PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 32068648-0 2021 B-Cell Precursor-Acute Lymphoblastic Leukemia With EBF1-PDGFRB Fusion Treated With Hematopoietic Stem Cell Transplantation and Imatinib: A Case Report and Literature Review. imatinib 127-135 EBF transcription factor 1 Homo sapiens 51-55 32068648-0 2021 B-Cell Precursor-Acute Lymphoblastic Leukemia With EBF1-PDGFRB Fusion Treated With Hematopoietic Stem Cell Transplantation and Imatinib: A Case Report and Literature Review. imatinib 127-135 platelet derived growth factor receptor beta Homo sapiens 56-62 31845621-3 2020 One case was severe with bilateral optic neuritis and transverse myelitis that was AQP4 IgG and myelin oligodendrocyte glycoprotein (MOG) IgG negative and improved after plasma exchange and withdrawal of imatinib. imatinib 204-212 myelin oligodendrocyte glycoprotein Homo sapiens 96-131 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 31950222-1 2020 The current study was designed to evaluate potential enhancement of the anticancer activity of imatinib mesylate (IM) with dipyridamole (DIP) and to investigate the underlying mechanisms of the combined therapy (IM/DIP) to reduce hepatotoxicity of IM in solid Ehrlich carcinoma (SEC)-bearing mice. imatinib 95-112 protein inhibitor of activated STAT 2 Mus musculus 137-140 31919789-0 2020 S2P peptide-conjugated PLGA-Maleimide-PEG nanoparticles containing Imatinib for targeting drug delivery to atherosclerotic plaques. imatinib 67-75 membrane bound transcription factor peptidase, site 2 Homo sapiens 0-3 31919789-1 2020 BACKGROUND: Imatinib is a platelet-derived growth factor receptor (PDGFR) inhibitor with very low water solubility. imatinib 12-20 platelet derived growth factor receptor beta Homo sapiens 26-65 31919789-1 2020 BACKGROUND: Imatinib is a platelet-derived growth factor receptor (PDGFR) inhibitor with very low water solubility. imatinib 12-20 platelet derived growth factor receptor beta Homo sapiens 67-72 31919789-5 2020 OBJECTIVES: The objective of this study is the targeting drug delivery to atherosclerotic plaques by using imatinib-loaded nanoparticles modified by S2P peptide. imatinib 107-115 membrane bound transcription factor peptidase, site 2 Homo sapiens 149-152 31950222-13 2020 DIP as an adjuvant therapy potentiated the cytotoxic effect of IM, ameliorated its hepatic toxicity, and showed synergistic effect with IM in vitro cell lines. imatinib 63-65 protein inhibitor of activated STAT 2 Mus musculus 0-3 31950222-13 2020 DIP as an adjuvant therapy potentiated the cytotoxic effect of IM, ameliorated its hepatic toxicity, and showed synergistic effect with IM in vitro cell lines. imatinib 136-138 protein inhibitor of activated STAT 2 Mus musculus 0-3 31950222-14 2020 Furthermore, the resistance against IM therapy may be overcome by the use of DIP independent on mdr-1 gene expression. imatinib 36-38 protein inhibitor of activated STAT 2 Mus musculus 77-80 31950222-14 2020 Furthermore, the resistance against IM therapy may be overcome by the use of DIP independent on mdr-1 gene expression. imatinib 36-38 malic enzyme complex, mitochondrial Mus musculus 96-101 31930541-0 2020 Betulinic acid restores imatinib sensitivity in BCR-ABL1 kinase-independent, imatinib-resistant chronic myeloid leukemia by increasing HDAC3 ubiquitination and degradation. imatinib 24-32 BCR activator of RhoGEF and GTPase Homo sapiens 48-56 31930541-3 2020 Furthermore, betulinic acid (BA), a lupane-type pentacyclic triterpenoid saponin isolated from birch trees, restored IM sensitivity in the BCR-ABL1 kinase-independent, IM-resistant primary cells and in K562R cells, as well as in primary CD34+ bone marrow cells from CML patients. imatinib 117-119 BCR activator of RhoGEF and GTPase Homo sapiens 139-147 31930541-4 2020 We found that BA restored IM sensitivity through inhibition of HDAC3 accumulation in cells, and that this was mediated by BA-dependent ubiquitination and degradation of HDAC3. imatinib 26-28 histone deacetylase 3 Homo sapiens 63-68 31930541-6 2020 Our findings demonstrated that HDAC3 is an essential factor in BCR-ABL1 kinase-independent IM resistance, and that BA in combination with IM may be a novel treatment strategy for overcoming IM resistance in CML. imatinib 91-93 histone deacetylase 3 Homo sapiens 31-36 31881245-0 2020 Lyn regulates creatine uptake in an imatinib-resistant CML cell line. imatinib 36-44 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 0-3 31881245-2 2020 We previously demonstrated that the imatinib-resistant CML cells (Myl-R) contained elevated Lyn activity and intracellular creatine pools compared to