title: Genomic imbalances in AIDS-related lymphomas: relation with tumoral Epstein-Barr virus status.
abstract: 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.
  
  
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Hospital Avicenne, University Paris 13, France.
authors.forename: Parissa
authors.initials: P
authors.lastname: Vaghefi
authors.forename: Antoine
authors.initials: A
authors.lastname: Martin
authors.forename: Sophie
authors.initials: S
authors.lastname: Prévot
authors.forename: Frédéric
authors.initials: F
authors.lastname: Charlotte
authors.forename: Sophie
authors.initials: S
authors.lastname: Camilleri-Broët
authors.forename: Elisabeth
authors.initials: E
authors.lastname: Barli
authors.forename: Frédéric
authors.initials: F
authors.lastname: Davi
authors.forename: Jean
authors.initials: J
authors.lastname: Gabarre
authors.forename: Martine
authors.initials: M
authors.lastname: Raphael
authors.forename: Hélène A
authors.initials: HA
authors.lastname: Poirel
mesh_terms: D000328:Adult; D000368:Aged; D002051:Burkitt Lymphoma / Q000150:complications / Q000235:genetics / Q000276:immunology; D018791:CD4 Lymphocyte Count; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D002869:Chromosome Aberrations; D002877:Chromosomes, Human / Q000235:genetics; D002999:Clone Cells / Q000276:immunology; D004279:DNA, Viral / Q000235:genetics; D020031:Epstein-Barr Virus Infections / Q000150:complications / Q000235:genetics* / Q000276:immunology; D005260:Female; D005814:Genes, Viral / Q000235:genetics / Q000276:immunology; D006801:Humans; D016483:Lymphoma, AIDS-Related / Q000150:complications / Q000235:genetics* / Q000276:immunology; D016403:Lymphoma, Large B-Cell, Diffuse / Q000150:complications / Q000235:genetics / Q000276:immunology; D016411:Lymphoma, T-Cell, Peripheral / Q000150:complications / Q000235:genetics / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009693:Nucleic Acid Hybridization / Q000379:methods
chemical_list: D004279:DNA, Viral