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Bax and Bcl‐2 protein expression in gastric precancerous lesions: Immunohistochemical study
Author(s) -
ANAGNOSTOPOULOS GEORGE K,
STEFANOU DIMITRIOS,
ARKOUMANI EVDOKIA,
SAKORAFAS GEORGE,
PAVLAKIS GEORGE,
ARVANITIDIS DIMITRIOS,
TSIANOS EPAMEIDAS,
AGNANTIS NIKI J
Publication year - 2005
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/j.1440-1746.2005.04057.x
Subject(s) - intestinal metaplasia , dysplasia , atrophic gastritis , immunohistochemistry , medicine , carcinogenesis , apoptosis , biopsy , pathology , metaplasia , gastritis , chronic gastritis , gastric mucosa , bcl 2 associated x protein , cancer research , cancer , stomach , gastroenterology , biology , programmed cell death , caspase 3 , biochemistry
Background and Aims: Bcl‐2 protein prolongs cell survival in the face of classical apoptotic stimuli, and is considered to be a suppressor of apoptosis. Bax plays a key role in apoptosis by accelerating cell death after an apoptotic stimulus. The aim of our study was to determine the roles of the Bax proapoptotic gene and the Bcl‐2 antiapoptotic gene in the carcinogenesis of gastric cancer. Methods: One hundred and forty‐five gastric biopsy specimens of chronic gastritis, atrophic gastritis, intestinal metaplasia and gastric dysplasia were studied. Using immunohistochemical methods, Bax and Bcl‐2 protein expression was observed. Results: Bax was expressed in epithelial cells in all cases of chronic gastritis. Bax was not detected in 26% of specimens of atrophic gastritis. As intestinal metaplasia develops, Bax is further suppressed. In biopsy samples with dysplasia, Bax expression was demonstrated only in 12% of biopsy samples. Although Bcl‐2 protein was not detected in chronic gastritis, aberrant expression was found in gastric epithelial intestinal metaplasia and dysplasia. Conclusions: The suppression of Bax and overexpression of Bcl‐2 protein is an early event in gastric tumorigenesis, before gastric dysplastic changes occur.