Immunodetection of apoptosis-regulating proteins in lymphomas from patients with and without human immunodeficiency virus infection
Autor: | Schlaifer, D., Krajewski, S., Galoin, S., Rigal-Huguet, F., Laurent, G., Massip, P., Pris, J., Delsol, G., Reed, J. C., Brousset, P. |
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Jazyk: | angličtina |
Rok vydání: | 1996 |
Předmět: |
Cytoplasm
Lymphoma Non-Hodgkin Nuclear Proteins Apoptosis Lymphoma T-Cell Hodgkin Disease Immunohistochemistry immune system diseases hemic and lymphatic diseases HIV Seronegativity Proto-Oncogene Proteins Biomarkers Tumor Humans Tumor Suppressor Protein p53 In Situ Hybridization Research Article Lymphoma AIDS-Related |
Popis: | The expression of the apoptosis-regulating genes Bcl-2, Bcl-x, Bax, Mcl-1, and p53 analyzed in 4 cases of human immunodeficiency virus (HIV)-associated Hodgkin's disease, in 36 cases of HIV-related non-Hodgkin's lymphomas (NHLs), and in 109 cases of non-HIV-related NHLs by using immunohistochemistry. HIV-associated Hodgkin's disease samples were positive for all markers. For the HIV-related NHL samples, 36, 66, 88, 100, and 94% of the cases were Bcl-2, Bcl-x, Bax, Mcl-1, and p53 were found to be expressed in 69, 65, 82, 83, and 42%, respectively. No significant differences were observed in Bax and Mcl-1 staining between HIV-unrelated NHLs of B cell and T cell types. In contrast, Bcl-2 was positive in 66/79 (83%) and 10/30 (33%) of B cell and T cell HIV-unrelated NHLs, respectively (P2 < 0.001). Peculiar patterns were observed for hairy cell leukemia (Bax+, Bcl-2+, Mcl-1-) and for anaplastic large cell lymphoma (Bax+, Mcl-1+, Bcl-2-) in HIV-unrelated NHLs. Of interest, all cases with a positive expression of Bax were also found to express either Mcl-1 and/or Bcl-2, suggesting that Mcl-1 and Bcl-2 may counteract the pro-apoptosis function of Bax in vivo by protein-protein interaction within the tumor cell, as demonstrated previously in vitro. These results suggest that apoptosis regulation may have a role in the pathogenesis of some HIV-related and HIV-unrelated NHLs. |
Databáze: | OpenAIRE |
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