Abstract:
:Mutant RAS-driven tumorigenesis was thought for decades to arise independently of wild-type RAS isoforms, but recent evidence indicates wild-type isoforms are involved. In this issue of Cancer Cell, Grabocka and colleagues report how the loss of wild-type RAS alters oncogenic signaling and dampens the DNA-damage response, thereby affecting tumor progression and chemosensitivity.
journal_name
Cancer Celljournal_title
Cancer cellauthors
Anastassiadis T,Brown EJdoi
10.1016/j.ccr.2014.01.029subject
Has Abstractpub_date
2014-02-10 00:00:00pages
137-8issue
2eissn
1535-6108issn
1878-3686pii
S1535-6108(14)00043-9journal_volume
25pub_type
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