Genomic imbalances in AIDS-related lymphomas: relation with tumoral Epstein-Barr virus status.
| Autor: | Vaghefi P; Hospital Avicenne, University Paris 13, France., Martin A, Prévot S, Charlotte F, Camilleri-Broët S, Barli E, Davi F, Gabarre J, Raphael M, Poirel HA |
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| Jazyk: | angličtina |
| Zdroj: | AIDS (London, England) [AIDS] 2006 Nov 28; Vol. 20 (18), pp. 2285-91. |
| DOI: | 10.1097/QAD.0b013e328010ac5b |
| Abstrakt: | 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. |
| Databáze: | MEDLINE |
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