PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 ATP binding cassette subfamily B member 1 Homo sapiens 93-98 34963561-9 2022 In addition, DNR induced the expression of drug exporter ABCB1 in K562 cells through the p38 MAPK/NFkappaB-mediated pathway, while imatinib or ABT-199 inhibited the DNR-induced effect. Imatinib Mesylate 131-139 ATP binding cassette subfamily B member 1 Homo sapiens 57-62 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 ATP binding cassette subfamily B member 1 Homo sapiens 69-74 34410954-0 2021 Combined Therapy of ATRA and Imatinib Mesylate Decreases BCR-ABL and ABCB1/MDR1 Expression Through Cellular Differentiation in a Chronic Myeloid Leukemia Model. Imatinib Mesylate 29-37 ATP binding cassette subfamily B member 1 Homo sapiens 75-79 34144313-9 2021 There was also a significant decrease in the mRNA levels of the major drug efflux genes (ABCB1, ABCB10, ABCC1 and ABCG2) when treated with a combination of imatinib and MBF in comparison to imatinib treatment alone. Imatinib Mesylate 156-164 ATP binding cassette subfamily B member 1 Homo sapiens 89-94 34144313-9 2021 There was also a significant decrease in the mRNA levels of the major drug efflux genes (ABCB1, ABCB10, ABCC1 and ABCG2) when treated with a combination of imatinib and MBF in comparison to imatinib treatment alone. Imatinib Mesylate 190-198 ATP binding cassette subfamily B member 1 Homo sapiens 89-94 35129779-4 2022 Imatinib is the only TKI whose absorption depends on both influx (OCT1 and OATP1A2) and efflux (ABCB1 and ABCG2) transporters, whereas the others rely only on efflux transporters. Imatinib Mesylate 0-8 ATP binding cassette subfamily B member 1 Homo sapiens 96-101 33565361-1 2022 BACKGROUND: Our study aimed to investigate the association between multidrug resistance (MDR1) C1236T, C3435T and G2677T/A polymorphisms and the response to imatinib (IM) in chronic myeloid leukemia (CML). Imatinib Mesylate 157-165 ATP binding cassette subfamily B member 1 Homo sapiens 89-93 33995081-1 2021 Imatinib is transported extracellularly by ABCB1 and ABCG2 efflux transporters and bound to alpha-1-acid glycoprotein (AGP) in the bloodstream. Imatinib Mesylate 0-8 ATP binding cassette subfamily B member 1 Homo sapiens 43-48 33995081-2 2021 However, the clinical and pharmacokinetic effects of ABCB1 and ABCG2 on imatinib were inconsistent in the previous literature and have not been confirmed. Imatinib Mesylate 72-80 ATP binding cassette subfamily B member 1 Homo sapiens 53-58 33995081-3 2021 Therefore, in the present study, we explored the effects of the ABCG2 and ABCB1 genetic polymorphisms on imatinib pharmacokinetics in association with plasma AGP levels in healthy subjects. Imatinib Mesylate 105-113 ATP binding cassette subfamily B member 1 Homo sapiens 74-79 33607534-10 2021 Furthermore, AZT and AZT/IMA combination decreased Pgp function in K562R cells in comparison with their controls. Imatinib Mesylate 25-28 ATP binding cassette subfamily B member 1 Homo sapiens 51-54 33607534-13 2021 One of the mechanisms underlying the potent anticancer effect of combined AZT/IMA could be its ability to inhibit Pgp function and increase intracellular accumulation of IMA which leads to the induction of apoptosis in K562R cells. Imatinib Mesylate 78-81 ATP binding cassette subfamily B member 1 Homo sapiens 114-117 33086089-8 2020 Imatinib mesylate (IM), P-gp substrate, was used as a model drug. Imatinib Mesylate 19-21 ATP binding cassette subfamily B member 1 Homo sapiens 24-28 33129240-3 2021 This study attempted to evaluate the influence of ABCB1 gene polymorphisms and smoking on CML risk and resistance to imatinib. Imatinib Mesylate 117-125 ATP binding cassette subfamily B member 1 Homo sapiens 50-55 33707832-10 2021 Also, results suggest that ABCB1 3435TT genotype increases imatinib resistance in CML and influence therapeutic outcome in B-ALL. Imatinib Mesylate 59-67 ATP binding cassette subfamily B member 1 Homo sapiens 27-32 31262905-10 2019 CONCLUSION: These findings provide valuable information regarding the sensitizing of drug-resistant cells and indicate that imatinib and erlotinib may be used in patients with potentially resistant cancer without any toxic effects from P-gp inhibition. Imatinib Mesylate 124-132 ATP binding cassette subfamily B member 1 Homo sapiens 236-240 32715517-0 2020 Overexpression of P-glycoprotein and resistance to Imatinib in chronic myeloid leukemia patients. Imatinib Mesylate 51-59 ATP binding cassette subfamily B member 1 Homo sapiens 18-32 32715517-1 2020 BACKGROUND: The P-glycoprotein (P-gp) is one of the mechanisms of Imatinib (IM) resistance in chronic myeloid leukemia (CML). Imatinib Mesylate 66-74 ATP binding cassette subfamily B member 1 Homo sapiens 16-30 32715517-1 2020 BACKGROUND: The P-glycoprotein (P-gp) is one of the mechanisms of Imatinib (IM) resistance in chronic myeloid leukemia (CML). Imatinib Mesylate 66-74 ATP binding cassette subfamily B member 1 Homo sapiens 32-36 32112424-0 2020 The potentiation of menadione on imatinib by down-regulation of ABCB1 expression. Imatinib Mesylate 33-41 ATP binding cassette subfamily B member 1 Homo sapiens 64-69 31759356-0 2019 Association between C1236T Genetic Variant of ABCB1 Gene and Molecular Response to Imatinib in Indonesian Chronic Myeloid Patients. Imatinib Mesylate 83-91 ATP binding cassette subfamily B member 1 Homo sapiens 46-51 31759356-3 2019 Mutation in ABCB1 efflux transporters is one of the known mechanisms of resistance to imatinib in chronic myeloid leukemia patients. Imatinib Mesylate 86-94 ATP binding cassette subfamily B member 1 Homo sapiens 12-17 31759356-4 2019 This study was aimed to investigate the association of ABCB1 C1236T polymorphism in Indonesian chronic myeloid patients with molecular response to imatinib treatment. Imatinib Mesylate 147-155 ATP binding cassette subfamily B member 1 Homo sapiens 55-60 33244077-4 2020 Patients carrying ABCB1-C1236T variants had high day29 plasma imatinib levels (P = 0.005), increased EMR at 3 months (P = 0.044) and a better 2 year FFS (P = 0.003) when compared to those with wild type genotype. Imatinib Mesylate 62-70 ATP binding cassette subfamily B member 1 Homo sapiens 18-23 33244077-5 2020 This translates to patients with lower ABCB1 mRNA expression having a significantly higher intracellular imatinib levels (P = 0.029). Imatinib Mesylate 105-113 ATP binding cassette subfamily B member 1 Homo sapiens 39-44 32415468-0 2020 Effect of Cytochrome P450 and ABCB1 Polymorphisms on Imatinib Pharmacokinetics After Single-Dose Administration to Healthy Subjects. Imatinib Mesylate 53-61 ATP binding cassette subfamily B member 1 Homo sapiens 30-35 32415468-3 2020 OBJECTIVE: To investigate whether polymorphisms in genes encoding cytochrome P450 (CYP) enzymes and ABCB1 transporter affect imatinib pharmacokinetic parameters. Imatinib Mesylate 125-133 ATP binding cassette subfamily B member 1 Homo sapiens 100-105 30956965-0 2019 ABCB1 and BMI1 mRNA expression in patients with chronic myeloid leukemia: impact on imatinib efficacy. Imatinib Mesylate 84-92 ATP binding cassette subfamily B member 1 Homo sapiens 0-5 30956965-2 2019 ABCB1 displays a high affinity for imatinib. Imatinib Mesylate 35-43 ATP binding cassette subfamily B member 1 Homo sapiens 0-5 30956965-13 2019 Conclusion: ABCB1 mRNA expression may serve as a predictor of the optimal response to imatinib treatment in patients with CML. Imatinib Mesylate 86-94 ATP binding cassette subfamily B member 1 Homo sapiens 12-17 30186389-0 2018 Decreased expression of microRNA-214 contributes to imatinib mesylate resistance of chronic myeloid leukemia patients by upregulating ABCB1 gene expression. Imatinib Mesylate 52-69 ATP binding cassette subfamily B member 1 Homo sapiens 134-139 29945498-6 2018 RESULTS: beta-catenin and NFkappaB-p65 proteins bound to DNA promoter regions of MDR1 in imatinib-sensitive and resistant CML cells, whereas any direct protein-protein interaction could not be found between NFkappaB-p65 and Akirin-2 or beta-catenin proteins. Imatinib Mesylate 89-97 ATP binding cassette subfamily B member 1 Homo sapiens 81-85 30186389-1 2018 The aim of the present study was to determine the expression of adenosine triphosphate binding cassette subfamily B member 1 (ABCB1) gene and its protein P-glycoprotein (PGP) in bone marrow mononuclear cells from chronic myeloid leukemia (CML) patients with imatinib mesylate (IM) resistance, or IM-resistant CML K562 cells. Imatinib Mesylate 258-275 ATP binding cassette subfamily B member 1 Homo sapiens 64-124 30186389-1 2018 The aim of the present study was to determine the expression of adenosine triphosphate binding cassette subfamily B member 1 (ABCB1) gene and its protein P-glycoprotein (PGP) in bone marrow mononuclear cells from chronic myeloid leukemia (CML) patients with imatinib mesylate (IM) resistance, or IM-resistant CML K562 cells. Imatinib Mesylate 258-275 ATP binding cassette subfamily B member 1 Homo sapiens 126-131 30186389-1 2018 The aim of the present study was to determine the expression of adenosine triphosphate binding cassette subfamily B member 1 (ABCB1) gene and its protein P-glycoprotein (PGP) in bone marrow mononuclear cells from chronic myeloid leukemia (CML) patients with imatinib mesylate (IM) resistance, or IM-resistant CML K562 cells. Imatinib Mesylate 258-275 ATP binding cassette subfamily B member 1 Homo sapiens 170-173 28762371-0 2018 Imatinib-induced ophthalmological side-effects in GIST patients are associated with the variations of EGFR, SLC22A1, SLC22A5 and ABCB1. Imatinib Mesylate 0-8 ATP binding cassette subfamily B member 1 Homo sapiens 129-134 28762371-5 2018 These results indicated that variants in EGFR, SLC22A1, SLC22A5 and ABCB1 influenced the incidence of Imatinib-induced ophthalmological toxicities, and polymorphism analyses in associated genes might be beneficial to optimize Imatinib treatment. Imatinib Mesylate 102-110 ATP binding cassette subfamily B member 1 Homo sapiens 68-73 28762371-5 2018 These results indicated that variants in EGFR, SLC22A1, SLC22A5 and ABCB1 influenced the incidence of Imatinib-induced ophthalmological toxicities, and polymorphism analyses in associated genes might be beneficial to optimize Imatinib treatment. Imatinib Mesylate 226-234 ATP binding cassette subfamily B member 1 Homo sapiens 68-73 28836054-0 2017 Molecular study of ABCB1 gene and its correlation with imatinib response in chronic myeloid leukemia. Imatinib Mesylate 55-63 ATP binding cassette subfamily B member 1 Homo sapiens 19-24 29808796-13 2018 Our results indicate that inhibition of apoptosis, induction of autophagy, overexpression of efflux gene MDR1 and down-regulation of influx gene OCT1 play crucial