Journal of Clinical Oncology, Vol 18, Issue 21
(November), 2000: 3707-3721
© 2000 American Society for Clinical Oncology
Molecular Biology of Burkitt’s Lymphoma
By Jonathan L. Hecht,
Jon C. Aster
From the Departments of Pathology, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA.
Address reprint requests to Jon C. Aster, MD, Brigham and Women’s Hospital, 75 Francis St, Boston, MA 02115.
ABSTRACT
The diagnostic category of Burkitt’s lymphoma encompasses a closely related group of aggressive B-cell tumors that includes sporadic, endemic, and human immunodeficiency virus–associated subtypes. All subtypes are characterized by chromosomal rearrangements involving the c-myc proto-oncogene that lead to its inappropriate expression. This review focuses on the roles of c-myc dysregulation and Epstein-Barr virus infection in Burkitt’s lymphoma. Although the normal function of c-Myc remains enigmatic, recent data indicate that it has a central role in several fundamental aspects of cellular biology, including proliferation, differentiation, metabolism, apoptosis, and telomere maintenance. We discuss new insights into the molecular mechanisms of these c-Myc activities and their potential relevance to the pathogenesis of Burkitt’s lymphoma and speculate on the role of Epstein-Barr virus.
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