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MEK inhibitors block growth of lung tumours with mutations in ataxia-telangiectasia mutated.

Abstract：

:Lung cancer is the leading cause of cancer deaths, and effective treatments are urgently needed. Loss-of-function mutations in the DNA damage response kinase ATM are common in lung adenocarcinoma but directly targeting these with drugs remains challenging. Here we report that ATM loss-of-function is synthetic lethal with drugs inhibiting the central growth factor kinases MEK1/2, including the FDA-approved drug trametinib. Lung cancer cells resistant to MEK inhibition become highly sensitive upon loss of ATM both in vitro and in vivo. Mechanistically, ATM mediates crosstalk between the prosurvival MEK/ERK and AKT/mTOR pathways. ATM loss also enhances the sensitivity of KRAS- or BRAF-mutant lung cancer cells to MEK inhibition. Thus, ATM mutational status in lung cancer is a mechanistic biomarker for MEK inhibitor response, which may improve patient stratification and extend the applicability of these drugs beyond RAS and BRAF mutant tumours.

journal_name

Nat Commun

journal_title

Nature communications

authors

Smida M,Fece de la Cruz F,Kerzendorfer C,Uras IZ,Mair B,Mazouzi A,Suchankova T,Konopka T,Katz AM,Paz K,Nagy-Bojarszky K,Muellner MK,Bago-Horvath Z,Haura EB,Loizou JI,Nijman SM

doi

10.1038/ncomms13701

subject

Has Abstract

pub_date

2016-12-06 00:00:00

pages

13701

issn

2041-1723

pii

ncomms13701

journal_volume

7

pub_type

杂志文章

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