PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33662676-11 2021 Yet, immunoassays revealed a suppression of the STAT5 phosphorylation status by co-application of the most active derivatives with imatinib. Imatinib Mesylate 131-139 signal transducer and activator of transcription 5A Homo sapiens 48-53 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 signal transducer and activator of transcription 5A Homo sapiens 53-58 33149116-0 2020 Correction: Imatinib mesylate inhibits STAT5 phosphorylation in response to IL-7 and promotes T cell lymphopenia in chronic myelogenous leukemia patients. Imatinib Mesylate 12-29 signal transducer and activator of transcription 5A Homo sapiens 39-44 27027438-0 2016 BM microenvironmental protection of CML cells from imatinib through Stat5/NF-kappaB signaling and reversal by Wogonin. Imatinib Mesylate 51-59 signal transducer and activator of transcription 5A Homo sapiens 68-73 31371410-2 2020 Peroxisome proliferator-activated receptor-gamma (PPARgamma) agonist pioglitazone downregulates signal transducer and activator of transcription 5 (STAT5) and in combination with imatinib induces complete molecular response in imatinib-refractory patients by eroding leukemia stem cells. Imatinib Mesylate 179-187 signal transducer and activator of transcription 5A Homo sapiens 148-153 31371410-2 2020 Peroxisome proliferator-activated receptor-gamma (PPARgamma) agonist pioglitazone downregulates signal transducer and activator of transcription 5 (STAT5) and in combination with imatinib induces complete molecular response in imatinib-refractory patients by eroding leukemia stem cells. Imatinib Mesylate 227-235 signal transducer and activator of transcription 5A Homo sapiens 148-153 32999163-0 2020 Emodin Inhibits Resistance to Imatinib by Downregulation of Bcr-Abl and STAT5 and Allosteric Inhibition in Chronic Myeloid Leukemia Cells. Imatinib Mesylate 30-38 signal transducer and activator of transcription 5A Homo sapiens 72-77 30516071-0 2019 MicroRNA-221 sensitizes chronic myeloid leukemia cells to imatinib by targeting STAT5. Imatinib Mesylate 58-66 signal transducer and activator of transcription 5A Homo sapiens 80-85 30516071-2 2019 In this study, we examined the STAT5-related miRNA-expression profile in CML cell lines (K562 and imatinib-resistant K562/G) by quantitative real-time reverse-transcriptase polymerase chain reactions. Imatinib Mesylate 98-106 signal transducer and activator of transcription 5A Homo sapiens 31-36 30516071-6 2019 MiR-221 restoration and STAT5 knockdown in K562/G cells increased the sensitivity of CML cells to imatinib by reducing the Bcl2: Bax ratio. Imatinib Mesylate 98-106 signal transducer and activator of transcription 5A Homo sapiens 24-29 30516071-7 2019 Collectively, our data suggested that miR-221-STAT5 axis played crucial roles in controlling the sensitivity of CML cells to imatinib. Imatinib Mesylate 125-133 signal transducer and activator of transcription 5A Homo sapiens 46-51 30687103-0 2018 A Novel Naphthoquinone-Coumarin Hybrid That Inhibits BCR-ABL1-STAT5 Oncogenic Pathway and Reduces Survival in Imatinib-Resistant Chronic Myelogenous Leukemia Cells. Imatinib Mesylate 110-118 signal transducer and activator of transcription 5A Homo sapiens 62-67 30687103-11 2018 Notably, NPQ-C6 maintained its activity on BCR-ABL1/STAT5/c-MYC/PIM-1 oncogenic pathway in imatinib-resistant cells. Imatinib Mesylate 91-99 signal transducer and activator of transcription 5A Homo sapiens 52-57 29777794-3 2018 The tLyp1 peptide-modified hybrid nanoparticles presented good stability and effective targeting to Treg cells, and they enhanced the effect of imatinib in downregulating Treg cell suppression through inhibition of STAT3 and STAT5 phosphorylation. Imatinib Mesylate 144-152 signal transducer and activator of transcription 5A Homo sapiens 225-230 29115375-0 2018 Persistent STAT5-mediated ROS production and involvement of aberrant p53 apoptotic signaling in the resistance of chronic myeloid leukemia to imatinib. Imatinib