fluorescein	188-199	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-80
26222440-9	2015	Secondary assays showed that one of these hit compounds, the antithrombotic drug dipyridamole, enhances ABL kinase activity in vitro to a greater extent than the previously described ABL agonist, DPH.	Dipyridamole	81-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-107
26222440-9	2015	Secondary assays showed that one of these hit compounds, the antithrombotic drug dipyridamole, enhances ABL kinase activity in vitro to a greater extent than the previously described ABL agonist, DPH.	Dipyridamole	81-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	183-186
26222440-9	2015	Secondary assays showed that one of these hit compounds, the antithrombotic drug dipyridamole, enhances ABL kinase activity in vitro to a greater extent than the previously described ABL agonist, DPH.	Phenytoin	196-199	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	183-186
26022079-1	2015	4-(Pyridin-3-yl)-1H-pyrazol-1-yl-phenyl-3-benzamide derivatives have been proposed as new BCR-ABL tyrosine kinase inhibitors by using combinational strategies of scaffold hopping and conformational constraint.	4-(pyridin-3-yl)-1h-pyrazol-1-yl-phenyl-3-benzamide	0-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
25825203-0	2015	A derivative of epigallocatechin-3-gallate induces apoptosis via SHP-1-mediated suppression of BCR-ABL and STAT3 signalling in chronic myelogenous leukaemia.	epigallocatechin gallate	16-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
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 Mesylate	167-175	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
25825203-6	2015	EGCG-MP induced Src-homology 2 domain-containing tyrosine phosphatase 1 (SHP-1) leading decreased oncogenic protein BCR-ABL and STAT3 phosphorylation in CML cells, compared with treatment with EGCG.	epigallocatechin gallate	0-4	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	116-123
25825203-8	2015	Conversely, depletion of SHP-1 or application of the tyrosine phosphatase inhibitor pervanadate blocked the ability of EGCG-MP to suppress phosphorylation of BCR-ABL and STAT3, and the expression of survival genes downstream of STAT3.	pervanadate	84-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-165
25825203-8	2015	Conversely, depletion of SHP-1 or application of the tyrosine phosphatase inhibitor pervanadate blocked the ability of EGCG-MP to suppress phosphorylation of BCR-ABL and STAT3, and the expression of survival genes downstream of STAT3.	egcg-mp	119-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-165
25825203-10	2015	Immunohistochemistry revealed increased caspase 3 and SHP-1 activity and decreased phosphorylation of BCR-ABL in the EGCG-MP-treated group relative to that in the EGCG-treated group.	epigallocatechin gallate	117-121	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
25825203-11	2015	CONCLUSIONS AND IMPLICATIONS: EGCG-MP induced SHP-1-mediated inhibition of BCR-ABL and STAT3 signalling in vitro and in vivo more effectively than EGCG.	epigallocatechin gallate	30-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-82
25963192-0	2015	CD-200 induces apoptosis and inhibits Bcr-Abl signaling in imatinib-resistant chronic myeloid leukemia with T315I mutation.	Imatinib Mesylate	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-45
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 Mesylate	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	182-189
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 Mesylate	104-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	186-189
25944899-4	2015	c-Abl and HIPK2 synergized in activating p53 on apoptotic promoters in a reporter assay, and c-Abl was required for endogenous HIPK2 accumulation and phosphorylation of p53 at Ser(46) in response to DNA damage by gamma- and UV radiation.	Serine	176-179	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
25944899-4	2015	c-Abl and HIPK2 synergized in activating p53 on apoptotic promoters in a reporter assay, and c-Abl was required for endogenous HIPK2 accumulation and phosphorylation of p53 at Ser(46) in response to DNA damage by gamma- and UV radiation.	Serine	176-179	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-98
25944899-8	2015	These data demonstrate a new mechanism for the induction of DNA damage-induced apoptosis by c-Abl and illustrate network interactions between serine/threonine and tyrosine kinases that dictate cell fate.	Serine	142-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-97
25944899-8	2015	These data demonstrate a new mechanism for the induction of DNA damage-induced apoptosis by c-Abl and illustrate network interactions between serine/threonine and tyrosine kinases that dictate cell fate.	Threonine	149-158	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	92-97
26458641-4	2015	All of them had the BCR-ABL fusion gene and responded well to treatment with imatinib mesylate.	Imatinib Mesylate	77-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27
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.	Hydroxyurea	191-202	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
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 Mesylate	207-215	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
26304076-0	2015	[The prognostic value of early BCR-ABL transcripts level in 251 patients with chronic myeloid leukemia after treatment with imatinib].	Imatinib Mesylate	124-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