roles in the progression of imatinib resistance. Imatinib Mesylate 191-199 ATP binding cassette subfamily B member 1 Homo sapiens 105-109 33177018-0 2018 [Effect of MDR1 and CYP3A5 gene polymorphisms on outcomes of patients receiving imatinib treatment for chronic myeloid leukemia]. Imatinib Mesylate 80-88 ATP binding cassette subfamily B member 1 Homo sapiens 11-15 33177018-1 2018 OBJECTIVE: To study the effect of MDR1 and CYP3A5 gene polymorphisms on the outcomes of imatinib treatment in patients with chronic myeloid leukemia (CML). Imatinib Mesylate 88-96 ATP binding cassette subfamily B member 1 Homo sapiens 34-38 33177018-9 2018 CONCLUSIONS: The risk of cytogenetic relapse of CML was significantly affected by SNPs of C1236T and C3435T loci of MDR1 gene and blood imatinib concentration. Imatinib Mesylate 136-144 ATP binding cassette subfamily B member 1 Homo sapiens 116-120 28836054-3 2017 Three single-nucleotide polymorphisms (C1236T, G2677T/A, C3435T) and/or mRNA expression changes of ABCB1 gene were demonstrated to be associated with inter-individual variability of imatinib response in CML patients. Imatinib Mesylate 182-190 ATP binding cassette subfamily B member 1 Homo sapiens 99-104 28836054-4 2017 In this study, we aimed to examine whether genetic variations and/or altered expression of ABCB1 gene may influence response to imatinib. Imatinib Mesylate 128-136 ATP binding cassette subfamily B member 1 Homo sapiens 91-96 28836054-12 2017 CONCLUSION: Furthermore, analyses of ABCB1 haplotypes should be taken into account to study the relationship between ABCB1 genotypes and imatinib efficacy. Imatinib Mesylate 137-145 ATP binding cassette subfamily B member 1 Homo sapiens 37-42 28836054-12 2017 CONCLUSION: Furthermore, analyses of ABCB1 haplotypes should be taken into account to study the relationship between ABCB1 genotypes and imatinib efficacy. Imatinib Mesylate 137-145 ATP binding cassette subfamily B member 1 Homo sapiens 117-122 28190319-8 2017 Overexpression of MEG3 in imatinib-resistant K562 cells markedly decreased cell proliferation, increased cell apoptosis, reversed imatinib resistance, and reduced the expression of MRP1, MDR1, and ABCG2. Imatinib Mesylate 26-34 ATP binding cassette subfamily B member 1 Homo sapiens 187-191 28367681-0 2017 Do polymorphisms in MDR1 and CYP3A5 genes influence the risk of cytogenetic relapse in patients with chronic myeloid leukemia on imatinib therapy? Imatinib Mesylate 129-137 ATP binding cassette subfamily B member 1 Homo sapiens 20-24 28330783-0 2017 Influence of MDR1 and CYP3A5 genetic polymorphisms on trough levels and therapeutic response of imatinib in newly diagnosed patients with chronic myeloid leukemia. Imatinib Mesylate 96-104 ATP binding cassette subfamily B member 1 Homo sapiens 13-17 28623111-0 2017 Reversal of ABCB1 mediated efflux by imatinib and nilotinib in cells expressing various transporter levels. Imatinib Mesylate 37-45 ATP binding cassette subfamily B member 1 Homo sapiens 12-17 28623111-1 2017 Recently, it has been suggested that imatinib (IM) and nilotinib (NIL) could be studied beyond their original application, as inhibitors of the drug efflux pump ABCB1 (P-glycoprotein, MDR1). Imatinib Mesylate 37-45 ATP binding cassette subfamily B member 1 Homo sapiens 161-166 28623111-1 2017 Recently, it has been suggested that imatinib (IM) and nilotinib (NIL) could be studied beyond their original application, as inhibitors of the drug efflux pump ABCB1 (P-glycoprotein, MDR1). Imatinib Mesylate 37-45 ATP binding cassette subfamily B member 1 Homo sapiens 168-182 28623111-1 2017 Recently, it has been suggested that imatinib (IM) and nilotinib (NIL) could be studied beyond their original application, as inhibitors of the drug efflux pump ABCB1 (P-glycoprotein, MDR1). Imatinib Mesylate 37-45 ATP binding cassette subfamily B member 1 Homo sapiens 184-188 28330783-2 2017 Aim of this study was to assess the influence of polymorphisms in MDR1 and CYP3A5 genes on imatinib trough levels, cytogenetic and molecular response in patients with CML. Imatinib Mesylate 91-99 ATP binding cassette subfamily B member 1 Homo sapiens 66-70 28330783-11 2017 Patients with GG genotype for CYP3A5-A6986G (P=0.016) and TT genotype for MDR1-C3435T (P=0.013) polymorphisms had significantly higher trough levels of imatinib. Imatinib Mesylate 152-160 ATP binding cassette subfamily B member 1 Homo sapiens 74-78 28330783-13 2017 Patients with CGC haplotype for MDR1 polymorphisms had significantly lower imatinib trough levels and were at a higher risk of imatinib failure [RR=1.547, 95% CI (1.324, 1.808), P<0.001]. Imatinib Mesylate 75-83 ATP binding cassette subfamily B member 1 Homo sapiens 32-36 28330783-13 2017 Patients with CGC haplotype for MDR1 polymorphisms had significantly lower imatinib trough levels and were at a higher risk of imatinib failure [RR=1.547, 95% CI (1.324, 1.808), P<0.001]. Imatinib Mesylate 127-135 ATP binding cassette subfamily B member 1 Homo sapiens 32-36 28330783-15 2017 To conclude, MDR1 and CYP3A5 genetic polymorphisms significantly influence plasma trough levels and therapeutic response of imatinib in patients with CML. Imatinib Mesylate 124-132 ATP binding cassette subfamily B member 1 Homo sapiens 13-17 27536777-6 2016 ABCB1 overexpression was also observed in cell lines as an intermediate step during development of resistance to imatinib and dasatinib in vitro. Imatinib Mesylate 113-121 ATP binding cassette subfamily B member 1 Homo sapiens 0-5 27875938-7 2017 RESULTS: Our results showed that lncRNA HOTAIR was greatly upregulated in the MRP1-high patients as well as in the K562-imatinib-resistant cells compared with control. Imatinib Mesylate 120-128 ATP binding cassette subfamily B member 1 Homo sapiens 78-82 27875938-8 2017 Knockdown of HOTAIR expression downregulated the MRP1 expression levels in the K562-imatinib cells and resulted in higher sensitivity to the imatinib treatment. Imatinib Mesylate 84-92 ATP binding cassette subfamily B member 1 Homo sapiens 49-53 27875938-8 2017 Knockdown of HOTAIR expression downregulated the MRP1 expression levels in the K562-imatinib cells and resulted in higher sensitivity to the imatinib treatment. Imatinib Mesylate 141-149 ATP binding cassette subfamily B member 1 Homo sapiens 49-53 27416909-0 2017 The clinical significance of ABCB1 overexpression in predicting outcome of CML patients undergoing first-line imatinib treatment. Imatinib Mesylate 110-118 ATP binding cassette subfamily B member 1 Homo sapiens 29-34 27416909-5 2017 Since the drug efflux transporter ABCB1 has previously been implicated in TKI resistance, we determined if early increases in ABCB1 mRNA expression (fold change from diagnosis to day 22 of imatinib therapy) predict for patient response. Imatinib Mesylate 189-197 ATP binding cassette subfamily B member 1 Homo sapiens 34-39 27416909-5 2017 Since the drug efflux transporter ABCB1 has previously been implicated in TKI resistance, we determined if early increases in ABCB1 mRNA expression (fold change from diagnosis to day 22 of imatinib therapy) predict for patient response. Imatinib Mesylate 189-197 ATP binding cassette subfamily B member 1 Homo sapiens 126-131 27418107-8 2016 Further concentration dependent studies showed that imatinib, nilotinib and pazopanib were potent Pgp inhibitors with IC50 values of 2.42, 6.11 and 8.06 mum, respectively. Imatinib Mesylate 52-60 ATP binding cassette subfamily B member 1 Homo sapiens 98-101 28289867-0 2017 Association of the hOCT1/ABCB1 genotype with efficacy and tolerability of imatinib in patients affected by chronic myeloid leukemia. Imatinib Mesylate 74-82 ATP binding cassette subfamily B member 1 Homo sapiens 25-30 28289867-4 2017 RESULTS: We found that a combination of two polymorphisms, namely hOCT1 c.480C>G (rs683369) and ABCB1 c.3435C>T (rs1045642), seems to play the role of predictor for imatinib in both efficacy and toxicity. Imatinib Mesylate 171-179 ATP binding cassette subfamily B member 1 Homo sapiens 99-104 27770655-0 2016 Low ABCB1 and high OCT1 levels play a favorable role in the molecular response to imatinib in CML patients in the community clinical practice. Imatinib Mesylate 82-90 ATP binding cassette subfamily B member 1 Homo sapiens 4-9 27770655-6 2016 Our results suggest that ABCB1 and OCT1 mRNA expressions may present biological relevance to identify responder and non-responder patients to imatinib treatment. Imatinib Mesylate 142-150 ATP binding cassette subfamily B member 1 Homo sapiens 25-30 27268766-0 2016 ABCB1 1199G>A polymorphism (rs2229109) affects the transport of imatinib, nilotinib and dasatinib. Imatinib Mesylate 67-75 ATP binding cassette subfamily B member 1 Homo sapiens 0-5 27405085-0 2016 Impact of ABCB1 1236C > T-2677G > T-3435C > T polymorphisms on the anti-proliferative activity of imatinib, nilotinib, dasatinib and ponatinib. Imatinib Mesylate 107-115 ATP binding cassette subfamily B member 1 Homo sapiens 10-15 27405085-3 2016 The most common ABCB1 variants are 1236C > T, 2677G > T, 3435C > T and have been associated with clinical response to imatinib in chronic myelogenous leukaemia (CML) in some studies. Imatinib Mesylate 127-135 ATP binding cassette subfamily B member 1 Homo sapiens 16-21 27405085-6 2016 Imatinib anti-proliferative effect and accumulation were decreased to a larger extent in cells expressing the ABCB1 wild-type protein compared with the 1236T-2677T-3435T variant relatively to control cells. Imatinib Mesylate 0-8 ATP binding cassette subfamily B member 1 Homo sapiens 110-115 27405085-8 2016 In conclusion, our data suggest that wild-type ABCB1 exports imatinib more efficiently than the 1236T-2677T-3435T variant protein, providing a molecular basis for the reported association between ABCB1 polymorphisms and the response to imatinib in CML. Imatinib Mesylate 61-69 ATP binding cassette subfamily B member 1 Homo sapiens 47-52 27405085-8 2016 In conclusion, our data suggest that wild-type ABCB1 exports imatinib more efficiently than the 1236T-2677T-3435T variant protein, providing a molecular basis for the reported association between ABCB1 polymorphisms and the response to imatinib in CML. Imatinib Mesylate 61-69 ATP binding cassette subfamily B member 1 Homo sapiens 196-201 27405085-8 2016 In conclusion, our data suggest that wild-type ABCB1 exports imatinib more efficiently than the 1236T-2677T-3435T variant protein, providing a molecular basis for the reported association between ABCB1 polymorphisms and the response to imatinib in CML. Imatinib Mesylate 236-244 ATP binding cassette subfamily B member 1 Homo sapiens 47-52 27405085-8 2016 In conclusion, our data suggest that wild-type ABCB1 exports imatinib more efficiently