EXPRESSION OF Bcl-2, Bcl-X, Bax AND p53 PROTEINS IN EPSTEIN BARR VIRUS POSITIVE AND NEGATIVE HODGKIN'S LYMPHOMA
DOI:
https://doi.org/10.5457/ams.v37i1.60Keywords:
Hodgkin’s lymphoma, bcl-2, bcl-X, bax, p53, Epstein Barr virusAbstract
Introduction: Reed-Sternberg cells are typical for Hodgkin's lymphoma. They are transformed post-germinative B cells that not achieve successful immunoglobulin gene rearrangement, and therefore predetermined to apoptosis. Several mechanisms, including latent Epstein Barr virus infection (EBV), enable survival of Hodgkin's lymphoma neoplastic cells. Goal of this study is correlation of Hodgkin's lymphoma EBV status with expression of apoptosis associated proteins in neoplastic cells. Association of Hodgkin's lymphoma with EBV was determined by chromogenic hybridization in situ detection of EBER1 and EBER2. Material and Methods: Presence of apoptosis associated proteins: bcl-2, bcl-X, bax and p53, were determined immunohistochemicaly in neoplastic cells of 39 EBV positive, and 42 EBV negative Hodgkin's lymphomas. Results: Bcl-2 protein was detected in neoplastic cells in 22.2%, Bcl-X in 87.7%, Bax in 80.2% and p53 in 67.8% of cases. In 44.4% cases simultaneous presence of Bcl-X, Bax and p53 protein was detected. Bcl-X is significantly more produced in mixed cellularity, and Bcl-X and Bax in nodular sclerosis. No significant difference was found in production of all four proteins between EBV positive and negative Hodgkin's lymphoma. Median intensity of p53, Bcl-2, Bcl-X and Bax staining of complete examined group, EBV positive and EBV negative group show significant difference, except between Bcl-X and Bax. Discussion: Survival capacity of Hodgkin's lymphoma neoplastic cells depends on activity of numerous regulators of programmed cell death. Expression of bcl-2, bcl-X, bax and p53 proteins is not different in neoplastic cells of EBV positive and EBV negative Hodgkin's lymphoma.
Downloads
Issue
Section
License
Copyright transfer
The listed authors warrant that they are the authors and sole owners of the submitted manuscript. The authors also warrant that the work is original; that it has not been previously published in print or electronic format and is not under consideration by another publisher or electronic medium; that it has not been previously transferred, assigned, or otherwise encumbered; and that the authors have full power to grant such rights. With respect to the results of this work, the manuscript of this or substantially similar content will not be submitted to any other journal until the review process in the Acta Medica Salinianana has been officially completed (acceptance or rejection of the manuscript). The paper will not be withdrawn from the review process by the Acta Medica Saliniana Editorial Board until the review process is completed. The authors will comply with the requests of the Acta Medica Saliniana Editors and reviewers to improve the paper for publication. The eventual disagreements will be submitted in a written form; the authors are aware that the disagreement(s) with the Acta Medica Saliniana requests may result in the rejection of the manuscript. The authors hereby grant to the Acta Medica Saliniana the right to edit, revise, abridge, and condense the manuscript. If the manuscript is accepted for publication in the Acta Medica Saliniana, the authors hereby transfer the copyright of the paper to the Acta Medica Saliniana. The authors permit the Acta Medica Saliniana to allow third parties to copy any part of the journal without asking for permission, provided that the reference to the source is given. For papers with more than one author: All other co-authors agree to allow the corresponding author to make decisions regarding prepublication release of the information in the paper to the media, federal agencies, or both.
