Genome wide DNA-profiling of HIV-related B-cell lymphomas.
Genome wide DNA-profiling of HIV-related B-cell lymphomas.
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DOI:
10.1111/j.1365-2141.2009.07943.x
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发表时间:
2010-01
影响因子:
6.5
通讯作者:
Bertoni F
中科院分区:
文献类型:
--
作者:
Capello D;Scandurra M;Poretti G;Rancoita PM;Mian M;Gloghini A;Deambrogi C;Martini M;Rossi D;Greiner TC;Chan WC;Ponzoni M;Moreno SM;Piris MA;Canzonieri V;Spina M;Tirelli U;Inghirami G;Rinaldi A;Zucca E;Favera RD;Cavalli F;Larocca LM;Kwee I;Carbone A;Gaidano G;Bertoni F
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.
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影响因子:
6.4
作者:
Agirre, X;Román-Gómez, J;Prósper, F
通讯作者:
Prósper, F
影响因子:
3.7
作者:
Hussain, A;Gutiérrez, MI;Bhatia, K
通讯作者:
Bhatia, K
影响因子:
64.8
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Compagno, Mara;Lim, Wei Keat;Grunn, Adina;Nandula, Subhadra V.;Brahmachary, Manisha;Shen, Qiong;Bertoni, Francesco;Ponzoni, Maurilio;Scandurra, Marta;Califano, Andrea;Bhagat, Govind;Chadburn, Amy;Dalla-Favera, Riccardo;Pasqualucci, Laura
通讯作者:
Pasqualucci, Laura
影响因子:
8
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Kameoka, Y;Tagawa, H;Seto, M
通讯作者:
Seto, M
影响因子:
3.4
作者:
Grogg, K. L.;Miller, R. F.;Dogan, A.
通讯作者:
Dogan, A.