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
AU - Mian, Michael
AU - Gloghini, Annunziata
AU - Deambrogi, Clara
AU - Martini, Maurizio
AU - Rossi, Davide
AU - Greine, Timothy
AU - Wing, Chan
AU - Ponzoni, Maurilio
AU - Moreno, Santiago
AU - Piris, Miguel
AU - Canzonieri, Vincenzo
AU - Spina, Michele
AU - Tirelli, Umberto
AU - Inghirami, Giorgio
AU - Rinaldi, Andrea
AU - Zucca, Emanuela
AU - Dalla Favera, Riccardo
AU - Cavalli, Franco
AU - Larocca, Luigi Maria
AU - Kwee, Ivo
AU - Carbone, Antonino
AU - Gaidano, Gianluca
AU - Bertoni, Francesco
PY - 2010
Y1 - 2010
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 - Burkitt Lymphoma
KW - Chromosome Aberrations
KW - DNA Methylation
KW - Gene Frequency
KW - Humans
KW - Lymphoma, AIDS-Related
KW - Lymphoma, Large B-Cell, Diffuse
KW - Microarray Analysis
KW - Polymerase Chain Reaction
KW - Polymorphism, Single Nucleotide
KW - Burkitt Lymphoma
KW - Chromosome Aberrations
KW - DNA Methylation
KW - Gene Frequency
KW - Humans
KW - Lymphoma, AIDS-Related
KW - Lymphoma, Large B-Cell, Diffuse
KW - Microarray Analysis
KW - Polymerase Chain Reaction
KW - Polymorphism, Single Nucleotide
UR - http://hdl.handle.net/10807/25860
U2 - 10.1111/j.1365-2141.2009.07943.x
DO - 10.1111/j.1365-2141.2009.07943.x
M3 - Article
SN - 1365-2141
VL - 148
SP - 245
EP - 255
JO - British Journal of Haematology
JF - British Journal of Haematology
ER -
