Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10415 (Bcl-2)
 33,771 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study investigates the extent of apoptosis in 53 testicular and ovarian germ cell tumors by using the in situ 3'-end DNA labeling technique on tumor sections. The tumors were also immunostained with antibodies to the p53 and bcl-2 proteins. The extent of apoptosis was highest in embryonal carcinoma (mean, 2.9%) followed by seminoma (mean, 1.1%), choriocarcinoma (mean, 0.7%) and immature teratoma (mean, 0.7%). In individual components of the mixed germ cell tumors the apoptotic index was in the same range as in the corresponding pure germ cell tumors. Mature teratomas rarely contained any apoptotic cells. Sixty-two percent of all the tumors expressed p53 protein. p53 expression was quantitatively strongest in embryonal carcinomas which also showed the highest level of apoptosis. Bcl-2 positivity could only be detected in some mesenchymal and epithelial components of the immature and mature teratomas; embryonal carcinomas, seminomas, or choriocarcinomas did not express bcl-2 at all. Our results show that the level of apoptosis in germ cell tumors associates with the histological type of the neoplastic component independent of whether it is singly present or a component of a mixed germ cell tumor. The results suggest that the quantity of p53 expression may contribute to the level of apoptosis in different tumor groups.
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PMID:Extent of apoptosis in relation to p53 and bcl-2 expression in germ cell tumors. 891 34

Apoptosis plays a crucial role in the regulation of spermatogenesis in male germ cells and is, at least in part, modulated by Bcl-2, Bax, and the Fas pathway. Seminomas have a favourable outcome and respond to radio-/chemotherapy with an increased rate of apoptosis. The expression of Bax, Bcl-2, Fas and Fas-ligand (Fas-L) in human seminoma was evaluated and correlated with the apoptotic index. Twenty-nine classical seminomas were examined by immunohistochemistry and Western blotting using antibodies against Bax, Bcl-2, Fas and Fas-L. Apoptosis was detected by in-situ end-labeling of fragmented DNA and the apoptotic index (AI) was determined. Expression of Fas was found in 26 (89.7%) of Fas-L in 24 seminomas (82.2%); none of the tumours expressed Bcl-2. No correlation between the AI and Fas, Fas-L or Bcl-2 expression was found. Bax was demonstrated in 20/29 tumours (69%). Bax-positive tumours showed an increased AI of 4.75 +/- 2.38% in contrast to 2.60 +/- 1.23% of the Bax-negative tumours (P = 0.002). The number of Bax-positive tumour cells and apoptotic cells revealed a significant correlation using chi2-test (P = 0.04) and linear regression (r = 0.54, P = 0.001). Therefore, Bax seems to play a determinant role in the modulation of apoptosis in human seminoma that may be linked to a favourable outcome.
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PMID:Bax, Bcl-2, fas and Fas-L antigen expression in human seminoma: correlation with the apoptotic index. 1258 39

Immunocytochemical study of 40 germ cell cancers, 31 bladder cancers and 27 squamous head and neck cancers using monoclonal antibodies (Mab) specific for p53, Bcl-2 and HSP70 was carried out. The results showed that 89% of germ cell cancer compared to 7% of bladder and 2% of squamous head and neck cancers were positive for p53 using Mab 240. In contrast only 60% of germ cell cancers (20% strong) but 100% of bladder (80% strong) and head and neck (75% strong) were positive for Bcl-2. There was a higher p53 positivity for the more chemoradiosensitive seminoma (82%, n=17) compared to non-seminoma (33%, n=6) and the inverse for Bcl-2 (53% vs. 83%). Taken together with emerging data that the putative stem cell for all germ cell cancers, the tetraploid pachytene primary spermatocyte normally expresses p53, these results support the view that near tetraploid overexpression of functional p53 in germ cell cancer may be a factor in why germ cell cancers are more chemosensitive than the common adult cancers. They also highlight the need for better understanding of the cell cycle check points during meiosis as possible molecular targets that would increase the chemosensitivity of non-germ cell cancers.
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PMID:Tetraploid arrest with overexpressed non-mutated p53 in germ cell cancers. 2152 47