TY - JOUR
T1 - Genome wide DNA-profiling of HIV-related B-cell lymphomas
AU - CAPELLO, Daniela
AU - Scandurra, M
AU - Poretti, G
AU - PM, Rancoita
AU - Mian, M
AU - Gloghini, A
AU - Deambrogi, C
AU - Martini, M
AU - ROSSI, Davide
AU - TC, Greiner
AU - WC, Chan
AU - Ponzoni, M
AU - SM, Moreno
AU - MA, Piris
AU - Canzonieri, V
AU - Spina, M
AU - Tirelli, U
AU - Inghirami, G
AU - Rinaldi, A
AU - Zucca, E
AU - Dalla, Favera R
AU - Cavalli, F
AU - LM, Larocca
AU - Kwee, I
AU - Carbone, A
AU - GAIDANO, Gianluca
AU - Bertoni, F.
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
UR - https://iris.uniupo.it/handle/11579/29917
U2 - 10.1111/j.1365-2141.2009.07943.x
DO - 10.1111/j.1365-2141.2009.07943.x
M3 - Article
SN - 0007-1048
VL - 148
SP - 245
EP - 255
JO - British Journal of Haematology
JF - British Journal of Haematology
IS - 2
ER -