26139550-2	2015	Nilotinib is a second generation TKI targeting the oncoprotein BCR-ABL used in patients in the chronic phase of CML.	nilotinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
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 Mesylate	92-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-55
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.	Dasatinib	105-114	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 Mesylate	38-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	265-268
25996455-6	2015	In contrast, Dasatinib binding to the active kinase form may activate a broader ensemble of allosteric pathways that are less dependent on the phosphorylation status of Abl and provide a better balance between the efficiency and resilience of signaling routes.	Dasatinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	169-172
26198949-0	2015	[Effect of indomethacin on BCR/ABL-Wnt/beta-catenin pathway in K562 cells].	Indomethacin	11-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-34
26198949-5	2015	Indomethacin treatment dose-dependently decreased the protein level of pBCR/ABL and total BCR/ABL without affecting bcr-abl mRNA expressions.	Indomethacin	0-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-79
26198949-5	2015	Indomethacin treatment dose-dependently decreased the protein level of pBCR/ABL and total BCR/ABL without affecting bcr-abl mRNA expressions.	Indomethacin	0-12	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
26198949-7	2015	CONCLUSION: Indomethacin inhibits the proliferation of K562 cells by suppressing the activity of bcr-abl-Wnt/beta-catenin pathway.	Indomethacin	12-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	101-104
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 Mesylate	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&gt;10%, &gt;1%-&lt;= 10% and &lt;= 1% were found in 92, 94 and 64 patients, their PFS were 53.3%, 71.3% and 86.2%, respectively.	Imatinib Mesylate	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&gt;10%, 50&gt;1% -&lt;= 10% and 110 &lt;= 1%, their PFS were 27.3% vs 66.0% vs 82.7% (P&lt;0.05), the OS of three groups were 86.4% vs 94.0% vs 100%.	Imatinib Mesylate	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 Mesylate	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 Mesylate	138-146	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	84-91
26126715-8	2015	When coexpressed in HEK293T cells, ABL phosphorylated DGCR8 at Tyr(267).	Tyrosine	63-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
26126715-11	2015	These results reveal a new pathway in the DNA damage response wherein ABL-dependent tyrosine phosphorylation of DGCR8 stimulates the processing of selective primary miRNAs.	Tyrosine	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-73
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 Mesylate	129-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
26106294-0	2015	Reactive oxygen species trigger motoneuron death in non-cell-autonomous models of ALS through activation of c-Abl signaling.	Reactive Oxygen Species	0-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	108-113
26106294-8	2015	Finally, we find that blocking the opening of the mitochondrial permeability transition pore with cyclosporine A, or inhibiting mitochondrial calcium uptake with Ru360, reduces ROS production and c-Abl activation.	Cyclosporine	98-112	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	196-201
26106294-8	2015	Finally, we find that blocking the opening of the mitochondrial permeability transition pore with cyclosporine A, or inhibiting mitochondrial calcium uptake with Ru360, reduces ROS production and c-Abl activation.	Calcium	142-149	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	196-201
26106294-8	2015	Finally, we find that blocking the opening of the mitochondrial permeability transition pore with cyclosporine A, or inhibiting mitochondrial calcium uptake with Ru360, reduces ROS production and c-Abl activation.	Ru 360	162-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	196-201
26106294-10	2015	ROS production, mediated at least in part through mitochondrial alterations, trigger c-Abl signaling and lead to motoneuron death.	Reactive Oxygen Species	0-3	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-90
26336545-7	2015	The time to ES occurrence was significantly longer in the ABL group than in the No ABL group (p=0.04).	Einsteinium	12-14	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-61
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 Mesylate	96-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-81
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 Mesylate	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 Mesylate	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
25856345-9	2015	Finally, a small scale in vitro kinase assay screen demonstrated that LB has a potent inhibitory effect on multiple kinases, including PI3K, Src, EGFR, Tie2, lck, lyn, RTK5, FGFR1, Abl, and Flt.	lb	70-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	181-184
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 Mesylate	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 Mesylate	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 Mesylate	29-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
25795725-0	2015	c-Abl mediated tyrosine phosphorylation of paxillin regulates LPS-induced endothelial dysfunction and lung injury.	Tyrosine	15-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
