PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 20059901-0 2010 Hot topic: Enhancing omega-3 fatty acids in milk fat of dairy cows by using stearidonic acid-enriched soybean oil from genetically modified soybeans. stearidonic acid 76-92 Weaning weight-maternal milk Bos taurus 44-48 20059901-3 2010 In utilizing SDA-enhanced soybean oil (SBO) derived from genetically modified soybeans, our objectives were to examine the potential to increase the n-3 fatty acid content of milk fat and to determine the efficiency of SDA uptake from the digestive tract and transfer to milk fat. stearidonic acid 13-16 Weaning weight-maternal milk Bos taurus 175-179 20059901-3 2010 In utilizing SDA-enhanced soybean oil (SBO) derived from genetically modified soybeans, our objectives were to examine the potential to increase the n-3 fatty acid content of milk fat and to determine the efficiency of SDA uptake from the digestive tract and transfer to milk fat. stearidonic acid 13-16 Weaning weight-maternal milk Bos taurus 271-275 20059901-11 2010 Transfer efficiency of SDA to milk fat represented 39.3% (range=36.8 to 41.9%) of the abomasally infused SDA and 47.3% (range=45.0 to 49.6%) when the n-3 fatty acids downstream from SDA were included. stearidonic acid 105-108 Weaning weight-maternal milk Bos taurus 30-34 20059901-11 2010 Transfer efficiency of SDA to milk fat represented 39.3% (range=36.8 to 41.9%) of the abomasally infused SDA and 47.3% (range=45.0 to 49.6%) when the n-3 fatty acids downstream from SDA were included. stearidonic acid 105-108 Weaning weight-maternal milk Bos taurus 30-34 20059901-12 2010 In contrast, transfer of ruminally infused SDA to milk fat averaged only 1.7% (range=1.3 to 2.1%), indicating extensive rumen biohydrogenation. stearidonic acid 43-46 Weaning weight-maternal milk Bos taurus 50-54 20059901-13 2010 Overall, results demonstrate the potential to use SDA-enhanced SBO from genetically modified soybeans combined with proper ruminal protection to achieve impressive increases in the milk fat content of SDA and other n-3 fatty acids that are beneficial for human health. stearidonic acid 50-53 Weaning weight-maternal milk Bos taurus 181-185 20059901-13 2010 Overall, results demonstrate the potential to use SDA-enhanced SBO from genetically modified soybeans combined with proper ruminal protection to achieve impressive increases in the milk fat content of SDA and other n-3 fatty acids that are beneficial for human health. stearidonic acid 201-204 Weaning weight-maternal milk Bos taurus 181-185 29670920-2 2018 We investigated the effects of methotrexate (MTX) alone and combined with 4-hydroperoxycyclophosphamide (4-HC) on P-gp expression in fibroblast-like synoviocytes (FLSs) from patients with RA and examined the signaling pathway involved. Methotrexate 45-48 ATP binding cassette subfamily B member 1 Homo sapiens 114-118 29170124-5 2018 LncRNA LUCAT1 and ABCB1 protein expression levels were both up-regulated when induced by different concentration of methotrexate. Methotrexate 116-128 ATP binding cassette subfamily B member 1 Homo sapiens 18-23 29170124-9 2018 Overall, results indicate the vital role of LUCAT1 in the methotrexate resistance regulation through miR-200c/ABCB1 pathway, providing a novel insight and treatment strategy for osteosarcoma drug resistance. Methotrexate 58-70 ATP binding cassette subfamily B member 1 Homo sapiens 110-115 28616661-0 2017 Clinical relevance of P-glycoprotein activity on peripheral blood mononuclear cells and polymorphonuclear neutrophils to methotrexate in systemic lupus erythematosus patients. Methotrexate 121-133 ATP binding cassette subfamily B member 1 Homo sapiens 22-36 28598776-5 2017 Expression of genes important to the transport (SLC19A1, ABCB1, ABCC1, ABCG2), metabolism (FPGS, GGH), and mechanism of action (TYMS, MTR, MTRR) of