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Genome wide DNA‐profiling of HIV‐related B‐cell lymphomas
Author(s) -
Capello Daniela,
Scandurra Marta,
Poretti Giulia,
Rancoita Paola M. V.,
Mian Michael,
Gloghini Annunziata,
Deambrogi Clara,
Martini Maurizio,
Rossi Davide,
Greiner Timothy C.,
Chan Wing C.,
Ponzoni Maurilio,
Moreno Santiago M.,
Piris Miguel A.,
Canzonieri Vincenzo,
Spina Michele,
Tirelli Umberto,
Inghirami Giorgio,
Rinaldi Andrea,
Zucca Emanuele,
Favera Riccardo D.,
Cavalli Franco,
Larocca Luigi Maria,
Kwee Ivo,
Carbone Antonino,
Gaidano Gianluca,
Bertoni Francesco
Publication year - 2010
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.2009.07943.x
Subject(s) - genome , dna , human immunodeficiency virus (hiv) , biology , computational biology , dna profiling , lymphoma , genetics , virology , cancer research , medicine , gene , immunology
Summary 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.