Abstract:
BACKGROUND AND AIMS:Juvenile polyps occur in several Mendelian disorders, whether in association with gastrointestinal cancer alone (juvenile polyposis syndrome, JPS) or as part of known syndromes (Cowden, Gorlin, and Bannayan-Zonana) in association with developmental abnormalities, dysmorphic features, or extraintestinal tumours. Recently, some JPS families were shown to harbour germline mutations in the SMAD4 (DPC4) gene, providing further evidence for the importance of the TGFbeta signalling pathway in colorectal cancer. There remains, however, considerable, unexplained genetic heterogeneity in JPS. Other members of the SMAD family are excellent candidates for JPS, especially SMAD2 (which, like SMAD4, is mutated somatically in colorectal cancers), SMAD3 (which causes colorectal cancer when "knocked out" in mice), SMAD5, and SMAD1. METHODS:SMAD1, SMAD2, SMAD3, and SMAD5 were screened for germline mutations in 30 patients with JPS and without SMAD4 mutations. RESULTS:No mutations were found in any of these genes. A G-A C89Y polymorphism with possible effects on protein function was found in SMAD3, but the frequencies of the G and A alleles did not differ between patients with JPS and controls. CONCLUSIONS:It remains to be determined whether or not this polymorphism is involved in a minor predisposition to colorectal or other carcinomas. SMAD4 may be the only member of the SMAD family which causes JPS when mutant in the germline. The other genes underlying JPS remain to be identified.
journal_name
Gutjournal_title
Gutauthors
Bevan S,Woodford-Richens K,Rozen P,Eng C,Young J,Dunlop M,Neale K,Phillips R,Markie D,Rodriguez-Bigas M,Leggett B,Sheridan E,Hodgson S,Iwama T,Eccles D,Bodmer W,Houlston R,Tomlinson Idoi
10.1136/gut.45.3.406keywords:
subject
Has Abstractpub_date
1999-09-01 00:00:00pages
406-8issue
3eissn
0017-5749issn
1468-3288journal_volume
45pub_type
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