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JNCI Monographs 1998 1998(23):95-100;
© 1998 by Oxford University Press
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Journal of the National Cancer Institute Monographs, No. 23, 95-100, 1998
© 1998 Oxford University Press

Genetic Basis of Acquired Immunodeficiency Syndrome-Related Lymphomagenesis

Gianluca Gaidano, Antonino Carbone, Riccardo Dalla-Favera*

* Affiliations of authors: G. Gaidano, Division of Internal Medicine, Department of Medical Sciences, University of Torino at Novara, Italy; A. Carbone, Division of Pathology, I.N.R.C.C.S., Centro di Riferimento Oncologico, Aviano, Italy; R. Dalla-Favera, Division of Oncology, Department of Pathology, College of Physicians & Surgeons, Columbia University, New York, NY

Correspondence to: Riccardo Dalla-Favera, M.D., Division of Oncology, Department of Pathology, College of Physicians & Surgeons, Columbia University, 630 W. 168th St., New York, NY 10032. E-mail: rd10{at}columbia.edu.

The molecular pathogenesis of systemic acquired immunodeficiency syndrome (AIDS)-related non-Hodgkin's lymphomas (AIDS-NHL) is a complex process involving both host factors and the accumulation of genetic lesions within the tumor clone. On the basis of the pattern of molecular lesions involved in these tumors, several distinct pathogenetic pathways can be presently identified in AIDS-related lymphomagenesis. These pathways selectively associate with the different clinicopathologic variants of AIDS-NHL. AIDS-related Burkitt's lymphoma is characterized by activation of c-MYC in all cases, disruption of p53 in 60% of the cases, and infection by Epstein-Barr virus (EBV) in 30% of the cases. AIDS-related diffuse large-cell lymphoma harbor frequent EBV infection (80%) and, in 20% of the cases, BCL-6 rearrangements. Finally, the pathogenesis of AIDS-related body cavity-based lymphoma involves infection by human herpesvirus-8 in all cases and frequently also the co-infection by EBV.


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