The expression of syndecan-1, tenascin-C, tumor-associated trypsin inhibitor (TATI), p53, p21 and bcl-2 was analyzed by immunohistochemistry informalin-fixed, paraffin-embedded specimens from 337 patients with gastric cancer.
Thus, Bcl-2 may play a very important role in carcinogenesis of gastric cancer and its knockdown may offer a new potential gene therapy approach for human gastric cancer in future.
To investigate the relationship between Helicobacter pylori (H.pylori) infection and the expressions of the p53, Rb, c-myc, bcl-2 and hTERT mRNA in a series of diseases from chronic gastritis (CG), intestinal metaplasia type I or II(IMI-II), intestinal metaplasia type III (IMIII), mild or modest dysplasia (DysI-II), severe dysplasia (DysIII) to gastric cancer(GC) and to elucidate the mechanism of gastric carcinogenesis relating to H.pylori infection.
Infection with H. pylori, especially that expressing CagA-positivity, is primum movens in developing GC and MALT-lymphoma and the upregulation of growth factors, particularly of gastrin, and COX-2 and dysregulation of the Bax/Bcl-2 system seem to contribute to gastric cancerogenesis.
Although expression of bcl-2 has been shown to correlate with a better prognosis in breast and lung carcinomas, information concerning the prognostic role of bcl-2 in gastric cancer on a considerable number of tumours is still lacking.
Our finding suggests that reduction of bcl-2 protein in gastric cancers, and possibly also in a variety of other tumors, may be a novel and rational approach to improve photosensitivity and the treatment outcome.
In addition, K-ras mutations, c-erbB-2 gene amplification, loss of heterozygosity (LOH) and mutations of the APC gene, LOH of the bcl-2 gene, and LOH at the DCC locus are preferentially associated with well differentiated gastric cancer.
On the other hand, 24% (5/21) of poorly differentiated stomach cancers overexpressed bcl-2 gene, whereas no overexpression was detected in well differentiated stomach cancer.