Activation of c-Ki-ras in human gastrointestinal dysplasias determined by direct sequencing of polymerase chain reaction products.

摘要: Activation of c-Ki-ras by point mutation within exon 1 was studied in 33 specimens dysplastic gastrointestinal lesions or cancers presumed to arise from dysplasia. Samples were obtained patients with underlying ulcerative colitis Barrett's esophagus, two diseases associated dysplasia and increased rates colonic esophageal adenocarcinoma, respectively. Genomic DNA amplified using primers bounding this the polymerase chain reaction. Polymerase reaction products analyzed direct dideoxy sequencing. Three mutations codon 13 found, all (two high-grade dysplasias one adenocarcinoma arising colitis). No observed second around codons 12, 13, 61 c-N-ras C-Ha-ras a partial sampling specimens. These data indicate that ras family protooncogene activation is an uncommon event at level malignant progression these disease states. Carcinogenesis esophagus may proceed via different pathways than sporadic colon cancer, perhaps involving loss inactivation suppressor genes.