PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 25475722-3 2015 In this study, we first established imatinib-resistant K562 CML cells, and then evaluated the effect of Adiponectin in reversing imatinib resistance. Imatinib Mesylate 129-137 adiponectin, C1Q and collagen domain containing Homo sapiens 104-115 26147296-0 2015 Adiponectin enhances Imatinib anti-tumour activity in human chronic myeloid leukaemia cells with serum levels associated with Imatinib efficacy in early chronic phase patients. Imatinib Mesylate 21-29 adiponectin, C1Q and collagen domain containing Homo sapiens 0-11 26147296-0 2015 Adiponectin enhances Imatinib anti-tumour activity in human chronic myeloid leukaemia cells with serum levels associated with Imatinib efficacy in early chronic phase patients. Imatinib Mesylate 126-134 adiponectin, C1Q and collagen domain containing Homo sapiens 0-11 26147296-5 2015 MATERIALS AND METHODS: Effects of recombinant adiponectin protein, in enhancing Imatinib anti-tumour activities, in K562 and MEG-01 CML cells, were examined in vitro and in vivo. Imatinib Mesylate 80-88 adiponectin, C1Q and collagen domain containing Homo sapiens 46-57 26147296-8 2015 RESULTS: Data presented here indicate that adiponectin enhanced Imatinib efficacy in vitro and in vivo. Imatinib Mesylate 64-72 adiponectin, C1Q and collagen domain containing Homo sapiens 43-54 26147296-10 2015 Most importantly, additional clinical data revealed that adiponectin plasma levels in CML ECP patients, correlated with Imatinib efficacy. Imatinib Mesylate 120-128 adiponectin, C1Q and collagen domain containing Homo sapiens 57-68 26147296-11 2015 CONCLUSIONS: Adiponectin enhanced Imatinib anti-tumour activity in human chronic myeloid leukaemia cells and its serum levels were associated with Imatinib efficacy, in early chronic phase patients. Imatinib Mesylate 34-42 adiponectin, C1Q and collagen domain containing Homo sapiens 13-24 26147296-11 2015 CONCLUSIONS: Adiponectin enhanced Imatinib anti-tumour activity in human chronic myeloid leukaemia cells and its serum levels were associated with Imatinib efficacy, in early chronic phase patients. Imatinib Mesylate 147-155 adiponectin, C1Q and collagen domain containing Homo sapiens 13-24 25475722-0 2015 Adiponectin signals through Adiponectin Receptor 1 to reverse imatinib resistance in K562 human chronic myeloid leukemia cells. Imatinib Mesylate 62-70 adiponectin, C1Q and collagen domain containing Homo sapiens 0-11 25475722-4 2015 The data presented here demonstrated that Adiponectin was able to reverse K562 resistance to imatinib in vitro and in vivo. Imatinib Mesylate 93-101 adiponectin, C1Q and collagen domain containing Homo sapiens 42-53 25475722-5 2015 Additional data with molecular approaches suggested that the reversion of Adiponectin in imatinib resistance signals through AdipoR1 but not AdipoR2 to downregulate Bcr-Abl expression and effect in imatinib-resistant K562 CML cells. Imatinib Mesylate 89-97 adiponectin, C1Q and collagen domain containing Homo sapiens 74-85 25475722-5 2015 Additional data with molecular approaches suggested that the reversion of Adiponectin in imatinib resistance signals through AdipoR1 but not AdipoR2 to downregulate Bcr-Abl expression and effect in imatinib-resistant K562 CML cells. Imatinib Mesylate 198-206 adiponectin, C1Q and collagen domain containing Homo sapiens 74-85 25475722-6 2015 Taken together, our data showed that Adiponectin can reverse imatinib resistance in CML, and to a certain extent elucidate the mechanism of Adiponectin reversing imatinib resistance that may provide a new and promising approach in imatinib resistance management in CML therapy. Imatinib Mesylate 61-69 adiponectin, C1Q and collagen domain containing Homo sapiens 37-48 25475722-6 2015 Taken together, our data showed that Adiponectin can reverse imatinib resistance in CML, and to a certain extent elucidate the mechanism of Adiponectin reversing imatinib resistance that may provide a new and promising approach in imatinib resistance management in CML therapy. Imatinib