Search for Correlations between K-ras Oncogene Activation and Pathology, in Sporadic and Familial Colonic Adenomas
The activation of K-ras oncogene by point mutation at its 12th codon has been reported as a molecular marker of tumor progression in colonic neoplasias (early event, correlated with the increasing size of adenomas, but not with dysplasia)1. The overall frequency of K-ras point mutations has probably been underestimated by the usual former techniques. Direct sequencing of PCR amplified K-ras oncogene demonstrated that 75% and 65% adenomas and adenocarcinomas, respectively, harbored a mutated allele of K-ras at codon 122. We described a new sensitive method for an easier detection of this mutation, based upon the introduction of an artificial restriction site in a modified primer for selective in vitro amplification3. This sensitive method, connected with the feasibility of PCR amplification of DNA in formalin-fixed and paraffin-embedded tissues, prompted us to reevaluate the frequency of K-ras point mutations at codon 12 in both sporadic and familial colonic adenomas.
KeywordsNucleic Acid Research Familial Polyposis Coli Colonic Neoplasia Homozygous Wild Type Sporadic Adenoma
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