Genotyping and Phenotyping of p53' Mutation in Dysplastic Epithelial Lesion of The Stomach

Yoon, Chong Mann; Rew, Jong Sun; Choi, Sung Kyu; Koo, Cheol; Kim, Tai Doo; Juhng, Sang Woo

Abstract

BACKGROUND AND AIMS: Gastric dysplasia or flat adenoma is regarded as a premalignant lesion in clinical practice. However, it is not clear yet whether the molecular events in colorectal adenomacarcinoma sequence are involved in the possible gastric dysplasia-carcinoma relationship. In this study, p53 mutation, the most common genetic alteration in human malignancies, was investigated in dysplastic epithelial lesions of the stomach by means of polymerase chain reaction-single strand confarmational polymarphism (PCR-SSCP) and immunohistochemistry.
METHODS
DNA was extracted from the paraffin-embedded tissue of 34 cases and served as template for PCR of exons 4, 5/6, 7 and 8/9. Among the 34 cases, 24 cases yielded PCR products for at least one of the exons and then, were subjected to SSCP: 21 cases for exon 4, 15 cases for exon 5/6, 23 cases for exon 7 and 18 cases for exon 8/9. The same paraffin-embedded tissue of the 24 cases was also used for immunohistochemisry of p53 protein. Normel full-term placental tissue and gastric carcinoma tissue served as control for wild type and mutant p53 gene or protein, respectively.
RESULTS
Histopathologically, 14 cases of dyplasia of moderate degree, 9 cases of rnoderate to severe degree and 1 case of severe degree were observed. By PCR-SSCP, only one case deonstrated an aberrant band of exon 7 in addition to the wild type bands of placental tissue. Immunocytochemistry revealed focal positivity in three cases of moderate dysplasia and diffuse positivity in one case of moderate to severe dysplasia, the case of mutant exon 7 shown by PCR-SSCP,
CONCLUSIONS
The low incidence of p53 mutation in gastric dysplasia suggest that p53 mutation does not play a major role in pathogenesis of dysplasia, and the mutation may occur in advanced stage of dysplasia or in carcinoma stage.