than the 1236T-2677T-3435T variant protein, providing a molecular basis for the reported association between ABCB1 polymorphisms and the response to imatinib in CML. Imatinib Mesylate 236-244 ATP binding cassette subfamily B member 1 Homo sapiens 196-201 27268766-2 2016 The purpose of this study was to evaluate in vitro the influence of the ABCB1 1199G>A SNP on ABCB1 transport activity toward selected TKIs (imatinib, nilotinib and dasatinib) that are currently used in chronic myelogenous leukemia. Imatinib Mesylate 143-151 ATP binding cassette subfamily B member 1 Homo sapiens 72-77 27268766-2 2016 The purpose of this study was to evaluate in vitro the influence of the ABCB1 1199G>A SNP on ABCB1 transport activity toward selected TKIs (imatinib, nilotinib and dasatinib) that are currently used in chronic myelogenous leukemia. Imatinib Mesylate 143-151 ATP binding cassette subfamily B member 1 Homo sapiens 96-101 27268766-7 2016 CONCLUSION: Imatinib, nilotinib and dasatinib are transported more efficiently by the ABCB1 variant (Asn400) compared with the wild-type (Ser400) protein. Imatinib Mesylate 12-20 ATP binding cassette subfamily B member 1 Homo sapiens 86-91 27168851-0 2016 Association between the concentration of imatinib in bone marrow mononuclear cells, mutation status of ABCB1 and therapeutic response in patients with chronic myelogenous leukemia. Imatinib Mesylate 41-49 ATP binding cassette subfamily B member 1 Homo sapiens 103-108 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 ATP binding cassette subfamily B member 1 Homo sapiens 0-30 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 ATP binding cassette subfamily B member 1 Homo sapiens 32-36 27168851-1 2016 Low concentrations of imatinib (IM) in bone marrow cells have been linked with poor prognosis in patients with chronic myeloid leukemia (CML), which may be caused by the emergence of ATP-binding cassette transporter B1 (ABCB1) mutations. Imatinib Mesylate 22-30 ATP binding cassette subfamily B member 1 Homo sapiens 183-218 27168851-1 2016 Low concentrations of imatinib (IM) in bone marrow cells have been linked with poor prognosis in patients with chronic myeloid leukemia (CML), which may be caused by the emergence of ATP-binding cassette transporter B1 (ABCB1) mutations. Imatinib Mesylate 22-30 ATP binding cassette subfamily B member 1 Homo sapiens 220-225 25908454-6 2015 Moreover, leukemia cell lines overexpressing ABCB1 have also been shown to be more resistant to the tyrosine kinase inhibitor imatinib mesylate. Imatinib Mesylate 126-143 ATP binding cassette subfamily B member 1 Homo sapiens 45-50 26634458-1 2015 Our study aimed to investigate the association between multidrug resistance (MDR1) gene polymorphisms and the response to imatinib (IM) in chronic myeloid leukemia (CML). Imatinib Mesylate 122-130 ATP binding cassette subfamily B member 1 Homo sapiens 77-81 25916699-3 2015 Our previous studies have highlighted the role of cyclooxygenase-2 (COX-2) in regulating the expression of multidrug resistant protein-1 (MDR1), P-gp, in imatinib-resistant K562 cells (IR-K562) via PGE2-cAMP-PKC-NF-kappaB pathway and inhibition of COX-2 by celecoxib, a COX-2 specific inhibitor, inhibits this pathway and reverses the drug resistance. Imatinib Mesylate 154-162 ATP binding cassette subfamily B member 1 Homo sapiens 107-136 25916699-3 2015 Our previous studies have highlighted the role of cyclooxygenase-2 (COX-2) in regulating the expression of multidrug resistant protein-1 (MDR1), P-gp, in imatinib-resistant K562 cells (IR-K562) via PGE2-cAMP-PKC-NF-kappaB pathway and inhibition of COX-2 by celecoxib, a COX-2 specific inhibitor, inhibits this pathway and reverses the drug resistance. Imatinib Mesylate 154-162 ATP binding cassette subfamily B member 1 Homo sapiens 138-142 25916699-4 2015 Studies have identified that not only MDR1 but other ATP-binding cassette transport proteins (ABC transporters) are involved in the development of imatinib resistance. Imatinib Mesylate 147-155 ATP binding cassette subfamily B member 1 Homo sapiens 38-42 26250462-11 2016 Patients with CC421 ABCG2/TT3435 ABCB1 and CC421 ABCG2/TT27157 XRCC1 diplotypes might be at higher risk to rapid and severe development of CML and have weaker response to treatments with imatinib. Imatinib Mesylate 187-195 ATP binding cassette subfamily B member 1 Homo sapiens 33-38 26546461-0 2015 A study to explore the correlation of ABCB1, ABCG2, OCT1 genetic polymorphisms and trough level concentration with imatinib mesylate-induced thrombocytopenia in chronic myeloid leukemia patients. Imatinib Mesylate 115-132 ATP binding cassette subfamily B member 1 Homo sapiens 38-43 26546461-3 2015 The present study was framed to explore the influence of common drug transporter gene polymorphisms of ABCB1, ABCG2, OCT1 and trough level concentration on commonly occurring adverse events in CML patients treated with imatinib mesylate. Imatinib Mesylate 219-236 ATP binding cassette subfamily B member 1 Homo sapiens 103-108 27294449-0 2015 C1236T polymorphism in MDR1 gene correlates with therapeutic response to imatinib mesylate in Indian patients with chronic myeloid leukaemia. Imatinib Mesylate 73-90 ATP binding cassette subfamily B member 1 Homo sapiens 23-27 27294449-4 2015 We therefore studied three polymorphisms (C1236T, G2677T and C3435T) in the human multidrug-resistance gene (MDR1) in 86 patients with chronic myeloid leukaemia treated with imatinib. Imatinib Mesylate 174-182 ATP binding cassette subfamily B member 1 Homo sapiens 109-113 27294449-7 2015 In conclusion, determination of C1236T MDR1 genotype may help to predict response to imatinib therapy in patients with chronic myeloid leukaemia. Imatinib Mesylate 85-93 ATP binding cassette subfamily B member 1 Homo sapiens 39-43 24954033-0 2014 Resistance to daunorubicin, imatinib, or nilotinib depends on expression levels of ABCB1 and ABCG2 in human leukemia cells. Imatinib Mesylate 28-36 ATP binding cassette subfamily B member 1 Homo sapiens 83-88 25245580-0 2015 ABCB1 polymorphisms predict imatinib response in chronic myeloid leukemia patients: a systematic review and meta-analysis. Imatinib Mesylate 28-36 ATP binding cassette subfamily B member 1 Homo sapiens 0-5 25482933-2 2015 In the present study, we determined the effect of dasatinib which was approved for imatinib resistant chronic myelogenous leukemia (CML) and (Ph(+)) acute lymphoblastic leukemia (ALL) treatment on P-gp-mediated MDR. Imatinib Mesylate 83-91 ATP binding cassette subfamily B member 1 Homo sapiens 197-201 25568846-12 2014 On the other hand, a higher expression level of ABCB1 in imatinib-exposed samples did not affect second-generation TKI responses but was correlated with poor imatinib responses. Imatinib Mesylate 57-65 ATP binding cassette subfamily B member 1 Homo sapiens 48-53 25568846-12 2014 On the other hand, a higher expression level of ABCB1 in imatinib-exposed samples did not affect second-generation TKI responses but was correlated with poor imatinib responses. Imatinib Mesylate 158-166 ATP binding cassette subfamily B member 1 Homo sapiens 48-53 25301112-0 2014 ABCB1 haplotypes but not individual SNPs predict for optimal response/failure in Egyptian patients with chronic-phase chronic myeloid leukemia receiving imatinib mesylate. Imatinib Mesylate 153-170 ATP binding cassette subfamily B member 1 Homo sapiens 0-5 25568846-5 2014 ABCB1 revealed highly variable expression levels before and after imatinib treatment. Imatinib Mesylate 66-74 ATP binding cassette subfamily B member 1 Homo sapiens 0-5 25568846-6 2014 In addition, median ABCB1 expression in follow-up samples was lower in patients achieving complete cytogenetic response or major molecular response during imatinib treatment than in failed patients. Imatinib Mesylate 155-163 ATP binding cassette subfamily B member 1 Homo sapiens 20-25 24954033-5 2014 We observed that the resistance to DRN and imatinib was proportional to the expression level of ABCB1. Imatinib Mesylate 43-51 ATP binding cassette subfamily B member 1 Homo sapiens 96-101 24954033-9 2014 Only cells which expression of ABCB1 or ABCG2 exceeded a certain level exhibited a significantly decreased intracellular level of imatinib, and this effect was accompanied by a significantly increased resistance to this drug. Imatinib Mesylate 130-138 ATP binding cassette subfamily B member 1 Homo sapiens 31-36 24589908-1 2014 The aim of the study was to investigate any possible influence of polymorphisms of transmembrane transporters human organic cation transporter 1 (hOCT1), ABCB1, ABCG2 on imatinib pharmacokinetics in 33 men and 27 women (median age and range, 56 and 27-79 years, respectively) affected by chronic myeloid leukemia. Imatinib Mesylate 170-178 ATP binding cassette subfamily B member 1 Homo sapiens 154-159 25089713-1 2014 One of the potential mechanisms of imatinib mesylate (IM) resistance in chronic myeloid leukemia (CML) is increased level of P-glycoprotein (Pgp). Imatinib Mesylate 35-52 ATP binding cassette subfamily B member 1 Homo sapiens 125-139 25089713-1 2014 One of the potential mechanisms of imatinib mesylate (IM) resistance in chronic myeloid leukemia (CML) is increased level of P-glycoprotein (Pgp). Imatinib Mesylate 35-52 ATP binding cassette subfamily B member 1 Homo sapiens 141-144 24472814-0 2014 MDR1 expression predicts outcome of Ph+ chronic phase CML patients on second-line nilotinib therapy after imatinib failure. Imatinib Mesylate 106-114 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 24472814-6 2014 (v) Nilotinib was able to impede proliferation of MDR1-overexpressing imatinib-resistant cells. Imatinib Mesylate 70-78 ATP binding cassette subfamily B member 1 Homo sapiens 50-54 24472814-7 2014 High MDR1 gene expression might identify patients whose mode of imatinib resistance is essentially determined by increased efflux activity of MDR1 and therefore can be overcome by second-line nilotinib treatment. Imatinib Mesylate 64-72 ATP binding cassette subfamily B member 1 Homo sapiens 5-9 24472814-7 2014 High MDR1 gene expression might identify patients whose mode of imatinib resistance is essentially determined by increased efflux activity of MDR1 and therefore can be overcome by second-line nilotinib treatment. Imatinib Mesylate 64-72 ATP binding cassette subfamily B member 1 Homo sapiens 142-146 24581936-0 2014 Association of genotypes and haplotypes of multi-drug transporter genes ABCB1 and ABCG2 with clinical response to imatinib mesylate in chronic myeloid leukemia patients. Imatinib Mesylate 114-122 ATP binding cassette subfamily B member 1 Homo sapiens 72-77 24667683-7 2014 Lovastatin does not influence influx but significantly inhibits efflux of imatinib