MTX, including for the adenosine receptors ADORA1, ADORA2A, ADORA2B, ADORA3 and ADORA3variant were quantitated by real-time PCR in each nodule sample. Methotrexate 148-151 ATP binding cassette subfamily B member 1 Homo sapiens 57-62 28616661-1 2017 To elucidate the relationship between P-glycoprotein activity on peripheral blood leukocytes of systemic lupus erythematosus (SLE) patients with lupus arthritis and the clinical response to methotrexate. Methotrexate 190-202 ATP binding cassette subfamily B member 1 Homo sapiens 38-52 28616661-8 2017 The prevalence of low fluorescence levels (<6 relative fluorescence units), signifying higher P-glycoprotein activity of both mononuclear cells and polymorphonuclear neutrophils, was higher in methotrexate responders than in non-responders (27.3 vs. 4.8%; p = 0.10 and 81.8 vs. 23.8%; p = 0.003, respectively). Methotrexate 196-208 ATP binding cassette subfamily B member 1 Homo sapiens 97-111 28616661-9 2017 In SLE patients with joint involvement treated with methotrexate, P-glycoprotein activity was higher in responders to methotrexate than in non-responders. Methotrexate 52-64 ATP binding cassette subfamily B member 1 Homo sapiens 66-80 28616661-9 2017 In SLE patients with joint involvement treated with methotrexate, P-glycoprotein activity was higher in responders to methotrexate than in non-responders. Methotrexate 118-130 ATP binding cassette subfamily B member 1 Homo sapiens 66-80 28616661-10 2017 Further studies are required to determine the mechanisms behind this finding and whether P-glycoprotein activity mediates alterations in methotrexate efficacy. Methotrexate 137-149 ATP binding cassette subfamily B member 1 Homo sapiens 89-103 28615105-0 2017 [Over-expression of mdr1/P-gp is associated with methotrexate resistance in patients with rheumatoid arthritis]. Methotrexate 49-61 ATP binding cassette subfamily B member 1 Homo sapiens 20-24 28710036-3 2017 Carriers of the ABCC4 934CC and ABCB1 1236TT genotypes received a lower percentage of the protocol-recommended starting dose of MTX (62.1 vs. 81.3% for 934CA carriers, p=0.001) and 6MP (73.1 vs. 87.7% for 1236CC/CT carriers; p=0.026), respectively. Methotrexate 128-131 ATP binding cassette subfamily B member 1 Homo sapiens 32-37 28693150-5 2017 Additionally, methotrexate and doxorubicin are the most widely used anticancer agents against osteosarcoma, and the observed enhanced chemoresistance of OS-TICs to these two agents could be associated with the upregulation of DHFR and MDR1. Methotrexate 14-26 ATP binding cassette subfamily B member 1 Homo sapiens 235-239 28615105-1 2017 Objective To investigate the relationship between the gene expression of multidrug resisitance 1 (mdr1)/P-glycoprotein (P-gp) in peripheral blood mononuclear cells (PBMCs) and methotrexate (MTX) resistance in patients with rheumatoid arthritis (RA). Methotrexate 176-188 ATP binding cassette subfamily B member 1 Homo sapiens 98-102 28615105-1 2017 Objective To investigate the relationship between the gene expression of multidrug resisitance 1 (mdr1)/P-glycoprotein (P-gp) in peripheral blood mononuclear cells (PBMCs) and methotrexate (MTX) resistance in patients with rheumatoid arthritis (RA). Methotrexate 176-188 ATP binding cassette subfamily B member 1 Homo sapiens 104-118 28615105-1 2017 Objective To investigate the relationship between the gene expression of multidrug resisitance 1 (mdr1)/P-glycoprotein (P-gp) in peripheral blood mononuclear cells (PBMCs) and methotrexate (MTX) resistance in patients with rheumatoid arthritis (RA). Methotrexate 190-193 ATP binding cassette subfamily B member 1 Homo sapiens 98-102 28615105-1 2017 Objective To investigate the relationship between the gene expression of multidrug resisitance 1 (mdr1)/P-glycoprotein (P-gp) in peripheral blood mononuclear cells (PBMCs) and methotrexate (MTX) resistance in patients with rheumatoid arthritis (RA). Methotrexate 190-193 ATP binding cassette subfamily B member 1 Homo sapiens 104-118 28615105-8 2017 Conclusion The over-expression of mdr1/P-gp in RA patients is related to the MTX resistance. Methotrexate 77-80 ATP binding cassette subfamily B member 1 Homo sapiens 34-38 27980801-4 2016 The purpose of this study was to investigate the allelic frequencies in different ethnic and/or population groups in the 10 polymorphisms of enzyme proteins and transporters related to the MTX response and pharmacokinetics including MTHFR, TYMS, RFC1, FPGS, GGH, ABCB1, ABCC2 and ABCG2 in unrelated healthy Japanese adults and patients with RA. Methotrexate 189-192 ATP binding cassette subfamily B member 1 Homo sapiens 263-268 27751863-9 2017 RESULTS: When taking MTX, those patients carrying the CC genotype of rs1045642 in ABCB1 showed significantly higher GPT levels (7.1+-2.0 U/L; P<.001). Methotrexate 21-24 ATP binding cassette subfamily B member 1 Homo sapiens 82-87 27751863-12 2017 DISCUSSION: Our data suggest that genotyping functional variants in FGPS and MTHFR enzymes and the transporter ABCB1 could help to identify patients with increased risk of MTX toxicity. Methotrexate 172-175 ATP binding cassette subfamily B member 1 Homo sapiens 111-116 27533339-8 2016 RESULTS: Individuals who were CC homozygotes at MDR1 rs1045642 had lower risk of having methotrexate plasma concentrations >1 muM and leukopenia grade I (odds ratio [OR] = 0.30; 95% CI = 0.13-0.72 and OR = 0.32; 95% CI = 0.14-0.72, respectively). Methotrexate 88-100 ATP binding cassette subfamily B member 1 Homo sapiens 48-52 27323187-7 2016 There was a positive linear correlation between the P-gp level in FLS cells and the duration of MTX treatment in the RRA group (G = 0.733, P < 0.05), whereas there was no significant correlation between the P-gp level and DAS28 scoring (G = 0.206, P > 0.05). Methotrexate 96-99 ATP binding cassette subfamily B member 1 Homo sapiens 52-56 27322261-8 2016 The latter feature of two TSPO ligand-MTX conjugates was also confirmed by in vitro permeability studies conducted on Madin-Darby canine kidney cells transfected with the human MDR1 gene (MDCK-MDR1) monolayers. Methotrexate 38-41 ATP binding cassette subfamily B member 1 Homo sapiens 177-181 27322261-8 2016 The latter feature of two TSPO ligand-MTX conjugates was also confirmed by in vitro permeability studies conducted on Madin-Darby canine kidney cells transfected with the human MDR1 gene (MDCK-MDR1) monolayers. Methotrexate 38-41 ATP binding cassette subfamily B member 1 Homo sapiens 188-197 26184955-9 2016 However, the analysis did indicate that MTX toxicity was associated with the ABCB1 C3435T polymorphism in RA under an overdominant model (TC vs. TT + CC; OR 0.483, 95 % CI 0.259-0.900, p = 0.022), evidencing a lower risk of MTX toxicity for heterozygotes (TC) than homozygotes (TT and CC). Methotrexate 40-43 ATP binding cassette subfamily B member 1 Homo sapiens 77-82 26184955-9 2016 However, the analysis did indicate that MTX toxicity was associated with the ABCB1 C3435T polymorphism in RA under an overdominant model (TC vs. TT + CC; OR 0.483, 95 % CI 0.259-0.900, p = 0.022), evidencing a lower risk of MTX toxicity for heterozygotes (TC) than homozygotes (TT and CC). Methotrexate 224-227 ATP binding cassette subfamily B member 1 Homo sapiens 77-82 26184955-10 2016 CONCLUSION: This meta-analysis demonstrated that the ABCB1 C3435T polymorphism may be not associated with responsiveness to DMARD therapy, but may be associated with MTX toxicity in RA. Methotrexate 166-169 ATP binding cassette subfamily B member 1 Homo sapiens 53-58 27323187-8 2016 P-gp might be upregulated during the progression of RRA, which possibly correlates with the development of resistance to MTX. Methotrexate 121-124 