25043303-5	2015	We show that phosphorylation of tyrosines 295 and 361 of Dok1 by Abl family kinases suppresses CrkI transforming activity, and that upon phosphorylation these tyrosines bind the SH2 domains of the Ras inhibitor p120 RasGAP.	Tyrosine	32-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-68
25795725-9	2015	Together, these results suggest that c-Abl mediated tyrosine phosphorylation of paxillin at Y31 and Y118 regulates LPS-mediated pulmonary vascular permeability and injury.	Tyrosine	52-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-42
25814671-6	2015	The Abl family kinases, c-Abl (Abl1) and Abl related gene (Arg, Abl2), phosphorylate several cytoskeletal effectors that mediate vascular permeability, including nonmuscle myosin light chain kinase, cortactin, vinculin, and beta-catenin.	Arginine	59-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-7
25946048-4	2015	Here we show that Abl family of non-receptor tyrosine kinases, comprised of Abl (ABL1) and Arg (ABL2), are activated downstream of the Met receptor, and that inhibition of Abl kinases dramatically suppresses HGF-induced cell scattering and tubulogenesis.	Arginine	91-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-21
25814671-6	2015	The Abl family kinases, c-Abl (Abl1) and Abl related gene (Arg, Abl2), phosphorylate several cytoskeletal effectors that mediate vascular permeability, including nonmuscle myosin light chain kinase, cortactin, vinculin, and beta-catenin.	Arginine	59-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-29
25814671-6	2015	The Abl family kinases, c-Abl (Abl1) and Abl related gene (Arg, Abl2), phosphorylate several cytoskeletal effectors that mediate vascular permeability, including nonmuscle myosin light chain kinase, cortactin, vinculin, and beta-catenin.	Arginine	59-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-35
25814671-6	2015	The Abl family kinases, c-Abl (Abl1) and Abl related gene (Arg, Abl2), phosphorylate several cytoskeletal effectors that mediate vascular permeability, including nonmuscle myosin light chain kinase, cortactin, vinculin, and beta-catenin.	Arginine	59-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-29
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	214-222	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-34
25882987-1	2015	BACKGROUND: Nilotinib inhibits the tyrosine kinase activity of ABL1/BCR-ABL1 and KIT, platelet-derived growth factor receptors (PDGFRs), and the discoidin domain receptor.	nilotinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-67
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 Mesylate	76-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-25
25754950-0	2015	Haematological cancer: BCL-ABL1 resistance mutation--breakthrough with axitinib.	Axitinib	71-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-31
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 Mesylate	140-148	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	22-26
25919613-1	2015	The hallmark of Philadelphia chromosome positive (Ph(+)) leukemia is the BCR/ABL kinase, which is successfully targeted by selective ATP competitors.	Adenosine Triphosphate	133-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-80
25644089-0	2015	Anti-cancer fatty-acid derivative induces autophagic cell death through modulation of PKM isoform expression profile mediated by bcr-abl in chronic myeloid leukemia.	Fatty Acids	12-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	129-136
25644089-4	2015	To develop a new strategy for the treatment of CML, we investigated the associations among bcr-abl, the cascade related to cancer energy metabolism, and autophagy induced by a fatty-acid derivative that we had previously reported as being an autophagy inducer.	Fatty Acids	176-186	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-98
25644089-5	2015	Here we report that a fatty-acid derivative, AIC-47, induced transcriptional repression of the bcr-abl gene and modulated the expression profile of PKM isoforms, resulting in autophagic cell death.	Fatty Acids	22-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-102
25897414-6	2015	Imatinib resistance was confirmed by a screening for ABL kinase domain E255K mutations, and dasatinib was administered.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-56
25770215-5	2015	Tyrosine phosphorylation of AKAP8 is induced by several tyrosine kinases, such as Src, Fyn, and c-Abl but not Syk.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-101
25894969-8	2015	One patient with lymphoid BC/Ph+ ALL who harbored a T315I ABL mutation and was treated with ponatinib was found to have developed a newly acquired V216M TP53 mutation (12% of transcripts) when becoming resistant to ponatinib.	ponatinib	92-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-61
25894969-9	2015	Ponatinib led to a decrease of ABL T315I positive transcripts from 47% before ponatinib treatment to 16% at the time of ponatinib resistance in this patient, suggesting that both TP53 and ABL mutations were present in the same clone and that the newly acquired TP53 mutation might have caused ponatinib resistance in this patient.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-34
25894969-9	2015	Ponatinib led to a decrease of ABL T315I positive transcripts from 47% before ponatinib treatment to 16% at the time of ponatinib resistance in this patient, suggesting that both TP53 and ABL mutations were present in the same clone and that the newly acquired TP53 mutation might have caused ponatinib resistance in this patient.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	188-191
