{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T09:24:13Z","timestamp":1792661053874,"version":"4.5.0"},"reference-count":44,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2019,6,3]],"date-time":"2019-06-03T00:00:00Z","timestamp":1559520000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Intl Journal of Cancer"],"published-print":{"date-parts":[[2019,12]]},"abstract":"\n Diffuse large B\u2010cell lymphoma (DLBCL) is up to 17\u2010fold more likely to occur, follows a more aggressive clinical course and frequently presents at advanced stages in HIV infected (+) individuals compared to HIV negative (\u2212) individuals. However, the molecular pathology underpinning the clinical features of DLBCL in HIV(+) patients relative to the general population is poorly understood. We performed a retrospective study examining the transcriptional, genomic and protein expression differences between HIV(+) and HIV(\u2212) germinal center B\u2010cell (GCB) DLBCL cases using digital gene expression analysis, array comparative genomic hybridization (CGH) and immunohistochemistry (IHC). Genes associated with cell cycle progression (\n CCNA2<\/jats:italic>\n ,\n CCNB1<\/jats:italic>\n ,\n CDC25A<\/jats:italic>\n ,\n E2F1<\/jats:italic>\n ), DNA replication (\n MCM2<\/jats:italic>\n ,\n MCM4<\/jats:italic>\n ,\n MCM7<\/jats:italic>\n ) and DNA damage repair, including eight Fanconi anemia genes (\n FANCA<\/jats:italic>\n ,\n FANCD1\/BRCA2<\/jats:italic>\n ,\n FANCE<\/jats:italic>\n ,\n FANCG<\/jats:italic>\n ,\n FANCR\/RAD51<\/jats:italic>\n ,\n FANCS\/BRCA1<\/jats:italic>\n ,\n FANCT\/UBE2T<\/jats:italic>\n ,\n FANCV\/MAD2L2<\/jats:italic>\n ), were significantly increased in HIV(+) GCB\u2010DLBCL tumors compared to HIV(\u2212) tumors. In contrast, genes associated with cell cycle inhibition (\n CDKN1A<\/jats:italic>\n ,\n CDKN1B<\/jats:italic>\n ) as well as apoptosis regulating BCL2 family members (\n BCL2<\/jats:italic>\n ,\n BAX<\/jats:italic>\n ,\n BIM<\/jats:italic>\n ,\n BMF<\/jats:italic>\n ,\n PUMA<\/jats:italic>\n ) were significantly decreased in the HIV(+) cohort. BCL2 IHC confirmed this expression. Array CGH data revealed that HIV(+) GCB\u2010DLBCL tumors have fewer copy number variations than their HIV(\u2212) counterparts, indicating enhanced genomic stability. Together, the results show that HIV(+) GCB\u2010DLBCL is a distinct molecular malignancy from HIV(\u2212) GCB\u2010DLBCL; with an increased proliferative capacity, confirmed by Ki67 IHC staining, and enhanced genomic stability, the latter of which is likely related to the enhanced expression of DNA repair genes.\n <\/jats:p>","DOI":"10.1002\/ijc.32381","type":"journal-article","created":{"date-parts":[[2019,5,2]],"date-time":"2019-05-02T01:24:06Z","timestamp":1556760246000},"page":"3078-3088","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["Enhanced DNA repair and genomic stability identify a novel HIV\u2010related diffuse large B\u2010cell lymphoma signature"],"prefix":"10.1002","volume":"145","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1193-5528","authenticated-orcid":false,"given":"Alanna","family":"Maguire","sequence":"first","affiliation":[{"name":"Department of Research Mayo Clinic Arizona Scottsdale 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