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 26652611-8 2016 CONCLUSION: FPGS and ABCB1 genetic variants can influence the outcome in RA patients receiving MTX monotherapy. Methotrexate 95-98 ATP binding cassette subfamily B member 1 Homo sapiens 21-26 25007187-1 2014 BACKGROUND: The aim of this study is to analyze polymorphisms in genes involved in 6-mercaptopurine detoxification (TPMT); methotrexate (MTX) metabolism including ABCB1 (or MDR1), ABCC2, SLC19A1 (or RFC1), and SLCO1B1; and the MTX effect mainly MTHFR and TYMS, and to assess whether these polymorphisms are predictors of treatment toxicity and/or MTX clearance. Methotrexate 227-230 ATP binding cassette subfamily B member 1 Homo sapiens 163-168 26353179-0 2015 Association of ABCB1, ABCC5 and xanthine oxidase genetic polymorphisms with methotrexate adverse reactions in Mexican pediatric patients with ALL. Methotrexate 76-88 ATP binding cassette subfamily B member 1 Homo sapiens 15-20 26353179-8 2015 Single nucleotide polymorphisms (SNPs) of ABCB1 1236C>T (OR 0.19, 95% CI: 0.03-0.9, p<0.05) and ABCC5 3933+313T>C (OR 0.12, 95% CI: 0.027-0.58, p<0.05) were associated with methotrexate ADRs. Methotrexate 185-197 ATP binding cassette subfamily B member 1 Homo sapiens 42-47 25074866-0 2014 Association of MDR1 C3435T and RFC1 G80A polymorphisms with methotrexate toxicity and response in Jordanian rheumatoid arthritis patients. Methotrexate 60-72 ATP binding cassette subfamily B member 1 Homo sapiens 15-19 25074866-2 2014 Genetic polymorphisms of reduced folate carrier (RFC1 G80A) and multi-drug resistance-1 (MDR1 C3435T) might affect MTX response and/or toxicity. Methotrexate 115-118 ATP binding cassette subfamily B member 1 Homo sapiens 58-87 25074866-2 2014 Genetic polymorphisms of reduced folate carrier (RFC1 G80A) and multi-drug resistance-1 (MDR1 C3435T) might affect MTX response and/or toxicity. Methotrexate 115-118 ATP binding cassette subfamily B member 1 Homo sapiens 89-93 25074866-5 2014 RESULTS: There was an association between RFC1 G80A and MDR1 C3435T polymorphisms with MTX toxicity. Methotrexate 87-90 ATP binding cassette subfamily B member 1 Homo sapiens 56-60 25074866-7 2014 Patients carrying at least one MDR1 3435T variant allele were at higher risk for MTX overall toxicity (p = 0.04), especially hepatotoxicity (p = 0.028). Methotrexate 81-84 ATP binding cassette subfamily B member 1 Homo sapiens 31-35 25007187-1 2014 BACKGROUND: The aim of this study is to analyze polymorphisms in genes involved in 6-mercaptopurine detoxification (TPMT); methotrexate (MTX) metabolism including ABCB1 (or MDR1), ABCC2, SLC19A1 (or RFC1), and SLCO1B1; and the MTX effect mainly MTHFR and TYMS, and to assess whether these polymorphisms are predictors of treatment toxicity and/or MTX clearance. Methotrexate 123-135 ATP binding cassette subfamily B member 1 Homo sapiens 163-168 25007187-1 2014 BACKGROUND: The aim of this study is to analyze polymorphisms in genes involved in 6-mercaptopurine detoxification (TPMT); methotrexate (MTX) metabolism including ABCB1 (or MDR1), ABCC2, SLC19A1 (or RFC1), and SLCO1B1; and the MTX effect mainly MTHFR and TYMS, and to assess whether these polymorphisms are predictors of treatment toxicity and/or MTX clearance. Methotrexate 123-135 ATP binding cassette subfamily B member 1 Homo sapiens 173-177 25007187-1 2014 BACKGROUND: The aim of this study is to analyze polymorphisms in genes involved in 6-mercaptopurine detoxification (TPMT); methotrexate (MTX) metabolism including ABCB1 (or MDR1), ABCC2, SLC19A1 (or RFC1), and SLCO1B1; and the MTX effect mainly MTHFR and TYMS, and to assess whether these polymorphisms are predictors of treatment toxicity and/or MTX clearance. Methotrexate 137-140 ATP binding cassette subfamily B member 1 Homo sapiens 163-168 25007187-1 2014 BACKGROUND: The aim of this study is to analyze