25894969-9	2015	Ponatinib led to a decrease of ABL T315I positive transcripts from 47% before ponatinib treatment to 16% at the time of ponatinib resistance in this patient, suggesting that both TP53 and ABL mutations were present in the same clone and that the newly acquired TP53 mutation might have caused ponatinib resistance in this patient.	ponatinib	78-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-34
25894969-9	2015	Ponatinib led to a decrease of ABL T315I positive transcripts from 47% before ponatinib treatment to 16% at the time of ponatinib resistance in this patient, suggesting that both TP53 and ABL mutations were present in the same clone and that the newly acquired TP53 mutation might have caused ponatinib resistance in this patient.	ponatinib	120-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-34
25894969-9	2015	Ponatinib led to a decrease of ABL T315I positive transcripts from 47% before ponatinib treatment to 16% at the time of ponatinib resistance in this patient, suggesting that both TP53 and ABL mutations were present in the same clone and that the newly acquired TP53 mutation might have caused ponatinib resistance in this patient.	ponatinib	120-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-34
25694432-0	2015	The interaction of protein-tyrosine phosphatase alpha (PTPalpha) and RACK1 protein enables insulin-like growth factor 1 (IGF-1)-stimulated Abl-dependent and -independent tyrosine phosphorylation of PTPalpha.	Tyrosine	27-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	139-142
25694432-5	2015	We found that PTPalpha binds to the scaffold protein RACK1 and that RACK1 coordinates the IGF-1 receptor, PTPalpha, and Abl in a complex to enable IGF-1-stimulated and Abl-dependent PTPalpha-Tyr-789 phosphorylation.	Tyrosine	191-194	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	120-123
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 Mesylate	78-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-76
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.	Lapatinib	98-107	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-76
25849484-7	2015	Our data revealed that Imatinib (IM) induced BCR-ABL inhibition results in significant (p&lt;0.05) upregulation of Notch activity, assessed by Hes1 expression.	Imatinib Mesylate	23-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
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 Mesylate	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 Mesylate	224-232	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
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 Mesylate	34-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
25803821-2	2015	ABL inhibition by the tyrosine kinase inhibitor nilotinib is a first-line treatment for this disease.	nilotinib	48-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
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 Mesylate	58-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	7-14
25082234-6	2015	It can bind to BCR-ABL in the cytosol, where it is phosphorylated on tyrosine residues, and it maintains the proper compartmentalization in the nuclear bodies, where it acts as part of a PML network to regulate PTEN de-ubiquitination.	Tyrosine	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
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 Mesylate	181-189	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-169
25249015-1	2015	The SH2-containing adaptor protein Grb10 was first identified in a yeast screen as a new binding partner for BCR-ABL and associates with BCR-ABL in a tyrosine-dependent manner.	Tyrosine	150-158	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
25249015-1	2015	The SH2-containing adaptor protein Grb10 was first identified in a yeast screen as a new binding partner for BCR-ABL and associates with BCR-ABL in a tyrosine-dependent manner.	Tyrosine	150-158	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	137-144
25662515-12	2015	The Src and BCR-Abl inhibitors saracatinib and AZD0424, along with the previous four drugs, are in clinical trials for a variety of solid tumors including breast and lung cancers.	saracatinib	31-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
25801024-2	2015	In the current work, we report that the Bcr-Abl inhibitor and anti-leukemia agent ponatinib is also a first-in-class dual inhibitor of RIPK1 and RIPK3.	ponatinib	82-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
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).	nilotinib	200-209	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
25662515-12	2015	The Src and BCR-Abl inhibitors saracatinib and AZD0424, along with the previous four drugs, are in clinical trials for a variety of solid tumors including breast and lung cancers.	AZD-0424	47-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
25809097-12	2015	Stat5 is activated in the nuclear and cytosolic compartments of K562 cells and the S5-DBD-PA inhibitor most likely affects the viability of Bcr-Abl+ K562 cells through the inhibition of canonical Stat5 induced target gene transcription.	dbd-pa	86-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
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).	Dasatinib	213-222	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
