BACKGROUND: bcl-2 protein encoded by the proto-oncogene bcl-2 confers to the cell a survival advantage by inhibiting apoptosis. Its aberrant expression has been reported in lymphomas and lung carcinoma. To determine if bcl-2 plays a role in the gastric carcinogenic sequence, the authors studied bcl-2 expression in gastric epithelial dysplasia (GED) and chronic atrophic gastritis with intestinal metaplasia (CAG-IM). METHODS: Immunohistochemical staining using monoclonal bcl-2 protein antibody, clone 124, was performed on archival material. RESULTS: bcl-2 staining was seen in 13 of 16 GEDs (81%). The staining was heterogeneous, suggesting that within the dysplastic epithelium, some cellular clones may have a survival advantage. When noted, the staining in IM was located in the proliferative zone, but some positivity could also be noted higher up along the cellular escalator. Normal gastric mucosa stained in the proliferative zone. CONCLUSIONS: The authors demonstrated that bcl-2 expression is noted in GED as well as in the extended proliferative zone of CAG-IM. This suggests that prolonged cell survival due to inhibition of apoptosis is instrumental in addition to increased cellular proliferation in the altered cellular homeostasis of the gastric carcinogenic sequence. Whether bcl-2 protein aberrant expression is an independent process or inherent to immaturity of the cells produced by the increased proliferation awaits further studies.
BACKGROUND:bcl-2 protein encoded by the proto-oncogene bcl-2 confers to the cell a survival advantage by inhibiting apoptosis. Its aberrant expression has been reported in lymphomas and lung carcinoma. To determine if bcl-2 plays a role in the gastric carcinogenic sequence, the authors studied bcl-2 expression in gastric epithelial dysplasia (GED) and chronic atrophic gastritis with intestinal metaplasia (CAG-IM). METHODS: Immunohistochemical staining using monoclonal bcl-2 protein antibody, clone 124, was performed on archival material. RESULTS:bcl-2 staining was seen in 13 of 16 GEDs (81%). The staining was heterogeneous, suggesting that within the dysplastic epithelium, some cellular clones may have a survival advantage. When noted, the staining in IM was located in the proliferative zone, but some positivity could also be noted higher up along the cellular escalator. Normal gastric mucosa stained in the proliferative zone. CONCLUSIONS: The authors demonstrated that bcl-2 expression is noted in GED as well as in the extended proliferative zone of CAG-IM. This suggests that prolonged cell survival due to inhibition of apoptosis is instrumental in addition to increased cellular proliferation in the altered cellular homeostasis of the gastric carcinogenic sequence. Whether bcl-2 protein aberrant expression is an independent process or inherent to immaturity of the cells produced by the increased proliferation awaits further studies.
Authors: Y Maor-Kendler; G Gabay; J Bernheim; T Naftali; I Lesin; G Leichtman; I Pomeranz; B Novis Journal: Dig Dis Sci Date: 1999-04 Impact factor: 3.199