polymorphisms in genes involved in 6-mercaptopurine detoxification (TPMT); methotrexate (MTX) metabolism including ABCB1 (or MDR1), ABCC2, SLC19A1 (or RFC1), and SLCO1B1; and the MTX effect mainly MTHFR and TYMS, and to assess whether these polymorphisms are predictors of treatment toxicity and/or MTX clearance. Methotrexate 137-140 ATP binding cassette subfamily B member 1 Homo sapiens 173-177 26715450-5 2015 METHODS: We have compared the functional Multidrug Activity Factors (MAF) of the MDR1 and MRP1 transporters of Peripheral Blood Leukocytes of 59 Rheumatoid Arthritis patients with various response rate to MTX-therapy (MTX-responder, MTX-resistant and MTX-intolerant RA-groups) and 47 non-RA controls in six different leukocyte subpopulations (neutrophil leukocytes, monocytes, lymphocytes, CD4+, CD8+ and CD19+ cells). Methotrexate 205-208 ATP binding cassette subfamily B member 1 Homo sapiens 81-85 26715450-5 2015 METHODS: We have compared the functional Multidrug Activity Factors (MAF) of the MDR1 and MRP1 transporters of Peripheral Blood Leukocytes of 59 Rheumatoid Arthritis patients with various response rate to MTX-therapy (MTX-responder, MTX-resistant and MTX-intolerant RA-groups) and 47 non-RA controls in six different leukocyte subpopulations (neutrophil leukocytes, monocytes, lymphocytes, CD4+, CD8+ and CD19+ cells). Methotrexate 218-221 ATP binding cassette subfamily B member 1 Homo sapiens 81-85 26715450-5 2015 METHODS: We have compared the functional Multidrug Activity Factors (MAF) of the MDR1 and MRP1 transporters of Peripheral Blood Leukocytes of 59 Rheumatoid Arthritis patients with various response rate to MTX-therapy (MTX-responder, MTX-resistant and MTX-intolerant RA-groups) and 47 non-RA controls in six different leukocyte subpopulations (neutrophil leukocytes, monocytes, lymphocytes, CD4+, CD8+ and CD19+ cells). Methotrexate 218-221 ATP binding cassette subfamily B member 1 Homo sapiens 81-85 26715450-5 2015 METHODS: We have compared the functional Multidrug Activity Factors (MAF) of the MDR1 and MRP1 transporters of Peripheral Blood Leukocytes of 59 Rheumatoid Arthritis patients with various response rate to MTX-therapy (MTX-responder, MTX-resistant and MTX-intolerant RA-groups) and 47 non-RA controls in six different leukocyte subpopulations (neutrophil leukocytes, monocytes, lymphocytes, CD4+, CD8+ and CD19+ cells). Methotrexate 218-221 ATP binding cassette subfamily B member 1 Homo sapiens 81-85 25921280-0 2015 ABCB1 polymorphisms correlate with susceptibility to adult acute leukemia and response to high-dose methotrexate. Methotrexate 100-112 ATP binding cassette subfamily B member 1 Homo sapiens 0-5 25921280-1 2015 The aim of this study is to investigate the association of ABCB1 polymorphisms with susceptibility to adult acute leukemia, and the influence of ABCB1 polymorphisms on the efficacy of high-dose methotrexate (HDMTX). Methotrexate 194-206 ATP binding cassette subfamily B member 1 Homo sapiens 145-150 26071279-0 2015 Multidrug resistance 1 (MDR1) 3435C>T gene polymorphism influences the clinical phenotype and methotrexate-induced adverse events in South Indian Tamil rheumatoid arthritis. Methotrexate 97-109 ATP binding cassette subfamily B member 1 Homo sapiens 0-22 26071279-0 2015 Multidrug resistance 1 (MDR1) 3435C>T gene polymorphism influences the clinical phenotype and methotrexate-induced adverse events in South Indian Tamil rheumatoid arthritis. Methotrexate 97-109 ATP binding cassette subfamily B member 1 Homo sapiens 24-28 26071279-10 2015 MDR1 3435CT genotype was associated with MTX-induced adverse events [p = 0.01, OR 2.01, 95% CI (1.15-3.52)], and the 3435 TT genotype remained protective for the development of adverse events [p = 0.009, OR 0.40, 95% CI (0.21-0.78)]. Methotrexate 41-44 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 26071279-12 