期刊
BRITISH JOURNAL OF HAEMATOLOGY
卷 148, 期 2, 页码 245-255出版社
WILEY
DOI: 10.1111/j.1365-2141.2009.07943.x
关键词
acquired immunodeficiency syndrome; Fragile Histidine Triad; WW domain-containing Oxidoreductase; diffuse large B-cell lymphoma; Affymetrix
类别
资金
- Swiss National Science Foundation [205321-112430, 205320-121886/1]
- Cantone Ticino ('Computational life science/Ticino in rete' program)
- Fondazione per la Ricerca e la Cura sui Linfomi (Lugano, Switzerland)
- Ricerca Sanitaria Finalizzata, Regione Piemonte, Torino, Italy
- VI Programma Nazionale di Ricerca sull'AIDS, ISS, Rome, Italy
- PRIN-MIUR 2006
- Novara-AIL Onlus, Novara, Italy
- Fondazione CRT, Torino, Italy
- Alto Adige Bolzano-AIL Onlus
- Cantone Ticino 'Ticino in rete'
- PHS [UO1 CA 114778]
- [OCS-1939-8-2006]
- NATIONAL CANCER INSTITUTE [U01CA114778] Funding Source: NIH RePORTER
P>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 center dot 032), whereas the median number of copy number changes was significantly higher in Epstein-Barr virus negative (EBV-) HIV-DLBCL (42 center dot 5, range 8-153) compared to EBV+ cases (22; range 3-41; P = 0 center dot 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.
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