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K-ras and p53 mutations in hereditary non-polyposis colorectal cancers

✍ Scribed by Lorena Losi; Maurizio Ponz de Leon; Josef Jiricny; Carmela Di Gregorio; Piero Benatti; Antonio Percesepe; Rossella Fante; Luca Roncucci; Monica Pedroni; Jean Benhattar

Publisher: John Wiley and Sons
Year: 1997
Tongue: French
Weight: 57 KB
Volume: 74
Category: Article
ISSN: 0020-7136
DOI: 10.1002/(sici)1097-0215(19970220)74:1<94::aid-ijc16>3.0.co;2-i

No coin nor oath required. For personal study only.

✦ Synopsis

Genetic instability related to defective DNA mismatch repair genes may be involved in the pathogenesis of carcinoma in Hereditary Non-Polyposis Colorectal Cancer (HN-PCC). To test that the targets of genetic instability could include critical transforming genes involved in colon tumor progression, we examined 23 colorectal carcinomas in patients with HNPCC in order to detect somatic mutations in K-ras and p53 genes. Using single strand conformation polymorphism followed by direct DNA sequencing, we detected 4 mutations in K-ras gene (17%) and 3 in p53 gene (13%) which change the aminoacid sequence of the protein p53. This is significantly lower than in sporadic cancer. Our data suggest that colon cancer in HNPCC might partly involve a distinct pathogenetic mechanism that involves other genes than those altered in sporadic tumors.

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