Mesylate 142-150 signal transducer and activator of transcription 5A Homo sapiens 11-16 29115375-3 2018 In the present study, it was observed that the mRNA levels of STAT5A and STAT5B were upregulated in patients with imatinib-resistant CML and in the imatinib-resistant K562/G CML cell line. Imatinib Mesylate 114-122 signal transducer and activator of transcription 5A Homo sapiens 62-68 29115375-3 2018 In the present study, it was observed that the mRNA levels of STAT5A and STAT5B were upregulated in patients with imatinib-resistant CML and in the imatinib-resistant K562/G CML cell line. Imatinib Mesylate 148-156 signal transducer and activator of transcription 5A Homo sapiens 62-68 29115375-4 2018 In addition, increased expression of STAT5 was observed in the BCR-ABL1 mutation group, compared with that in the non-BCR-ABL1 mutation group, regardless of patient imatinib resistance state. Imatinib Mesylate 165-173 signal transducer and activator of transcription 5A Homo sapiens 37-42 29115375-10 2018 Taken together, these findings suggest that the resistance of CML to the tyrosine kinase inhibitor, imatinib, may be associated with persistent STAT5-mediated ROS production, and the abnormality of the p53 pathway. Imatinib Mesylate 100-108 signal transducer and activator of transcription 5A Homo sapiens 144-149 28403213-4 2017 Recently, we showed that in neoplastic mast cells that endogenously express an imatinib-resistant Kit mutant, Kit causes oncogenic activation of the phosphatidylinositol 3-kinase-Akt (PI3K-Akt) pathway and the signal transducer and activator of transcription 5 (STAT5) but only on endolysosomes and on the endoplasmic reticulum (ER), respectively. Imatinib Mesylate 79-87 signal transducer and activator of transcription 5A Homo sapiens 210-260 28403213-4 2017 Recently, we showed that in neoplastic mast cells that endogenously express an imatinib-resistant Kit mutant, Kit causes oncogenic activation of the phosphatidylinositol 3-kinase-Akt (PI3K-Akt) pathway and the signal transducer and activator of transcription 5 (STAT5) but only on endolysosomes and on the endoplasmic reticulum (ER), respectively. Imatinib Mesylate 79-87 signal transducer and activator of transcription 5A Homo sapiens 262-267 32272420-9 2020 However, the repression of the STAT5 phosphorylation relates with the possibility to sensitize K562-resistant CML cells to imatinib treatment. Imatinib Mesylate 123-131 signal transducer and activator of transcription 5A Homo sapiens 31-36 31952546-0 2020 De-regulated STAT5A/miR-202-5p/USP15/Caspase-6 regulatory axis suppresses CML cell apoptosis and contributes to Imatinib resistance. Imatinib Mesylate 112-120 signal transducer and activator of transcription 5A Homo sapiens 13-19 28387753-0 2017 Imatinib mesylate inhibits STAT5 phosphorylation in response to IL-7 and promotes T cell lymphopenia in chronic myelogenous leukemia patients. Imatinib Mesylate 0-17 signal transducer and activator of transcription 5A Homo sapiens 27-32 27272942-6 2016 The increased IL-7 was secreted by mesenchymal stem cells (MSC) in the bone marrow, which may protect leukemic cells from apoptosis induced by imatinib through JAK1/STAT5 signaling pathway. Imatinib Mesylate 143-151 signal transducer and activator of transcription 5A Homo sapiens 165-170 27027438-1 2016 Constitutive Stat5 activation enhanced cell survival and resistance to imatinib (IM) in chronic myelogenous leukemia (CML) cells. Imatinib Mesylate 71-79 signal transducer and activator of transcription 5A Homo sapiens 13-18 22895079-11 2012 Our data showed that oridonin remarkably suppressed activations of Akt/mTOR, Raf/MEK and STAT5 pathway in these primary specimens and oridonin with imatinib exerted synergetic suppressive effects on mTOR, STAT5 and LYN signaling in one imatinib resistant patient specimen. Imatinib Mesylate 148-156 signal transducer and activator of transcription 5A Homo sapiens 205-210 25953263-0 2015 Revealing genome-wide mRNA and microRNA expression patterns in leukemic