Article
No mutations of the Smad2 gene in human sporadic gastric carcinomas.
Japanese journal of clinical oncology - 1 Jan 1999
Shitara Y, Yokozaki H, Yasui W, Takenoshita S, Kuwano H, Nagamachi Y, Tahara E
Abstract excerpt
BACKGROUND: The majority of cancer cells escape from TGF-beta-mediated growth control. However, the mechanism of resistance to the growth inhibitory effects by TGF-beta is not clear. TGF-beta signaling is initiated when the type I receptor phosphorylates the SMAD proteins, Smad2 and Smad3. Recently, mutations of Smad2 have been detected in human colon and lung cancers. Mutation of coding sequences of Smad2 in...
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