imatinib-sensitive Myl cells. imatinib 36-44 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 92-95 31930541-0 2020 Betulinic acid restores imatinib sensitivity in BCR-ABL1 kinase-independent, imatinib-resistant chronic myeloid leukemia by increasing HDAC3 ubiquitination and degradation. imatinib 24-32 histone deacetylase 3 Homo sapiens 135-140 31930541-0 2020 Betulinic acid restores imatinib sensitivity in BCR-ABL1 kinase-independent, imatinib-resistant chronic myeloid leukemia by increasing HDAC3 ubiquitination and degradation. imatinib 77-85 BCR activator of RhoGEF and GTPase Homo sapiens 48-56 31930541-2 2020 Through in vitro studies, we observed that HDAC3 levels were elevated in BCR-ABL1 kinase-independent, IM-resistant primary cells from CML patients and in IM-resistant K562 (K562R) cells and that downregulation of HDAC3 could enhance IM efficacy in K562R cells. imatinib 102-104 histone deacetylase 3 Homo sapiens 43-48 31930541-2 2020 Through in vitro studies, we observed that HDAC3 levels were elevated in BCR-ABL1 kinase-independent, IM-resistant primary cells from CML patients and in IM-resistant K562 (K562R) cells and that downregulation of HDAC3 could enhance IM efficacy in K562R cells. imatinib 102-104 BCR activator of RhoGEF and GTPase Homo sapiens 73-81 31930541-2 2020 Through in vitro studies, we observed that HDAC3 levels were elevated in BCR-ABL1 kinase-independent, IM-resistant primary cells from CML patients and in IM-resistant K562 (K562R) cells and that downregulation of HDAC3 could enhance IM efficacy in K562R cells. imatinib 154-156 histone deacetylase 3 Homo sapiens 43-48 31930541-2 2020 Through in vitro studies, we observed that HDAC3 levels were elevated in BCR-ABL1 kinase-independent, IM-resistant primary cells from CML patients and in IM-resistant K562 (K562R) cells and that downregulation of HDAC3 could enhance IM efficacy in K562R cells. imatinib 154-156 histone deacetylase 3 Homo sapiens 43-48 31857719-0 2020 TAS-116 inhibits oncogenic KIT signalling on the Golgi in both imatinib-naive and imatinib-resistant gastrointestinal stromal tumours. imatinib 63-71 KIT proto-oncogene receptor tyrosine kinase Mus musculus 27-30 31857719-1 2020 BACKGROUND: Despite the effectiveness of imatinib mesylate (IM), most gastrointestinal stromal tumours (GISTs) develop IM resistance, mainly due to the additional kinase-domain mutations accompanied by concomitant reactivation of KIT tyrosine kinase. imatinib 119-121 KIT proto-oncogene receptor tyrosine kinase Mus musculus 230-233 31857719-6 2020 RESULTS: TAS-116 inhibited growth and induced apoptosis in both IM-naive and IM-resistant GIST cell lines with KIT activation. imatinib 77-79 KIT proto-oncogene receptor tyrosine kinase Mus musculus 111-114 31833955-5 2020 Targeted therapies of KIT-altered melanoma patients is based in KIT inhibitor (mostly imatinib, nilotinib), although for both melanoma subtypes, results are for now disappointing as compared with BRAF and MEK inhibitors in BRAF-mutated melanoma. imatinib 86-94 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 22-25 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 31747806-0 2020 Acquired neuro-secretory defect in growth hormone secretion due to Imatinib mesylate and the efficacy of growth hormone therapy in children with chronic myeloid leukemia. imatinib 67-84 growth hormone 1 Homo sapiens 35-49 31747806-2 2020 The study was planned to assess the GHRH-GH-IGF1 axis in children with CML, receiving Imatinib and to evaluate the efficacy of human growth hormone (hGH) therapy. imatinib 86-94 growth hormone releasing hormone Homo sapiens 36-40 31747806-2 2020 The study was planned to assess the GHRH-GH-IGF1 axis in children with CML, receiving Imatinib and to evaluate the efficacy of human growth hormone (hGH) therapy. imatinib 86-94 insulin like growth factor 1 Homo sapiens 44-48 31955347-4 2020 Considering the relationship between ATP and cancer, we aimed to evaluate the influence of imatinib mesylate on the expressions and functions of the NTPDase and ecto-5"-nucleotidase (CD73) enzymes in imatinib-sensitive and -resistant K-562 cell lines. imatinib 91-108 5'-nucleotidase ecto Homo sapiens 161-181 31955347-4 2020 Considering the relationship between ATP and cancer, we aimed to evaluate the influence of imatinib mesylate on the expressions and functions of the NTPDase and ecto-5"-nucleotidase (CD73) enzymes in imatinib-sensitive and -resistant K-562 cell lines. imatinib 91-108 5'-nucleotidase ecto Homo sapiens 183-187 31955347-4 2020 Considering the relationship between ATP and cancer, we aimed to evaluate the influence of imatinib mesylate on the