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Journal of Tropical Pediatrics 1990 36(3):114-120; doi:10.1093/tropej/36.3.114
© 1990 by Oxford University Press
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Burkitt's Lymphoma and the Role of Epstein–Barr Virus

Jayne A. Goldstein, BSc and R. L. Bernstein, PhD

Department of Biological Sciences, San Francisco State University 1600 Holloway Avenue, San Francisco, USA

Correspondence: Jayne A. Goldstein, Department of Pathology, School of Medicine, University of Washington, Seattle, WA 98195, USA.

Burkitt's lymphoma is the most common childhood cancer in Africa. Most prevalent in areas endemic for malaria, the disease, a malignant growth of lymphoid tissue, usually presents itself as a large tumour of the jaw. When first characterized in the 1950s, the lymphoma was thought to spread by some infectious agent. Subsequent research indicates that the frequent involvement of an infectious agent is but one factor in a more complex aetiology. Today, Burkitt's lymphoma is considered an example of multistep carcinogenesis. Each step in the process results from a different agent. The agent in the first step is the Epstein–Barr virus, which infects B cells of the immune system causing a proliferation of these cells. The second step, malarial infection, furthers the proliferation of B cells providing a large population of cells available for a chromosomal translocation which represents the third step in the formation of the lymphoma. The chromosomal translocation places a cancer causing gene, c-myc, in close proximity to an active antibody-encoding its proliferation resulting in a cell capable of unlimited growth which serves as the nucleus of a B cell lymphoma.


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