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Associations of classic Kaposi sarcoma with common variants in genes that modulate host immunity

  1. Author:
    Brown, E. E.
    Fallin, D.
    Ruczinski, I.
    Hutchinson, A.
    Staats, B.
    Vitale, F.
    Lauria, C.
    Serraino, D.
    Rezza, G.
    Mbisa, G.
    Whitby, D.
    Messina, A.
    Goedert, J. J.
    Chanock, S. J.
    Kaposi Sarcoma Working, G.

  2. Author Address

    NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Rockville, MD 20852 USA. Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA. NCI, Core Genotyping Facil, Ctr Adv Technol, SAIC Frederick Inc, Frederick, MD 21701 USA. Univ Palermo, Dipartimento Igiene & Microbiol Giuseppe Alessand, Palermo, Italy. Lega Italiana Lotta Contro & Tumori, Sez Ragusa, Ragusa, Italy. Ist Ricovero & Cura Carattere Sci, Ctr Riferimento Oncol, Serv Epidemiol & Biostat, Aviano, Italy. Ist Super Sanita, Reparto Epidemiol, Dipartimento Malattie Infett Parassitarie & Immun, I-00161 Rome, Italy. NCI, Viral Epidemiol Sect, AIDS Vaccine Program, Sci Applicat Int Corp, Frederick, MD 21701 USA. Univ Catania, Dipartimento Sci Biomed, Catania, Italy. NCI, Pediat Oncol Branch, Canc Res Ctr, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA. Fdn G Pascale, Ist Tumori Napoli, Unita Operat Epidemiol, Naples, Italy. IRCCS, INMI Lazzaro Spallanzani, Rome, Italy. Ist Dermatopat Immacolata, Rome, Italy. San Gallicano Hosp, Rome, Italy. Res Triangle Inst, Rockville, MD USA. NCI, Biostat Branch, Div Canc Epidemiol & Genet, Rockville, MD USA. NCI, Core Genotyping Facil, NIH, Dept Hlth & Human Serv, Gaithersburg, MD USA.;Brown, EE, NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, 6120 Execut Blvd,EPS 8005 MSC 7248, Rockville, MD 20852 USA.;brownbe@mail.nih.gov
    1. Year: 2006
    2. Date: May
  2. Journal: Cancer Epidemiology Biomarkers & Prevention
    1. 15
    2. 5
    3. Pages: 926-934
  4. Type of Article: Article
  5. ISSN: 1055-9965
  1. Abstract:

    Classic Kaposi sarcoma (CKS) is an inflammatory-mediated neoplasm primarily caused by Kaposi sarcoma-associated herpesvirus (KSHV). Kaposi sarcoma lesions are characterized, in part, by the presence of proinflammatory cytokines and growth factors thought to regulate KSHV replication and CKS pathogenesis. Using genomic DNA extracted from 133 CKS cases and 172 KSHV-Iatent nuclear antigen-positive, population-based controls in Italy without HIV infection, we examined the risk of CKS associated with 28 common genetic variants in 14 immune-modulating genes. Haplotypes were estimated for IL1A, IL1B, IL4, IL8, IL8RB, IL10, IL12A, IL13, and TNF. Compared with controls, CKS risk was decreased with 1235T/-1010G-containing diplotypes of IL8RB (odds ratio, 0.49; 95% confidence interval, 0.30-0.78; P = 0.003), whereas risk was increased with diplotypes of IL13 containing the promoter region variant 98A (rs20541, alias +130; odds ratio, 1.88; 95% confidence interval, 1.15-3.08; P = 0.01) when considered in multivariate analysis. Risk estimates did not substantially vary by age, sex, incident disease, or disease burden. Our data provide preliminary evidence for variants in immune-modulating genes that could influence the risk of CKS. Among KSHV-seropositive Italians, CKS risk was associated with diplotypes of IL8RB and IL13, supporting laboratory evidence of immune-mediated pathogenesis.

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External Sources

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  2. DOI: 10.1158/1055-9965.epi-05-0791
  3. PMID: 16702372
  4. View record in Web of Science®
  5. WOS: 000237713200016

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