Genomic imbalances in AIDS-related lymphomas: relation with tumoral Epstein-Barr virus status.

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.