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 Mesylate	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.	nilotinib	78-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-61
25547679-6	2015	Surprisingly, oligomycin-A sensitized leukemia cells to BCR-ABL inhibition at concentrations of 100- to 1,000-fold below those required for inhibition of respiration.	oligomycin A	14-26	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
25547679-2	2015	Through a large-scale synthetic lethal RNAi screen, we identified pyruvate dehydrogenase, the limiting enzyme for pyruvate entry into the mitochondrial tricarboxylic acid cycle, as critical for the survival of chronic myelogenous leukemia (CML) cells upon BCR-ABL inhibition.	Pyruvic Acid	66-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	256-263
25686603-0	2015	Axitinib effectively inhibits BCR-ABL1(T315I) with a distinct binding conformation.	Axitinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-38
25686603-2	2015	Introduction of ABL1 kinase inhibitors (for example, imatinib) has markedly improved patient survival, but acquired drug resistance remains a challenge.	Imatinib Mesylate	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-20
25686603-4	2015	The BCR-ABL1 kinase domain gatekeeper mutation Thr315Ile (T315I) confers resistance to all approved ABL1 inhibitors except ponatinib, which has toxicity limitations.	ponatinib	123-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-12
25686603-6	2015	Axitinib potently inhibited BCR-ABL1(T315I), at both biochemical and cellular levels, by binding to the active form of ABL1(T315I) in a mutation-selective binding mode.	Axitinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-36
25686603-6	2015	Axitinib potently inhibited BCR-ABL1(T315I), at both biochemical and cellular levels, by binding to the active form of ABL1(T315I) in a mutation-selective binding mode.	Axitinib	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-123
25686603-9	2015	Taken together, our findings demonstrate an unexpected opportunity to repurpose axitinib, an anti-angiogenic drug approved for renal cancer, as an inhibitor for ABL1 gatekeeper mutant drug-resistant leukaemia patients.	Axitinib	80-88	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	161-165
25742608-0	2015	Correction: ATRA-induced cellular differentiation and CD38 expression inhibits acquisition of BCR-ABL mutations for CML acquired resistance.	Tretinoin	12-16	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
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 Mesylate	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 Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
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 Mesylate	190-198	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
25547679-8	2015	Importantly, oligomycin-A enhanced elimination of BCR-ABL(+) leukemia cells by TKI in a mouse model and in primary blast crisis CML samples.	oligomycin A	13-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	50-57
25501124-0	2015	Dual inhibition of Bcr-Abl and Hsp90 by C086 potently inhibits the proliferation of imatinib-resistant CML cells.	Imatinib Mesylate	84-92	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
25575688-1	2015	Imatinib resistance has been associated with BCR-ABL alterations, but other mechanisms might be involved, like drug transporters.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
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 Mesylate	128-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	7-14
25499760-2	2015	Despite major advances in the treatment of this highly aggressive disease with potent inhibitors of the BCR-ABL kinase such as dasatinib, patients in remission frequently relapse due to persistent minimal residual disease possibly supported, at least in part, by salutary cytokine-driven signaling within the hematopoietic microenvironment.	Dasatinib	127-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
25499760-3	2015	Using a mouse model of Ph+ ALL that accurately mimics the genetics, clinical behavior, and therapeutic response of the human disease, we show that a combination of 2 agents approved by the US Food and Drug Administration (dasatinib and ruxolitinib, which inhibit BCR-ABL and Janus kinases, respectively), significantly extends survival by targeting parallel signaling pathways.	ruxolitinib	236-247	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	263-270
27308396-0	2015	Imatinib may be ABL to improve anti-angiogenic therapy.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-19
25526365-5	2015	Then, the dasatinib derivatives were synthesized and labeled with the fluorescent dye Alexa 488, and the binding and dissociation processes of Alexa 488-dasatinib and ABL1 were systematically investigated.	Dasatinib	10-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-171
25526365-6	2015	The dissociation constant and the dissociation rate for the Alexa 488-dasatinib-ABL1 complex were determined.	Alexa-488	60-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-84
25526365-6	2015	The dissociation constant and the dissociation rate for the Alexa 488-dasatinib-ABL1 complex were determined.	Dasatinib	70-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-84
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 Mesylate	59-67	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	107-114
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 Mesylate	177-185	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
