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当守护者变成敌人:在PTEN缺陷型癌症中靶向ATM

When the guardian becomes the enemy: Targeting ATM in PTEN-deficient cancers.

作者信息

McCabe Nuala, Walker Steven M, Kennedy Richard D

机构信息

Centre for Cancer Research and Cell Biology, Queens University Belfast, Northern Ireland; Almac Diagnostics, Craigavon, Northern Ireland.

出版信息

Mol Cell Oncol. 2015 Jun 10;3(1):e1053595. doi: 10.1080/23723556.2015.1053595. eCollection 2016 Jan.

Abstract

Ataxia telangiectasia mutated (ATM) is an important signaling molecule in the DNA damage response and inhibitors of ATM are under clinical development. We identified a synthetic lethal interaction between ATM inhibition and phosphatase and tensin homolog (PTEN) loss that was the result of increased oxidative stress. Inhibition of ATM therefore represents a novel strategy to target PTEN-associated cancers.

摘要

共济失调毛细血管扩张症突变基因(ATM)是DNA损伤反应中的一种重要信号分子,ATM抑制剂正处于临床开发阶段。我们发现ATM抑制与磷酸酶和张力蛋白同源物(PTEN)缺失之间存在合成致死相互作用,这是氧化应激增加的结果。因此,抑制ATM代表了一种针对PTEN相关癌症的新策略。

相似文献

1
When the guardian becomes the enemy: Targeting ATM in PTEN-deficient cancers.当守护者变成敌人:在PTEN缺陷型癌症中靶向ATM
Mol Cell Oncol. 2015 Jun 10;3(1):e1053595. doi: 10.1080/23723556.2015.1053595. eCollection 2016 Jan.

本文引用的文献

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PTEN: Multiple Functions in Human Malignant Tumors.PTEN:人类恶性肿瘤中的多种功能。
Front Oncol. 2015 Feb 16;5:24. doi: 10.3389/fonc.2015.00024. eCollection 2015.
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ATM activation by oxidative stress.氧化应激激活 ATM。
Science. 2010 Oct 22;330(6003):517-21. doi: 10.1126/science.1192912.

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