Akt抑制剂如何抑制乳腺癌和乳腺癌转移:从小鼠研究中获得的经验教训

N. Hay
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引用次数: 0

摘要

PI3K/Akt信号通路在不同类型的乳腺癌中经常过度激活。在过去的二十年里,人们一直在努力开发这一途径的抑制剂来治疗癌症患者。然而,这种途径在进化上最保守的功能是在细胞和有机体代谢中,被癌细胞劫持。因此,当靶向PI3K或Akt时,预期会产生不良的代谢后果。这些代谢后果,特别是高胰岛素血症,可能会阻碍治疗的效果。本文综述了最近在小鼠中进行的基因研究,这些研究可能为利用Akt抑制剂有效治疗乳腺癌和乳腺癌转移铺平道路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
How to inhibit breast cancer and breast cancer metastasis with Akt inhibitors: Lessons learned from studies in mice
The PI3K/Akt signaling pathway is frequently hyperactivated in different types of breast cancer. In the past two decades, major efforts have been made to develop inhibitors of this pathway to treat cancer patients. However, the most evolutionarily conserved function of this pathway is in cellular and organismal metabolism, which is hijacked by cancer cells. Thus, adverse metabolic consequences are expected when PI3K or Akt is targeted. These metabolic consequences, particularly hyperinsulinemia, could impede the efficacy of treatment. This review summarizes recent genetic studies in mice that could pave the way to efficient breast cancer and breast cancer metastasis treatment with Akt inhibitors.
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