25620702-5	2015	c-Abl/Arg regulates cellular proteasome abundance by controlling the PSMA7 subunit supply.	Arginine	6-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
25620702-7	2015	In response to oxidative stress, the c-Abl-mediated upregulation of proteasome level compensates for the proteasomal activity impairment induced by reactive oxygen species.	Reactive Oxygen Species	148-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-42
25450971-0	2015	Imatinib restores VASP activity and its interaction with Zyxin in BCR-ABL leukemic cells.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
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 Mesylate	20-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
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.	Doxorubicin	42-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
26218127-3	2015	As compared with a drug alone, co-treatment with IM and DOX loaded in nanoparticles allowed a sustained downregulation of BCR-ABL and significant CML stem cell death.	Doxorubicin	56-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
25450971-8	2015	Imatinib induced an increase in phosphorylation at Ser157 of VASP and decreased VASP and BCR-ABL interaction.	Imatinib Mesylate	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
25411098-3	2015	We evaluated the efficacy and safety of bosutinib, a tyrosine kinase inhibitor that potently inhibits Src and Abl, in patients with recurrent glioblastoma.	bosutinib	40-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-113
25075558-2	2015	Kinome-wide selectivity profiling of the library resulted in the identification of a series of 4-substituted 1H-pyrrolo[2,3-b]pyridines that exhibited potent inhibitory activity against two mitogen-activated protein kinases (MAPKs), TAK1 (MAP3K7) and MAP4K2, as well as pharmacologically well interrogated kinases such as p38alpha (MAPK14) and ABL.	substituted 1h-pyrrolo[2,3-b]pyridines	97-135	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	344-347
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 Mesylate	111-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
25469771-3	2015	Recently, the pyrazolo[3,4-d]pyrimidine 3 was reported as a dual c-Src/Abl inhibitor.	pyrazolo(3,4-d)pyrimidine	14-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	71-74
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 Mesylate	37-45	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96
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 Mesylate	44-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
25406390-0	2015	Studies of N(9)-arenthenyl purines as novel DFG-in and DFG-out dual Src/Abl inhibitors using 3D-QSAR, docking and molecular dynamics simulations.	n(9)-arenthenyl purines	11-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-75
25406390-2	2015	In order to explore the different structural features impacting the Src and Abl inhibitory activities of N(9)-arenethenyl purines and to investigate the molecular mechanisms of ligand-receptor interactions, a molecular modeling study combining the three-dimensional quantitative structure-activity relationship (3D-QSAR), molecular docking and molecular dynamics (MD) simulations was performed.	n(9)-arenethenyl purines	105-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-79
25406390-7	2015	In an energetic analysis, the MM-PBSA (molecular mechanics Poisson-Boltzmann surface) energy decomposition revealed that the van der Waals interactions were the major driving force for the binding of the DFG-in and DFG-out compounds to Src and Abl, especially the hydrophobic interactions between ligands and residues Ala403/380, Asp404/381, and Phe405/382 in DFG-out Src and Abl complexes.	poly(tetramethylene succinate-co-tetramethylene adipate)	33-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	244-247
25406390-7	2015	In an energetic analysis, the MM-PBSA (molecular mechanics Poisson-Boltzmann surface) energy decomposition revealed that the van der Waals interactions were the major driving force for the binding of the DFG-in and DFG-out compounds to Src and Abl, especially the hydrophobic interactions between ligands and residues Ala403/380, Asp404/381, and Phe405/382 in DFG-out Src and Abl complexes.	poly(tetramethylene succinate-co-tetramethylene adipate)	33-37	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	376-379
25406390-7	2015	In an energetic analysis, the MM-PBSA (molecular mechanics Poisson-Boltzmann surface) energy decomposition revealed that the van der Waals interactions were the major driving force for the binding of the DFG-in and DFG-out compounds to Src and Abl, especially the hydrophobic interactions between ligands and residues Ala403/380, Asp404/381, and Phe405/382 in DFG-out Src and Abl complexes.	1,3-Diphenylguanidine	204-207	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	244-247
25406390-7	2015	In an energetic analysis, the MM-PBSA (molecular mechanics Poisson-Boltzmann surface) energy decomposition revealed that the van der Waals interactions were the major driving force for the binding of the DFG-in and DFG-out compounds to Src and Abl, especially the hydrophobic interactions between ligands and residues Ala403/380, Asp404/381, and Phe405/382 in DFG-out Src and Abl complexes.	1,3-Diphenylguanidine	204-207	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	376-379
