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

Activation of c-Ki-ras by point mutation within exon 1 was studied in 33 specimens of dysplastic gastrointestinal lesions or of cancers presumed to arise from dysplasia. Samples were obtained from patients with underlying ulcerative colitis or Barrett's esophagus, two diseases associated with d...

Full description

Saved in:
Bibliographic Details
Published in:Cancer research (Chicago, Ill.) Ill.), 1990-06, Vol.50 (12), p.3627-3630
Main Authors: MELTZER, S. J, MANE, S. M, WOOD, P. K, RESAU, J. H, NEWKIRK, C, TERZAKIS, J. A, KORELITZ, B. I, WEINSTEIN, W. M, NEEDLEMAN, S. W
Format: Article
Language:English
Subjects:
Adenocarcinoma - genetics
Biological and medical sciences
Codon
Colitis, Ulcerative - genetics
DNA, Neoplasm - analysis
Esophageal Neoplasms - genetics
Esophagus - analysis
Esophagus - pathology
Gastroenterology. Liver. Pancreas. Abdomen
gastrointestinal tract
Genes, ras
Humans
Medical sciences
Mutation
Other diseases. Semiology
Polymerase Chain Reaction
Stomach. Duodenum. Small intestine. Colon. Rectum. Anus
ulcerative colitis
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Activation of c-Ki-ras by point mutation within exon 1 was studied in 33 specimens of dysplastic gastrointestinal lesions or of cancers presumed to arise from dysplasia. Samples were obtained from patients with underlying ulcerative colitis or Barrett's esophagus, two diseases associated with dysplasia and increased rates of colonic or esophageal adenocarcinoma, respectively. Genomic DNA was amplified using primers bounding this exon in the polymerase chain reaction. Polymerase chain reaction products were analyzed by direct dideoxy sequencing. Three point mutations in codon 13 of c-Ki-ras were found, all in colonic specimens (two high-grade dysplasias and one adenocarcinoma arising in ulcerative colitis). No point mutations were observed in the second exon of c-Ki-ras or in and around codons 12, 13, and 61 of c-N-ras and C-Ha-ras in a partial sampling of the specimens. These data indicate that ras family protooncogene activation is an uncommon event at this level of malignant progression in these disease states. Carcinogenesis in ulcerative colitis and Barrett's esophagus may proceed via different pathways than in sporadic colon cancer, perhaps involving loss or inactivation of suppressor genes.
ISSN:0008-5472
1538-7445