Immunohistochemical Analysis of BAD Protein Expression in Gastric Carcinomas.
10.5230/jkgca.2003.3.2.75
- Author:
Nam Jin YOO
1
;
Jong Woo LEE
;
Won Sang PARK
;
Jung Young LEE
;
Sug Hyung LEE
Author Information
1. Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, Korea. suhulee@catholic.ac.kr
- Publication Type:Original Article
- Keywords:
Stomach cancer;
Gastric carcinoma;
BAD;
Apoptosis
- MeSH:
Adenocarcinoma;
Apoptosis;
Apoptosis Regulatory Proteins;
bcl-Associated Death Protein*;
Humans;
Immunohistochemistry;
Stomach Neoplasms
- From:Journal of the Korean Gastric Cancer Association
2003;3(2):75-79
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Evidence exists that dysregulation of apoptosis is involved in the pathogenesis of cancer development. The Bcl-XL/Bcl-2-associated death promoter (BAD), a member of the Bcl-2 family, is a critical regulatory component of the intrinsic cell-death pathway that exerts its pro-apoptotic effect upon heterodimerization with anti-apoptotic proteins Bcl-2 and Bcl-XL. Expression of the BAD protein has been reported in several cancer types, but not in stomach cancer. The aim of this study was to explore the expression status of the BAD protein in gastric carcinomas. MATERIALS AND METHODS: In the current study, we analyzed the expression of the BAD protein in 60 advanced gastric adenocarcinomas by using immunohistochemistry and a tissue microarray approach. RESULTS: Immunopositivity (defined as > or =30%) was observed for the BAD protein in 57 (95%) of the 60 cancers. Normal gastric mucosal cells showed weaker expressions of the BAD protein than gastric carcinomas. CONCLUSION: Taken together, these results suggest that stomach cancer cells in vivo may need BAD protein expression for apoptosis. Also, the higher expression of the BAD protein in stomach cancer cells than in normal gastric mucosal cells suggests that apoptosis might be easily triggered in susceptible stomach cancer cells, thereby producing selective pressure to make more apoptosis-resistant cells during tumor development.