Mesylate 162-170 adiponectin, C1Q and collagen domain containing Homo sapiens 140-151 25475722-6 2015 Taken together, our data showed that Adiponectin can reverse imatinib resistance in CML, and to a certain extent elucidate the mechanism of Adiponectin reversing imatinib resistance that may provide a new and promising approach in imatinib resistance management in CML therapy. Imatinib Mesylate 162-170 adiponectin, C1Q and collagen domain containing Homo sapiens 140-151 20466781-0 2010 Plasma adiponectin levels are markedly elevated in imatinib-treated chronic myeloid leukemia (CML) patients: a mechanism for improved insulin sensitivity in type 2 diabetic CML patients? Imatinib Mesylate 51-59 adiponectin, C1Q and collagen domain containing Homo sapiens 7-18 20466781-4 2010 We therefore hypothesized that imatinib therapy would be associated with an increase in peripheral and intramedullary adiposity and elevated plasma adiponectin levels. Imatinib Mesylate 31-39 adiponectin, C1Q and collagen domain containing Homo sapiens 148-159 20466781-5 2010 RESEARCH DESIGN AND METHODS: Adiponectin levels in CML patient plasma, at diagnosis and then during imatinib mesylate therapy, was measured using an ELISA. Imatinib Mesylate 100-108 adiponectin, C1Q and collagen domain containing Homo sapiens 29-40 20466781-9 2010 CONCLUSIONS: Elevated adiponectin levels in imatinib-treated CML patients provide a possible mechanism for improved glucose and lipid metabolism reported for some imatinib-treated patients. Imatinib Mesylate 44-52 adiponectin, C1Q and collagen domain containing Homo sapiens 22-33 20466781-9 2010 CONCLUSIONS: Elevated adiponectin levels in imatinib-treated CML patients provide a possible mechanism for improved glucose and lipid metabolism reported for some imatinib-treated patients. Imatinib Mesylate 163-171 adiponectin, C1Q and collagen domain containing Homo sapiens 22-33 22474082-0 2012 Suppression of PDGF-induced PI3 kinase activity by imatinib promotes adipogenesis and adiponectin secretion. Imatinib Mesylate 51-59 adiponectin, C1Q and collagen domain containing Homo sapiens 86-97 22474082-2 2012 We recently reported that plasma levels of adiponectin, an important regulator of insulin sensitivity, are elevated following imatinib therapy in CML patients, which could account for these improved metabolic outcomes. Imatinib Mesylate 126-134 adiponectin, C1Q and collagen domain containing Homo sapiens 43-54 22474082-3 2012 Adiponectin is secreted exclusively from adipocytes, suggesting that imatinib modulates adiponectin levels directly, by transcriptional upregulation of adiponectin in pre-existing adipocytes, and/or indirectly, by stimulating adipogenesis. Imatinib Mesylate 69-77 adiponectin, C1Q and collagen domain containing Homo sapiens 0-11 22474082-3 2012 Adiponectin is secreted exclusively from adipocytes, suggesting that imatinib modulates adiponectin levels directly, by transcriptional upregulation of adiponectin in pre-existing adipocytes, and/or indirectly, by stimulating adipogenesis. Imatinib Mesylate 69-77 adiponectin, C1Q and collagen domain containing Homo sapiens 88-99 22474082-3 2012 Adiponectin is secreted exclusively from adipocytes, suggesting that imatinib modulates adiponectin levels directly, by transcriptional upregulation of adiponectin in pre-existing adipocytes, and/or indirectly, by stimulating adipogenesis. Imatinib Mesylate 69-77 adiponectin, C1Q and collagen domain containing Homo sapiens 152-163 22474082-4 2012 In this report, we have demonstrated that imatinib promotes adipogenic differentiation of human mesenchymal stromal cells (MSCs), which in turn secrete high-molecular-weight adiponectin. Imatinib Mesylate 42-50 adiponectin, C1Q and collagen domain containing Homo sapiens 174-185 22474082-10 2012 Taken together, our results suggest that imatinib increases plasma adiponectin levels by promoting adipogenesis through the suppression of PI3 kinase signalling downstream of PDGFR. Imatinib Mesylate 41-49 adiponectin, C1Q and collagen domain containing Homo sapiens 67-78