| Cytokine signaling pathway polymorphisms and AIDS-related non-Hodgkin lymphoma risk in the multicenter AIDS cohort study. | |
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MedLine Citation:
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PMID: 20299965 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Cytokine stimulation of B-cell proliferation may be an important causative mechanism for acquired immunodeficiency syndrome (AIDS)-related non-Hodgkin lymphoma (NHL). The Epstein-Barr virus (EBV) may be a co-factor, particularly for primary central nervous system (CNS) tumors, which are uniformly EBV-positive in the setting of AIDS. Thus, we examined associations of genetic variation in IL10 and related cytokine-signaling molecules (IL10RA, CXCL12, IL13, IL4, IL4R, CCL5 and BCL6) with AIDS-related NHL risk and evaluated differences between primary CNS and systemic tumors. PATIENTS AND MATERIALS: We compared 160 Multicenter AIDS Cohort Study (MACS) participants with incident lymphomas, of which 90 followed another AIDS diagnosis, to HIV-1-seropositive controls matched on duration of lymphoma-free survival post-HIV-1 infection (N = 160) or post-AIDS diagnosis (N = 90). We fit conditional logistic regression models to estimate odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: Carriage of at least one copy of the T allele for the IL10 rs1800871 (as compared to no copies) was associated with decreased AIDS-NHL risk specific to lymphomas arising from the CNS (CC vs. CT/TT: OR = 0.3; 95% CI 0.1, 0.7) but not systemically (CC vs. CT/TT: OR = 1.0; 95% CI 0.5, 1.9) (Pheterogeneity = 0.03). Carriage of two copies of the 'low IL10' haplotype rs1800896_A/rs1800871_T/rs1800872_A was associated with decreased lymphoma risk that varied by number of copies (Ptrend = 0.02). None of the ORs for the other studied polymorphisms was significantly different from 1.0. CONCLUSION: Excessive IL10 response to HIV-1 infection may be associated with increased risk of NHL, particularly in the CNS. IL10 dysregulation may be an important causative pathway for EBV-related lymphomagenesis. |
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Authors:
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Hui-Lee Wong; Elizabeth C Breen; Ruth M Pfeiffer; Brahim Aissani; Jeremy J Martinson; Joseph B Margolick; Richard A Kaslow; Lisa P Jacobson; Richard F Ambinder; Stephen Chanock; Otoniel Martínez-Maza; Charles S Rabkin |
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Publication Detail:
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Type: Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural |
Journal Detail:
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Title: AIDS (London, England) Volume: 24 ISSN: 1473-5571 ISO Abbreviation: AIDS Publication Date: 2010 Apr |
Date Detail:
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Created Date: 2010-04-13 Completed Date: 2011-01-21 Revised Date: 2011-02-01 |
Medline Journal Info:
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Nlm Unique ID: 8710219 Medline TA: AIDS Country: England |
Other Details:
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Languages: eng Pagination: 1025-33 Citation Subset: IM; X |
Affiliation:
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National Cancer Institute, Rockville, Maryland, USA. huilee.wong@fda.hhs.gov |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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B-Lymphocytes Case-Control Studies Central Nervous System Neoplasms / genetics, virology Cytokines / genetics*, metabolism HIV Infections / genetics*, pathology, virology HIV-1 / genetics* Herpesvirus 4, Human / genetics* Humans Interleukin-10 / genetics, metabolism Lymphoma, AIDS-Related / genetics*, pathology, virology Male Multicenter Studies as Topic Polymorphism, Genetic Risk Factors Signal Transduction / genetics |
| Grant Support | |
ID/Acronym/Agency:
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5-M01-RR-00722/RR/NCRR NIH HHS; P50-CA-096888/CA/NCI NIH HHS; R01-CA57152/CA/NCI NIH HHS; R01-CA73475/CA/NCI NIH HHS; UO1-AI-35039/AI/NIAID NIH HHS; UO1-AI-35040/AI/NIAID NIH HHS; UO1-AI-35041/AI/NIAID NIH HHS; UO1-AI-35042/AI/NIAID NIH HHS; UO1-AI-35043/AI/NIAID NIH HHS; UO1-AI-37613/AI/NIAID NIH HHS; UO1-AI-37984/AI/NIAID NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Cytokines; 130068-27-8/Interleukin-10 |
| Comments/Corrections | |
Erratum In:
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AIDS. 2010 Jul 31;24(12):1973 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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