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Bornkamm, G.W.

Epstein-Barr virus and its role in the pathogenesis of Burkitt's lymphoma: An unresolved issue.

Semin. Cancer Biol. 19, 351-365 (2009)

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Open Access Green as soon as Postprint is submitted to ZB.

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For several reasons Burkitt's lymphoma (BL) has become a paradigm in cancer research: for its particular geographical distribution, the presence of Epstein-Barr virus (EBV) in the cases in high incidence areas, and for the activation of the proto-oncogene c-myc by chromosomal translocation in one of the immunoglobulin gene loci. As c-MYC activates both, proliferation and apoptosis, at least two events have to cooperate in lymphomagenesis: Activation of c-MYC and a shift in the balance from apoptosis towards survival. Antigenic and/or polyclonal stimulation of the B cell receptor, genetic instability imposed by activation induced deaminase (AID), as well as the viral gene products EBNA1 and several small non-coding non-polyadenylated RNAs are the main factors suspected to play an important role in the pathogenesis of BL Despite intensive research, the role of the virus has remained largely elusive in the past decades, but the discovery of two viral microRNA clusters that are expressed in EBV associated tumors including BL has raised new hopes and expectations that EBV is going to reveal its mystery. This review focuses on the interplay between cellular and viral factors and puts special emphasis on mouse models and experimental cell culture systems that address these points.

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Publication type Article: Journal article

Document type Scientific Article

Corresponding Author

Keywords c-myc/Ig translocations; Apoptosis; Activation induced deaminase; Tonic B cell receptor signal; Malaria; HIV; EBNA1; EBER1 and EBER2; MicroRNAs; Mouse models

ISSN (print) / ISBN 1044-579X

e-ISSN 1096-3650

Journal Seminars in Cancer Biology

Quellenangaben Volume: 19, Issue: 6, Pages: 351-365

Publisher Saunders

Publishing Place Philadelphia, Pa.

Non-patent literature Publications

Reviewing status Peer reviewed

Institute(s) Institute of Clinical Molecular Biology and Tumor Genetics (K.MOLBI)