expressions and functions of the NTPDase and ecto-5"-nucleotidase (CD73) enzymes in imatinib-sensitive and -resistant K-562 cell lines. imatinib 91-99 5'-nucleotidase ecto Homo sapiens 161-181 31955347-4 2020 Considering the relationship between ATP and cancer, we aimed to evaluate the influence of imatinib mesylate on the expressions and functions of the NTPDase and ecto-5"-nucleotidase (CD73) enzymes in imatinib-sensitive and -resistant K-562 cell lines. imatinib 91-99 5'-nucleotidase ecto Homo sapiens 183-187 31955347-6 2020 However, when treated with imatinib mesylate for 24 h, the expression of ENTPD1, -2, -3 and -5 increased, leading to a higher nucleotides hydrolysis rate. imatinib 27-44 ectonucleoside triphosphate diphosphohydrolase 1 Homo sapiens 73-94 31955347-8 2020 On the other hand, we observed that imatinib-resistant K-562 cells presented a decrease in nucleotide hydrolysis and expressions of ENTPD1 and -5. imatinib 36-44 ectonucleoside triphosphate diphosphohydrolase 1 Homo sapiens 132-145 31926242-9 2020 Imatinib administration exhibited significant decreases in serum lipid parameters, CRP, ALT, AST and ALP. imatinib 0-8 C-reactive protein Oryctolagus cuniculus 83-86 31995156-0 2020 Treatment-free remission in FIP1L1-PDGFRA-positive myeloid/lymphoid neoplasms with eosinophilia after imatinib discontinuation. imatinib 102-110 factor interacting with PAPOLA and CPSF1 Homo sapiens 28-34 31995156-1 2020 FIP1L1-PDGFRA-positive myeloid/lymphoid neoplasms with eosinophilia (MLN-eo) are exquisitely sensitive to imatinib. imatinib 106-114 factor interacting with PAPOLA and CPSF1 Homo sapiens 0-6 31995156-1 2020 FIP1L1-PDGFRA-positive myeloid/lymphoid neoplasms with eosinophilia (MLN-eo) are exquisitely sensitive to imatinib. imatinib 106-114 platelet derived growth factor receptor alpha Homo sapiens 7-13 31995156-10 2020 Our data demonstrate that imatinib can be safely stopped in FIP1L1-PDGFRA-positive MLN-eo because of a high treatment-free remission at 12 and 24 months and because most patients achieve a rapid second CMR after restart of imatinib. imatinib 26-34 factor interacting with PAPOLA and CPSF1 Homo sapiens 60-66 31995156-10 2020 Our data demonstrate that imatinib can be safely stopped in FIP1L1-PDGFRA-positive MLN-eo because of a high treatment-free remission at 12 and 24 months and because most patients achieve a rapid second CMR after restart of imatinib. imatinib 26-34 platelet derived growth factor receptor alpha Homo sapiens 67-73 31999327-0 2020 A cryptic imatinib-sensitive G3BP1-PDGFRB rearrangement in a myeloid neoplasm with eosinophilia. imatinib 10-18 cripto, FRL-1, cryptic family 1 Homo sapiens 2-9 31999327-0 2020 A cryptic imatinib-sensitive G3BP1-PDGFRB rearrangement in a myeloid neoplasm with eosinophilia. imatinib 10-18 G3BP stress granule assembly factor 1 Homo sapiens 29-34 31999327-0 2020 A cryptic imatinib-sensitive G3BP1-PDGFRB rearrangement in a myeloid neoplasm with eosinophilia. imatinib 10-18 platelet derived growth factor receptor beta Homo sapiens 35-41 31926242-10 2020 Additionally, imatinib induced significant decreases for aortic and hepatic MDA, aortic NO and hepatic PDGFR-beta, while significantly exhibited elevations in aortic and hepatic GSH, SOD and hepatic PPARgamma1 compared with HC animals. imatinib 14-22 platelet-derived growth factor receptor beta Oryctolagus cuniculus 103-113 31926242-10 2020 Additionally, imatinib induced significant decreases for aortic and hepatic MDA, aortic NO and hepatic PDGFR-beta, while significantly exhibited elevations in aortic and hepatic GSH, SOD and hepatic PPARgamma1 compared with HC animals. imatinib 14-22 peroxisome proliferator-activated receptor gamma Oryctolagus cuniculus 199-209 31926242-12 2020 Interestingly, imatinib could return serum CRP, ALP, hepatic SOD and PDGFR-beta to basal values. imatinib 15-23 C-reactive protein Oryctolagus cuniculus 43-46 31926242-12 2020 Interestingly, imatinib could return serum CRP, ALP, hepatic SOD and PDGFR-beta to basal values. imatinib 15-23 platelet-derived growth factor receptor beta Oryctolagus cuniculus 69-79 31957165-6 2020 Knockout of BRD4 in vitro suppressed KIT expression, which led to inactivation of the KIT/PI3K/AKT/mTOR pathway, impeded migration and cell growth and made the resistant GIST cells sensitive to imatinib. imatinib 194-202 bromodomain containing 4 Homo sapiens 12-16 32024476-9 2020 KIT secondary mutations were the only mechanism of resistance found across 10 imatinib-resistant GIST patients progressing to sunitinib or regorafenib. imatinib 78-86 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 0-3 31831854-4 