25406390-7	2015	In an energetic analysis, the MM-PBSA (molecular mechanics Poisson-Boltzmann surface) energy decomposition revealed that the van der Waals interactions were the major driving force for the binding of the DFG-in and DFG-out compounds to Src and Abl, especially the hydrophobic interactions between ligands and residues Ala403/380, Asp404/381, and Phe405/382 in DFG-out Src and Abl complexes.	1,3-Diphenylguanidine	215-218	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	244-247
25406390-7	2015	In an energetic analysis, the MM-PBSA (molecular mechanics Poisson-Boltzmann surface) energy decomposition revealed that the van der Waals interactions were the major driving force for the binding of the DFG-in and DFG-out compounds to Src and Abl, especially the hydrophobic interactions between ligands and residues Ala403/380, Asp404/381, and Phe405/382 in DFG-out Src and Abl complexes.	1,3-Diphenylguanidine	215-218	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	376-379
25406390-7	2015	In an energetic analysis, the MM-PBSA (molecular mechanics Poisson-Boltzmann surface) energy decomposition revealed that the van der Waals interactions were the major driving force for the binding of the DFG-in and DFG-out compounds to Src and Abl, especially the hydrophobic interactions between ligands and residues Ala403/380, Asp404/381, and Phe405/382 in DFG-out Src and Abl complexes.	1,3-Diphenylguanidine	215-218	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	244-247
25406390-7	2015	In an energetic analysis, the MM-PBSA (molecular mechanics Poisson-Boltzmann surface) energy decomposition revealed that the van der Waals interactions were the major driving force for the binding of the DFG-in and DFG-out compounds to Src and Abl, especially the hydrophobic interactions between ligands and residues Ala403/380, Asp404/381, and Phe405/382 in DFG-out Src and Abl complexes.	1,3-Diphenylguanidine	215-218	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	376-379
25406390-9	2015	These results can offer useful references for designing novel potential DFG-in and DFG-out dual Src/Abl inhibitors.	1,3-Diphenylguanidine	72-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-103
25406390-9	2015	These results can offer useful references for designing novel potential DFG-in and DFG-out dual Src/Abl inhibitors.	1,3-Diphenylguanidine	83-86	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-103
25831762-0	2015	[Inhibitors for ABL, KIT and PDGFR tyrosine kinases--imatinib, nitotinib, and dasatinib].	Imatinib Mesylate	53-61	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-19
25831762-0	2015	[Inhibitors for ABL, KIT and PDGFR tyrosine kinases--imatinib, nitotinib, and dasatinib].	Dasatinib	78-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	16-19
25483100-2	2015	Bcr-Abl/T315I is the predominant mutation that causes resistance to Imatinib.	Imatinib Mesylate	68-76	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
25548962-0	2015	Computational study of the "DFG-flip" conformational transition in c-Abl and c-Src tyrosine kinases.	1,3-Diphenylguanidine	28-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	67-72
25548962-3	2015	The conformation of a three-residue motif Asp-Phe-Gly (DFG) near the N-terminus of the long "activation" loop covering the catalytic site is known to have a critical impact on the activity of c-Abl and c-Src tyrosine kinases.	DFG peptide	42-53	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	192-197
25548962-3	2015	The conformation of a three-residue motif Asp-Phe-Gly (DFG) near the N-terminus of the long "activation" loop covering the catalytic site is known to have a critical impact on the activity of c-Abl and c-Src tyrosine kinases.	1,3-Diphenylguanidine	55-58	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	192-197
25548962-5	2015	In the present study, the string method with swarms-of-trajectories was used to computationally determine the reaction pathway connecting the two end-states, and umbrella sampling calculations were carried out to characterize the thermodynamic factors affecting the conformations of the DFG motif in c-Abl and c-Src kinases.	1,3-Diphenylguanidine	287-290	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	300-305
25548962-6	2015	According to the calculated free energy landscapes, the DFG-out conformation is clearly more favorable in the case of c-Abl than that of c-Src.	1,3-Diphenylguanidine	56-59	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	118-123
25548962-7	2015	The calculations also show that the protonation state of the aspartate residue in the DFG motif strongly affects the in/out conformational transition in c-Abl, although it has a much smaller impact in the case of c-Src due to local structural differences.	Aspartic Acid	61-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-158
25548962-7	2015	The calculations also show that the protonation state of the aspartate residue in the DFG motif strongly affects the in/out conformational transition in c-Abl, although it has a much smaller impact in the case of c-Src due to local structural differences.	1,3-Diphenylguanidine	86-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-158
25305453-0	2015	MiR-30e induces apoptosis and sensitizes K562 cells to imatinib treatment via regulation of the BCR-ABL protein.	Imatinib Mesylate	55-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	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 Mesylate	89-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	165-172
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 Mesylate	178-186	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	83-90