cells highlighted "hsa-miR-2278" as a tumor suppressor for regain of chemotherapeutic imatinib response due to targeting STAT5A. Imatinib Mesylate 158-166 signal transducer and activator of transcription 5A Homo sapiens 193-199 25098340-4 2014 Constitutive activation of STAT5 and STAT3 are associated with imatinib resistance on leukemia cells. Imatinib Mesylate 63-71 signal transducer and activator of transcription 5A Homo sapiens 27-32 25098340-5 2014 Development of drugs targeting SH2 domains of STAT5 and STAT3 provides a novel strategy for the treatment of the imatinib-resistant CML. Imatinib Mesylate 113-121 signal transducer and activator of transcription 5A Homo sapiens 46-51 23400594-9 2013 STAT5A attenuation was also active at inhibiting growth of CML CD34(+) cells from patients with acquired resistance to imatinib. Imatinib Mesylate 119-127 signal transducer and activator of transcription 5A Homo sapiens 0-6 25953263-3 2015 In this study, we aimed to determine differing genome-wide microRNA (miRNA) and messenger RNA (mRNA) expression profiles in imatinib resistant (K562/IMA-3 muM) and parental cells by targeting STAT5A via small interfering RNA (siRNA) applications. Imatinib Mesylate 124-132 signal transducer and activator of transcription 5A Homo sapiens 192-198 24675360-4 2014 Moreover, ST2 overexpression is normalized following imatinib mesylate therapy, whereas IL-33 counteracts in vitro imatinib mesylate-induced growth arrest in CML CD34(+) progenitors via reactivation of the STAT5 pathway, thus supporting the notion that IL-33 may impede the antiproliferative effects of imatinib mesylate on CD34(+) progenitors in CML. Imatinib Mesylate 115-132 signal transducer and activator of transcription 5A Homo sapiens 206-211 24675360-4 2014 Moreover, ST2 overexpression is normalized following imatinib mesylate therapy, whereas IL-33 counteracts in vitro imatinib mesylate-induced growth arrest in CML CD34(+) progenitors via reactivation of the STAT5 pathway, thus supporting the notion that IL-33 may impede the antiproliferative effects of imatinib mesylate on CD34(+) progenitors in CML. Imatinib Mesylate 115-132 signal transducer and activator of transcription 5A Homo sapiens 206-211 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 signal transducer and activator of transcription 5A Homo sapiens 106-112 23370613-8 2013 Considering that STAT5 is a BCR-ABL molecular target that plays a key role in the pathogenesis of CML as well as in BCR-ABL-mediated resistance to apoptosis, TR120 could potentially be a useful novel agent in the treatment of imatinib-resistant CML. Imatinib Mesylate 226-234 signal transducer and activator of transcription 5A Homo sapiens 17-22 25436685-3 2012 Indirect strategies have yielded potent agents, such as imatinib, AC2207, and EXEL823 which effectively silence STAT5 activity but which suffer from off-target effects and toxicity. Imatinib Mesylate 56-64 signal transducer and activator of transcription 5A Homo sapiens 112-117 20201032-7 2010 However, Stat5- but not Stat3-deletion induces G(0)/G(1) cell cycle arrest and apoptosis of imatinib-sensitive and imatinib-resistant stable leukaemic cells in vitro. Imatinib Mesylate 92-100 signal transducer and activator of transcription 5A Homo sapiens 9-14 21356308-0 2011 Activation of STAT5 confers imatinib resistance on leukemic cells through the transcription of TERT and MDR1. Imatinib Mesylate 28-36 signal transducer and activator of transcription 5A Homo sapiens 14-19 21356308-4 2011 Conversely, silencing of endogenous STAT5 expression by siRNA significantly reduced both the expression of P-glycoprotein and telomerase activity and resulted in the recovery of the imatinib sensitivity of K562-ADM cells. Imatinib Mesylate 182-190 signal transducer and activator of transcription 5A Homo sapiens 36-41 21224473-5 2011 Imatinib antagonized Stat5 phosphorylation. Imatinib Mesylate 0-8 signal transducer and activator of transcription 5A Homo sapiens 21-26 21299849-8 2011 STAT5, ERK1/2 and