Selective killing of ATM- or p53-deficient cancer cells through inhibition of ATR

被引：0

作者：

Reaper, Philip M. ^{[1
]}

Griffiths, Matthew R. ^{[1
]}

Long, Joanna M. ^{[1
]}

Charrier, Jean-Damien ^{[1
]}

MacCormick, Somhairle ^{[1
]}

Charlton, Peter A. ^{[1
]}

Golec, Julian M. C. ^{[1
]}

Pollard, John R. ^{[1
]}

机构：

[1] Vertex Pharmaceut Europe, Abingdon, Oxon, England

来源：

NATURE CHEMICAL BIOLOGY | 2011年 / 7卷 / 07期

关键词：

DOUBLE-STRAND BREAKS; DNA-DAMAGE RESPONSE; LUNG-CANCER; CISPLATIN; ACTIVATION; CARCINOMA; CHROMATIN; REPAIR; MODEL; CHK2;

D O I：

10.1038/NCHEMBIO.573

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Here we report a comprehensive biological characterization of a potent and selective small-molecule inhibitor of the DNA damage response (DDR) kinase ATR. We show a profound synthetic lethal interaction between ATR and the ATM-p53 tumor suppressor pathway in cells treated with DNA-damaging agents and establish ATR inhibition as a way to transform the outcome for patients with cancer treated with ionizing radiation or genotoxic drugs.

引用

页码：428 / 430

页数：3

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