mediated by ATP-binding cassette (ABC) transporters: ABCB1 and ABCG2. Imatinib Mesylate 74-82 ATP binding cassette subfamily B member 1 Homo sapiens 136-141 24660038-0 2014 ABCB1 haplotypes are associated with P-gp activity and affect a major molecular response in chronic myeloid leukemia patients treated with a standard dose of imatinib. Imatinib Mesylate 158-166 ATP binding cassette subfamily B member 1 Homo sapiens 0-5 23683876-0 2014 Association of MDR1 gene polymorphism (G2677T) with imatinib response in Egyptian chronic myeloid leukemia patients. Imatinib Mesylate 52-60 ATP binding cassette subfamily B member 1 Homo sapiens 15-19 23683876-14 2014 CONCLUSION: Determination of MDR1 polymorphisms (G2677T) might be useful in response prediction to therapy with imatinib in patients with CML. Imatinib Mesylate 112-120 ATP binding cassette subfamily B member 1 Homo sapiens 29-33 24660038-0 2014 ABCB1 haplotypes are associated with P-gp activity and affect a major molecular response in chronic myeloid leukemia patients treated with a standard dose of imatinib. Imatinib Mesylate 158-166 ATP binding cassette subfamily B member 1 Homo sapiens 37-41 24019750-2 2013 ABCB1 SNPs and haplotypes have been suggested to influence the pharmacokinetics and therapeutic outcome of the tyrosine kinase inhibitor (TKI) imatinib, used for treatment of chronic myeloid leukemia (CML). Imatinib Mesylate 143-151 ATP binding cassette subfamily B member 1 Homo sapiens 0-5 24088895-11 2014 Furthermore, the same inhibition level of multidrug resistance 1 expression was observed in cells treated with activin A alone, treated sequentially with activin A and imatinib, or treated simultaneously with activin A and imatinib. Imatinib Mesylate 168-176 ATP binding cassette subfamily B member 1 Homo sapiens 42-64 24088895-11 2014 Furthermore, the same inhibition level of multidrug resistance 1 expression was observed in cells treated with activin A alone, treated sequentially with activin A and imatinib, or treated simultaneously with activin A and imatinib. Imatinib Mesylate 223-231 ATP binding cassette subfamily B member 1 Homo sapiens 42-64 23891189-0 2013 XIAP and P-glycoprotein co-expression is related to imatinib resistance in chronic myeloid leukemia cells. Imatinib Mesylate 52-60 ATP binding cassette subfamily B member 1 Homo sapiens 9-23 23891189-4 2013 Imatinib increased XIAP and Pgp expression in K562-Lucena cells, while in K562 cells a downregulation of these proteins was observed, suggesting that imatinib induces an increment of MDR phenotype of CML cells that previously exhibit high levels of Pgp/XIAP co-expression. Imatinib Mesylate 0-8 ATP binding cassette subfamily B member 1 Homo sapiens 28-31 23891189-4 2013 Imatinib increased XIAP and Pgp expression in K562-Lucena cells, while in K562 cells a downregulation of these proteins was observed, suggesting that imatinib induces an increment of MDR phenotype of CML cells that previously exhibit high levels of Pgp/XIAP co-expression. Imatinib Mesylate 0-8 ATP binding cassette subfamily B member 1 Homo sapiens 249-252 23891189-4 2013 Imatinib increased XIAP and Pgp expression in K562-Lucena cells, while in K562 cells a downregulation of these proteins was observed, suggesting that imatinib induces an increment of MDR phenotype of CML cells that previously exhibit high levels of Pgp/XIAP co-expression. Imatinib Mesylate 150-158 ATP binding cassette subfamily B member 1 Homo sapiens 249-252 24798723-1 2014 BACKGROUND: MDR1 gene polymorphisms were demonstrated to be associated with interindividual variability of imatinib response for chronic myeloid leukemia (CML) patients in several studies; however, the results have been inconclusive. Imatinib Mesylate 107-115 ATP binding cassette subfamily B member 1 Homo sapiens 12-16 24798723-2 2014 MATERIALS & METHODS: To clarify the effect of common MDR1 variants on clinical response to imatinib, we performed a meta-analysis to quantify the accumulated information from genetic association studies. Imatinib Mesylate 95-103 ATP binding cassette subfamily B member 1 Homo sapiens 57-61 24798723-3 2014 After a thorough search of the published literature, we undertook a meta-analysis to evaluate the effect of MDR1 C1236T, G2677T and C3435T polymorphisms on imatinib response. Imatinib Mesylate 156-164 ATP binding cassette subfamily B member 1 Homo sapiens 108-112 24798723-4 2014 RESULTS: Our pooled data showed a significant association between MDR1 C1236T polymorphism and the increasing risk of imatinib resistance in Asian CML patients. Imatinib Mesylate 118-126 ATP binding cassette subfamily B member 1 Homo sapiens 66-70 24798723-6 2014 CONCLUSION: The synonymous MDR1 C1236T polymorphism might be a risk factor for nonoptimal clinical response to imatinib in Asian CML patients. Imatinib Mesylate 111-119 ATP binding cassette subfamily B member 1 Homo sapiens 27-31 24107928-0 2014 Interaction of the efflux transporters ABCB1 and ABCG2 with imatinib, nilotinib, and dasatinib. Imatinib Mesylate 60-68 ATP binding cassette subfamily B member 1 Homo sapiens 39-44 24107928-1 2014 The efflux transporters adenosine triphosphate (ATP)-binding cassette (ABC)B1 and ABCG2 have been demonstrated to interact with the tyrosine kinase inhibitors (TKIs) imatinib, nilotinib, and dasatinib. Imatinib Mesylate 166-174 ATP binding cassette subfamily B member 1 Homo sapiens 71-77 25087954-0 2014 Distinct interaction of nilotinib and imatinib with P-Glycoprotein in intracellular accumulation and cytotoxicity in CML Cell Line K562 cells. Imatinib Mesylate 38-46 ATP binding cassette subfamily B member 1 Homo sapiens 52-66 25087954-7 2014 Nilotinib was found to accumulate in imatinib-resistant K562 (K562/IM) cells overexpressing the efflux transporter P-glycoprotein (P-gp), although cytotoxic assays showed that K562/IM cells displayed 20000-fold greater resistance to nilotinib over the parent K562 cells. Imatinib Mesylate 37-45 ATP binding cassette subfamily B member 1 Homo sapiens 115-129 25087954-7 2014 Nilotinib was found to accumulate in imatinib-resistant K562 (K562/IM) cells overexpressing the efflux transporter P-glycoprotein (P-gp), although cytotoxic assays showed that K562/IM cells displayed 20000-fold greater resistance to nilotinib over the parent K562 cells. Imatinib Mesylate 37-45 ATP binding cassette subfamily B member 1 Homo sapiens 131-135 24019750-4 2013 Functional studies of variant ABCB1 transport of imatinib as well as other TKIs might aid the interpretation of results from in vivo association studies, but are currently lacking. Imatinib Mesylate 49-57 ATP binding cassette subfamily B member 1 Homo sapiens 30-35 24019750-5 2013 The aim of this study was to investigate the consequences of ABCB1 variant haplotypes for transport and efficacy of TKIs (imatinib, its major metabolite N-desmethyl imatinib [CGP74588], dasatinib, nilotinib, and bosutinib) in CML cells. Imatinib Mesylate 122-130 ATP binding cassette subfamily B member 1 Homo sapiens 61-66 24019750-8 2013 It was found that dasatinib and the imatinib metabolite CGP74588 are effectively transported by ABCB1, while imatinib, nilotinib, and bosutinib are comparatively weaker ABCB1 substrates. Imatinib Mesylate 36-44 ATP binding cassette subfamily B member 1 Homo sapiens 96-101 24019750-8 2013 It was found that dasatinib and the imatinib metabolite CGP74588 are effectively transported by ABCB1, while imatinib, nilotinib, and bosutinib are comparatively weaker ABCB1 substrates. Imatinib Mesylate 109-117 ATP binding cassette subfamily B member 1 Homo sapiens 169-174 22845311-0 2013 Degree of kinase inhibition achieved in vitro by imatinib and nilotinib is decreased by high levels of ABCB1 but not ABCG2. Imatinib Mesylate 49-57 ATP binding cassette subfamily B member 1 Homo sapiens 103-108 22845311-1 2013 Imatinib and nilotinib interact with ABCB1 and ABCG2. Imatinib Mesylate 0-8 ATP binding cassette subfamily B member 1 Homo sapiens 37-42 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 ATP binding cassette subfamily B member 1 Homo sapiens 78-83 22845311-4 2013 High levels of ABCB1 protein in K562-Dox cells resulted in a significantly increased 50% inhibitory concentration (IC(50)) compared with parental K562 cells for imatinib (IC(50)(IM); 9 microM to 19 microM, p = 0.002) and nilotinib (IC(50)(NIL); 345 nM to 620 nM, p = 0.013). Imatinib Mesylate 161-169 ATP binding cassette subfamily B member 1 Homo sapiens 15-20 22845311-8 2013 Imatinib and nilotinib appear to be transported by ABCB1 but do not interact strongly with ABCG2. Imatinib Mesylate 0-8 ATP binding cassette subfamily B member 1 Homo sapiens 51-56 21718141-8 2011 In contrast, three imatinib-resistant K562 Dox lines exhibited only a further increase in ABCB1 expression. Imatinib Mesylate 19-27 ATP binding cassette subfamily B member 1 Homo sapiens 90-95 23257429-7 2012 It is concluded that the inhibiton of NHE1 can significantly decrease the protein expression of Pgp in K562/DOX and K562/G01 cells, increase the accumulation of Rhodamine123 and doxorubicin in the cells of advanced patients and enhance the sensitivity of cells to imatinib in which the p38 MAPK signal transduction pathways involves. Imatinib Mesylate 264-272 ATP binding cassette subfamily B member 1 Homo sapiens 96-99 23230732-0 2012 [Multidrug resistant gene MDR1 contributes to development of imatinib-resistance in Ph (+) acute lymphoblastic leukemia cell line SUP-BS15RI]. Imatinib Mesylate 61-69 ATP binding cassette subfamily B member 1 Homo sapiens 26-30 23230732-1 2012 OBJECTIVE: To investigate the contribution of multidrug-resistant gene MDR1 to development of imatinib-resistance in Ph(+) acute lymphoblastic leukemia cell line SUP-B15/RI. Imatinib Mesylate 94-102 ATP binding cassette subfamily B member 1 Homo sapiens 71-75 22883199-0 2012 [Effects of hOCT1 and ABCB1 gene on the efficacy of imatinib mesylate in chronic myelocytic leukemia]. Imatinib Mesylate 52-69 ATP binding cassette subfamily B member 1 Homo sapiens 22-27 22781602-21 2012 Imatinib concentration was regulated by AGP and the activities of hOCT1 and ABCB1. Imatinib Mesylate 0-8 ATP binding cassette subfamily B member 1 Homo sapiens 76-81 22134106-0 2012 ABCB1 haplotype is associated with major molecular response in chronic myeloid leukemia patients treated with standard-dose of imatinib. Imatinib Mesylate 127-135 ATP binding cassette subfamily B member 1 Homo sapiens 0-5 22098951-0 2012 Overexpression of P-glycoprotein induces acquired resistance to imatinib in chronic myelogenous leukemia cells. Imatinib Mesylate 64-72 ATP binding cassette subfamily B member 1 Homo sapiens 18-32 22098951-7 2012 Western blot analysis and reverse transcription-polymerase chain