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Multiple genetic lesions in acquired immunodeficiency syndrome-related
non-Hodgkin's lymphoma
P Ballerini, G Gaidano, JZ Gong, V Tassi, G Saglio, DM Knowles and R Dalla-Favera
Department of Pathology, College of Physicians & Surgeons, Columbia
University, New York, NY 10032.
Non-Hodgkin's lymphoma (NHL) develops in about 5% to 10% of acquired
immunodeficiency syndrome (AIDS) patients. The vast majority of AIDS- NHL
are clinically aggressive B-cell NHL that are histologically classified as
small noncleaved cell lymphoma (SNCCL), large cell immunoblastic
plasmacytoid lymphoma (LC-IBPL), and large noncleaved cell lymphoma
(LNCCL). In an attempt to understand the molecular pathogenesis of these
tumors, we have investigated the involvement of dominantly acting oncogenes
(c-myc, N-, K-, H-Ras), tumor suppressor genes (p53, RB1), and Epstein-Barr
virus (EBV) infection in 27 AIDS-NHL samples (16 SNCCL, 5 LC-IBP, and 6
LNCCL). The following lesions were detected in AIDS-NHL: EBV infection
(10/24; 41.6%), c-myc rearrangement (19/24; 79.1%), Ras mutation (4/27;
14.8%), and p53 loss/mutation (10/27; 37.0%). These lesions are not
uniformly distributed, but, rather, cluster with specific types of
AIDS-NHL: EBV infection is preferentially associated with LC-IBPL (4/4;
100%), while it is present in only a fraction of SNCCL (5/16; 31.2%) and
LNCCL (1/4; 25%); c-myc oncogene activation clusters with SNCCL (16/16;
100%), whereas it is less frequent in LC-IBPL (1/4; 25%) and LNCCL (2/4;
50%); p53 inactivation is restricted to SNCCL (10/16; 62.5%) and
consistently associated with c-myc activation. These data show that
AIDS-NHL are associated with multiple genetic lesions that involve both
proto- oncogenes and tumor suppressor genes and may accumulate in the
relatively short period of time (4 to 6 years) between human
immunodeficiency virus infection and AIDS-NHL development. These genetic
lesions differ in the various AIDS-NHL subtypes, suggesting the involvement
of distinct molecular pathway.
Volume 81,
Issue 1,
pp. 166-176,
01/01/1993
Copyright © 1993 by The American Society of Hematology
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