2010年03月05日

Targeting KRAS cancers

Mutations in genes of the RAS family are preset on about 20% of human cancers, making RAS proteins prime potential targets for cancer therapy.

Direct targeting of RAS proteins has not so far been productive, but two papers published in this issue offer the prospect of alternative targets in a signalling pathway downstream of RAS.

Using a synthetic lethality RNAi screen, Barbie et al.
identify TBK1 as a kinase in the NF-KB signalling pathway that is essential for the survial of KRAS-transformed cells.

TBK1 induces anti-apoptotic signals and may be a therapeutic cancer target.

And in an elegant mouse model for lung cancer driven by Kras mutation and loss of p53, Meylan et al.
show that NF-KB signalling is a activated by the concerted actions of these two alterations and required for tumour initiation and tumour maintenance.


### database ###
nature 462,1-126 5 November 2009 Issue no.7269
Letter pp.104 / Requirement for NF-KB signalling in a mouse model of lung adenocarcinoma / E meylan et al. (Massachusetts Institute Technology)
Letter pp.108 / Systematic RNA interference reveals that oncogennic KRAS-driven cancers require TBK1 / D A Barbie et al.
news and views p.44 / Cancer : A tumour gene's fatal flaws / Julian Downward


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