2020 The expression level of MLF2 was related to the proliferation, colony-formation ability, and sensitivity to imatinib in K562 cells. imatinib 108-116 myeloid leukemia factor 2 Homo sapiens 24-28 31676982-11 2020 Interestingly, binding of Imatinib inside the catalytic domain of PARP-1 also suggests that it has caspase-independent properties in promoting cancer cell deaths. imatinib 26-34 poly (ADP-ribose) polymerase 1 Rattus norvegicus 66-72 31558067-0 2020 Efficacy of imatinib and chemotherapy in a pediatric patient with Philadelphia-like acute lymphoblastic leukemia with Ebf1-Pdgfrb fusion transcript. imatinib 12-20 EBF transcription factor 1 Homo sapiens 118-122 31558067-0 2020 Efficacy of imatinib and chemotherapy in a pediatric patient with Philadelphia-like acute lymphoblastic leukemia with Ebf1-Pdgfrb fusion transcript. imatinib 12-20 platelet derived growth factor receptor beta Homo sapiens 123-129 31957165-6 2020 Knockout of BRD4 in vitro suppressed KIT expression, which led to inactivation of the KIT/PI3K/AKT/mTOR pathway, impeded migration and cell growth and made the resistant GIST cells sensitive to imatinib. imatinib 194-202 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 37-40 31957165-7 2020 The expression of KIT was repressed by a BRD4 inhibitor JQ1, which also induced myristoylated-AKT-suppressible caspases 3 and 9 activities, induced LC3-II, exhibited dose-dependent therapeutic synergy with imatinib and attenuated the activation of the PI3K/AKT/mTOR pathway. imatinib 206-214 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 18-21 31957165-7 2020 The expression of KIT was repressed by a BRD4 inhibitor JQ1, which also induced myristoylated-AKT-suppressible caspases 3 and 9 activities, induced LC3-II, exhibited dose-dependent therapeutic synergy with imatinib and attenuated the activation of the PI3K/AKT/mTOR pathway. imatinib 206-214 bromodomain containing 4 Homo sapiens 41-45 31957165-7 2020 The expression of KIT was repressed by a BRD4 inhibitor JQ1, which also induced myristoylated-AKT-suppressible caspases 3 and 9 activities, induced LC3-II, exhibited dose-dependent therapeutic synergy with imatinib and attenuated the activation of the PI3K/AKT/mTOR pathway. imatinib 206-214 AKT serine/threonine kinase 1 Homo sapiens 94-97 31957165-8 2020 In comparison with their single therapy, the combination of JQ1/imatinib more efficiently suppressed the growth of xenografts and exhibited a reduction in KIT phosphorylation, a decrease in Ki-67 and in the levels of phosphorylated PI3K/AKT/mTOR and enhanced TUNEL staining. imatinib 64-72 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 155-158 31957165-8 2020 In comparison with their single therapy, the combination of JQ1/imatinib more efficiently suppressed the growth of xenografts and exhibited a reduction in KIT phosphorylation, a decrease in Ki-67 and in the levels of phosphorylated PI3K/AKT/mTOR and enhanced TUNEL staining. imatinib 64-72 AKT serine/threonine kinase 1 Homo sapiens 237-240 31957165-8 2020 In comparison with their single therapy, the combination of JQ1/imatinib more efficiently suppressed the growth of xenografts and exhibited a reduction in KIT phosphorylation, a decrease in Ki-67 and in the levels of phosphorylated PI3K/AKT/mTOR and enhanced TUNEL staining. imatinib 64-72 mechanistic target of rapamycin kinase Homo sapiens 241-245 31897102-5 2020 According to western blot analysis, the protein expression levels of Nrf2 and HO-1 were obviously higher in the other three groups than those in sham operation group (P<0.05), and they were remarkably higher in imatinib group than those in model group and inhibitor group (P<0.05). imatinib 214-222 heme oxygenase 1 Rattus norvegicus 78-82 31672491-7 2020 This suggests a potential clinical benefit of the metformin/imatinib combination by allowing the reduction in dose intensity of standard chemotherapy without compromising survival outcome and represents a potential faster track application for EwS patients. imatinib 60-68 EWS RNA binding protein 1 Homo sapiens 244-247 31914467-8 2020 CONCLUSIONS: In summary, Loeffler"s endocarditis caused by a myeloid and lymphoid neoplasm associated with eosinophilia and abnormalities of FIP1L1-PDGFRA rearrangement could be treated successfully with oral anticoagulation therapy and the tyrosine-kinase inhibitor imatinib. imatinib 268-276 factor interacting with PAPOLA and CPSF1 Homo sapiens 142-148 31914467-8 2020 CONCLUSIONS: In summary, Loeffler"s endocarditis caused by a myeloid and lymphoid neoplasm associated with eosinophilia and abnormalities of FIP1L1-PDGFRA rearrangement could be treated