reaction(RT-PCR) demonstrated that P-glycoprotein(P-gp) and MDR1 mRNA levels were increased in K562-imatinib cells. Imatinib Mesylate 165-173 ATP binding cassette subfamily B member 1 Homo sapiens 100-114 22098951-7 2012 Western blot analysis and reverse transcription-polymerase chain reaction(RT-PCR) demonstrated that P-glycoprotein(P-gp) and MDR1 mRNA levels were increased in K562-imatinib cells. Imatinib Mesylate 165-173 ATP binding cassette subfamily B member 1 Homo sapiens 125-129 23272163-0 2012 SLC22A1-ABCB1 haplotype profiles predict imatinib pharmacokinetics in Asian patients with chronic myeloid leukemia. Imatinib Mesylate 41-49 ATP binding cassette subfamily B member 1 Homo sapiens 8-13 23272163-1 2012 OBJECTIVE: This study aimed to explore the influence of SLC22A1, PXR, ABCG2, ABCB1 and CYP3A5 3 genetic polymorphisms on imatinib mesylate (IM) pharmacokinetics in Asian patients with chronic myeloid leukemia (CML). Imatinib Mesylate 121-138 ATP binding cassette subfamily B member 1 Homo sapiens 77-82 23383209-0 2013 Imatinib reverses doxorubicin resistance by affecting activation of STAT3-dependent NF-kappaB and HSP27/p38/AKT pathways and by inhibiting ABCB1. Imatinib Mesylate 0-8 ATP binding cassette subfamily B member 1 Homo sapiens 139-144 23383209-6 2013 In contrast, imatinib prevents acquired resistance by inhibiting upregulation of the ABC drug transporter, ABCB1, directly inhibiting ABCB1 function, and abrogating survival signaling. Imatinib Mesylate 13-21 ATP binding cassette subfamily B member 1 Homo sapiens 107-112 23383209-6 2013 In contrast, imatinib prevents acquired resistance by inhibiting upregulation of the ABC drug transporter, ABCB1, directly inhibiting ABCB1 function, and abrogating survival signaling. Imatinib Mesylate 13-21 ATP binding cassette subfamily B member 1 Homo sapiens 134-139 23230732-8 2012 CONCLUSION: The overexpression of MDR1 mRNA and higher activity of P-gp is partially responsible for acquiring of imatinib resistance in SUP-B15/RI cell line. Imatinib Mesylate 114-122 ATP binding cassette subfamily B member 1 Homo sapiens 34-38 21225261-0 2011 Interactions of N-desmethyl imatinib, an active metabolite of imatinib, with P-glycoprotein in human leukemia cells. Imatinib Mesylate 28-36 ATP binding cassette subfamily B member 1 Homo sapiens 77-91 21663515-0 2011 Development of imatinib and dasatinib resistance: dynamics of expression of drug transporters ABCB1, ABCC1, ABCG2, MVP, and SLC22A1. Imatinib Mesylate 15-23 ATP binding cassette subfamily B member 1 Homo sapiens 94-99 21185600-0 2011 Correlation between genetic polymorphisms of the hOCT1 and MDR1 genes and the response to imatinib in patients newly diagnosed with chronic-phase chronic myeloid leukemia. Imatinib Mesylate 90-98 ATP binding cassette subfamily B member 1 Homo sapiens 59-63 21185600-1 2011 The association between seven polymorphisms in the genes hOCT1 and MDR1, encoding for imatinib transporter proteins, and the response to imatinib 400mg/daily was investigated in 65 patients newly diagnosed with chronic-phase chronic myeloid leukemia. Imatinib Mesylate 86-94 ATP binding cassette subfamily B member 1 Homo sapiens 67-71 21185600-1 2011 The association between seven polymorphisms in the genes hOCT1 and MDR1, encoding for imatinib transporter proteins, and the response to imatinib 400mg/daily was investigated in 65 patients newly diagnosed with chronic-phase chronic myeloid leukemia. Imatinib Mesylate 137-145 ATP binding cassette subfamily B member 1 Homo sapiens 67-71 21185600-4 2011 Beside, the MDR1 haplotype 1236T-2677G-3435C was more frequently found in patients primarily resistant to imatinib. Imatinib Mesylate 106-114 ATP binding cassette subfamily B member 1 Homo sapiens 12-16 21225261-7 2011 Our results indicate that CGP74588 could hardly positively contribute to the treatment of chronic myeloid leukemia (CML) where ABCB1 gene overexpression represents a possible mechanism of resistance to imatinib in vivo. Imatinib Mesylate 202-210 ATP binding cassette subfamily B member 1 Homo sapiens 127-132 21356308-0 2011 Activation of STAT5 confers imatinib resistance on leukemic cells through the transcription of TERT and MDR1. Imatinib Mesylate 28-36 ATP binding cassette subfamily B member 1 Homo sapiens 104-108 21520403-5 2011 In the K562-Lucena cell line, Pgp positive, imatinib caused an enhancing in Pgp expression at protein and mRNA levels, whereas in the Pgp negative cell line, this drug was capable of decreasing MDR1/Pgp mRNA levels. Imatinib Mesylate 44-52 ATP binding cassette subfamily B member 1 Homo sapiens 30-33 21520403-5 2011 In the K562-Lucena cell line, Pgp positive, imatinib caused an enhancing in Pgp expression at protein and mRNA levels, whereas in the Pgp negative cell line, this drug was capable of decreasing MDR1/Pgp mRNA levels. Imatinib Mesylate 44-52 ATP binding cassette subfamily B member 1 Homo sapiens 76-79 21520403-5 2011 In the K562-Lucena cell line, Pgp positive, imatinib caused an enhancing in Pgp expression at protein and mRNA levels, whereas in the Pgp negative cell line, this drug was capable of decreasing MDR1/Pgp mRNA levels. Imatinib Mesylate 44-52 ATP binding cassette subfamily B member 1 Homo sapiens 76-79 21520403-5 2011 In the K562-Lucena cell line, Pgp positive, imatinib caused an enhancing in Pgp expression at protein and mRNA levels, whereas in the Pgp negative cell line, this drug was capable of decreasing MDR1/Pgp mRNA levels. Imatinib Mesylate 44-52 ATP binding cassette subfamily B member 1 Homo sapiens 194-198 21520403-5 2011 In the K562-Lucena cell line, Pgp positive, imatinib caused an enhancing in Pgp expression at protein and mRNA levels, whereas in the Pgp negative cell line, this drug was capable of decreasing MDR1/Pgp mRNA levels. Imatinib Mesylate 44-52 ATP binding cassette subfamily B member 1 Homo sapiens 76-79 21261505-8 2011 Nef is a candidate chemical that can increase STI571 chemosensitivity in STI571-resistant K562 cells by inhibition of P-gp expression and increasing intracellular STI571 accumulation. Imatinib Mesylate 46-52 ATP binding cassette subfamily B member 1 Homo sapiens 118-122 21311410-0 2011 Association of genetic polymorphisms in the influx transporter SLCO1B3 and the efflux transporter ABCB1 with imatinib pharmacokinetics in patients with chronic myeloid leukemia. Imatinib Mesylate 109-117 ATP binding cassette subfamily B member 1 Homo sapiens 98-103 21311410-5 2011 Patients with the ABCB1 3435CC genotype had significantly higher imatinib clearance (12.7 +- 3.0 L/hr; n = 7) compared with patients with ABCB1 3435CT and TT genotypes (7.9 +- 2.7 L/hr; n = 27) (P = 0.035). Imatinib Mesylate 65-73 ATP binding cassette subfamily B member 1 Homo sapiens 18-23 21311410-6 2011 In conclusion, the present study suggests that single nucleotide polymorphisms of the influx transporter SLCO1B3 and the efflux transporter ABCB1 were functionally associated with individual variability of imatinib pharmacokinetics in Japanese patients with chronic myeloid leukemia. Imatinib Mesylate 206-214 ATP binding cassette subfamily B member 1 Homo sapiens 140-145 20204543-4 2011 We investigated the MDR1 T1236C, G 2677T/A, and C3435T polymorphism in 52 patients with chronic myeloid leukemia treated with imatinib. Imatinib Mesylate 126-134 ATP binding cassette subfamily B member 1 Homo sapiens 20-24 20204543-10 2011 In conclusion, determination of 1236T, C3435T, and G2677T MDR1 polymorphisms might be useful in response prediction to therapy with imatinib in patients with CML. Imatinib Mesylate 132-140 ATP binding cassette subfamily B member 1 Homo sapiens 58-62 20204543-0 2011 Multidrug resistance gene (MDR1) polymorphisms correlate with imatinib response in chronic myeloid leukemia. Imatinib Mesylate 62-70 ATP binding cassette subfamily B member 1 Homo sapiens 27-31 21183698-0 2010 Polymorphisms in the multidrug resistance gene MDR1 (ABCB1) predict for molecular resistance in patients with newly diagnosed chronic myeloid leukemia receiving high-dose imatinib. Imatinib Mesylate 171-179 ATP binding cassette subfamily B member 1 Homo sapiens 47-51 20204543-3 2011 Imatinib is a substrate of P-gp-mediated efflux. Imatinib Mesylate 0-8 ATP binding cassette subfamily B member 1 Homo sapiens 27-31 21163869-6 2011 In vitro experiments show a significant role of ABCB1 and ABCG2 in cellular uptake and retention of imatinib, although pharmacokinetic and pharmacogenetic data are still scarce and contradictory. Imatinib Mesylate 100-108 ATP binding cassette subfamily B member 1 Homo sapiens 48-53 21183698-0 2010 Polymorphisms in the multidrug resistance gene MDR1 (ABCB1) predict for molecular resistance in patients with newly diagnosed chronic myeloid leukemia receiving high-dose imatinib. Imatinib Mesylate 171-179 ATP binding cassette subfamily B member 1 Homo sapiens 53-58 20206383-1 2010 Our previous studies have shown that overexpression of MDR1 and cyclooygenase-2 (COX-2) resulted in resistance development to imatinib in chronic myelogenous leukemia (CML) K562 (IR-K562) cells. Imatinib Mesylate 126-134 ATP binding cassette subfamily B member 1 Homo sapiens 55-59 20423956-3 2010 We compared the interactions of the TKIs imatinib, nilotinib, and dasatinib with ABCB1 and ABCG2 in ex vivo and in vitro systems. Imatinib Mesylate 41-49 ATP binding cassette subfamily B member 1 Homo sapiens 81-86 20423956-10 2010 Taken together, the results suggest that therapeutic doses of imatinib and nilotinib may diminish the potential of ABCB1 and ABCG2 to limit oral absorption or confer resistance. Imatinib Mesylate 62-70 ATP binding cassette subfamily B member 1 Homo sapiens 115-120 20507731-12 2010 CONCLUSIONS: The MDR of K562/A02 cells may be partially reversed by imatinib or BrTet, and the mechanism may be related to the downregulation of mdr1 mRNA and P-gp expression and the upregulation of the rate of apoptosis in K562/A02 cells. Imatinib Mesylate 68-76 ATP binding cassette subfamily B member 1 Homo sapiens 145-149 20658364-0 2010 [Expression of MDR1 and KIT in imatinib-resistant gastrointestinal stromal tumor cells]. Imatinib Mesylate 31-39 ATP binding cassette subfamily B member 1 Homo sapiens 15-19 20658364-1 2010 OBJECTIVE: To explore the relationship between imatinib resistance and genes MDR1 and KIT in gastrointestinal stromal tumor (GIST) cells. Imatinib Mesylate 47-55 ATP binding cassette subfamily B member 1 Homo sapiens 77-81 20658364-8 2010 CONCLUSIONS: Over-expression of gene MDR1 may be associated with imatinib resistance in GIST. Imatinib Mesylate 65-73 ATP binding cassette subfamily B member 1 Homo sapiens 37-41 20507731-12 2010 CONCLUSIONS: The MDR of K562/A02 cells may be partially reversed by imatinib or BrTet, and