Recurrent chromosomal alterations in molecularly classified AIDS-related lymphomas: an integrated analysis of DNA copy number and gene expression.
J Acquir Immune Defic Syndr, 2010/5/01;54(1):18-26.
Deffenbacher KE[1], Iqbal J, Liu Z, Fu K, Chan WC
Affiliations
PMID: 20216076DOI: 10.1097/QAI.0b013e3181d3d9eb
Abstract
HIV-infected individuals have a significantly increased risk of developing an aggressive B-cell Non-Hodgkin Lymphoma relative to HIV(-) persons. Due to their aggressive nature, AIDS-related lymphomas (ARL) can also be more difficult to classify. Genetic abnormalities are known to play a significant role in HIV(-) lymphomagenesis. To aid in case classification and identify key pathogenetic events in ARL, we analyzed gene expression data and somatic DNA copy number changes by high-resolution array comparative genomic hybridization in tumors from 20 B-cell derived ARL (B-ARL) patients. Gene expression-based predictors robustly classified the B-ARL cases, distinguishing Burkitt lymphoma and diffuse large B-cell lymphoma, and identifying activated B-cell like and germinal center B-cell like molecular subtypes of diffuse large B-cell lymphoma. Array comparative genomic hybridization analysis revealed 13 recurrent losses and 16 recurrent gains in the B-ARL cases, including gain of 19p13.2 and loss of 16q23, not previously reported in B-ARL. The WWOX tumor suppressor gene was characterized as a candidate gene for the 16q23.1 locus and showed gene silencing or truncated transcript in 9 of 16 cases. These data demonstrate the ability to molecularly classify B-ARL lymphomas by gene expression and identified DNA copy number alterations targeted in B-ARL.
MeSH terms
Adult; Burkitt Lymphoma; Chromosome Aberrations; Comparative Genomic Hybridization; Diagnosis, Differential; Female; Gene Dosage; Gene Expression; HIV Infections; Humans; Lymphoma, AIDS-Related; Lymphoma, Large B-Cell, Diffuse; Male; Middle Aged; Young Adult
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