successfully with oral anticoagulation therapy and the tyrosine-kinase inhibitor imatinib. imatinib 268-276 platelet derived growth factor receptor alpha Homo sapiens 149-155 31648125-1 2020 Recent studies examined the possibility to overcome imatinib resistance in chronic myeloid leukemia (CML) patients by combination therapy with peroxisome proliferator-activated receptor gamma (PPARgamma) ligands. imatinib 52-60 peroxisome proliferator activated receptor gamma Homo sapiens 143-191 31648125-1 2020 Recent studies examined the possibility to overcome imatinib resistance in chronic myeloid leukemia (CML) patients by combination therapy with peroxisome proliferator-activated receptor gamma (PPARgamma) ligands. imatinib 52-60 peroxisome proliferator activated receptor gamma Homo sapiens 193-202 31897102-0 2020 Imatinib inhibits oxidative stress response in spinal cord injury rats by activating Nrf2/HO-1 signaling pathway. imatinib 0-8 NFE2 like bZIP transcription factor 2 Rattus norvegicus 85-89 31897102-0 2020 Imatinib inhibits oxidative stress response in spinal cord injury rats by activating Nrf2/HO-1 signaling pathway. imatinib 0-8 heme oxygenase 1 Rattus norvegicus 90-94 31897102-1 2020 Effect of imatinib on rats with spinal cord injury (SCI) was investigated through the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. imatinib 10-18 NFE2 like bZIP transcription factor 2 Rattus norvegicus 86-129 31969553-5 2020 CASE REPORT We present case of 68-year-old female with chordoma, who underwent multiple surgical resections, radiotherapy session, and had course complication by disease progression on imatinib and local recurrence. imatinib 185-193 CHDM Homo sapiens 55-63 31935370-0 2020 Loss or Inhibition of Stromal-Derived PlGF Prolongs Survival of Mice with Imatinib-Resistant Bcr-Abl1+ Leukemia. imatinib 74-82 placental growth factor Mus musculus 38-42 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 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 31897102-5 2020 According to western blot analysis, the protein expression levels of Nrf2 and HO-1 were obviously higher in the other three groups than those in sham operation group (P<0.05), and they were remarkably higher in imatinib group than those in model group and inhibitor group (P<0.05). imatinib 214-222 NFE2 like bZIP transcription factor 2 Rattus norvegicus 69-73 31908570-5 2020 A single dose administration of imatinib (20 and 40 mg/kg) attenuated ischemia-reperfusion-induced behavioral deficits and the extent of cerebral infarction along with the restoration of connexin 43 and p-STAT3 levels. imatinib 32-40 gap junction protein, alpha 1 Mus musculus 187-198 31908570-5 2020 A single dose administration of imatinib (20 and 40 mg/kg) attenuated ischemia-reperfusion-induced behavioral deficits and the extent of cerebral infarction along with the restoration of connexin 43 and p-STAT3 levels. imatinib 32-40 signal transducer and activator of transcription 3 Mus musculus 205-210 31908570-6 2020 However, administration of AG490, a selective Janus-activated kinase 2 (JAK2)/STAT3 inhibitor, abolished the neuroprotective actions of imatinib and decreased the expression of connexin 43 and p-STAT3. imatinib 136-144 Janus kinase 2 Mus musculus 46-70 31908570-6 2020 However, administration of AG490, a selective Janus-activated kinase 2 (JAK2)/STAT3 inhibitor, abolished the neuroprotective actions of imatinib and decreased the expression of connexin 43 and p-STAT3. imatinib 136-144 Janus kinase 2 Mus musculus 72-76 31908570-6 2020 However, administration of AG490, a selective Janus-activated kinase 2 (JAK2)/STAT3 inhibitor, abolished the neuroprotective actions of imatinib and decreased the expression of connexin 43 and p-STAT3. imatinib 136-144 signal transducer and activator of transcription 3 Mus musculus 78-83 31908570-7 2020 It is concluded that imatinib has the potential of attenuating global ischemia-reperfusion-induced cerebral injury, which may be possibly attributed to activation of JAK2/STAT3 signaling pathway along with the increase in the expression of connexin 43. imatinib 21-29 Janus kinase 2 Mus musculus 166-170 31908570-7 2020 It is concluded that imatinib has the potential of attenuating global ischemia-reperfusion-induced cerebral injury, which may be possibly attributed to activation of JAK2/STAT3 signaling pathway along with the increase in the expression of connexin 43. imatinib 21-29 signal transducer and activator of transcription 3 Mus musculus 171-176 31908570-7 2020 It is concluded that imatinib has the potential of attenuating global ischemia-reperfusion-induced cerebral injury, which may