the mechanism may be related to the downregulation of mdr1 mRNA and P-gp expression and the upregulation of the rate of apoptosis in K562/A02 cells. Imatinib Mesylate 68-76 ATP binding cassette subfamily B member 1 Homo sapiens 159-163 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 ATP binding cassette subfamily B member 1 Homo sapiens 124-146 20446917-2 2010 By using RNA interference-mediated knockdown of MDR1, we have investigated and compared the specific functional consequence of Pgp on the cellular disposition of the major clinically in use TKIs imatinib, dasatinib, nilotinib, sunitinib and sorafenib. Imatinib Mesylate 195-203 ATP binding cassette subfamily B member 1 Homo sapiens 127-130 20446917-4 2010 In these conditions, abrogating specifically Pgp-mediated efflux in vitro revealed the remarkable and statistically significant cellular accumulation of imatinib (difference in cellular levels between Pgp-expressing and silenced cells, at high and low incubation concentration, respectively: 6.1 and 6.6), dasatinib (4.9 and 5.6), sunitinib (3.7 and 7.3) and sorafenib (1.2 and 1.4), confirming that these TKIs are all substrates of Pgp. Imatinib Mesylate 153-161 ATP binding cassette subfamily B member 1 Homo sapiens 45-48 20446917-4 2010 In these conditions, abrogating specifically Pgp-mediated efflux in vitro revealed the remarkable and statistically significant cellular accumulation of imatinib (difference in cellular levels between Pgp-expressing and silenced cells, at high and low incubation concentration, respectively: 6.1 and 6.6), dasatinib (4.9 and 5.6), sunitinib (3.7 and 7.3) and sorafenib (1.2 and 1.4), confirming that these TKIs are all substrates of Pgp. Imatinib Mesylate 153-161 ATP binding cassette subfamily B member 1 Homo sapiens 201-204 20446917-4 2010 In these conditions, abrogating specifically Pgp-mediated efflux in vitro revealed the remarkable and statistically significant cellular accumulation of imatinib (difference in cellular levels between Pgp-expressing and silenced cells, at high and low incubation concentration, respectively: 6.1 and 6.6), dasatinib (4.9 and 5.6), sunitinib (3.7 and 7.3) and sorafenib (1.2 and 1.4), confirming that these TKIs are all substrates of Pgp. Imatinib Mesylate 153-161 ATP binding cassette subfamily B member 1 Homo sapiens 201-204 18669873-7 2008 Both dasatinib and imatinib were transported from the basal to the apical layer, indicating that they were transported by ABCB1, which was confirmed using the ABCB1 inhibitor PSC833 (P = .001 and P < .001, respectively). Imatinib Mesylate 19-27 ATP binding cassette subfamily B member 1 Homo sapiens 122-127 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 ATP binding cassette subfamily B member 1 Homo sapiens 99-104 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 ATP binding cassette subfamily B member 1 Homo sapiens 125-129 19785662-2 2009 It has been documented that ABCB1 and ABCG2 interact with several first-generation, small-molecule, tyrosine kinase inhibitors (TKIs), including the Bcr-Abl fusion kinase inhibitor imatinib, used for the treatment of chronic myeloid leukaemia. Imatinib Mesylate 181-189 ATP binding cassette subfamily B member 1 Homo sapiens 28-33 19584153-2 2009 Several cellular and genetic mechanisms of imatinib resistance have been proposed, including amplification and overexpression of the BCR/ABL gene, the tyrosine kinase domain point mutations, and MDR1 gene overexpression. Imatinib Mesylate 43-51 ATP binding cassette subfamily B member 1 Homo sapiens 195-199 19394750-1 2009 OBJECTIVE: To investigate the interaction of imatinib mesylate (IM) with the clinically relevant adenosine triphosphate-binding cassette efflux transporter MDR1 (ABCB1) in cells from patients with chronic myeloid leukemia (CML) and to explore whether inhibition of this transporter would improve IM"s efficacy in the elimination of CML CD34(+) cells by increasing cell-associated drug accumulation. Imatinib Mesylate 45-62 ATP binding cassette subfamily B member 1 Homo sapiens 156-160 19394750-1 2009 OBJECTIVE: To investigate the interaction of imatinib mesylate (IM) with the clinically relevant adenosine triphosphate-binding cassette efflux transporter MDR1 (ABCB1) in cells from patients with chronic myeloid leukemia (CML) and to explore whether inhibition of this transporter would improve IM"s efficacy in the elimination of CML CD34(+) cells by increasing cell-associated drug accumulation. Imatinib Mesylate 45-62 ATP binding cassette subfamily B member 1 Homo sapiens 162-167 18669873-7 2008 Both dasatinib and imatinib were transported from the basal to the apical layer, indicating that they were transported by ABCB1, which was confirmed using the ABCB1 inhibitor PSC833 (P = .001 and P < .001, respectively). Imatinib Mesylate 19-27 ATP binding cassette subfamily B member 1 Homo sapiens 159-164 17495881-7 2007 ABCB1 genotype was associated with steady-state CL/F due to an apparent genotype-specific influence of imatinib on elimination. Imatinib Mesylate 103-111 ATP binding cassette subfamily B member 1 Homo sapiens 0-5 18524988-0 2008 Multidrug resistance gene (MDR1) polymorphisms are associated with major molecular responses to standard-dose imatinib in chronic myeloid leukemia. Imatinib Mesylate 110-118 ATP binding cassette subfamily B member 1 Homo sapiens 27-31 18524988-4 2008 We analyzed the 3 most relevant single nucleotide polymorphisms of MDR1 in 90 CML patients treated with imatinib. Imatinib Mesylate 104-112 ATP binding cassette subfamily B member 1 Homo sapiens 67-71 18294126-0 2008 Role of P-glycoprotein in evolution of populations of chronic myeloid leukemia cells treated with imatinib. Imatinib Mesylate 98-106 ATP binding cassette subfamily B member 1 Homo sapiens 8-22 18294126-3 2008 The goal of this study was to investigate the role of a multidrug resistance protein, P-glycoprotein (Pgp), in the evolution of CML treated with imatinib. Imatinib Mesylate 145-153 ATP binding cassette subfamily B member 1 Homo sapiens 86-100 18294126-3 2008 The goal of this study was to investigate the role of a multidrug resistance protein, P-glycoprotein (Pgp), in the evolution of CML treated with imatinib. Imatinib Mesylate 145-153 ATP binding cassette subfamily B member 1 Homo sapiens 102-105 18294126-4 2008 We demonstrate here that although imatinib is a substrate for Pgp, cultured CML cells (strain K562/i-S9), overexpressing active Pgp, do not exhibit imatinib resistance. Imatinib Mesylate 34-42 ATP binding cassette subfamily B member 1 Homo sapiens 62-65 18294126-5 2008 Studies of CML patients in the accelerated phase have shown variations in the number of Pgp-positive cells (Pgp+) among individual patients treated with imatinib. Imatinib Mesylate 153-161 ATP binding cassette subfamily B member 1 Homo sapiens 88-91 18294126-5 2008 Studies of CML patients in the accelerated phase have shown variations in the number of Pgp-positive cells (Pgp+) among individual patients treated with imatinib. Imatinib Mesylate 153-161 ATP binding cassette subfamily B member 1 Homo sapiens 108-111 18294126-6 2008 During treatment of patients with imatinib for 6-12 months, the number of Pgp-positive cells significantly increased in most patients. Imatinib Mesylate 34-42 ATP binding cassette subfamily B member 1 Homo sapiens 74-77 18294126-12 2008 Our data suggest that treatment with imatinib causes selection of leukemic stem cells characterized by expression of Pgp and other ABC transporters. Imatinib Mesylate 37-45 ATP binding cassette subfamily B member 1 Homo sapiens 117-120 18083230-0 2008 Imatinib-resistant K562 cells are more sensitive to celecoxib, a selective COX-2 inhibitor: role of COX-2 and MDR-1. Imatinib Mesylate 0-8 ATP binding cassette subfamily B member 1 Homo sapiens 110-115 18083230-4 2008 Further studies revealed the over-expression of COX-2 and MDR-1 in IR-K562 cells suggesting the possible involvement of COX-2 in the development of resistance to imatinib. Imatinib Mesylate 162-170 ATP binding cassette subfamily B member 1 Homo sapiens 58-63 18398725-2 2008 Imatinib is transported out of cells by the efflux transporter ABCB1 (MDR1, whose product is p-glycoprotein). Imatinib Mesylate 0-8 ATP binding cassette subfamily B member 1 Homo sapiens 63-68 18398725-2 2008 Imatinib is transported out of cells by the efflux transporter ABCB1 (MDR1, whose product is p-glycoprotein). Imatinib Mesylate 0-8 ATP binding cassette subfamily B member 1 Homo sapiens 70-74 18398725-2 2008 Imatinib is transported out of cells by the efflux transporter ABCB1 (MDR1, whose product is p-glycoprotein). Imatinib Mesylate 0-8 ATP binding cassette subfamily B member 1 Homo sapiens 93-107 17934801-0 2008 Constitutive overexpression of P-glycoprotein, rather than breast cancer resistance protein or organic cation transporter 1, contributes to acquisition of imatinib-resistance in K562 cells. Imatinib Mesylate 155-163 ATP binding cassette subfamily B member 1 Homo sapiens 31-45 17934801-12 2008 CONCLUSIONS: P-gp, rather than BCRP or OCT1, is partially responsible for the development of imatinib-resistance due to constitutive and functional overexpression, leading to reduced intracellular accumulation of imatinib in K562/IM. Imatinib Mesylate 93-101 ATP binding cassette subfamily B member 1 Homo sapiens 13-17 17934801-12 2008 CONCLUSIONS: P-gp, rather than BCRP or OCT1, is partially responsible for the development of imatinib-resistance due to constitutive and functional overexpression, leading to reduced intracellular accumulation of imatinib in K562/IM. Imatinib Mesylate 213-221 ATP binding cassette subfamily B member 1 Homo sapiens 13-17 18337118-3 2008 Imatinib is transported by human and rodent ATP-binding cassette (ABC) transporters like P-glycoprotein (Pgp) and the breast cancer resistance protein (BCRP). Imatinib Mesylate 0-8 ATP binding cassette subfamily B member 1 Homo sapiens 89-103 18337118-3 2008 Imatinib is transported by human and rodent ATP-binding cassette (ABC) transporters like P-glycoprotein (Pgp) and the breast cancer resistance protein (BCRP). Imatinib Mesylate 0-8 ATP binding cassette subfamily B member 1 Homo sapiens 105-108 17690695-0 2008 Evidence for the interaction of imatinib at the transport-substrate site(s) of the multidrug-resistance-linked ABC drug transporters ABCB1 (P-glycoprotein) and ABCG2. Imatinib Mesylate 32-40 ATP binding cassette subfamily B member 1 Homo sapiens 133-138 17690695-0 2008 Evidence for the interaction of imatinib at the transport-substrate site(s) of the multidrug-resistance-linked ABC drug transporters ABCB1 (P-glycoprotein) and ABCG2. Imatinib Mesylate 32-40 ATP binding cassette subfamily B member 1 Homo sapiens 140-154 