TY - JOUR
T1 - Genome wide DNA-profiling of HIV-related B-cell lymphomas
AU - Capello, Daniela
AU - Scandurra, Marta
AU - Poretti, Giulia
AU - Rancoita, Paola M.V.
AU - Mian, Michael
AU - Gloghini, Annunziata
AU - Deambrogi, Clara
AU - Martini, Maurizio
AU - Rossi, Davide
AU - Greiner, Timothy C.
AU - Chan, Wing C.
AU - Ponzoni, Maurilio
AU - Moreno, Santiago M.
AU - Piris, Miguel A.
AU - Canzonieri, Vincenzo
AU - Spina, Michele
AU - Tirelli, Umberto
AU - Inghirami, Giorgio
AU - Rinaldi, Andrea
AU - Zucca, Emanuele
AU - Favera, Riccardo D.
AU - Cavalli, Franco
AU - Larocca, Luigi Maria
AU - Kwee, Ivo
AU - Carbone, Antonino
AU - Gaidano, Gianluca
AU - Bertoni, Francesco
PY - 2010/1
Y1 - 2010/1
N2 - Non-Hodgkin lymphomas (NHL) represent a frequent complication of human immunodeficiency virus (HIV) infection. To elucidate HIV-NHL pathogenesis, we performed a genome-wide DNA profiling based on a single nucleotide polymorphism-based microarray comparative genomic hybridization in 57 HIV-lymphomas and, for comparison, in 105 immunocompetent diffuse large B-cell lymphomas (IC-DLBCL). Genomic complexity varied across HIV-NHL subtypes. HIV-Burkitt lymphoma showed a significantly lower number of lesions than HIV-DLBCL (P = 0·032), whereas the median number of copy number changes was significantly higher in Epstein-Barr virus negative (EBV-) HIV-DLBCL (42·5, range 8-153) compared to EBV+ cases (22; range 3-41; P = 0·029). Compared to IC-DLBCL, HIV-DLBCL displayed a distinct genomic profile with no gains of 18q and specific genetic lesions. Fragile sites-associated genes, including FHIT (FRA3B), WWOX (FRA16D), DCC (FRA18B) and PARK2 (FRA6E) were frequently inactivated in HIV-NHL by interstitial deletions, and a significantly higher prevalence of FHIT alterations was observed in HIV-DLBCL compared to IC-DLBCL. The same genes involved by fragile site deletions were also frequently affected by aberrant methylation of regulative regions.
AB - Non-Hodgkin lymphomas (NHL) represent a frequent complication of human immunodeficiency virus (HIV) infection. To elucidate HIV-NHL pathogenesis, we performed a genome-wide DNA profiling based on a single nucleotide polymorphism-based microarray comparative genomic hybridization in 57 HIV-lymphomas and, for comparison, in 105 immunocompetent diffuse large B-cell lymphomas (IC-DLBCL). Genomic complexity varied across HIV-NHL subtypes. HIV-Burkitt lymphoma showed a significantly lower number of lesions than HIV-DLBCL (P = 0·032), whereas the median number of copy number changes was significantly higher in Epstein-Barr virus negative (EBV-) HIV-DLBCL (42·5, range 8-153) compared to EBV+ cases (22; range 3-41; P = 0·029). Compared to IC-DLBCL, HIV-DLBCL displayed a distinct genomic profile with no gains of 18q and specific genetic lesions. Fragile sites-associated genes, including FHIT (FRA3B), WWOX (FRA16D), DCC (FRA18B) and PARK2 (FRA6E) were frequently inactivated in HIV-NHL by interstitial deletions, and a significantly higher prevalence of FHIT alterations was observed in HIV-DLBCL compared to IC-DLBCL. The same genes involved by fragile site deletions were also frequently affected by aberrant methylation of regulative regions.
KW - Acquired immunodeficiency syndrome
KW - Affymetrix
KW - Diffuse large B-cell lymphoma
KW - Fragile Histidine Triad
KW - WW domain-containing Oxidoreductase
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U2 - 10.1111/j.1365-2141.2009.07943.x
DO - 10.1111/j.1365-2141.2009.07943.x
M3 - Article
C2 - 19832807
AN - SCOPUS:72649089121
SN - 0007-1048
VL - 148
SP - 245
EP - 255
JO - British Journal of Haematology
JF - British Journal of Haematology
IS - 2
ER -