be possibly attributed to activation of JAK2/STAT3 signaling pathway along with the increase in the expression of connexin 43. imatinib 21-29 gap junction protein, alpha 1 Mus musculus 240-251 31897102-1 2020 Effect of imatinib on rats with spinal cord injury (SCI) was investigated through the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. imatinib 10-18 NFE2 like bZIP transcription factor 2 Rattus norvegicus 131-135 31897102-1 2020 Effect of imatinib on rats with spinal cord injury (SCI) was investigated through the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. imatinib 10-18 heme oxygenase 1 Rattus norvegicus 137-153 31897102-1 2020 Effect of imatinib on rats with spinal cord injury (SCI) was investigated through the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. imatinib 10-18 heme oxygenase 1 Rattus norvegicus 155-159 31897102-4 2020 Compared with those in model group and inhibitor group, the positive expression level of Bax was distinctly lower, while that of Bcl-2 was notably increased in imatinib group (P<0.05). imatinib 160-168 BCL2, apoptosis regulator Rattus norvegicus 129-134 31897102-7 2020 Based on ELISA, the other three groups exhibited notably raised content of IL-6, TNF-alpha, ROS and SOD compared with sham operation group (P<0.05), and imatinib group displayed remarkably decreased content of IL-6, TNF-alpha and ROS and markedly elevated SOD content in comparison with model group and inhibitor group (P<0.05). imatinib 156-164 interleukin 6 Rattus norvegicus 213-217 31897102-7 2020 Based on ELISA, the other three groups exhibited notably raised content of IL-6, TNF-alpha, ROS and SOD compared with sham operation group (P<0.05), and imatinib group displayed remarkably decreased content of IL-6, TNF-alpha and ROS and markedly elevated SOD content in comparison with model group and inhibitor group (P<0.05). imatinib 156-164 tumor necrosis factor Rattus norvegicus 219-228 31897102-9 2020 Imatinib inhibits oxidative stress response in SCI rats by activating the Nrf2/HO-1 signaling pathway, thus repressing apoptosis and inflammation. imatinib 0-8 NFE2 like bZIP transcription factor 2 Rattus norvegicus 74-78 31897102-9 2020 Imatinib inhibits oxidative stress response in SCI rats by activating the Nrf2/HO-1 signaling pathway, thus repressing apoptosis and inflammation. imatinib 0-8 heme oxygenase 1 Rattus norvegicus 79-83 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 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 31699612-5 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 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 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 31938055-5 2020 Results: We found that specific impairment of PDGFRbeta kinase activity by 1-NaPP1 treatment efficiently suppressed growth in tumors with high expression of PDGF-BB, i.e. LLC and B16/PDGF-BB, while the clinically used PDGFRbeta kinase inhibitor imatinib did not suppress tumor growth. imatinib 245-253 platelet derived growth factor receptor, beta polypeptide Mus musculus 46-55 31938055-7 2020 Inhibition of PDGFRbeta by either drug impaired tumor vascularization and also affected pericyte coverage; however, specific targeting of PDGFRbeta by 1-NaPP1 resulted in a more pronounced decrease in vessel function with increased vessel apoptosis in high PDGF-BB expressing tumors, compared to treatment with imatinib. imatinib 311-319 platelet derived growth factor receptor, beta polypeptide Mus musculus 138-147 31576676-8 2019 LY294002 and imatinib were used to inhibit the activity of PI3K/Akt and platelet-derived growth factor receptor (PDGFR) beta. imatinib 13-21 AKT serine/threonine kinase 1 Homo sapiens 64-67 31576676-8 2019 LY294002 and imatinib were used to inhibit the activity of PI3K/Akt and platelet-derived growth factor receptor (PDGFR) beta. imatinib 13-21 platelet derived growth factor receptor beta Homo sapiens 113-124 31638261-5 2019 In the present, down regulation of RAD51 by shRNA and imatinib sensitized Jurkat cells to etoposide by decreasing the activity of homologous recombination (HR). imatinib 54-62 RAD51 recombinase Homo sapiens 35-40 31638261-7 2019 Importantly, downregulation of RAD51 by imatinib obviously increased the apoptosis of Jurkat cell after etoposide treatment. imatinib 40-48 RAD51 recombinase Homo sapiens 31-36 31708372-2 2019 Imatinib mesylate (IM), which inhibits both KIT and PDGFRA receptors, significantly improved treatment of advanced (metastatic, recurrent, and/or inoperable) GISTs. imatinib 0-17 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 44-47 31708372-2 2019 Imatinib mesylate (IM), which