Activation of c-Ki-ras in Human Gastrointestinal Dysplasias Determined by Direct Sequencing of Polymerase Chain Reaction Products

Stephen J. Meltzer, Shrikant M. Mane, Patrick K. Wood, James H. Resau, Carnell Newkirk, John A. Terzakis, Burton I. Korelitz, Wilfred M. Weinstein, Samuel W. Needleman

Research output: Contribution to journalArticlepeer-review

Abstract

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-nu 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.

Original languageEnglish (US)
Pages (from-to)3627-3630
Number of pages4
JournalCancer Research
Volume50
Issue number12
StatePublished - Jun 15 1990
Externally publishedYes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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