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 ATP binding cassette subfamily B member 1 Homo sapiens 106-136 18401881-5 2008 There are a number of BCR-ABL-independent mechanisms of imatinib resistance, including the efflux protein multidrug resistance protein-1, of which imatinib is a substrate. Imatinib Mesylate 147-155 ATP binding cassette subfamily B member 1 Homo sapiens 106-136 17429432-0 2007 Resistance reversal by RNAi silencing of MDR1 in CML cells associated with increase in imatinib intracellular levels. Imatinib Mesylate 87-95 ATP binding cassette subfamily B member 1 Homo sapiens 41-45 17180388-3 2007 The purpose of this study was to investigate in vitro, whether hydroxyurea could enhance the central nervous system penetration of imatinib, by inhibition of the ATP-dependent transporter proteins P-glycoprotein (ABCB1; MDR1; Pgp) and Breast Cancer Resistance Protein (ABCG2; BCRP), or by inhibition of cytochrome P450 3A (CYP3A) metabolism of imatinib. Imatinib Mesylate 131-139 ATP binding cassette subfamily B member 1 Homo sapiens 197-211 17180388-3 2007 The purpose of this study was to investigate in vitro, whether hydroxyurea could enhance the central nervous system penetration of imatinib, by inhibition of the ATP-dependent transporter proteins P-glycoprotein (ABCB1; MDR1; Pgp) and Breast Cancer Resistance Protein (ABCG2; BCRP), or by inhibition of cytochrome P450 3A (CYP3A) metabolism of imatinib. Imatinib Mesylate 131-139 ATP binding cassette subfamily B member 1 Homo sapiens 213-218 17180388-3 2007 The purpose of this study was to investigate in vitro, whether hydroxyurea could enhance the central nervous system penetration of imatinib, by inhibition of the ATP-dependent transporter proteins P-glycoprotein (ABCB1; MDR1; Pgp) and Breast Cancer Resistance Protein (ABCG2; BCRP), or by inhibition of cytochrome P450 3A (CYP3A) metabolism of imatinib. Imatinib Mesylate 131-139 ATP binding cassette subfamily B member 1 Homo sapiens 220-224 17180388-3 2007 The purpose of this study was to investigate in vitro, whether hydroxyurea could enhance the central nervous system penetration of imatinib, by inhibition of the ATP-dependent transporter proteins P-glycoprotein (ABCB1; MDR1; Pgp) and Breast Cancer Resistance Protein (ABCG2; BCRP), or by inhibition of cytochrome P450 3A (CYP3A) metabolism of imatinib. Imatinib Mesylate 344-352 ATP binding cassette subfamily B member 1 Homo sapiens 197-211 17180388-3 2007 The purpose of this study was to investigate in vitro, whether hydroxyurea could enhance the central nervous system penetration of imatinib, by inhibition of the ATP-dependent transporter proteins P-glycoprotein (ABCB1; MDR1; Pgp) and Breast Cancer Resistance Protein (ABCG2; BCRP), or by inhibition of cytochrome P450 3A (CYP3A) metabolism of imatinib. Imatinib Mesylate 344-352 ATP binding cassette subfamily B member 1 Homo sapiens 213-218 17180388-3 2007 The purpose of this study was to investigate in vitro, whether hydroxyurea could enhance the central nervous system penetration of imatinib, by inhibition of the ATP-dependent transporter proteins P-glycoprotein (ABCB1; MDR1; Pgp) and Breast Cancer Resistance Protein (ABCG2; BCRP), or by inhibition of cytochrome P450 3A (CYP3A) metabolism of imatinib. Imatinib Mesylate 344-352 ATP binding cassette subfamily B member 1 Homo sapiens 220-224 16890580-1 2006 OBJECTIVE: Our objective was to explore the relationships between imatinib pharmacokinetics and 9 allelic variants in 7 genes coding for adenosine triphosphate-binding cassette transporters (ABCB1 and ABCG2) and enzymes (cytochrome P450 [CYP] 2C9, CYP2C19, CYP2D6, CYP3A4, and CYP3A5) of putative relevance for imatinib. Imatinib Mesylate 66-74 ATP binding cassette subfamily B member 1 Homo sapiens 191-196 16890580-1 2006 OBJECTIVE: Our objective was to explore the relationships between imatinib pharmacokinetics and 9 allelic variants in 7 genes coding for adenosine triphosphate-binding cassette transporters (ABCB1 and ABCG2) and enzymes (cytochrome P450 [CYP] 2C9, CYP2C19, CYP2D6, CYP3A4, and CYP3A5) of putative relevance for imatinib. Imatinib Mesylate 311-319 ATP binding cassette subfamily B member 1 Homo sapiens 191-196 15970668-0 2005 Chronic imatinib mesylate exposure leads to reduced intracellular drug accumulation by induction of the ABCG2 (BCRP) and ABCB1 (MDR1) drug transport pumps. Imatinib Mesylate 8-25 ATP binding cassette subfamily B member 1 Homo sapiens 121-126 16620554-1 2005 OBJECTIVE: To elucidate the mechanisms of imatinib resistance involved in some chronic myeloid leukemia (CML) cells overexpressing P-glycoprotein (P-gp). Imatinib Mesylate 42-50 ATP binding cassette subfamily B member 1 Homo sapiens 131-145 16620554-1 2005 OBJECTIVE: To elucidate the mechanisms of imatinib resistance involved in some chronic myeloid leukemia (CML) cells overexpressing P-glycoprotein (P-gp). Imatinib Mesylate 42-50 ATP binding cassette subfamily B member 1 Homo sapiens 147-151 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 ATP binding cassette subfamily B member 1 Homo sapiens 49-53 16157201-1 2005 Different mechanisms could sustain Imatinib resistance, including overexpression of MDR1, a gene already known to be responsible for multidrug resistance in other hematologic malignancies. Imatinib Mesylate 35-43 ATP binding cassette subfamily B member 1 Homo sapiens 84-88 16157201-6 2005 Reported data maintain that MDR1 expression would play an important role in Imatinib resistance when the disease is not fully controlled (e.g., progressive disease or during the first months of treatment). Imatinib Mesylate 76-84 ATP binding cassette subfamily B member 1 Homo sapiens 28-32 15970668-0 2005 Chronic imatinib mesylate exposure leads to reduced intracellular drug accumulation by induction of the ABCG2 (BCRP) and ABCB1 (MDR1) drug transport pumps. Imatinib Mesylate 8-25 ATP binding cassette subfamily B member 1 Homo sapiens 128-132 15970668-2 2005 We investigated whether the intended chronic oral administration of imatinib might lead to the induction of the intestinal ABC transport proteins ABCB1, ABCC1 (MRP1), ABCC2 (MRP2) and ABCG2. Imatinib Mesylate 68-76 ATP binding cassette subfamily B member 1 Homo sapiens 146-151 15970668-3 2005 Using Caco2 cells as an in vitro model for intestinal drug transport, we found that continuous exposure (up to 100 days) with imatinib (10 microM) specifically upregulates the expression of ABCG2 (maximal approximately 17-fold) and ABCB1 (maximal approximately 5-fold). Imatinib Mesylate 126-134 ATP binding cassette subfamily B member 1 Homo sapiens 232-237 15970668-5 2005 Importantly, chronic imatinib exposure of Caco2 cells resulted in a approximately 50% decrease in intracellular accumulation of imatinib, probably by enhanced ABCG2- and ABCB1-mediated efflux, as a result of upregulated expression of these drug pumps. Imatinib Mesylate 21-29 ATP binding cassette subfamily B member 1 Homo sapiens 170-175 15970668-5 2005 Importantly, chronic imatinib exposure of Caco2 cells resulted in a approximately 50% decrease in intracellular accumulation of imatinib, probably by enhanced ABCG2- and ABCB1-mediated efflux, as a result of upregulated expression of these drug pumps. Imatinib Mesylate 128-136 ATP binding cassette subfamily B member 1 Homo sapiens 170-175 15970668-6 2005 Both ABCG2 and ABCB1 are normally expressed in the gastrointestinal tract and it might be anticipated that drug-induced upregulation of these intestinal pumps could reduce the oral bioavailability of imatinib, representing a novel mechanism of acquired pharmacokinetic drug resistance in cancer patients that are chronically treated with imatinib. Imatinib Mesylate 200-208 ATP binding cassette subfamily B member 1 Homo sapiens 15-20 15970668-6 2005 Both ABCG2 and ABCB1 are normally expressed in the gastrointestinal tract and it might be anticipated that drug-induced upregulation of these intestinal pumps could reduce the oral bioavailability of imatinib, representing a novel mechanism of acquired pharmacokinetic drug resistance in cancer patients that are chronically treated with imatinib. Imatinib Mesylate 338-346 ATP binding cassette subfamily B member 1 Homo sapiens 15-20 15963852-0 2005 RNAi-mediated knockdown of P-glycoprotein using a transposon-based vector system durably restores imatinib sensitivity in imatinib-resistant CML cell lines. Imatinib Mesylate 98-106 ATP binding cassette subfamily B member 1 Homo sapiens 27-41 15963852-0 2005 RNAi-mediated knockdown of P-glycoprotein using a transposon-based vector system durably restores imatinib sensitivity in imatinib-resistant CML cell lines. Imatinib Mesylate 122-130 ATP binding cassette subfamily B member 1 Homo sapiens 27-41 15963852-3 2005 METHODS: We constructed a nonviral, transposon-based vector system for the stable knockdown of PgP in chronic myeloid leukemia cell lines resistant to imatinib and doxorubicin. Imatinib Mesylate 151-159 ATP binding cassette subfamily B member 1 Homo sapiens 95-98 15963852-7 2005 CONCLUSION: Using chronic myeloid leukemia as a model, we show that PgP-mediated resistance to imatinib and anthracyclines can be durably reversed by nonviral, transposon-based knockdown of PgP in malignant cells. Imatinib Mesylate 95-103 ATP binding cassette subfamily B member 1 Homo sapiens 68-71 15963852-7 2005 CONCLUSION: Using chronic myeloid leukemia as a model, we show that PgP-mediated resistance to imatinib and anthracyclines can be durably reversed by nonviral, transposon-based knockdown of PgP in malignant cells. Imatinib Mesylate 95-103 ATP binding cassette subfamily B member 1 Homo sapiens 190-193 15805252-0 2005 The effect of Bcrp1 (Abcg2) on the in vivo pharmacokinetics and brain penetration of imatinib mesylate (Gleevec): implications for the use of breast cancer resistance protein and P-glycoprotein inhibitors to enable the brain penetration of imatinib in patients. Imatinib Mesylate 85-102 ATP binding cassette subfamily B member 1 Homo sapiens 179-193 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 ATP binding cassette subfamily B member 1 Homo sapiens 114-128 15902298-0 2005 Synergistic activity of imatinib and 17-AAG in imatinib-resistant CML cells overexpressing BCR-ABL--Inhibition of P-glycoprotein function by 17-AAG. Imatinib Mesylate 47-55 ATP binding cassette subfamily B member 1 Homo sapiens 114-128 15902298-1 2005 Overexpression of BCR-ABL and P-glycoprotein (Pgp) are two of the known mechanisms of imatinib resistance. Imatinib Mesylate 86-94 ATP binding cassette subfamily B member 1 Homo sapiens 30-44 15902298-1 2005 Overexpression of BCR-ABL and P-glycoprotein (Pgp) are two of the known mechanisms of imatinib resistance. Imatinib Mesylate 86-94 ATP