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 Mesylate	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 Mesylate	116-124	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
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 Mesylate	274-282	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-38
26618175-0	2015	Doxorubicin Differentially Induces Apoptosis, Expression of Mitochondrial Apoptosis-Related Genes, and Mitochondrial Potential in BCR-ABL1-Expressing Cells Sensitive and Resistant to Imatinib.	Doxorubicin	0-11	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	134-138
25881828-0	2015	ABL kinase inhibitory and antiproliferative activity of novel picolinamide based benzothiazoles.	picolinamide	62-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
25881828-0	2015	ABL kinase inhibitory and antiproliferative activity of novel picolinamide based benzothiazoles.	Benzothiazoles	81-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-3
25881828-1	2015	A series of novel picolinamide based benzothiazoles (17 final compounds), targeting both wild-type and the most resistant T315I mutant of Bcr-Abl kinase, has been designed and synthesized.	picolinamide	18-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
25881828-1	2015	A series of novel picolinamide based benzothiazoles (17 final compounds), targeting both wild-type and the most resistant T315I mutant of Bcr-Abl kinase, has been designed and synthesized.	Benzothiazoles	37-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
25196702-1	2015	Bosutinib is an oral, dual SRC/ABL1 tyrosine kinase inhibitor for resistant/intolerant chronic myeloid leukaemia (CML).	bosutinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-35
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 Mesylate	119-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
25608112-8	2015	In particular, BCR-ABL promotes Casein Kinase II-mediated PTEN tail phosphorylation with consequent inhibition of the phosphatase activity toward PIP3.	PIP3	146-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
25351958-6	2015	Bosutinib and dasatinib were originally developed as inhibitors of the protein tyrosine kinases Bcr-Abl and Src but we show that, surprisingly, the effects of bosutinib and dasatinib on macrophage polarization are the result of the inhibition of the salt-inducible kinases.	bosutinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-111
25351958-6	2015	Bosutinib and dasatinib were originally developed as inhibitors of the protein tyrosine kinases Bcr-Abl and Src but we show that, surprisingly, the effects of bosutinib and dasatinib on macrophage polarization are the result of the inhibition of the salt-inducible kinases.	Dasatinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-111
25351958-6	2015	Bosutinib and dasatinib were originally developed as inhibitors of the protein tyrosine kinases Bcr-Abl and Src but we show that, surprisingly, the effects of bosutinib and dasatinib on macrophage polarization are the result of the inhibition of the salt-inducible kinases.	bosutinib	159-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-111
25351958-6	2015	Bosutinib and dasatinib were originally developed as inhibitors of the protein tyrosine kinases Bcr-Abl and Src but we show that, surprisingly, the effects of bosutinib and dasatinib on macrophage polarization are the result of the inhibition of the salt-inducible kinases.	Dasatinib	173-182	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-111
26291130-1	2015	We previously showed that incubation of chronic myeloid leukemia (CML) cells in very low oxygen selects a cell subset where the oncogenetic BCR/Abl protein is suppressed and which is thereby refractory to tyrosine kinase inhibitors used for CML therapy.	Oxygen	89-95	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
26291130-5	2015	Surprisingly, the drug also concentration-dependently enforced the maintenance of BCR/Abl signaling in low oxygen, an effect which was paralleled by the rescue of sensitivity of stem cell potential to IM.	Oxygen	107-113	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
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 Mesylate	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 Mesylate	54-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	11-15
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 Mesylate	39-56	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
31388478-1	2015	Introduction: Bosutinib is a dual ABL1 and SRC third generation tyrosine kinase inhibitor (TKI) indicated for the treatment of patients with chronic myelogenous leukemia (CML) resistant to or intolerant of other BCR-ABL1 inhibitors.	bosutinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-38
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 Mesylate	36-44	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
25821558-0	2015	HSP90 inhibitor AUY922 induces cell death by disruption of the Bcr-Abl, Jak2 and HSP90 signaling network complex in leukemia cells.	5-(2,4-dihydroxy-5-isopropylphenyl)-4-(4-morpholin-4-ylmethylphenyl)isoxazole-3-carboxylic acid ethylamide	16-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
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 Mesylate	170-178	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-169
25821558-6	2015	Tyrosine phosphorylation of Bcr-Abl showed a dose-dependent decrease in 32Dp210T315I following AUY922 treatment for 16h.	Tyrosine	0-8	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-35