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

Abstract:

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 of RAS-dependent cancers. Using this novel reagent, we have specifically targeted RAS signalling in a transgenic mouse model of lung cancer by directly blockading RAS-effector interactions with an antibody ...

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Publisher copy:
10.1038/onc.2010.346
Journal:
Oncogene More from this journal
Volume:
29
Issue:
45
Pages:
6064-6070
Publication date:
2010-11-01
DOI:
EISSN:
1476-5594
ISSN:
0950-9232
Language:
English
Keywords:
Pubs id:
pubs:324307
UUID:
uuid:619b40d9-cc4c-418d-8704-1428a874ed46
Local pid:
pubs:324307
Source identifiers:
324307
Deposit date:
2013-11-16

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