Point Mutation of c‐Ki‐ras Oncogene in Gastric Adenoma and Adenocarcinoma with Tubular Differentiation

The presence of point mutation at codons 12,13 and 61 of the c‐Ki‐ras oncogene was investigated in 7 cases of gastric adenoma and 35 cases of gastric adenocarcinoma using DNA samples from formalin‐fixed and paraffin‐embedded tissues. Oligonucleotides encompassing the three codons were amplified by u...

Full description

Saved in:
Bibliographic Details
Published in:Cancer science 1991-03, Vol.82 (3), p.308-314
Main Authors: Kihana, Toshimasa, Tsuda, Hitoshi, Hirota, Teruyuki, Shimosato, Yukio, Sakamoto, Hiromi, Terada, Masaaki, Hirohashi, Setsuo
Format: Article
Language:English
Subjects:
Adenocarcinoma
Adenocarcinoma - genetics
Adenocarcinoma - pathology
Adenoma
Adenoma - genetics
Adenoma - pathology
Aged
Amino Acid Sequence
Antisense Elements (Genetics)
Base Sequence
Biological and medical sciences
Carcinogenesis
Carcinoma
Cell Differentiation
Codon - genetics
Codons
c‐Ki‐ras oncogene
Female
Gastric cancer
Gastroenterology. Liver. Pancreas. Abdomen
Genes, ras
Histogenesis of gastric cancer
Human gastric cancer
Humans
Hybridization
Male
Medical sciences
Middle Aged
Molecular Sequence Data
Mutation
Nucleic Acid Hybridization
Oligonucleotide Probes
Oligonucleotides
Oncogenes
Paraffin
Point mutation
Polymerase chain reaction
Polymerase Chain Reaction - methods
Stomach Neoplasms - genetics
Stomach Neoplasms - pathology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The presence of point mutation at codons 12,13 and 61 of the c‐Ki‐ras oncogene was investigated in 7 cases of gastric adenoma and 35 cases of gastric adenocarcinoma using DNA samples from formalin‐fixed and paraffin‐embedded tissues. Oligonucleotides encompassing the three codons were amplified by using the polymerase chain reaction (PCR), and then examined for point mutation by the selective oligonucleotide hybridization technique. Point mutation was detected in three of the 7 adenomas (43%) and three of the 35 carcinomas (9%). All the gastric adenomas showed the histology of tubular adenoma, being very similar to that of colonic adenoma. The 35 cases of gastric adenocarcinoma were classified into 17 cases of differentiated type and 17 cases of undifferentiated type including signet‐ring cell carcinoma. The point mutation of c‐Ki‐ras oncogene was detected only in the differentiated type (3/17, 18%), and there was no case with point mutation in the undifferentiated type. These results suggest that the genetic mechanism of carcinogenesis differs between the differentiated type and the undifferentiated type of gastric adenocarcinoma, and also that c‐Ki‐ros activation is possibly involved in a relatively early step of the “adenoma‐carcinoma sequence,” which leads to the development of a portion of differentiated adenocarcinomas in the stomach.
ISSN:0910-5050
1347-9032
1349-7006
1876-4673
DOI:10.1111/j.1349-7006.1991.tb01847.x