the ribosomal S6 protein (RPS6) are BCR-ABL1 downstream effectors, and all three proteins are dephosphorylated by imatinib in sensitive cell lines. Imatinib Mesylate 132-140 signal transducer and activator of transcription 5A Homo sapiens 0-5 21299849-15 2011 These cell lines are unique as they dephosphorylate ERK1/2 and STAT5 after treatment with imatinib, while PI3K/AKT1/mTOR activity remains unaffected. Imatinib Mesylate 90-98 signal transducer and activator of transcription 5A Homo sapiens 63-68 20849385-0 2010 Suppression of STAT5A increases chemotherapeutic sensitivity in imatinib-resistant and imatinib-sensitive K562 cells. Imatinib Mesylate 64-72 signal transducer and activator of transcription 5A Homo sapiens 15-21 20849385-0 2010 Suppression of STAT5A increases chemotherapeutic sensitivity in imatinib-resistant and imatinib-sensitive K562 cells. Imatinib Mesylate 87-95 signal transducer and activator of transcription 5A Homo sapiens 15-21 20849385-3 2010 The XTT cell proliferation assay showed that both sensitive and resistant K562 cells were sensitized to imatinib upon transfection with STAT5A siRNA. Imatinib Mesylate 104-112 signal transducer and activator of transcription 5A Homo sapiens 136-142 21220747-0 2011 High STAT5 levels mediate imatinib resistance and indicate disease progression in chronic myeloid leukemia. Imatinib Mesylate 26-34 signal transducer and activator of transcription 5A Homo sapiens 5-10 21220747-2 2011 Here we show that the expression level of the transcription factor STAT5 is another parameter that determines the sensitivity of BCR-ABL1(+) cells against tyrosine kinase inhibitors (TKIs), such as imatinib, nilotinib, or dasatinib. Imatinib Mesylate 198-206 signal transducer and activator of transcription 5A Homo sapiens 67-72 21220747-5 2011 In support of this concept, under imatinib treatment and with disease progression, STAT5 mRNA and protein levels increased in patients with Ph(+) chronic myeloid leukemia. Imatinib Mesylate 34-42 signal transducer and activator of transcription 5A Homo sapiens 83-88 21220747-9 2011 It also suggests that STAT5 may serve as an attractive target to overcome imatinib resistance in BCR-ABL1(+) leukemia. Imatinib Mesylate 74-82 signal transducer and activator of transcription 5A Homo sapiens 22-27 21233313-10 2011 Simultaneously inhibiting STAT5 with pimozide and the kinase inhibitors imatinib or nilotinib shows enhanced effects in inhibiting STAT5 phosphorylation and in inducing apoptosis. Imatinib Mesylate 72-80 signal transducer and activator of transcription 5A Homo sapiens 26-31 21233313-10 2011 Simultaneously inhibiting STAT5 with pimozide and the kinase inhibitors imatinib or nilotinib shows enhanced effects in inhibiting STAT5 phosphorylation and in inducing apoptosis. Imatinib Mesylate 72-80 signal transducer and activator of transcription 5A Homo sapiens 131-136 21091189-6 2011 Thus, our study provides support for STAT5 as a potential target downstream of BCR-ABL for CML treatment and helps establish the concept of targeting STAT5 by decoy ODN as a novel therapy approach for imatinib-resistant CML. Imatinib Mesylate 201-209 signal transducer and activator of transcription 5A Homo sapiens 37-42 21091189-6 2011 Thus, our study provides support for STAT5 as a potential target downstream of BCR-ABL for CML treatment and helps establish the concept of targeting STAT5 by decoy ODN as a novel therapy approach for imatinib-resistant CML. Imatinib Mesylate 201-209 signal transducer and activator of transcription 5A Homo sapiens 150-155 20201032-7 2010 However, Stat5- but not Stat3-deletion induces G(0)/G(1) cell cycle arrest and apoptosis of imatinib-sensitive and imatinib-resistant stable leukaemic cells in vitro. Imatinib Mesylate 115-123 signal transducer and activator of transcription 5A Homo sapiens 9-14 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 signal transducer and activator of transcription 5A Homo sapiens 132-137 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 signal