binding cassette subfamily B member 1 Homo sapiens 46-49 15902298-8 2005 Monotherapy with 17-AAG decreased P-glycoprotein activity, which may increase intracellular imatinib levels and contribute to the sensitization of CML cells to imatinib. Imatinib Mesylate 92-100 ATP binding cassette subfamily B member 1 Homo sapiens 34-48 15902298-8 2005 Monotherapy with 17-AAG decreased P-glycoprotein activity, which may increase intracellular imatinib levels and contribute to the sensitization of CML cells to imatinib. Imatinib Mesylate 160-168 ATP binding cassette subfamily B member 1 Homo sapiens 34-48 15918555-9 2005 Interestingly, recent molecular-targeted drugs, such as imatinib and gefitinib, were very recently found to be substrates for P-glycoprotein and/or BCRP. Imatinib Mesylate 56-64 ATP binding cassette subfamily B member 1 Homo sapiens 126-140 15251980-3 2004 Indeed, several molecular mechanisms leading to imatinib resistance have already been reported, including overexpression of the MDR1/ABCB1 drug pump. Imatinib Mesylate 48-56 ATP binding cassette subfamily B member 1 Homo sapiens 128-132 15315971-11 2004 Differential expression of influx (hOCT1) and efflux (MDR1) transporters may be a critical determinant of intracellular drug levels and, hence, resistance to imatinib. Imatinib Mesylate 158-166 ATP binding cassette subfamily B member 1 Homo sapiens 54-58 15611623-0 2004 Pharmacokinetic resistance to imatinib mesylate: role of the ABC drug pumps ABCG2 (BCRP) and ABCB1 (MDR1) in the oral bioavailability of imatinib. Imatinib Mesylate 137-145 ATP binding cassette subfamily B member 1 Homo sapiens 93-98 15611623-0 2004 Pharmacokinetic resistance to imatinib mesylate: role of the ABC drug pumps ABCG2 (BCRP) and ABCB1 (MDR1) in the oral bioavailability of imatinib. Imatinib Mesylate 137-145 ATP binding cassette subfamily B member 1 Homo sapiens 100-104 15251980-3 2004 Indeed, several molecular mechanisms leading to imatinib resistance have already been reported, including overexpression of the MDR1/ABCB1 drug pump. Imatinib Mesylate 48-56 ATP binding cassette subfamily B member 1 Homo sapiens 133-138 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 ATP binding cassette subfamily B member 1 Homo sapiens 104-108 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 ATP binding cassette subfamily B member 1 Homo sapiens 69-74 14724652-0 2004 P-glycoprotein-mediated drug efflux is a resistance mechanism of chronic myelogenous leukemia cells to treatment with imatinib mesylate. Imatinib Mesylate 118-135 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 14724652-3 2004 Here, we show by a novel high-performance liquid chromatography-based method that intracellular levels of imatinib decrease in P-glycoprotein (Pgp)-positive leukemic cells. Imatinib Mesylate 106-114 ATP binding cassette subfamily B member 1 Homo sapiens 127-141 14724652-3 2004 Here, we show by a novel high-performance liquid chromatography-based method that intracellular levels of imatinib decrease in P-glycoprotein (Pgp)-positive leukemic cells. Imatinib Mesylate 106-114 ATP binding cassette subfamily B member 1 Homo sapiens 143-146 14724652-4 2004 In a model of K562 cells with gradually increasing Pgp expression, a Pgp-dependent decline of intracellular imatinib levels was observed. Imatinib Mesylate 108-116 ATP binding cassette subfamily B member 1 Homo sapiens 51-54 14724652-4 2004 In a model of K562 cells with gradually increasing Pgp expression, a Pgp-dependent decline of intracellular imatinib levels was observed. Imatinib Mesylate 108-116 ATP binding cassette subfamily B member 1 Homo sapiens 69-72 14724652-6 2004 The modulation of Pgp by cyclosporin A (CSA) readily restored imatinib cytotoxicity in these cells. Imatinib Mesylate 62-70 ATP binding cassette subfamily B member 1 Homo sapiens 18-21 14724652-7 2004 Finally, we provide first data showing a biological effect of Pgp modulation in the imatinib treatment of a patient with BCR-ABL-positive ALL. Imatinib Mesylate 84-92 ATP binding cassette subfamily B member 1 Homo sapiens 62-65 14724652-8 2004 MDR1 overexpression must therefore be considered as an important clinical mechanism in the diversity of resistance development to imatinib treatment. Imatinib Mesylate 130-138 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 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 ATP binding cassette subfamily B member 1 Homo sapiens 84-88 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 ATP binding cassette subfamily B member 1 Homo sapiens 83-87 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 ATP binding cassette subfamily B member 1 Homo sapiens 69-74 12824882-10 2003 These findings suggest that STI571 is a substrate for P-gp, but is less efficiently transported by P-gp than VCR, and STI571 is not a substrate for MRP1. Imatinib Mesylate 28-34 ATP binding cassette subfamily B member 1 Homo sapiens 99-103 12975485-0 2003 Interaction of imatinib mesilate with human P-glycoprotein. Imatinib Mesylate 15-32 ATP binding cassette subfamily B member 1 Homo sapiens 44-58 12975485-1 2003 The interaction of imatinib mesilate with P-glycoprotein (P-gp) was examined using pig kidney epithelial LLC-PK1 cells versus L-MDR1 cells, which overexpress human P-gp on the apical membrane. Imatinib Mesylate 19-36 ATP binding cassette subfamily B member 1 Homo sapiens 42-56 12975485-1 2003 The interaction of imatinib mesilate with P-glycoprotein (P-gp) was examined using pig kidney epithelial LLC-PK1 cells versus L-MDR1 cells, which overexpress human P-gp on the apical membrane. Imatinib Mesylate 19-36 ATP binding cassette subfamily B member 1 Homo sapiens 58-62 12975485-6 2003 The rhodamine 123 efflux assay showed that the efflux of rhodamine 123 in K562/DXR cells, which overexpress human P-gp, could be blocked markedly by imatinib mesilate in a dose-dependent fashion. Imatinib Mesylate 149-166 ATP binding cassette subfamily B member 1 Homo sapiens 114-118 12975485-7 2003 The Ki values for the inhibition of P-gp function by cyclosporin A and imatinib mesilate were estimated to be 6.1 and 18.3 muM, respectively, using a calcein-AM efflux assay. Imatinib Mesylate 71-88 ATP binding cassette subfamily B member 1 Homo sapiens 36-40 12975485-8 2003 These observations demonstrate that imatinib mesilate is a substrate as well as a modulator of human P-gp, suggesting that imatinib mesilate drug interactions may occur via P-gp. Imatinib Mesylate 36-53 ATP binding cassette subfamily B member 1 Homo sapiens 101-105 12975485-8 2003 These observations demonstrate that imatinib mesilate is a substrate as well as a modulator of human P-gp, suggesting that imatinib mesilate drug interactions may occur via P-gp. Imatinib Mesylate 36-53 ATP binding cassette subfamily B member 1 Homo sapiens 173-177 12975485-8 2003 These observations demonstrate that imatinib mesilate is a substrate as well as a modulator of human P-gp, suggesting that imatinib mesilate drug interactions may occur via P-gp. Imatinib Mesylate 123-140 ATP binding cassette subfamily B member 1 Homo sapiens 101-105 12975485-8 2003 These observations demonstrate that imatinib mesilate is a substrate as well as a modulator of human P-gp, suggesting that imatinib mesilate drug interactions may occur via P-gp. Imatinib Mesylate 123-140 ATP binding cassette subfamily B member 1 Homo sapiens 173-177 12975485-9 2003 It is necessary to consider the pharmacokinetic and pharmacodynamic interactions of imatinib mesilate with other drugs via P-gp. Imatinib Mesylate 84-101 ATP binding cassette subfamily B member 1 Homo sapiens 123-127 12963124-0 2003 Anti-proliferative effect of the abl tyrosine kinase inhibitor STI571 on the P-glycoprotein positive K562/ADM cell line. Imatinib Mesylate 63-69 ATP binding cassette subfamily B member 1 Homo sapiens 77-91 12963124-2 2003 We addressed whether STI571 is effective for the CML blastic crisis cell line K562 and the P-glycoprotein (P-gp) positive, multidrug resistance cell line K562/ADM. Imatinib Mesylate 21-27 ATP binding cassette subfamily B member 1 Homo sapiens 91-105 12963124-3 2003 The present results demonstrate that P-gp positive K562/ADM cells were more resistant than K562 cells to the anti-proliferative and apoptotic effect of STI571, but the co-addition of a P-gp modulator augmented the sensitivity of K562/ADM cells to STI571. Imatinib Mesylate 152-158 ATP binding cassette subfamily B member 1 Homo sapiens 37-41 12963124-4 2003 For patients in CML blastic crisis, simultaneous use of a P-gp modulator may increase the efficacy of STI571. Imatinib Mesylate 102-108 ATP binding cassette subfamily B member 1 Homo sapiens 58-62 12869489-0 2003 Functional consequence of MDR1 expression on imatinib intracellular concentrations. Imatinib Mesylate 45-53 ATP binding cassette subfamily B member 1 Homo sapiens 26-30 12824882-4 2003 STI571 inhibited the [(125)I]azidoagosterol A-photolabeling of P-gp, but not that of MRP1. Imatinib Mesylate 0-6 ATP binding cassette subfamily B member 1 Homo sapiens 63-67 12824882-5 2003 K562/MDR cells that overexpress P-gp were 3.67 times more resistant to STI571 than the parental Philadelphia-chromosome-positive (Ph +) CML K562 cells, and this resistance was most effectively reversed by cepharanthine among the tested reversing agents. Imatinib Mesylate 71-77 ATP binding cassette subfamily B member 1 Homo sapiens 32-36 12824882-7 2003 In KB-G2 cells that overexpress P-gp, but not Bcr-Abl, 2.5 micro M STI571 partly reversed the resistance to vincristine (VCR), paclitaxel, etoposide (VP-16) and actinomycin D (ACD) but not to Adriamycin (ADM) or colchicine. Imatinib Mesylate 67-73 ATP binding cassette subfamily B member 1 Homo sapiens 32-36 12824882-10 2003 These findings suggest that STI571 is a substrate for P-gp, but is less efficiently transported by P-gp than VCR, and STI571 is not a substrate for MRP1. Imatinib Mesylate 28-34 ATP binding cassette subfamily B member 1 Homo sapiens 54-58 12824882-11 2003 Among the tested reversing agents that interact with P-gp, cepharanthine was the most effective agent for the reversal of the resistance to STI571 in K562/MDR cells. Imatinib Mesylate 140-146 ATP binding cassette subfamily B member 1 Homo sapiens 53-57 12824882-12 2003 Furthermore, STI571 itself was a potent reversing agent for MDR in P-gp-expressing KB-G2 cells. Imatinib Mesylate 13-19 ATP binding cassette subfamily B member 1 Homo sapiens 67-71 12609962-0 2003 MDR1 gene overexpression confers resistance to imatinib mesylate in leukemia cell line models. Imatinib Mesylate 47-64 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 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 ATP binding cassette subfamily B member 1 Homo sapiens 76-80