inhibits both KIT and PDGFRA receptors, significantly improved treatment of advanced (metastatic, recurrent, and/or inoperable) GISTs. imatinib 0-17 platelet derived growth factor receptor alpha Homo sapiens 52-58 31708372-2 2019 Imatinib mesylate (IM), which inhibits both KIT and PDGFRA receptors, significantly improved treatment of advanced (metastatic, recurrent, and/or inoperable) GISTs. imatinib 19-21 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 44-47 31708372-2 2019 Imatinib mesylate (IM), which inhibits both KIT and PDGFRA receptors, significantly improved treatment of advanced (metastatic, recurrent, and/or inoperable) GISTs. imatinib 19-21 platelet derived growth factor receptor alpha Homo sapiens 52-58 31708372-11 2019 Secondary KIT mutations were detected in 10 from 133 (7 %) patients treated with IM. imatinib 81-83 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 10-13 31540978-1 2019 BCR-ABL1 transcripts at imatinib cessation were quantified by droplet digital PCR (ddPCR) for 175 patients on the STIM2 trial. imatinib 24-32 BCR activator of RhoGEF and GTPase Homo sapiens 0-8 31566580-10 2019 Treatment with imatinib restored VE-cadherin/adherens junctions, inhibited vascular permeability, and significantly reduced colonic inflammation in experimental colitis. imatinib 15-23 cadherin 5 Homo sapiens 33-44 31689840-0 2019 Combination of pembrolizumab and imatinib in a patient with double KIT mutant melanoma: A case report. imatinib 33-41 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 67-70 31689840-10 2019 Combining Imatinib with checkpoint inhibitors may be efficacious in patients with metastatic melanoma and KIT mutations. imatinib 10-18 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 106-109 31673329-1 2019 Background: Imatinib shows limited efficacy in patients with gastrointestinal stromal tumors (GISTs) carrying secondary KIT mutations. imatinib 12-20 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 120-123 31614827-7 2019 PAK1 was inhibited by small-molecule inhibitor IPA-3 (p21-activated kinase inhibitor III), PAK2 was downregulated by specific short hairpin RNA (shRNA), and BCR-ABL1 tyrosine kinase was inhibited by imatinib (IM). imatinib 199-207 p21 (RAC1) activated kinase 1 Homo sapiens 0-4 31614827-7 2019 PAK1 was inhibited by small-molecule inhibitor IPA-3 (p21-activated kinase inhibitor III), PAK2 was downregulated by specific short hairpin RNA (shRNA), and BCR-ABL1 tyrosine kinase was inhibited by imatinib (IM). imatinib 199-207 p21 (RAC1) activated kinase 2 Homo sapiens 91-95 31614827-7 2019 PAK1 was inhibited by small-molecule inhibitor IPA-3 (p21-activated kinase inhibitor III), PAK2 was downregulated by specific short hairpin RNA (shRNA), and BCR-ABL1 tyrosine kinase was inhibited by imatinib (IM). imatinib 199-207 BCR activator of RhoGEF and GTPase Homo sapiens 157-165 31614827-7 2019 PAK1 was inhibited by small-molecule inhibitor IPA-3 (p21-activated kinase inhibitor III), PAK2 was downregulated by specific short hairpin RNA (shRNA), and BCR-ABL1 tyrosine kinase was inhibited by imatinib (IM). imatinib 209-211 p21 (RAC1) activated kinase 1 Homo sapiens 0-4 31614827-7 2019 PAK1 was inhibited by small-molecule inhibitor IPA-3 (p21-activated kinase inhibitor III), PAK2 was downregulated by specific short hairpin RNA (shRNA), and BCR-ABL1 tyrosine kinase was inhibited by imatinib (IM). imatinib 209-211 p21 (RAC1) activated kinase 2 Homo sapiens 91-95 31614827-7 2019 PAK1 was inhibited by small-molecule inhibitor IPA-3 (p21-activated kinase inhibitor III), PAK2 was downregulated by specific short hairpin RNA (shRNA), and BCR-ABL1 tyrosine kinase was inhibited by imatinib (IM). imatinib 209-211 BCR activator of RhoGEF and GTPase Homo sapiens 157-165 31614827-9 2019 Herein, we show that inhibition of the activity of PAK1 and/or PAK2 enhanced the effect of IM against CML cells without affecting the normal cells. imatinib 91-93 p21 (RAC1) activated kinase 1 Homo sapiens 51-55 31614827-9 2019 Herein, we show that inhibition of the activity of PAK1 and/or PAK2 enhanced the effect of IM against CML cells without affecting the normal cells. imatinib 91-93 p21 (RAC1) activated kinase 2 Homo sapiens 63-67 31614827-14 2019 Based on our results, we hypothesize that IM, a BCR-ABL1 tyrosine kinase inhibitor, combined with a PAK1/2 inhibitor facilitates eradication of CML-CP cells. imatinib 42-44 BCR activator of RhoGEF and GTPase Homo sapiens 48-56 31601938-3 2019 Imatinib mesylate (IM) blocks the CSF-1 receptor. imatinib 0-17 colony stimulating factor 1 receptor Homo sapiens 34-48 31601938-3 2019 Imatinib mesylate (IM) blocks