transducer and activator of transcription 5A Homo sapiens 69-74 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 signal transducer and activator of transcription 5A Homo sapiens 49-54 17533047-6 2007 RESULTS: Imatinib showed a specific time- and dose-dependent growth inhibitory effect on FDCP cells expressing JAK2(V617F), wherein we observed imatinib"s inactivation of JAK2, STAT5 and cKIT proteins. Imatinib Mesylate 9-17 signal transducer and activator of transcription 5A Homo sapiens 177-182 17533047-6 2007 RESULTS: Imatinib showed a specific time- and dose-dependent growth inhibitory effect on FDCP cells expressing JAK2(V617F), wherein we observed imatinib"s inactivation of JAK2, STAT5 and cKIT proteins. Imatinib Mesylate 144-152 signal transducer and activator of transcription 5A Homo sapiens 177-182 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 signal transducer and activator of transcription 5A Homo sapiens 360-365 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 signal transducer and activator of transcription 5A Homo sapiens 138-143 15277706-8 2004 Concomitantly, constitutive phosphorylation of Stat5 and FKHRL1 was significantly inhibited by imatinib, and the inhibition was canceled by the addition of GM-CSF, accompanied by upregulation of Bcl-xL and downregulation of p27/Kip1. Imatinib Mesylate 95-103 signal transducer and activator of transcription 5A Homo sapiens 47-52 17259998-8 2007 Phosphorylation of MAPK and STAT5 was also inhibited by imatinib at the same concentration, in cells expressing Val559Asp but not in those expressing Val559Ile. Imatinib Mesylate 56-64 signal transducer and activator of transcription 5A Homo sapiens 28-33 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 signal transducer and activator of transcription 5A Homo sapiens 122-127 14604282-5 2003 Imatinib mesylate inhibited activation of Stat5 rather than the MEK-ERK1/2 pathway. Imatinib Mesylate 0-17 signal transducer and activator of transcription 5A Homo sapiens 42-47 12804638-4 2003 Phosphorylated STAT5 was found to measure 2.22+/-0.09 relative fluorescence units (RFU) falling to 0.925+/-0.005RFU in the presence of STI571. Imatinib Mesylate 135-141 signal transducer and activator of transcription 5A Homo sapiens 15-20 12764361-0 2003 In BCR-ABL-positive cells, STAT-5 tyrosine-phosphorylation integrates signals induced by imatinib mesylate and Ara-C. Imatinib Mesylate 89-106 signal transducer and activator of transcription 5A Homo sapiens 27-33 12764361-3 2003 Here, we investigated the effects of imatinib mesylate and cytosine arabinoside (Ara-C) on STAT-5 tyrosine-phosphorylation, cellular proliferation and induction of apoptosis in cell lines and primary hematopoietic cells. Imatinib Mesylate 37-54 signal transducer and activator of transcription 5A Homo sapiens 91-97 12764361-4 2003 Imatinib mesylate treatment strongly suppressed STAT-5 tyrosine-phosphorylation in K562 and primary CML blasts. Imatinib Mesylate 0-17 signal transducer and activator of transcription 5A Homo sapiens 48-54 12764361-9 2003 Treatment of K562 cells with Ara-C in combination with imatinib mesylate revealed synergistic effects at the level of STAT-5 tyrosine-phosphorylation and DNA binding, Hck tyrosine-phosphorylation, cell growth and induction of apoptosis. Imatinib Mesylate 55-72 signal transducer and activator of transcription 5A Homo sapiens 118-124 12764361-10 2003 Overall, in this report we demonstrate that STAT-5 tyrosine-phosphorylation is a specific target of imatinib mesylate and Ara-C. Imatinib Mesylate 100-117 signal transducer and activator of transcription 5A Homo sapiens 44-50 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 signal transducer and activator of transcription 5A Homo sapiens 27-32 11313280-6 2001 STI-571-mediated apoptosis correlated with the inhibition of Stat-5 and MAP kinase activation and a reduction in overexpressed bcl-x(L) but not in PTP1B. Imatinib Mesylate 0-7 signal transducer and activator of transcription 5A Homo sapiens 61-67