2017
DOI: 10.1158/0008-5472.can-17-0899
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Abstract: Acquired and intrinsic resistance to receptor tyrosine kinase inhibitors (RTKi) represent a major hurdle in improving the management of clear cell renal cell carcinoma (ccRCC). Recent reports suggest that drug resistance is driven by tumor adaptation via epigenetic mechanisms that activate alternative survival pathways. The histone methyl transferase EZH2 is frequently altered in many cancers including ccRCC. To evaluate its role in ccRCC resistance to RTKi, we established and characterized a spontaneously met… Show more

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Cited by 66 publications
(58 citation statements)
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“…Indeed, our in vitro and in vivo data indicate that RCC cells exposed to sunitinib show increased serine 81 phosphorylated AR. There is evidence that Src activation is one of the alternative pathways induced by RTKi resistance (28,35), and this kinase is involved in AR phosphorylation (13). Our data suggest that CDK1 may also be induced upon sunitinib resistance.…”
Section: Discussionmentioning
confidence: 54%
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“…Indeed, our in vitro and in vivo data indicate that RCC cells exposed to sunitinib show increased serine 81 phosphorylated AR. There is evidence that Src activation is one of the alternative pathways induced by RTKi resistance (28,35), and this kinase is involved in AR phosphorylation (13). Our data suggest that CDK1 may also be induced upon sunitinib resistance.…”
Section: Discussionmentioning
confidence: 54%
“…We have recently reported that sunitinib resistance induces epigenetic-driven kinome reprogramming in RCC models, leading to increased global serine and tyrosine phosphorylation (28). In view of these findings, we hypothesized that the increased AR activation/expression, initially observed in our sunitinib-resistant PDX model by RPPA, was due to the phosphorylation of AR from sunitinib-induced kinase activation.…”
Section: Discussionmentioning
confidence: 74%
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“…Kinome reprogramming is a powerful barrier to a durable treatment response to kinase inhibition [10][11][12]. These signaling adaptations occur as a result of the compensatory activation of evolutionarily conserved signaling pathways that drive growth and proliferation, especially when central pathways such as RAS/MEK and PI3K/mTOR are blocked by drugs [13].…”
Section: Introductionmentioning
confidence: 99%