RESUMO
BACKGROUND: The pathologic heterogeneity of AIDS related lymphomas (ARL) reflects several pathogenic mechanisms: chronic antigenic stimulation, Epstein-Barr virus (EBV) infection, and genomic abnormalities. Genetic abnormalities, known to play a major role in lymphomas of non-immunocompromised patients, are not well characterized in ARL. OBJECTIVE: Characterization of the DNA copy number change (CNC) in ARL and comparison of our findings with tumoral EBV and immune status. DESIGN AND METHODS: We have studied by comparative genomic hybridization (CGH), 28 ARL well characterized for histopathologic, clonality and EBV findings. RESULTS: DNA-CNC were detected in 50% of cases. Gains of chromosomal material were much more frequent than losses and involved chromosomes 9p, 11q, 12q, 17q, and 19q recurrently. DNA-CNC tended to be more frequent in EBV-positive lymphomas with latency type II/III than in EBV-positive latency I or EBV-negative lymphomas. Most chromosomal regions affected in HIV-related lymphoma were similar to those already reported in HIV-negative lymphomas. CONCLUSION: This CGH study allowed the identification of non-random chromosomal alterations in ARL. The results suggested an inverse relationship between EBV infection (latency II/III), associated with deep acquired immune suppression, and the number of chromosomal alterations which may be explained by a direct role of viral proteins in lymphomagenesis by activation of signalling pathways without needing several genomic alterations.