2015 CONCLUSION: MDR1 3435C>T gene polymorphism influences the clinical phenotype and adverse events to MTX in the South Indian cohort of patients with RA. Methotrexate 102-105 ATP binding cassette subfamily B member 1 Homo sapiens 12-16 25303299-9 2014 Patients with MTHFR C677T and ABCB1 C3435T polymorphisms appear to have significantly higher MTX plasma concentrations (p < 0.05). Methotrexate 93-96 ATP binding cassette subfamily B member 1 Homo sapiens 30-35 25007187-1 2014 BACKGROUND: The aim of this study is to analyze polymorphisms in genes involved in 6-mercaptopurine detoxification (TPMT); methotrexate (MTX) metabolism including ABCB1 (or MDR1), ABCC2, SLC19A1 (or RFC1), and SLCO1B1; and the MTX effect mainly MTHFR and TYMS, and to assess whether these polymorphisms are predictors of treatment toxicity and/or MTX clearance. Methotrexate 227-230 ATP binding cassette subfamily B member 1 Homo sapiens 163-168 24680847-4 2014 Dioscin enhanced the intracellular concentration of MTX by down-regulating MDR1 expression through a mechanism that involves NF-kappaB signaling pathway inhibition in Caco-2 cells. Methotrexate 52-55 ATP binding cassette subfamily B member 1 Homo sapiens 75-79 24595806-9 2014 Folate deprivation markedly increased growth inhibitory effects of the established MRP1 substrates daunorubicin (~twofold), doxorubicin (~fivefold), and methotrexate (~83-fold) in MRP1-overexpressing cells, proportional to MRP1 expression. Methotrexate 153-165 ATP binding cassette subfamily B member 1 Homo sapiens 180-184 24595806-9 2014 Folate deprivation markedly increased growth inhibitory effects of the established MRP1 substrates daunorubicin (~twofold), doxorubicin (~fivefold), and methotrexate (~83-fold) in MRP1-overexpressing cells, proportional to MRP1 expression. Methotrexate 153-165 ATP binding cassette subfamily B member 1 Homo sapiens 180-184 23095111-9 2012 There was a significant association between the presence of both the T allele at MTHFR C677T (p=0.006), and the C allele at ABCB1 C3435T (p=0.046), with toxicity development after 12 months of MTX treatment. Methotrexate 193-196 ATP binding cassette subfamily B member 1 Homo sapiens 124-129 24229684-9 2013 Real-time PCR and Western blotting assays demonstrated that curcumin down-regulated P-gp expression of MNNG/HOS/MTX cells. Methotrexate 112-115 ATP binding cassette subfamily B member 1 Homo sapiens 84-88 23095111-11 2012 These data suggest that the presence of the MTHFR C677T and ABCB1 C3435T SNPs contribute to MTX toxicity in patients with RA. Methotrexate 92-95 ATP binding cassette subfamily B member 1 Homo sapiens 60-65 22859359-0 2012 ABCB1 and ABCC3 gene polymorphisms are associated with first-year response to methotrexate in juvenile idiopathic arthritis. Methotrexate 78-90 ATP binding cassette subfamily B member 1 Homo sapiens 0-5 22859359-7 2012 RESULTS: MTX response was more often achieved by patients variant for the adenosine triphosphate-binding cassette transporter B1 (ABCB1) gene polymorphism rs1045642 (OR 3.80, 95% CI 1.70-8.47, p = 0.001) and patients variant for the ABCC3 gene polymorphism rs4793665 (OR 3.10, 95% CI 1.49-6.41, p = 0.002) than by patients with other genotypes. Methotrexate 9-12 ATP binding cassette subfamily B member 1 Homo sapiens 130-135 22859359-9 2012 CONCLUSION: ABCB1 rs1045642, ABCC3 rs4793665, and SLC19A1 rs1051266 polymorphisms were associated with response to MTX in 287 patients with JIA studied longitudinally. Methotrexate 115-118 ATP binding cassette subfamily B member 1 Homo sapiens 12-17 22104130-9 2012 In conclusion, the ABCB1 3435C>T, ABCB1 2677G>A/T, and MTHFR 1298A>C polymorphisms influenced the efficacy of MTX monotherapy. Methotrexate 119-122 ATP binding cassette subfamily B member 1 Homo sapiens 19-24 22796246-0 2012 ABCB1 C3435T genetic polymorphism on population