{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,5,10]],"date-time":"2024-05-10T18:55:49Z","timestamp":1715367349400},"reference-count":35,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2013,7,27]],"date-time":"2013-07-27T00:00:00Z","timestamp":1374883200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Intl Journal of Cancer"],"published-print":{"date-parts":[[2014,1,15]]},"abstract":"<jats:p>Like other members of the \u03b3\u2010herpesvirus family, human herpes virus 8, the etiologic agent of classic and HIV\u2010related Kaposi's sarcoma (HIV\u2010KS) acquired and evolved several human genes with key immune modulatory and cellular growth control functions. The encoded viral homologs substitute for their human counterparts but escape cellular regulation, leading to uncontrolled cell proliferation. We postulated that DNA variants in the human homologs of viral genes that potentially alter the expression or the binding of the encoded factors controlling the antiviral response may facilitate viral interference. To test whether cellular homologs are candidate susceptibility genes, we evaluated the association of DNA variants in 92 immune\u2010related genes including seven cellular homologs with the risk for HIV\u2010KS in a matched case and control study nested in the Multicenter AIDS Cohort Study. Low\u2010 and high\u2010risk gene\u2010by\u2010gene interactions were estimated by multifactor dimensionality reduction and used as predictors in conditional logistic models. Among the most significant gene interactions at risk (OR\u2009=\u20092.84\u20133.92; Bonferroni\u2010 adjusted <jats:italic>p<\/jats:italic>\u2009=\u20099.9 \u00d7 10<jats:sup>\u22123<\/jats:sup>\u2013 2.6 \u00d7 10<jats:sup>\u22124<\/jats:sup>), three comprised human homologs of two latently expressed viral genes, cyclin D1 (<jats:italic>CCND1<\/jats:italic>) and interleukin\u20106 (<jats:italic>IL\u20106<\/jats:italic>), in conjunction with angiogenic genes (<jats:italic>VEGF<\/jats:italic>, <jats:italic>EDN\u20101<\/jats:italic> and <jats:italic>EDNRB<\/jats:italic>). At lower significance thresholds (adjusted <jats:italic>p<\/jats:italic> &lt; 0.05), human homologs related to apoptosis (<jats:italic>CFLAR<\/jats:italic>) and chemotaxis (<jats:italic>CCL2<\/jats:italic>) emerged as candidates. This \u201cproof of concept\u201d study identified human homologs involved in the regulation of type I interferon\u2010induced signaling, cell cycle and apoptosis potentially as important determinants of HIV\u2010KS<\/jats:p>","DOI":"10.1002\/ijc.28351","type":"journal-article","created":{"date-parts":[[2013,7,1]],"date-time":"2013-07-01T13:06:29Z","timestamp":1372683989000},"page":"397-404","source":"Crossref","is-referenced-by-count":5,"title":["A candidate gene approach for virally induced cancer with application to HIV\u2010related Kaposi's sarcoma"],"prefix":"10.1002","volume":"134","author":[{"given":"Brahim","family":"Aissani","sequence":"first","affiliation":[{"name":"Department of Epidemiology University of Alabama Birmingham AL"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Howard W.","family":"Wiener","sequence":"additional","affiliation":[{"name":"Department of Epidemiology University of Alabama Birmingham 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