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PI3-激酶和Akt信号的乳腺癌化疗耐药机制

Breast Cancer Chemoresistance Mechanisms Through PI 3-Kinase and Akt Signaling

作者:Toker, A.; Brown, K. 加工时间:2015-08-23 信息来源:科技报告(AD) 索取原文[10 页]
关键词:乳腺癌细胞(生物学);化疗;死亡
摘 要:We have discovered that the Akt pathway modulates breast cancer cell survival in response to genotoxic agents, and discovered a new substrate of Akt, MERIT40, that is phosphorylated upon exposure of cells to chemotherapeutic drugs. We propose that this represents a major mechanism by which cells exposed to these drugs evade cell death by apoptosis and thus become resistant to the damaging effects of clinically-relevant chemotherapy agents. These findings have important ramifications for the use of chemotherapy drugs in breast cancer patients, and many also suggest that MERIT40 may be used as a clinically relevant biomarker for resistance to doxorubicin.
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