p53 mutations and microsatellite instabilities in the subtype of intestinal metaplasia of the stomach.
To investigate the potential implication of the subtype of intestinal metaplasia in the progression to the gastric carcinoma, we analyzed the mutations of the p53 gene and microsatellite instability (MSI) both in the complete type (type I) and in the sulphomucin-secreting incomplete type (type III) intestinal metaplasia located adjacent to the gastric carcinoma. p53 mutations were observed in 13.3% of type I, in 6.6% of type III intestinal metaplasia, and in 40% of gastric carcinoma. The difference between p53 mutations observed in type I and type III intestinal metaplasia was not statistically significant. No identical mutation of the p53 gene was found in the intestinal metaplasia and carcinoma specimens from the patients. There was no case of intestinal metaplasia showing MSI. In gastric carcinomas, MSI was observed in six cases (40%). The cases harboring BAT-26 instability did not have the mutation of the p53 gene. These data suggest that intestinal metaplasia adjacent to gastric carcinoma, irrespective of its subtype, do not have the genetic alterations as showing in their carcinoma tissues.
Kim
Sung Soo
SS
Division of Gastroenterology, Department of Internal Medicine, College of Medicine, Catholic University of Korea, Seoul, Korea.
Bhang
Choon Sang
CS
Min
Ki Ouk
KO
Chae
Hiun Suk
HS
Choi
Sang Wook
SW
Lee
Chang Don
CD
Lim
Keun Woo
KW
Chung
In Sik
IS
Park
Doo Ho
DH
D002277:Carcinoma / Q000235:genetics / Q000473:pathology; D005091:Exons; D016158:Genes, p53; D006801:Humans; D008679:Metaplasia / Q000235:genetics / Q000473:pathology; D018895:Microsatellite Repeats; D009154:Mutation; D011230:Precancerous Conditions; D013270:Stomach / Q000473:pathology*; D013274:Stomach Neoplasms / Q000235:genetics / Q000473:pathology; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism
D016159:Tumor Suppressor Protein p53