2018
DOI: 10.1016/j.canlet.2018.04.037
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Cyclin E overexpression confers resistance to the CDK4/6 specific inhibitor palbociclib in gastric cancer cells

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Cited by 61 publications
(67 citation statements)
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“…15 – 19 Here, we identified CCNE1 as an additional potential marker of de novo resistance in a large panel of pan-cancer and BC cell lines. To date, the role of cyclin E1 as a marker of de novo resistance has been demonstrated in other tumor types such as ovarian and gastric cancer 37 , 38 but only suggested in BC. 33 , 39 Our data suggest that both CCNE1 and the CCNE1/RB1 ratio, which evaluates both CCNE1 and RB1 , might serve as “pan-cancer” markers of de novo resistance to palbociclib and that the CCNE1 / RB1 ratio might serve as better marker compared to the single biomarkers CCNE1 and RB1 used separately, both in BC and in other cancer types.…”
Section: Discussionmentioning
confidence: 99%
“…15 – 19 Here, we identified CCNE1 as an additional potential marker of de novo resistance in a large panel of pan-cancer and BC cell lines. To date, the role of cyclin E1 as a marker of de novo resistance has been demonstrated in other tumor types such as ovarian and gastric cancer 37 , 38 but only suggested in BC. 33 , 39 Our data suggest that both CCNE1 and the CCNE1/RB1 ratio, which evaluates both CCNE1 and RB1 , might serve as “pan-cancer” markers of de novo resistance to palbociclib and that the CCNE1 / RB1 ratio might serve as better marker compared to the single biomarkers CCNE1 and RB1 used separately, both in BC and in other cancer types.…”
Section: Discussionmentioning
confidence: 99%
“…[80][81][82][83][84][85][86] These aberrations associated with targeted therapy resistance could be used to develop an effective treatment sequence to delay disease progression. The majority of patients with advanced or ER-positive MBC will be treated with a CDK4/6 or mTOR inhibitor in combination with ET during the course of their disease.…”
Section: Preclinical Strategies To Identify Actionable Targets In Esrmentioning
confidence: 99%
“…Indeed, several studies now demonstrate differential mechanisms of acquired resistance to either mTOR or CDK4/6 inhibitors in breast and other cancers, including upregulation of MAPK signaling in everolimus-and palbociclib-resistant models, as well as mutations in RB1, and upregulation of CDK2, CCNE1, or PDK1 in palbociclib-resistant cells. [80][81][82][83][84][85][86] These aberrations associated with targeted therapy resistance could be used to develop an effective treatment sequence to delay disease progression. Certainly, several recent and ongoing clinical trials testing investigational agents are recruiting patients who have been treated previously with mTOR or CDK4/6 inhibitors, and comparison of response between these patient populations is necessary to provide insight into whether certain patient populations benefit from sequencing of targeted therapies or are inherently resistant to therapy.…”
Section: Preclinical Strategies To Identify Actionable Targets In Esrmentioning
confidence: 99%
“…CDK4/CDK6 inhibitors are now used for hormone receptor (HR)-positive and human epidermal growth factor receptor 2 (HER2)-negative breast cancer [29]. The palbociclib and abemaciclib were known to target the ATP binding site of CDK4 and CDK6 inhibit the phosphorylation of the retinoblastoma protein (RB) [30]. We found that inhibit CDK4 by small interference RNA or speci c CDK4 inhibitors could reverse the cell proliferation induced by WTAP in prostate cancer cell lines.…”
Section: Discussionmentioning
confidence: 99%