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Japanese Journal of Clinical Oncology, Vol 29, Issue 1 3-7, Copyright © 1999 by Foundation for Promotion of Cancer Research

ORIGINAL ARTICLE

No mutations of the Smad2 gene in human sporadic gastric carcinomas

Y Shitara, H Yokozaki, W Yasui, S Takenoshita, H Kuwano, Y Nagamachi and E Tahara
First Department of Pathology, Hiroshima University School of Medicine, Japan.

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 gastric carcinomas has not yet been elucidated adequately. METHODS: PCR-SSCP analysis of the entire coding region of Smad2 in 35 human sporadic gastric cancers and eight gastric cancer cell lines was performed using 11 sets of intron-based primers. RESULTS: No mutations of Smad2 were detected in any tumor or cell line. CONCLUSIONS: The results suggest that mutation of Smad2 does not play a key role in human stomach carcinogenesis.
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