the CSF-1 receptor. imatinib 19-21 colony stimulating factor 1 receptor Homo sapiens 34-48 31994093-7 2017 ROCK inhibitor (fasudil) and PDGF inhibitor (imatinib) caused significant decreases in NGF mRNA and protein content when administered alone, with no further effects noted when used in combination. imatinib 45-53 nerve growth factor Rattus norvegicus 87-90 31581474-0 2019 Structural Basis for the Regulation of PPARgamma Activity by Imatinib. imatinib 61-69 peroxisome proliferator activated receptor gamma Homo sapiens 39-48 31934053-0 2019 Rearrangement of PDGFRbeta gene in a patient with Ph-negative chronic myeloid leukemia t(5;12)(q33;p13) in imatinib mesylate treatment-free remission: a case report. imatinib 107-124 platelet derived growth factor receptor beta Homo sapiens 17-26 31934053-0 2019 Rearrangement of PDGFRbeta gene in a patient with Ph-negative chronic myeloid leukemia t(5;12)(q33;p13) in imatinib mesylate treatment-free remission: a case report. imatinib 107-124 H3 histone pseudogene 6 Homo sapiens 99-102 31934053-5 2019 A promising result was achieved, in which TEL-PDGFRbeta fusion gene could not be effectively detected during imatinib treatment, demonstrating complete molecular biologic remission. imatinib 109-117 platelet derived growth factor receptor beta Homo sapiens 46-55 31938099-3 2018 In this study, we discovered that knock-down of SARI expression suppressed cell growth and colony formation, inhibited invasion, enhanced imatinib (STI571)-mediated apoptosis, and induced G0/G1 and G2/M arrest in human K562 myeloid leukemia cells. imatinib 138-146 basic leucine zipper ATF-like transcription factor 2 Homo sapiens 48-52 31581474-2 2019 Interestingly, when an FDA-approved drug library was tested for agents that block peroxisome proliferator-activated receptor gamma (PPARgamma) phosphorylation at Ser245 to evaluate possibilities of antidiabetic drug repositioning, imatinib was determined as a PPARgamma antagonist ligand. imatinib 231-239 peroxisome proliferator activated receptor gamma Homo sapiens 82-130 31581474-3 2019 However, it is not well understood how imatinib binds to PPARgamma or would improve insulin sensitivity without classical agonism. imatinib 39-47 peroxisome proliferator activated receptor gamma Homo sapiens 57-66 31581474-4 2019 Here, we report the crystal structure of the PPARgamma R288A mutant in complex with imatinib. imatinib 84-92 peroxisome proliferator activated receptor gamma Homo sapiens 45-54 31581474-5 2019 Imatinib bound to Arm2 and Arm3 regions in the ligand-binding domain (LBD) of PPARgamma, of which the Arm3 region is closely related to the inhibition of PPARgamma phosphorylation at Ser245. imatinib 0-8 Jupiter microtubule associated homolog 1 Homo sapiens 18-22 31581474-5 2019 Imatinib bound to Arm2 and Arm3 regions in the ligand-binding domain (LBD) of PPARgamma, of which the Arm3 region is closely related to the inhibition of PPARgamma phosphorylation at Ser245. imatinib 0-8 peroxisome proliferator activated receptor gamma Homo sapiens 78-87 31581474-5 2019 Imatinib bound to Arm2 and Arm3 regions in the ligand-binding domain (LBD) of PPARgamma, of which the Arm3 region is closely related to the inhibition of PPARgamma phosphorylation at Ser245. imatinib 0-8 peroxisome proliferator activated receptor gamma Homo sapiens 154-163 31581474-8 2019 Our study provides new structural insights into the PPARgamma regulation by imatinib and may contribute to the development of new antidiabetic drugs targeting PPARgamma while minimizing known side effects. imatinib 76-84 peroxisome proliferator activated receptor gamma Homo sapiens 52-61 31581474-8 2019 Our study provides new structural insights into the PPARgamma regulation by imatinib and may contribute to the development of new antidiabetic drugs targeting PPARgamma while minimizing known side effects. imatinib 76-84 peroxisome proliferator activated receptor gamma Homo sapiens 159-168 31550821-9 2019 It is known that approximately 30% of PDGFRA mutations may be sensitive to imatinib, and patients with such tumors may benefit from imatinib, so imatinib treatment should not be empirically denied in these patients. imatinib 75-83 platelet derived growth factor receptor alpha Homo sapiens 38-44 31577092-0 2019 Imatinib mesylate inhibits proliferation and promotes apoptosis of chronic myeloid leukemia cells via STAT3 pathway. imatinib 0-17 signal transducer and activator of transcription 3 Homo sapiens 102-107 31723757-0 2018 Imatinib Treatment of Chronic Myeloid Leukemia Reveals a Preexisting CALR-mutated Essential Thrombocythemia. imatinib 0-8 calreticulin Homo sapiens 69-73