pharmacokinetics of methotrexate after hematopoietic stem cell transplantation in Korean patients: a prospective analysis. Methotrexate 68-80 ATP binding cassette subfamily B member 1 Homo sapiens 0-5 21887680-9 2012 Methotrexate toxicity was increased in variants of MTHFR c.1298A>C p.Glu(429)Ala (P = .038), ABCB1 c.3435T>C Ile(145)Ile (P = .027), and ABCC2 c.3563T>A p.Val(1188)Glu (P = .028). Methotrexate 0-12 ATP binding cassette subfamily B member 1 Homo sapiens 96-101 22104130-9 2012 In conclusion, the ABCB1 3435C>T, ABCB1 2677G>A/T, and MTHFR 1298A>C polymorphisms influenced the efficacy of MTX monotherapy. Methotrexate 119-122 ATP binding cassette subfamily B member 1 Homo sapiens 37-42 21509569-1 2011 PURPOSE: The objectives of this study were (1) to develop a population pharmacokinetic model of high-dose methotrexate (HD-MTX) in children with acute lymphoblastic leukaemia (ALL) and malignant lymphoma (ML) in order to investigate the influence of common polymorphisms in SLC19A1, MTHFR and ABCB1 on plasma levels of MTX and (2) to estimate MTX exposure in individual patients to study the association of genetic variability in the folate metabolic pathway with MTX toxicity. Methotrexate 106-118 ATP binding cassette subfamily B member 1 Homo sapiens 293-298 21948322-10 2011 The results suggest that even a low concentration of Tween 80 is sufficient for enhancing the transport of MTX from the NPs across MDCKII-MDR1 cells. Methotrexate 107-110 ATP binding cassette subfamily B member 1 Homo sapiens 138-142 21868524-5 2011 RESULTS: siRNA down-regulated MDR1 mRNA expression by 50% in breast carcinoma and osteosarcoma cell lines, and significantly inhibited tumor cell proliferation up to 90% (p<0.01), when co-administered with doxorubicin or methotrexate, despite the known chemoresistance of the cell lines. Methotrexate 224-236 ATP binding cassette subfamily B member 1 Homo sapiens 30-34 21387541-6 2011 PROCEDURE: We analyzed 10 polymorphisms in seven genes (MTHFR, TS, SHMT1, RFC1, ABCB1, ABCG2, and SLCO1B1) from the MTX metabolism in 115 Spanish pediatric B-ALL patients, using MTX plasma concentration as an objective and quantifiable marker of toxicity. Methotrexate 116-119 ATP binding cassette subfamily B member 1 Homo sapiens 80-85 21062675-7 2011 In addition to its immunosuppressive activity, CSA results may also be related to MTX/SSA effect restoration through P-gp inhibition. Methotrexate 82-85 ATP binding cassette subfamily B member 1 Homo sapiens 117-121 19915943-2 2010 However, infliximab with methotrexate (MTX) can overcome P-gp-mediated drug resistance. Methotrexate 25-37 ATP binding cassette subfamily B member 1 Homo sapiens 57-61 19915943-2 2010 However, infliximab with methotrexate (MTX) can overcome P-gp-mediated drug resistance. Methotrexate 39-42 ATP binding cassette subfamily B member 1 Homo sapiens 57-61 19915943-11 2010 Etanercept is useful for overcoming P-gp-mediated treatment resistance in intractable RA patients who have to discontinue infliximab or are intolerant to MTX. Methotrexate 154-157 ATP binding cassette subfamily B member 1 Homo sapiens 36-40 21062675-4 2011 Here, P-gp function before and after CSA administration in three psoriatic arthritis (PsA) patients, who developed a resistance to MTX/SSA, has been evaluated. Methotrexate 131-134 ATP binding cassette subfamily B member 1 Homo sapiens 6-10 20533531-0 2010 In vivo expansion of MDR1-transduced cells accompanied by a post-transplantation chemotherapy regimen with mitomycin C and methotrexate. Methotrexate 123-135 ATP binding cassette subfamily B member 1 Homo sapiens 21-25 20533531-7 2010 A remarkable increase in MDR1 transgene-positive cells was observed on day 532, during combination chemotherapy with mitomycin C and methotrexate. Methotrexate 133-145 ATP binding cassette subfamily B member 1 Homo sapiens 25-29