Interfering with RAS-effector protein interactions prevent RAS-dependent tumour initiation and causes stop-start control of cancer growth.

RAS mutations are the most common gain-of-function change in human cancer and promise to be a critical therapy target. As a new approach, we have used a surrogate to drug the 'undruggable' (that is, RAS-effector protein-protein interactions inside cancer cells) in pre-clinical mouse models...

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Bibliographic Details
Main Authors: Tanaka, T, Rabbitts, T
Format: Journal article
Language:English
Published: 2010